MALARIA IN COLONIAL

SOUTH ASIA

This book highlights the role of acute hunger in malaria lethality in colonial
South Asia and investigates how this understanding came to be lost in
modern medical, epidemic, and historiographic thought.
Using the case studies of colonial Punjab, Sri Lanka, and Bengal, it traces
the loss of fundamental concepts and language of hunger in the inter-war
period with the reductive application of the new specialisms of nutritional
science and immunology, and a parallel loss of the distinction between
infection (transmission) and morbid disease. The study locates the final
demise of the ‘Human Factor’ (hunger) in malaria history within pre- and
early post-WW2 international health institutions – the International Health
Division of the Rockefeller Foundation and the nascent WHO’s Expert
Committee on Malaria. It examines the implications of this epistemic
shift for interpreting South Asian health history, and reclaims a broader
understanding of common endemic infection (endemiology) as a prime
driver, in the context of subsistence precarity, of epidemic mortality history
and demographic change.
This book will be useful to scholars and researchers of public health,
social medicine and social epidemiology, imperial history, epidemic and
demographic history, history of medicine, medical sociology, and sociology.

Sheila Zurbrigg is a physician and independent scholar based in Toronto,

Canada. Her health history research investigates rising life expectancy in
South Asian history in relation to food security. She has served as Short-Term
Epidemiologist for the World Health Organization, Smallpox Eradication
Program, Uttar Pradesh, and Coordinator, Village Health Worker Program,
Madurai, Tamil Nadu, India. She has held appointments as Adjunct Professor,
International Development Studies, Dalhousie University, Halifax, Nova
Scotia, Canada; Visiting Scholar, York University, Toronto, Canada; and
Visiting Scholar, Jawaharlal Nehru University, New Delhi, India. Her work
with traditional village midwives in rural Tamil Nadu (1975–1979) led to the
analysis of child survival in contemporary India in relation to food security
and conditions of women’s work. In 1985, she turned to South Asian health
history research, funded by the Social Sciences and Humanities Research
Council (Ottawa). Among her published work is the book Epidemic Malaria
and Hunger in Colonial Punjab: ‘Weakened by Want’ (2019).
MALARIA IN COLONIAL
SOUTH ASIA
Uncoupling Disease and Destitution

Sheila Zurbrigg
First published 2020
by Routledge
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© 2020 Sheila Zurbrigg
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has been asserted by her in accordance with sections 77 and 78 of the
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 FOR THE VILLAGE MIDWIVES OF
RAMNAD DISTRICT, REMEMBERED
 CONTENTS

List of figuresviii
List of tablesix
Abbreviations and acronymsx
Glossaryxii
Preface and acknowledgmentsxiv

Introduction 1

1 The ‘Human Factor’ transformed 18

2 The 1934–1935 Ceylon epidemic and its epistemic

aftermath43

3 Hunger eclipsed: nutritional science in colonial South Asia 78

4 The larger sanitationist context 113

5 Colonial retrenchment and ‘selling’ vector control 143

6 Malaria and the W.H.O.: the ‘Human Factor’ set aside 169

7 Allure and legacies of the germ paradigm 200

8 What was lost 229

Appendix I: malaria transmission in Punjab262

Appendix II: an epidemiological approach to
hunger in history264
Bibliography268
Index294
vii
 FIGURES

0.1 Mean annual Oct.–Dec. fever death rate (per 1,000),

1868–1940, 23 plains districts, Punjab 3
2.1 Mean annual rainfall (inches), Ceylon 46
2.2 Spleen rate (per cent), Ceylon, 1922–1923 47
2.3 Nov.–Apr. death rate per 1,000, Ceylon, 1934–1935 49
2.4 Per cent increase in total mortality, by division, Ceylon,
Nov. 1934 to Apr. 1935 51
2.5 ‘Epidemic Figure’ map of 1934–1935 Ceylon malaria epidemic 56
3.1 Mortality, by month, Bengal province, July 1943–June 1944 95
7.1 Mean annual crude death rate, crude birth rate (per 1,000),
11 plains districts, (East) Punjab, 1920–60 210

viii
 TABLES

2.1 Crude death rate (per 1,000 population), infant mortality

rate (per 1,000 live births), Nov. 1934–Apr. 1935, extent
harvest failure, by district, Ceylon [Sri Lanka] 53
2.2 Infant mortality rate, estate and non-estate sectors, Kegalla
district, Ceylon [Sri Lanka], 1930–1940 57
7.1 Death rates (all causes) in the malarious and non-malarious
areas of Ceylon [Sri Lanka] during the second semesters,
1944–1948 and 1953 212
7.2 Percentage of population protected against malaria by
residual spraying of insecticides and semestral death rates
(all causes), Ceylon, 1944–1953 212

ix
 ABBREVIATIONS AND
ACRONYMS

AIIHPH All-India Institute of Hygiene and Public

Health
AJPH American Journal of Public Health
CBR crude birth rate (annual births per 1,000
population)
CDR crude death rate (annual deaths per 1,000
population)
DDT dichloro-diphenyl-trichloroethane
ECM Expert Committee on Malaria
EPW Economic and Political Weekly
FAO Food and Agriculture Organization
GDP Gross Domestic Product
GHLC Good Health at Low Cost
GOI Government of India
GOI-PHC Annual Report of the Public Health Com-
missioner with the Government of India
[1922–1947]
GOI-SCR Annual Report of the Sanitary Commissioner
with the Government of India [1868–1921]
GoP Government of Punjab
HMSO Her Majesty’s Stationery Office
IC Interim Commission (WHO)
ICMR Indian Council of Medical Research
IJMR Indian Journal of Medical Research
IESHR Indian Economic and Social History Review
IHB International Health Board (Rockefeller
Foundation)
IHD International Health Division (Rockefeller
Foundation)
IJM Indian Journal of Malariology
IMG Indian Medical Gazette
IMS Indian Medical Service

x
 A B B R E V I AT I O N S A N D A C R O N Y M S

IRFA Indian Research Fund Association

JMII Journal of the Malaria Institute of India
LN League of Nations
LNHO League of Nations Health Organisation
LNMC League of Nations Malaria Commission
LNMC-India report Report of the Malaria Commission on its
Study Tour of India, Geneva, 1930
LSHTM London School of Hygiene and Tropical
Medicine
MBD Malaria as a Block to Development
MSCR Report of the Sanitary Commissioner for
Madras
NNMB National Nutrition Monitoring Bureau
NNSO National Sample Survey Organisation
PLGP Proc. of the Lieutenant-Governor of the
Punjab, in the Home Dept (Sanitary)
PPHA Report on the Public Health Administration of
the Punjab [1922–47]
PSCR Report on the Sanitary Administration of the
Punjab [1868–1921]
QBHO Quarterly Bulletin of the Health Organisation
of the League of Nations
RF Rockefeller Foundation
RCAI Report of the Royal Commission on Agricul-
ture in India
RMSI Records of the Malaria Survey of India
Sci. Mem. Off. Scientific Memoirs by Officers of the
Med. San. Dep. Medical and Sanitary Departments of the
Government of India (New Series)
Season and Crops Report Report on the Season and Crops of the Punjab
[1901–1944]
Stat. Abst. Statistical abstract relating to British India
(London: HMSO, 1840–1920)
Trans. Bombay Congress Transactions of the Bombay Medical Con-
gress, 1909
UNRRA United Nations Relief and Rehabilitation
Administration
WHO World Health Organization

xi
 GLOSSARY

anthropophilic propensity of the female mosquito to seek blood meals

from humans rather than animals
basal metabolic rate that level of caloric intake required for all internal
metabolic and physiological functions in a state of complete rest
bonification a term applied by early twentieth-century Italian malaria
workers for agricultural improvement programs in malarious regions
case fatality rate the proportion of deaths within a designated popula-
tion of ‘cases’ (people with a medical condition) over the course of the
disease
crore ten million
crude death rate annual number of deaths from all causes in a given year
per 1,000 population
dalit term for the lowest (‘out-caste’) level in the Hindu social hierarchy
exophily the mosquito habit of resting outdoors after a human blood meal
rather than inside
gametocyte the reproductive stage of the malaria parasite, transmitted
from the human host to the female vector mosquito during its blood
meal
holoendemic a state of near year-round malaria transmission resulting in
high levels of acquired immunity in the local population such that clini-
cal symptoms of infection are minimal amongst all but young children
hyperendemic highly intense but seasonal malaria transmission, associ-
ated with high parasite and spleen (splenomegaly) rates (> 50%), with
acquired immunity levels sufficient to keep regular re-infection largely
asymptomatic in adults and older children
infant mortality rate number of infant deaths in the first year of life, per
1,000 live born
parasite rate that proportion of persons found with microscopically con-
firmed parasites in the bloodstream (parasitemia)
premunity a sufficient level of naturally acquired immunity where clinical
symptoms from continuing re-infection are limited or nil

xii
 G L O S S A RY

protozoa a single-celled microscopic animal with a defined nucleus

species sanitation the targeting of anti-mosquito operations specifically to
those anopheline species responsible for transmission in a region
spleen rate generally considered the per cent of children under the age of
10 years in a population with an enlarged spleen (splenomegaly)
splenomegaly enlargement of the spleen sufficient to be palpable below
the left rib cage
sporozoite the infective stage of the malaria parasite that is passed to the
human host from the salivary glands of the female mosquito during a
blood meal
thana subdivision of a rural district, under a subinspector of police
zamindar landowner who leases land for cultivation by tenant farmers
zoophilic propensity of the female mosquito to seek blood meals from ani-
mals rather than humans
zymotic a nineteenth-century term for acute febrile infectious diseases
believed to be caused by atmospheric vapours (miasma) resulting from
fermentation of organic matter

xiii
 PREFACE AND
ACKNOWLEDGMENTS

This exploration into the loss in understanding of hunger in South Asian

malaria history could not have been completed without the support and
experience of many people, as was the case with the first stage of this health
history project, published as Epidemic Malaria and Hunger in Colonial
Punjab: ‘Weakened by Want.’ The origins of the study lie in five years of
privileged acquaintance with many of the traditional village midwives of
Tiruppuvanam Block, Ramnad district in southern Tamil Nadu, women
who allowed me a glimpse into their midwifery skills and their lives as daily-
wage agricultural labourers. Returning to Canada in 1980, I found develop-
ment literatures where mortality decline in the ‘global south’ was interpreted
largely in terms of the transfer of modern medical techniques. From the per-
spective of these women’s lives and the general inaccessibility of rural health
services still apparent in the late 1970s, this reading was unconvincing. In
time, the question led me to explore the historical experience of mortality
decline in South Asia through the lens of malaria as pre-eminent trigger of
mortality across much of the period of British rule. I was surprised to find
how clearly the hunger-malaria lethality relationship had been documented
in the colonial records. But also by how fully this understanding seemed to
have been lost by the mid-twentieth century. This left me puzzled in turn by
the many larger epistemic questions as to how.
I am indebted first of all to the late Prof Biswamoy Pati for his immediate,
encouraging response to the proposed publication of this study – though my
gratitude is accompanied by deep regret that I was unable to convey this in
person before his untimely death. For financial support in the early years of
this research as a private scholar I remain grateful to the Social Sciences and
Humanities Research Council of Canada. Throughout, scholarly support
has come from many people. For their interest, expressed in the earliest days
of this exploration into South Asian health history, I am grateful to the late
Ian Catanach, Nigel Crook, Bill Owen, and John Farley, who gave crucial
support along the way, and in John’s case, invaluable commentary on first
drafts of many chapters. Feedback from Neeladri Bhattacharya on my ini-
tial writing was invaluable, as was generous encouragement mid-way from

xiv
 PREFACE AND ACKNOWLEDGMENTS

José-Antonio Ortega Osona. I thank them greatly. My gratitude to Douglas

Hay, Jim Phillips, and Paul Antze is enormous for their painstaking com-
mentary on the study overview, and for their insistent assurance of its coher-
ence. In all respects, the critical contemporary health analysis of Imrana
Qadeer, Mohan Rao, and Debabar Banerji at the Centre for Social Medicine
and Community Health, Jawaharlal Nehru University, New Delhi, has been,
and remains, an important touchstone.
For many Madurai friends who made possible my introduction to the
subsistence realities of rural Tamil Nadu, my respect and gratitude are abid-
ing. Among them, the late Prof K.A. Krishnamurthy, Mrs Janaki Ramas-
wamy, her elder brother, Dr G. Venkataswamy, and their extended family
are remembered fondly. The practical experience of those years was made
possible through the dedication, daily support, and treasured friendship of
Anusuya Andichamy and Shahnawaz Ghouse. Personal funding support
during these years came from the Canadian International Development
Agency and the remarkable Head of its Health Division, the late Dr Bill
Jeanes. For onerous editing support for my early efforts in putting pen to
paper I remain profoundly indebted to John Desrochers and the late John
Maliekal of the Bangalore Social Action Trust. It was their encouragement
that convinced me to pursue the Ramnad midwives’ insights into an under-
standing of the broader determinants of health.
The published work of many historians provided essential stepping stones
as I sought to place the expanding questions and historical subdisciplines
into a larger whole. Central to comprehending the demise in understand-
ing of the ‘Human Factor’ in malaria historiography has been Christopher
Hamlin’s 1998 analysis of the wider epistemic content of Edwin Chadwick’s
1842 Sanitary Report. It is a story with close parallels a century later to
that of malaria in South Asia, and his insights into this earlier stage of the
‘uncoupling of disease and destitution’ in nineteenth-century Britain have
provided critical context to this study. Important also has been the work of
Randall Packard, John Farley, and Socrates Litsios on the role of malaria in
the shaping of the nascent World Health Organization and related influence
of the Rockefeller Foundation.
Much of this study however has necessarily been a solitary journey
because so much of the extensive colonial South Asian malaria research
literature and records at the time had yet to be explored. Inevitably, there
will be many aspects that have been left incomplete, and I look forward to
critical commentary and additions to this work.
Once again, I thank the librarian staff of Dalhousie University in Halifax,
Nova Scotia – Gwyn Pace, Joe Wickens, Kellie Hawley, Marlyn McCann,
and Catherine Pickett – for their painstaking work in locating obscure docu-
ments. For many summers of assistance, I thank as well the staff of the India
Office Library, now housed within the British Library, and also the National
Archives of India, and York University, Toronto.

xv
 PREFACE AND ACKNOWLEDGMENTS

Throughout, the support of Heidi Williams, Barbara Lent, Sandi With-

erspoon, Paul and Sandra Odegaard, Christine Davidson, Jeanette Neeson,
Betty Peterson, Fatima and Ismail Cajee, and Carolyn van Gurp have sus-
tained me through the toughest writing times.
Especially, I thank Daniel and Gabe, for their confidence, their indispen-
sable computer skills, and the joy they give. For Philip’s editorial and moral
support that has never wavered through this project, and for much more,
I thank my lucky stars.

xvi
 INTRODUCTION

In September 1952, a leading British malaria researcher completed an analy-

sis of epidemic malaria in the Punjab plains of British India by conclud-
ing that the ‘notorious’ epidemics of the colonial period ‘were associated
with certain rainfall characteristics and with an inadequate immunity in
the local population.’1 Referencing a 1911 enquiry report entitled Malaria
in the Punjab, commissioned by the then colonial Government of India,
George Macdonald noted that the earlier study’s quantitative correlations
between monsoon rainfall and autumn malaria mortality were ‘so close that
they formed an obvious basis for forecasting future epidemics.’2 Here, by
periodic epidemics Macdonald was addressing the marked surges in malaria
deaths that episodically afflicted the malaria-endemic Punjab region. And
by ‘inadequate immunity’ he was referring to insufficient acquired (malaria-
specific) immunity.3 Wide annual variation in rainfall and malaria transmis-
sion in the region, he reasoned, led to varying numbers of ‘non-immunes’
among the population, and in turn to a corresponding fluctuation in suscep-
tibility of the population to the infection.
If a seemingly small and unremarkable detail in the overall body of
research conducted on malaria by the mid-twentieth century, this reading of
Punjab malaria history nonetheless revealed a fundamental shift in under-
standing of the region’s epidemic history. More broadly, it exemplified the
epistemic transformation in Western epidemic thought that had taken place
over the preceding century. The original study to which Macdonald referred
had pointed to quite a different factor underlying malaria mortality patterns
in colonial Punjab. What distinguished ‘fulminant’ malaria years, its author,
S.R. Christophers (1873–1978), had concluded, was markedly increased
human destitution, a condition that he referred to in his 1911 enquiry report
as the ‘Human Factor.’ The vast regional epidemics of malaria mortality
that afflicted the Punjab plains across the first half of the colonial period,
Christophers had shown, were correlated with preceding harvest failure,
soaring foodgrain prices (‘scarcity’) and, in particular years, overt condi-
tions of famine, a relationship he metaphorically encapsulated as malaria
‘merely reap[ing] a harvest prepared for it by the famine.’4

1
 INTRODUCTION

In detailed thana-level mapping of several major epidemics over the

1868–1908 period, Christophers had demonstrated that the epidemics were
not spatially related to varying malaria endemicity in the province. Rather,
the distinctive geographic distribution of mortality in each case suggested
instead a pattern of harvest failure (acute hunger) across the province, des-
titution often compounded by flooding with return of the rains.5 Adequate
rainfall was a necessary factor for widespread transmission of malaria infec-
tion in the province: failure of the annual monsoon rains limited malaria
incidence in any given year.6 But preceding economic stress predicted where,
when good rains ultimately returned, lethality of malaria infection would
soar to ‘disastrous’ epidemic proportions. Acute hunger then was an essen-
tial predisposing factor underlying malaria’s ‘fulminant’ or ‘exalted’ form
in the region.7 As the 1911 report also noted, a determining role for semi-
or frank starvation in the region’s recurring malaria epidemics was a com-
monplace in the nineteenth-century sanitary records, not only in Punjab but
more widely in British India, as well as in popular experience.8
Between the 1952 Macdonald reading of Punjab malaria history and the
original 1911 report lay an epistemic chasm. By the mid-twentieth century,
understanding of the ‘Human Factor’ in malaria epidemicity in South Asia
had come to be transformed from a condition of the human host – acute
hunger that undermined general immune capacity to mount a successful
response to future infection9 – to one of vector transmission: limited previ-
ous exposure to malaria and thus a lack of acquired, or specific, immunity.
In the process, malaria in the general medical literature had also come to
be considered a primary cause of hunger and underdevelopment: the nature
of the relationship documented in 1911 had been narrowed and in effect
turned upside down.10
This study explores how understanding of the role of acute hunger in
South Asian malaria mortality history came to be lost in modern medical
thought. It examines the conceptual consequences of this loss for interpret-
ing the region’s health history, and considers the larger epistemic implica-
tions for the study of mortality decline in history more generally.
In earlier work, I have explored, and corroborated, the conclusions of Chris-
tophers’s 1911 study that causally linked epidemic malaria in colonial Punjab
to acute hunger.11 In the process of quantitatively testing Christophers’s thesis,
it became clear as well that malaria death rates in the province fell very sub-
stantially after 1920, a decline that predated by more than three decades the
1950s DDT-based control of malaria transmission in the region (Figure 0.1).
Yet there was little evidence of a decrease in malaria transmission or sever-
ity of flooding in the province between 1920 and 1950, or shifts in acquired
immunity, to explain this decline. Nor does there appear to have been substan-
tial improvement in rural access to treatment (quinine). The conquest of ‘ful-
minant’ malaria in the region thus appears to have been temporally associated
instead with the control of epidemic destitution (‘famine’).12

2
 INTRODUCTION

25

Oct-Dec fever death rate (per 1000)

20

15

10

0
1860 1870 1880 1890 1900 1910 1920 1930 1940

Figure 0.1 Mean annual Oct.–Dec. fever death rate (per 1,000), 1868–1940, 23 plains
districts, Punjab
Source: PSCR, 1868–1921; PPHA, 1922–40. See S. Zurbrigg, Epidemic Malaria and Hunger
in Colonial Punjab, Fig. 4.1, p. 124. For an explanation of the Oct.–Dec. fever death rate as
an approximate measure of annual malaria mortality in Punjab, see ibid., pp. 10, 55–56, 200.
Note: 1918 omitted due to confounding influenza deaths.

In reinterpreting epidemic malaria patterns in South Asia in terms of

acquired immunity, Macdonald was hardly alone among malaria research-
ers of the period. Immunological aspects to infectious disease epidemicity
were at the forefront of medical and public health research from the final
decades of the nineteenth century, an interest evident also in British Indian
sanitary deliberations by the turn of the century.13 Macdonald’s particular
focus on the germ-transmission side of the ‘epidemic equation’ in analyzing
South Asian malaria epidemicity thus reflected a more general narrowing
framework in Western epidemic thought, a process already well in train
when Christophers penned his enquiry report in 1911. What was anoma-
lous at this point, then, was the latter’s detailed attention to conditions of
the human ‘host’ in his interpretation of malaria lethality.
In his efforts to explain the historical patterns of malaria mortality in
South Asia, Christophers had found himself plumbing terminology belong-
ing to a much earlier, pre-sanitationist body of medical theory, epidemio-
logical concepts that by the early 1900s had faded from academic medical
discourse. In speaking of the ‘Human Factor’ as ‘physiological poverty,’ he
was applying an earlier medical framework of epidemic causation in which
the relationship between infection (exposure to a specific microbe) and dis-
ease (clinical morbidity and associated mortality) was understood as often
mediated by predisposing factors.14 Paramount among such factors were
conditions of physical exhaustion in the human host through insufficient
food: in the words of the 1884 Gazetteer of Gurgaon district, ‘weakened by
want.’15 Malaria in the Punjab was quietly inserting the human host back
into the epidemic equation, the enquiry report a meeting ground in effect

3
 INTRODUCTION

between the modern biomedical and the pre-germ theory eras of epidemic
thought. Christophers, himself a leading Indian Medical Service epidemi-
ologist and entomologist in the emerging field of vector-borne disease, was
straddling both, demonstrating there was no contradiction between them:
indeed, that both were essential to understanding patterns and determinants
of malaria’s mortality burden in South Asia.
If reclaimed in the 1911 Punjab study, and administratively acknowledged
in fundamental famine relief policy reforms at the time, recognition of this
larger predispositionist framework to the phenomenon of ‘fulminant’ malaria
would not be sustained. To the limited extent that the 1911 malaria enquiry
report appears in modern medical literature, its conclusions continue to be
interpreted in immuno-entomological terms, with epidemic malaria under-
stood as a function of decline in acquired immunity: in other words, in terms
of vector transmission.16 Indeed, by the late twentieth century, malaria had
come to be categorized within the historiographic literature as belonging to
that group of inherently virulent epidemic diseases such as bubonic plague
for which ‘nutrition’ played little role in their historical mortality patterns,17
a view that continues to inform historical demographic and health analysis.18
The demise of the ‘Human Factor’ as a central epidemiological concept
in malaria research is remarkable in light of the professional stature of the
scientist who confirmed its importance in South Asia. But it is equally so
in light of the work of the League of Nations Malaria Commission, where
leading researchers in the 1920s studied and ultimately concurred with
the view arrived at by malaria workers both in India and in much of still
malaria-endemic regions of Europe19 as to the central role of improved eco-
nomic conditions in markedly reducing malaria’s mortality burden.
The question of how earlier insights into the role of acute hunger in malaria
history came to be lost is thus a compelling one. Given the prominence of malaria
as a leading trigger of historical mortality in South Asia, the loss is unfortunate
also in its larger consequences for understanding the region’s health history. But
the epistemic significance of the question for health historiography arguably
extends well beyond South Asia to other once malaria-endemic regions of the
world, and as well, potentially to endemic infective diseases other than malaria.20
How this understanding was lost is explored in this study. It attempts to
trace the conceptual steps involved in the eclipse of acute hunger in malaria
mortality historiography. In this endeavour, the period of Britain’s colonial
rule (1858–1947) offers a particularly important ‘window,’ provided by the
relative wealth and span of available administrative, medical, vital registra-
tion, and malaria research records. The book’s primary focus is the inter-
war and immediate post-WW2 years during which understanding of the
malaria-hunger relationship came to be inverted.21 It explores the impact in
these years of the emerging subdisciplines of immunology and nutritional
science on medical thought within British India, and in twentieth-century
institutions of international health, as key intellectual loci of this epistemic

4
 INTRODUCTION

shift. Across this period these medical specialisms offered new channels of
laboratory research and intriguing theoretic possibilities for interpreting
epidemic patterns in the microbiologic realm, an influence that extended
well beyond Punjab malaria analysis.
As elsewhere, the impact of the new science of nutrition was particularly
marked, as medical attention in British India rapidly shifted in the early
twentieth century from hunger – staple foods and their (in)sufficiency – to
micronutrient deficiency states in the wake of the discovery of vitamins in
the 1910s and 1920s. By the 1930s, the term ‘malnutrition’ (nutrient imbal-
ance) had come increasingly to dominate medical discussion and interest,22
and hunger as a public health issue receded both conceptually and investi-
gationally. One thus sees the remarkable juxtaposition of a colonial medical
literature increasingly directed to questions of ‘hidden hunger’ (subclinical
micronutrient deficiencies) with annual public health reports still prefaced as
they had been from the late 1860s with observations on harvest conditions
and foodgrain prices, data still considered by local public health officials as
central to anticipating mortality conditions in any given year. Those medi-
cal colleagues on the ‘frontlines’ of public health practice in India and those
within medical research and academia were now speaking two quite different
languages, and practising in effect two quite different preventive medicines.
Beyond the general terminology of hunger, what was being lost in the final
decades of colonial rule was a way of thinking about human subsistence in con-
crete, epidemiological terms: an understanding of hunger as expressed histori-
cally in terms of meals per day. Here, two meals a day reflected consumption
of staple foods ‘sufficient to satisfy hunger’; one, indicated undernourish-
ment (‘chronic’ hunger); and zero, acute hunger (semi- or frank starvation).
As detailed in an earlier work, and summarized in Appendix II below, such
categories encompass in general terms the relative prevalence of acute and
‘chronic’ hunger in populations over time – the term ‘prevalence’ here being
used in its epidemiological sense of frequency, duration, and social extent.
Along with micronutrient discoveries, the inter-war years in British India
also witnessed severe imperial retrenchment, creating a climate where to
maintain minimum research funding many malaria workers found themselves
pushed to ‘sell’ aggressively the importance of malaria transmission control for
the Indian economy: malaria as a cause of India’s poverty. Advocates of vector
transmission control turned to increasingly hyperbolic arguments for vector
control programs, with malaria now framed as a primary ‘block’ to economic
development in the subcontinent, what in contemporary public health analysis
has come to be referred to as the ‘malaria-as-a-block-to-development’ (MBD)
thesis.23 These fiscal pressures in turn fed aspirations for external philanthropic
sources of funding for medical research, opportunities that appeared to be at
hand through the recently established International Health Board of the Rock-
efeller Foundation, itself founded with a pedagogical mandate premised on a
unifocal view of disease as the cause of world poverty.

5
 INTRODUCTION

At the international level, fundamental divisions within the League of

Nations Malaria Commission had arisen between those malaria workers who
sought to control malaria transmission per se, and those who saw malaria
mortality as the pressing priority, a public health problem amenable to basic
agricultural improvements, reforms, and assured access to treatment. These
divisions threatened to undermine the work of the Malaria Commission and
the League’s larger Health Organisation as well, and appear to have led to a
notable muting of discussions of the broader economic dimensions to health.
Moreover, by the early 1930s, malaria concerns were being overshadowed
by the global economic Depression. ‘Nutrition’ would soon be at the fore-
front of the work of the League’s Health Organisation. But here, analysis
was increasingly directed to issues of dietary quality – declining consumption
of ‘protective’ foods among Anglo-European populations – and attention
to global hunger and its structural causes receded. Research on methods of
vector transmission control however continued to be initiated and funded by
the International Health Division of the Rockefeller Foundation, work that
would soon culminate in the international sphere in the post-WW2 prioriti-
sation of global malaria transmission control by the World Health Organiza-
tion (WHO). Here, India also figures prominently, if somewhat ironically. For
it would be Paul F. Russell, Rockefeller Foundation consultant, who would
carry the mantle of South Asian malaria expertise into the nascent WHO on
the basis of his several years of vector control trials in southern India in the
dying days of British rule. Under Russell’s unofficial leadership of the WHO’s
Expert Committee on Malaria,24 the previous four decades of epidemiologi-
cal analysis of malaria in relation to hunger, both in India and in the 1920s
work of the League of Nations Malaria Commission, were set aside.
The demise of the ‘Human Factor’ in international malaria delibera-
tions is an important institutional story in its own right. But it is significant
for health historiography also because malaria was one of the few major
endemic diseases, alongside tuberculosis, for which extensive evidence of its
socio-economic determinants was readily at hand in the post-war lead-up to
the creation of the World Health Organization. Much of this documentation
derived from research conducted in the Indian subcontinent. Indeed, of any
global region, it was the early twentieth-century epidemiological studies of
malaria in India that challenged the thesis of malaria as a major cause of
global poverty, the central argument that would be offered for proceeding
with the 1950s global malaria eradication program. In effect, the colonial
experience in the Indian subcontinent would be appropriated to underwrite
a fundamentally inverted interpretation of the malaria-hunger relationship,
one that would manifest in the singular germ-transmission framework of
much of the early years of the World Health Organization’s work.
Within recent international health historiography, the epistemic impact of
the new subdiscipline of nutritional science has been explored by Michael
Worboys in his analysis of the ‘discovery of malnutrition’ in the inter-war

6
 INTRODUCTION

period in British colonies in Africa: how, in its application, the new science of
nutrition was allowed to overshadow central realities of hunger.25 In the case
of British India, the emergence of nutritional science between the wars has
also been explored by V.R. Muraleedharan and David Arnold26 in accounts
of research undertaken into the prevalence of micronutrient deficiencies
and ‘unbalanced’ dietaries. Their work also notes several 1930s household
income surveys that indicated grossly insufficient calorie consumption levels
(undernourishment) among major portions of the population, both rural
and urban. Less explored in this important work however is the extent to
which the new nutritional science’s focus on dietary quality (micronutrients
and ‘protective’ foods) came to supplant that on quantitative sufficiency and
ultimately divert academic and administrative attention away from hunger
and subsistence precarity, realities so starkly highlighted in the household
income studies. This question has been explored more recently by C. Sathy-
amala in relation to the post-colonial legacy of the new ‘dietary’ science.27
Important historiographic research has also been undertaken in recent years
into the emergence of the League of Nations Health Organisation in the early
inter-war period as the first major international health agency with a mandate
that extended beyond international epidemic surveillance. This work has cast a
renewed spotlight upon the inter-war ‘contest’ between European and Anglo-
American members of the Malaria Commission of the League of Nations
Health Organisation in approaches to the global ‘malaria problem,’ a debate
that appeared to pit vector-control techniques against socio-economic measures
in the route to malaria mortality control.28 It has highlighted as well the semi-
nal role malaria continued to play in the shaping of the nascent World Health
Organization following the Second World War, and the role of the Rockefeller
Foundation in the organization’s prioritizing of global malaria control.29
Less explored in this literature, however, has been the question of how,
institutionally, this shift came about – beyond, that is, the ideational power
of the paradigm itself and general scientific ‘optimism’ of the period. For,
as will be seen in Chapter 4, the reductive rewriting of disease theory did
not proceed unopposed. While the complex interplay among actors within
and without the League of Nations Malaria Commission and nascent WHO
agencies has begun to be explored,30 only limited historiographic attention
has been directed to the underlying economic claims for malaria eradica-
tion: how the malaria ‘burden’ itself came to be redefined solely in terms of
malaria transmission in the days immediately following the close of WW2.31
Most importantly, what remains unaddressed in the current historiog-
raphy is what was set aside in the post-WW2 embrace of the ‘malaria as
obstacle to development’ thesis: which is to say, the extensive empirical and
narrative experience underlying interpretation of malaria as a ‘social disease’
in much of the world, its burden to a large extent a function of intense pov-
erty. Largely invisible have been the detailed accounts of malaria in relation
to hunger, a relationship traced in the early years of work of the League of

7
 INTRODUCTION

Nations Malaria Commission, and in greater epidemiological detail before

that in the South Asian sanitary records. The colonial public health adminis-
tration and malaria research records of British India make it possible to ana-
lyze with considerable clarity how this broader understanding was lost. They
offer critical insights into twentieth-century medical, intellectual, and geopo-
litical history across a period that represents a final stage in the ‘uncoupling’
of disease and destitution, one that saw a fundamental transformation in epi-
demiological concepts, language, and understanding of human subsistence
(daily ‘bread’), health and disease, and their once-manifest interrelationship.
How specific application of the new medical specialisms of entomology,
immunology, and nutritional science research in this period contributed to
the academic sidelining of subsistence precarity in malaria analysis takes
us beyond any single technology to consider broader spheres of cultural,
institutional, and political history of this period, what Worboys has termed,
in relation to similar developments in British colonies in Africa, an era of
the ‘scientizing’ or ‘medicalizing’ of social problems.32 The consequences
for South Asian malaria historiography have been considerable. With cen-
tral concepts and language of hunger largely superceded, its incorporation
within epidemic analysis became increasingly difficult in academic delibera-
tions, and in turn in discussions of malaria mortality.
An important inter-war example of the waning visibility of hunger in mod-
ern malaria analysis can be seen in relation to Sri Lankan malaria historiogra-
phy. Here, too, Western medical analysis has figured largely in this epistemic
loss: both in the interpretation of the factors underlying the malaria epidemic
of 1934–1935 in Sri Lanka (colonial Ceylon) where famine conditions gener-
ally were sidelined;33 and conversely, one decade later where improvements
in food security were overlooked in the interpretation of post-WW2 mortal-
ity decline in favour of DDT-based control of malaria transmission, despite
Sri Lankan analysts’ questioning of such a reading.34 The 1934–1935 Ceylon
epidemic takes on added historiographic significance for being a temporal
meeting point between the modern and historical malaria literatures: mod-
ern medical analysis of epidemic malaria reaches back to the 1934–1935
epidemic but little further; and historical South Asian malaria research gener-
ally extends little beyond. In both cases, the significance of malaria mortality
decline in the region between 1920 and 1950 has generally been unrecog-
nized – the period, in a sense, bifurcated and unexplored. It is the continuing
prominence of a vector transmission–based reading of modern Sri Lankan
malaria history that makes consideration of the epidemic experience of
India’s southeastern neighbour an important aspect to this larger study.
Without in any way gainsaying the mortality risk inherent to malarial
infection, falciparum malaria in particular,35 one can point to limited appre-
ciation within the historiographic literature of the wide range in disease
lethality associated with seasonal malaria transmission.36 This spectrum
varies from a week or so of intermittent fever, on the one hand – ‘ordinary’

8
 INTRODUCTION

post-monsoon malarial fever with a relatively low mortality rate in his-

torical terms – to extreme prostration and death, on the other. In years
of good rains in Punjab, falciparum malaria was widespread. But it was
markedly more lethal only in particular circumstances. These, Christophers
concluded, related directly to subsistence conditions of the human host, the
‘Human Factor,’ and indirectly through consequent possible dose effects.37
In the absence of this broader perspective, South Asian malaria historiogra-
phy has been limited largely to the domain of vector transmission, the disease’s
historical mortality burden presumed, it seems, primarily a function of the
plasmodial parasite. One example of the epistemic consequences is seen in
the view that little was achieved in the realm of ‘malaria control’ through the
colonial period.38 Save for desultory quinine distribution, the malaria problem
is seen as having remained largely unchanged to the end of British rule39 – even
though the 1920–1950 period saw ‘fulminant’ malaria epidemics decline dra-
matically in Punjab, and quite possibly elsewhere in the subcontinent. What
stands out, then, in much of the historiographic literature is an inadvertent
conflation of malaria infection (transmission) and malarial disease (mortality).
The interpretative consequences of this conflation can be seen in the atten-
tion directed to the ‘malariogenic’ effects of canal irrigation.40 While there
is little question that irrigation channels offered highly favourable sites for
larval development of Anopheles culicifacies – the principal rural malaria
vector in the plains of the subcontinent – malaria was endemic to all of
rural Punjab quite independent of the vast canal irrigation systems engi-
neered under the British Raj, and indeed across the vast plains of the Indian
subcontinent.41 Unfortunately, with attention directed primarily toward
malaria transmission, patterns of actual mortality from the disease have
remained unexamined, indeed largely invisible. In this sense, the conflation
of the two has served to foreclose essential avenues for incorporating the
overall impacts of colonial canal irrigation projects into analysis of histori-
cal mortality trends in the region, or indeed for understanding post-1920
mortality decline in Punjab and South Asia more widely.
Profound ecological problems unquestionably were associated with canal irri-
gation.42 The detrimental effects of soil alkalization and impact of canal embank-
ments on rural drainage patterns in the province were real, extensive, and in
the case of surface drainage obstruction, often preventable.43 But where malaria
developed as a major mortality problem in the canal tracts, it was related to the
economic effects of waterlogging rather than entomological conditions: underly-
ing decline in agricultural productivity and marked impoverishment. Here, fail-
ure to differentiate malaria infection from malaria mortality epidemiologically
has left the region’s malaria historiography at an impasse, with seemingly little to
study regarding malaria’s burden under colonial rule until the arrival of the pow-
erful residual insecticides in the 1950s period – and little also, it seems, thereafter.
The current ‘malariogenic’ critique of canal irrigation stands in notable
contrast to earlier colonial-period understanding of malaria’s mortality

9
 INTRODUCTION

burden in South Asia, and mirrors a narrowed framework to malaria anal-

ysis across the final years of British rule. This reductive trajectory was
challenged in the inter-war period, both by public figures and by several
leading researchers. Yet South Asian epidemic historiography still remains
constrained in important areas by the limitations of the modern germ-
paradigm, despite what the region’s ample historical resources reveal to the
contrary. This book attempts to reclaim that earlier understanding of the
relationship between hunger and disease through a study of how it was lost.

This study
It is at the moment of formal acknowledgement by the colonial administra-
tion of the role of hunger in the malaria mortality burden of British India
that this study begins. Chapter 1 explores the extent to which the economic
conclusions to Christophers’s Malaria in the Punjab report, publicly released
in 1911, had come to be taken seriously by the colonial Government of
India and, subsequently, by the League of Nations Malaria Commission in
the inter-war period. It then identifies and traces the conceptual shifts that
took place in the 1930s colonial malaria literature that underlay reinterpre-
tation of Christophers’s ‘Human Factor’ in immunological terms: from hun-
ger-induced weakened immune capacity in the human host, to fluctuating
levels of acquired immunity – now a function of vector transmission. This
shift took prominent expression in Western medical commentary on the
1934–1935 malaria epidemic in Sri Lanka (colonial Ceylon), an epidemic
that is examined in Chapter 2. Here the central role of famine conditions44
underlying the epidemic of malaria deaths is analyzed; then, their subse-
quent omission in expatriate academic interpretations, an omission to which
Christophers would call attention in ensuing Royal Society deliberations.
Chapter 3 then traces a parallel inter-war shift in medical attention from
quantitative to qualitative (micronutrient) hunger in medical research and
writing with the emergence of nutritional science in 1920s South Asia. The
epistemic impact of the new dietary science is traced in key government docu-
ments through the Bengal Famine Commission (1945) and Bhore Committee
(1946) reports,45 and at the international level within the League of Nations
Health Organisation. Highlighted, as well, are the contemporaneous efforts
of nascent trade unions, members of the Indian public, and a handful of
medical workers – largely ‘unsung’ figures, South Asian and Anglo-Indian46 –
who queried what they saw as increasingly reductive trends in the applica-
tion of the new biomedical subdisciplines and who strove to document the
commonplace relationship between malaria lethality and human destitution.
These medical subdisciplinary developments are then placed in the broader
context of nineteenth-century sanitationist and bacteriological developments
in the metropole and their impact on medical thought in colonial South Asia
(chapter four). The chapter draws on the work of Christopher Hamlin, who

10
 INTRODUCTION

has traced the efforts of leading medical figures in industrializing Britain who
challenged the 1842 Sanitary Report’s selective focus on ‘environmental’ filth
as the cause of recurring typhus epidemics to the exclusion of predisposing
conditions of ‘physiological poverty’ (destitution).47 The pages of the annual
Punjab sanitary and public health reports reveal a similarly reasoned reluc-
tance on the part of nineteenth-century health officials to embrace an exclusiv-
ist germ-transmission theory of epidemic causation; and resistance in the early
twentieth century to the inverted thesis of malaria as cause of India’s poverty.
Such questioning, however, would be overshadowed by the more immedi-
ate challenges presented by post-WWI fiscal retrenchment to all aspects of
medical research in India, the constraints and consequences of which are
explored in Chapter 5. Growing aspirations on the part of colonial research-
ers for alternate sources of funding would be accompanied by the expanding
influence of the Rockefeller Foundation’s International Health Rural Divi-
sion on public health deliberations in South Asia, ultimately leading to vec-
tor control trials in southern India in 1938–1941 undertaken by Rockefeller
consultant Paul F. Russell – work that would facilitate Russell’s rapid rise to
prominence as an authority on global malaria.
The influence of the Rockefeller Foundation in shaping an exclusively
transmission-based (vector control) framework for the subsequent WHO
malaria control program is traced in Chapter 6. Russell’s early and pre-
eminent membership on the organization’s Expert Committee on Malaria
would underlie the designation of malaria transmission control as a global
health priority in the earliest deliberations of the nascent WHO’s Interim
Commission in 1946. This decision, leveraged through UNRRA funding
conditionalities (United Nations Relief and Rehabilitation Administration),
was accompanied by the sidelining of the extensive South Asian epidemio-
logical malaria research from discussion of the nature of the global malaria
mortality problem, and the final eclipse of hunger (the ‘Human Factor’) in
understanding of its epidemiology.
Chapter 7 examines the allure of a germ model of malaria shorn of con-
siderations of the human host; the varied professional and often political
conveniences of a purely technical approach to vector transmission control
in the case of malaria; and the model’s ongoing legacy in modern malaria
historiography – a legacy evident in the limited visibility of subsistence
precarity in modern global mortality decline analysis. As one illustration,
the contested assessment of the mortality impact of post-WW2 insecticide-
based malaria eradication in Sri Lanka (colonial Ceylon) is revisited.
Chapter 8 considers the on-going legacy of the narrowed epidemic par-
adigm, seen in the relative invisibility of hunger that continues in mod-
ern health historiography. It examines a prominent 1985 study of rapid
mortality decline in several low-income countries and queries the limited
attention directed to the role of shifts in food security underlying these
achievements.48

11
 INTRODUCTION

Finally, the study draws attention to the exceptional discerning powers

of medical observers in nineteenth-century Britain49 and early twentieth-
century South Asia50 who challenged the reductive trend in health analysis
and sought to re-incorporate subsistence conditions of the human host in
interpreting mortality patterns of common endemic diseases in their socie-
ties. For them, a reclaiming of this broader ‘endemiology’ was not a dismissal
of science itself. Indeed, many were pre-eminent medical researchers them-
selves. Their advocacy thus powerfully reminds us, as does Roy Macleod,
that ‘[i]t is clearly possible to examine the culture of western medicine with-
out questioning the benefits of modern [medical] science.’51

Notes
1 G. Macdonald, ‘The Analysis of Equilibrium in Malaria,’ Tropical Diseases Bul-
letin, 49, 1952, 814, 819–828; reprinted in L. Bruce-Chwatt, and V.J. Glanville,
eds., Dynamics of Tropical Diseases: The Late George Macdonald (London:
Oxford University Press, 1973), 132.
2 Ibid.
3 See ch. 1, text accompanying note 84.
4 S.R. Christophers, ‘Malaria in the Punjab,’ Scientific Memoirs by Officers of the
Medical and Sanitary Departments of the Government of India (New Series),
No. 46 (Calcutta: Superintendent Govt Printing, 1911), 109.
5 For details, see S. Zurbrigg, Epidemic Malaria and Hunger in Colonial Punjab
(London and New Delhi: Routledge, 2019), ch. 2.
6 For a summary of malaria transmission bionomics in Punjab, see Appendix I.
7 Christophers, ‘Malaria in the Punjab,’ 113, 127, 133; S.R. Christophers, and
C.A. Bentley, Malaria in the Duars. Being the Second Report to the Advisory
Committee Appointed by the Government of India to Conduct an Enquiry
Regarding Blackwater and Other Fevers Prevalent in the Duars (Simla: Govern-
ment Monotype Press, 1909), 5, 7.
8 The distinction between acute hunger and lesser degrees of undernourishment
(‘chronic’ hunger) is discussed in Appendix II; as well, in Zurbrigg, Epidemic
Malaria and Hunger, chs.1, 3. Malaria lethality in South Asia appears to have
been heightened mainly by acute hunger and less so by lesser degrees of under-
nourishment, the latter affecting mortality rates from a range of other common
endemic infections; ibid. To this extent, malaria mortality history offers only a
partial ‘window’ on the role of hunger underlying very high pre-modern mortal-
ity levels. Nonetheless, because of its historical prevalence in much of the world,
malaria figures prominently in human health history.
9 Malaria mortality ‘was increased by the enfeeblement of health which a prolonged
period of privation had produced’; Christophers, ‘Malaria in the Punjab,’ 108–109.
10 P. Russell, L.S. West, and R.D. Manwell, Practical Malariology (Philadelphia:
W.B. Saunders, 1946), 375; J.A. Sinton, ‘What Malaria Costs India, Nation-
ally, Socially and Economically,’ Records of the Malaria Survey of India, 5, 3,
Sept. 1935, 223–264; Sinton, ‘What Malaria Costs India,’ 5, 4, Dec. 1935, 413–
489; Sinton, ‘What Malaria Costs India,’ 6, 1, Mar. 1936, 92–169 [hereafter
RMSI]; I.A. McGregor, ‘Malaria and Nutrition,’ in W.H. Wernsdorfer, and I.A.
McGregor, eds., Malaria: Principles and Practice of Malariology (Edinburgh:
Churchill Livingstone, 1988), 754–777, at 754.
11 Zurbrigg, Epidemic Malaria and Hunger, ch. 4.

12
 INTRODUCTION

12 Ibid., chs. 12, 9–11.

13 E.L. Perry, Recent Additions to Our Knowledge of Malaria in the Punjab.
A paper read before the Punjab Branch of the British Medical Association at
Simla, on Jul. 17, 1914 (Simla: Thacker, Spink & Co, 1914); C.A. Gill, ‘Epi-
demic or Fulminant Malaria Together with a Preliminary Study of the Part
Played by Immunity in Malaria’, Indian Journal of Medical Research, 2, 1, Jul.
1914, 268–314 [hereafter, IJMR]. See ch. 2, below.
14 ‘Physiological concepts of disease imply that a disease cannot be understood
apart from a particular individual suffering from it. . . . [Whereas w]ithin the
ontological tradition, disease is posited to be some sort of entity which befalls
a previously healthy person’; W. Bynum, ‘Nosology,’ in W. Bynum, and R. Por-
ter, Companion Encyclopedia of the History of Medicine (London: Routledge,
1993), 335–356.
15 Punjab Govt, Gazetteer of the Gurgaon District, 1883–1884 (Lahore: Govern-
ment Press, 1884), 131–132.
16 In 1967, Emilio Pampana, former permanent member of the early WHO Sec-
retariat and secretary to the Malaria Committee advised, ‘epidemics can take
place only in populations without malaria or malaria endemicity at a very low
level. . . .[I]f this large proportion of non-immunes does not exist the epidemic
cannot materialize’; E. Pampana, and E.J. Pampana, A Textbook of Malaria
Eradication (London: Oxford University Press, 1969), 92–93. See also M.J.
Bouma, and H. van der Kaay, ‘The El Niño Southern Oscillation and the histori-
cal malaria epidemics on the Indian subcontinent and Sri Lanka: An early warn-
ing system for future epidemics?,’ Tropical Medicine and International Health,
1, 1, Feb. 1996, 86–96. The phenomenon of fluctuating acquired immunity lev-
els in a population and suggested epidemic propensity would come to be denoted
as ‘unstable’ malaria.
17 R.I. Rotberg, ‘Nutrition and History,’ Journal of Interdisciplinary History, 14,
3, 1983, 199–204.
18 S.J. Kunitz, ‘Mortality since Malthus,’ in R. Scofield, and D. Coleman, The State
of Population Theory: Forward from Malthus (Oxford: Basil Blackwell, 1986),
279–302; T. Bengtsson, C. Campbell, J.Z. Lee, et al., eds., Life Under Pressure:
Mortality and Living Standards in Europe and Asia, 1700–1900 (Cambridge,
MA: MIT Press, 2004), 42–44.
19 See, e.g., A. Celli, ‘The Restriction of Malaria in Italy,’ in Transactions of the
Fifteenth International Congress on Hygiene and Demography, Washington,
September 23–28, 1912 (Washington, D.C., 1913), 516–531.
20 Here, the term ‘infective’ is used to include those microbial infections that
are not primarily communicable (i.e., ‘infectious’), such as many forms of
pneumonia, where heightened mortality risk is seen particularly among the
immune-compromised.
21 For analysis of the evolution of colonial malaria control policy leading up to,
and following, the 1909 Imperial Malaria Conference at Simla, see Zurbrigg,
Epidemic Malaria and Hunger, chs. 7–8.
22 R. McCarrison, Studies in Deficiency Diseases (London: Henry Frowde, Hod-
der & Stoughton, 1921); S.C. Seal, ‘Diet and the Incidence of Disease in India,’
Indian Medical Gazette, May 1938, 291–301.
23 P.J. Brown, ‘Malaria, Miseria, and Underpopulation in Sardinia: The “Malaria
Blocks Development” Cultural Model,’ Medical Anthropology, 17, 3, May 1997,
239–254.
24 Expert Committee on Malaria, ‘Summary Minutes of the First Session,’ 22–25
April 1947, WHO.IC/Mal./6, 1–45 [hereafter, ECM]; ECM, ‘Report on the First
Session,’ Geneva, 22–25 April 1947, WHO.IC/Mal./4, 3.

13
 INTRODUCTION

25 M. Worboys, ‘The Discovery of Colonial Malnutrition Between the Wars,’ in D.

Arnold, Imperial Medicine and Indigenous Societies (Manchester: Manchester
University Press, 1988), 208–225. The interpretative power of the microbiologic
framework in modern epidemic analysis has been explored as well in relation to
the 1970s thesis of ‘refeeding malaria’ in which starvation is considered to pro-
tect from malaria. For a critique, see S. Zurbrigg, ‘Did Starvation Protect from
Malaria? Distinguishing Between Severity and Lethality of Infectious Disease in
Colonial India,’ Social Science History, 21, 1, 1997, 27–58.
26 V.R. Muraleedharan, ‘Diet, Disease and Death in Colonial South India,’ Eco-
nomic and Political Weekly, Jan. 1–8, 1994, 55–63; D. Arnold, ‘The “Discov-
ery” of Malnutrition and Diet in Colonial India,’ Indian Economic and Social
History Review, 31, 1, 1994, 1–26 [hereafter, IESHR].
27 C. Sathyamala, ‘Nutrition as a Public Health Problem (1990–1947),’ Interna-
tional Institute of Social Studies, Working Paper No. 510, Dec. 2010.
28 J.A. Nájera aptly refers to the ‘two schools’ as the ‘anti-parasite’ group and the
‘anti-disease’ group, highlighting the central distinction between infection (trans-
mission) and disease (‘pernicious’ morbidity and mortality); in ‘The control of
tropical diseases and socio-economic development (with special reference to
malaria and its control),’ Parassitologia, 36, 17–33, 1994. See also S. Litsios,
‘Malaria Control, the Cold War, and the Postwar Reorganization of Interna-
tional Assistance,’ Medical Anthropology, 17, 1997, 255–278; J. Farley, Brock
Chisholm, the World Health Organization, and the Cold War (Vancouver: Uni-
versity of British Columbia Press, 2008); H. Evans, ‘European Malaria Policy in
the 1920s and 1930s: The Epidemiology of Minutiae,’ Isis, 80, 1, Mar. 1989,
40–59.
29 See, J. Gillespie, ‘Europe, America, and the Space of International Health,’ in S.
Gross Solomon, L. Murand, and P. Zylberman, eds., Shifting Boundaries in Pub-
lic Health: Europe in the Twentieth Century (Rochester: University of Rochester
Press, 2008), 114–137; J. Gillespie, ‘Social Medicine, Social Security and Inter-
national Health, 1940–60,’ in Esteban Rodriguez-Ocana, ed., The Politics of the
Healthy Life: An International Perspective (Sheffield: European Association for
the History of Medicine and Health, 2002), 219–253; S. Amrith, Decolonizing
International Health: India and Southeast Asia, 1930–65 (Basingstoke: Palgrave
Macmillan, 2006); J. Farley, To Cast Out Disease: A History of the Interna-
tional Health Division of the Rockefeller Foundation (1913–1951) (New York:
Oxford University Press, 2004). See also, I. Borowy, ‘International Social Medi-
cine between the Wars: Positioning a Volatile Concept,’ Hygiea Internationalis,
6, 2, 2007, 13–35, at 29–30.
30 With regard to the challenges faced by Ludwik Rajchman, LNHO Director,
and Andrija Stampar as prominent ‘social medicine’ advocates in the LNHO,
see Farley, Brock Chisholm; P. Weindling, ‘Philanthropy and World Health:
The Rockefeller Foundation and the League of Nations Health Organisation,’
Minerva, 35, 3, 1997, 269–281; Gillespie, ‘Social Medicine, Social Security and
International Health,’ 219–253.
31 Packard points out how weak the evidence was for the original premise of MBD,
in R.M. Packard, ‘Malaria Dreams: Postwar Visions of Health and Development
in the Third World,’ Medical Anthropology, 17, 1997, 279–296, at 284–286;
R.M. Packard, ‘ “Roll Back Malaria”? Reassessing the Economic Burden of
Malaria,’ Population and Development Review, 35, 1, Mar. 2009, 53–87.
32 M. Worboys, ‘The Discovery of Colonial Malnutrition Between the Wars,’ in D.
Arnold, ed., Imperial Medicine and Indigenous Societies (Manchester: Manches-
ter University Press, 1988), 208–225.

14
 INTRODUCTION

33 P.F. Russell, Malaria: Basic Principles Briefly Stated (Oxford: Blackwell Scientific
Publs, 1952), 100; G. Macdonald, ‘The Analysis of Equilibrium in Malaria,’ in
L. Bruce-Chwatt, and V.J. Glanville, eds., Dynamics of Tropical Diseases: The
Late George Macdonald (London: Oxford University Press, 1973), 132; C.L.
Dunn, Malaria in Ceylon: An Enquiry into its Causes (London: Bailliere, Tindall
and Cox, 1936).
34 K.N. Sarkar, The Demography of Ceylon (Colombo: Govt Press, 1958), 123;
S.A. Meegama, ‘The Decline in Maternal and Infant Mortality and its relation to
Malaria Eradication,’ Population Studies, 23, 2, 1969, 289–302.
35 The two main malaria species transmitted in Punjab were P. vivax (‘benign ter-
tian’) and P. falciparum (‘malignant’ or ‘sub-tertian’ malaria), the latter associ-
ated with greater morbidity and mortality related to greater parasitization of red
blood cells in the human host, potentially causing cerebral malaria also among
the well-nourished. Even in falciparum infections, however, historical lethality
(case fatality rate) varied greatly depending on previous exposure (‘acquired’
immunity); immuno-competence (factors affecting general immune capacity or
its suppression); strain of plasmodium; and possibly, dose of infection. The lat-
ter may have contributed to the lethality of infection among Europeans in their
exposure to transmission conditions in holoendemic regions of sub-Saharan
west Africa, where the prime vector (Anopheles gambiae) is a highly anthropo-
philic species resulting in extreme inoculation rates and high levels of protective
acquired immunity among the adult population but intense infection rates in the
as yet non-immune.
36 Variation in lethality of microbial infections is acknowledged theoretically in
modern epidemiology in the concepts of ‘case fatality rate’ and ‘epidemic equa-
tion’, the latter expressing the interplay between germ (pathogen) exposure and
human host response or resistance. Marked differentials in child survival rates
in relation to undernourishment have been documented in R. Martorell, and T.J.
Ho, ‘Malnutrition, Morbidity and Mortality,’ in H. Mosley, and L. Chen, eds.,
Child Survival: Strategies for Research, Supplement to vol. 10, Population and
Development Review, 1984, 49–68. Historians generally acknowledge a hunger-
infection lethality link, but the question is rarely pursued for paucity of mortality
and infection incidence data. An important exception is the field of historical
nutritional anthropometry: undernourishment prevalence tracked through his-
torical trends in mean adult stature; see, e.g., R. Floud, R. Fogel, B. Harris,
and Sok Chul Hong, eds., The Changing Body: Health, Nutrition, and Human
Development in the Western World since 1700 (Cambridge: Cambridge Univer-
sity Press, 2011). Awareness of the wide range in lethality of common endemic
infections in the pre-modern era centrally informed Thomas McKeown’s explo-
ration of the determinants of mortality decline in England and Wales; The Mod-
ern Rise of Population (London: Edward Arnold, 1976), 73.
37 Based on his sparrow experiments, Christophers considered ‘dose’ of infection to
be the number of sporozoites injected by an infected mosquito during a human
blood meal. He appears to have hypothesized that immune-suppression among
the famished led to higher parasite levels in vector mosquitoes and in turn in the
dose of subsequent human infections. On this, see Zurbrigg, Epidemic Malaria
and Hunger, 78–82, 192–194.
38 W. Bynum, ‘Malaria in inter-war British India,’ Parassitologia, 42, 2000, 25–31;
M. Harrison, ‘ “Hot Beds of Disease”: Malaria and Civilization in Nineteenth-
Century British India,’ Parassitologia, 40, 1998, 11–18; S. Polu, Infectious Dis-
ease in India, 1892–1940: Policy-Making and the Perceptions of Risk (London:
Palgrave Macmillan, 2012); D. Arnold, ‘Crisis and Contradiction in India’s

15
 INTRODUCTION

Public Health,’ in D. Porter, ed., The History of Public Health and the Modern
State (Amsterdam: Rodopi, 1994), 335–355; V.R. Muraleedharan, and D. Vee-
raraghavan, ‘Anti-malaria Policy in the Madras Presidency: An Overview of the
Early Decades of the Twentieth Century,’ Medical History, 36, 1992, 290–305.
39 This assumption appears in much recent writing on the malaria burden, with
Sinton’s mortality estimates from early twentieth-century experience tending to
inform perceptions of the pre-DDT South Asian malaria experience; V.P. Sharma,
and K.N. Mehrotra, ‘Malaria Resurgence in India: A Critical Study,’ Social Sci-
ence Medicine, 22, 1986, 835–845, at 835; V.P. Sharma, ‘Battling Malaria Ice-
berg Incorporating Strategic Reforms in Achieving Millennium Development
Goals & Malaria Elimination In India,’ IJMR, 136, Dec. 2012, 907–925.
40 S. Watts, ‘British Development Policies and Malaria in India 1897-c.1929,’ Past
and Present, 165, 1999, 141–181; E. Whitcombe, ‘The Environmental Costs of
Irrigation in British India: Waterlogging, Salinity, Malaria,’ in D. Arnold, and R.
Guha, eds., Nature, Culture, Imperialism: Essays on the Environmental History
of South Asia (New Delhi: Oxford University Press, 1995), 237–259; I. Klein,
‘Malaria and Mortality in Bengal,’ 1840–1921,’ IESHR, 9, 2, 1972, 132–160;
I. Klein, ‘Development and Death: Reinterpreting Malaria, Economics and Ecol-
ogy in British India,’ IESHR, 38, 2, 2001, 147–179; K. Wakimura, ‘Epidemic
Malaria and “Colonial Development”: Reconsidering the Cases of Northern
and Western India,’ Economic History Congress XIII, Buenos Aires, Argentina,
July 2002, mimeo.
41 The western canal tracts generally were less affected by the fulminant form of
malaria than other regions of the province. Moreover, on-going expansion of
the canal networks in the western half of the province in the final decades of the
colonial period was associated not with heightened mortality but rather with
declining crude death rates, in step with trends across the province; Zurbrigg,
Epidemic Malaria and Hunger, chs. 2, 4, and 6.
42 See, for example, I. Agnihotri, ‘Ecology, Land Use and Colonisation: The Canal
Colonies of Punjab,’ IESHR, 33, 1, 1996, 37–58; I. Stone, Canal Irrigation in
British India: Perspectives on Technological Changes in a Peasant Economy
(Cambridge: Cambridge University Press, 1984); E. Whitcombe, Agrarian Con-
ditions in Northern India, I, The United Provinces Under British Rule, 1860–
1900 (Berkeley: University of California Press, 1972); E. Whitcombe, ‘The
Environmental Costs of Irrigation’; Klein, ‘Development and Death.’
43 Zurbrigg, Epidemic Malaria and Hunger, 282–286. In large tracts of western
deltaic Bengal also, the effects of rail and road infrastructure construction on
agriculture productivity were catastrophic, heightened malaria intensity follow-
ing in train; C.A Bentley, ‘Some Economic Aspects of Bengal Malaria,’ IMG,
Sept. 1922, 321–326; C.A Bentley, in Report of the Royal Commission on
Agriculture in India, vol. IV, Bengal Evidence (London: HMSO, 1928), 240–
247. Nor is it suggested that criticism of the colonial government’s inaction on
malaria ‘control’ is unwarranted. Even in highly localised urban malarious areas,
such as Bombay municipality, feasible transmission-control efforts were under-
funded, at best erratic, and frequently abandoned. See also Muraleedharan and
Veeraraghavan, ‘Anti-malaria policy in the Madras Presidency.’
44 R. Briercliffe, The Ceylon Malaria Epidemic, 1934–35. Report by the Director of
Medical and Sanitary Service (Colombo: Ceylon Govt Press, Sept. 1935), 27, 43.
45 Famine Inquiry Commission, India, Report on Bengal, (New Delhi: GOI, 1945);
Report of the Health Survey and Development Committee (New Delhi: GOI,
1946).

16
 INTRODUCTION

46 See ch. 3, 114.

47 C. Hamlin, ‘Predisposing Causes and Public Health in Early Nineteenth-
Century Medical Thought,’ Society for the Social History of Medicine, 5, 1,
Apr. 1992, 43–70; C. Hamlin, Public Health and Social Justice in the Age of
Chadwick (Cambridge: Cambridge University Press, 1998). Similar concerns
emerged among early twentieth-century analysts in the industrialized West who
also ­recognized the limitations of a public health mandate selectively directed
to germ-­transmission control and elimination of micronutrient deficiencies; I.
Galdston, ‘Humanism and Public Health,’ Bulletin of the History of Medicine,
Jan. 1940, 1032–1039; E. Ackerknecht, ‘Hygiene in France, 1815–1848,’ Bulle-
tin of the History of Medicine, 22, 1948, 117–155. For analysis of the continued
dominance of biomedical theories of disease, and of broader social epidemiologi-
cal frameworks that have emerged in response, see for example, T.K.S. Ravin-
dran, and R. Gaitonde, eds., Health Inequities in India: A Synthesis of Recent
Evidence (Singapore: Springer, 2018); N. Krieger, Epidemiology and the People’s
Health: Theory and Context (Oxford: Oxford University Press, 2011); A.-E.
Birn, Y. Pillay, and T.H. Holtz, Textbook of Global Health, 4th ed. (Oxford:
Oxford University Press, 2017); I. Qadeer, K. Sen, and K.R. Nayar, eds., Public
Health and the Poverty of Reforms (New Delhi: Sage, 2001).
48 S.B. Halstead, J.A. Walsh, and K.S. Warren, Good Health at Low Cost (New
York: Rockefeller Foundation, 1985); D. Balabanova, M. McKee, and A. Mills,
eds., ‘Good Health at Low Cost’: Twenty Years On (London: London School of
Hygiene and Tropical Medicine, 2011).
49 C. Hamlin, ‘William Pulteney Alison, the Scottish Philosophy, and the Making
of a Political Medicine,’ Journal of the History of Medicine and Allied Sciences,
61, 2, 2006, 144–186.
50 N. Gangulee, Health and Nutrition in India (London: Faber and Faber, 1939);
S.R. Christophers, and C.A. Bentley, ‘The Human Factor: An Extension of our
Knowledge regarding the Epidemiology of Malarial Disease,’ in W.E. Jennings,
ed., Transactions of the Bombay Medical Congress, 1909, (Bombay: Bennett,
Coleman & Co., 1910), 78–83.
51 R. Macleod, ‘Introduction,’ in R. Macleod, and M. Lewis, eds., Disease, Medi-
cine and Empire (London: Routledge, 1988), 12.

17
 1
THE ‘HUMAN FACTOR’
TRANSFORMED

Certainly by 1908 with the commissioning of the Punjab malaria enquiry

report,1 the colonial administration in India was taking seriously the grow-
ing notoriety associated with the ‘exalted’ form of malaria in the country,
and was attempting to decipher, and at some level grapple with, the spec-
trum of causal factors underlying that lethality. Here, by way of context to
the Human Factor’s ultimate demise, the circumstances leading up to the
1911 enquiry report, and the remarkable (if brief) period of transparency
thereafter regarding the hunger-malaria relationship, are outlined.
The preceding decade had been one in which the British Raj was com-
ing to terms with mounting expectations for vector ‘extirpation’ from both
the colonial and metropolitan medical professions, expectations triggered in
1897–1898 by Ross’s confirmation of mosquitoes as malaria vector. A six-
year trial program of intensive mosquito destruction operations (1902–
1908) at the Mian Mir rural cantonment in central Punjab, however, had
manifestly failed to eliminate malaria. The severe epidemic in the autumn of
1908 had swept through the cantonment as dramatically as elsewhere in the
province and made it clear that there was no ready ‘fix’ on the horizon for
the control of malaria transmission in the vast rural areas of the subconti-
nent where the disease took its principal toll. Adding to the administration’s
malaria policy predicament, professional and public concerns about the
safety of quinine were compounding the crisis of sanitary legitimacy already
made acute with the outbreak of plague a decade earlier.
Mounting public calls in the British and Indian medical press for mos-
quito extirpation had left the colonial administration little choice but to
take into confidence senior medical, sanitary, and military officials regarding
the broader economic dimensions to the malaria problem in the subconti-
nent. It did so through two detailed epidemiological studies of malaria mor-
tality in relation to mass destitution, the findings of which were presented at
two medical conferences: the Bombay Medical Congress in February 19092
where the conclusions of a recent enquiry into the extreme malaria lethality
on the Duars tea plantations were presented (Malaria in the Duars, 1909);3
and the October 1909 Imperial Malaria conference at Simla4 where S.R.

18
 THE ‘HUMAN FACTOR’ TRANSFORMED

Christophers’s findings regarding the ‘disastrous’ 1908 malaria epidemic in

Punjab framed the proceedings.5
The emergence of a concerted malaria policy in colonial South Asia can
be traced in large part to the epidemiological findings presented at these
two medical gatherings. Though subject to undoubted editing, published
proceedings from these meetings open up for historians much more complex
aspects to the malaria deliberations taking place within the administration at
this point than the vector extirpationist ‘versus’ ameliorationist (‘quininist’)
framework that had come to characterize public malaria policy discussion in
the immediate post-1897 years. They provide, in turn, essential context for
interpreting the impact of malaria policy across the final decades of colonial
rule, policy directed primarily to reducing malaria’s mortality burden.
At the Bombay Medical Congress, a report on the disconcerting results of
the Mian Mir trial6 was followed by a paper entitled ‘The Human Factor: An
Extension of our Knowledge regarding the Epidemiology of Malarial Dis-
ease,’ co-authored by Christophers and C.A. Bentley (1873–1949), former
chief medical officer of the Empire of India and Ceylon Tea Company.7 The
paper summarized the findings of their recent investigation into blackwater
fever on the northeastern Duars tea plantations, and their wider implica-
tions. Blackwater fever was a generally uncommon but serious medical syn-
drome associated with malaria involving sudden red blood cell destruction
(hemolysis). Considered to be triggered by repeated, often irregular, quinine
use, it was seen typically in areas of very high malaria endemicity among
those with ready access to the drug. More problematic for the adminis-
tration, the increasing notoriety associated with blackwater fever on the
Duars estates was rapidly undermining medical and public confidence in the
therapeutic safety of quinine – and by extension, the principal anti-malarial
policy that the government then had at hand.
The Duars enquiry examined two questions. First, the pathophysiology
of the syndrome and its relationship to quinine consumption, findings that
were immediately published in the prestigious Scientific Memoirs series as
an official report.8 And second, analysis of the factors underlying the pecu-
liarly intense (‘exalted’) form of malaria observed among the Duars plan-
tations’ labour population. This second report was a scathing account of
conditions of frank destitution among this group, and the role of the labour
recruitment system under prevailing indentured labour law in creating and
perpetuating such conditions.9 ‘Physiologic misery,’10 the two investigators
had concluded, played an overriding role in the ‘intense’ form of malaria
seen on the Duars estates, the effects of which were spilling over to the non-
immune European managerial staff in the form of inordinate quinine use
and cases of blackwater fever in turn. Their conclusions, in other words,
extended far beyond questions of quinine safety and bore profound impli-
cations for understanding malaria mortality patterns more generally in the
subcontinent.

19
 THE ‘HUMAN FACTOR’ TRANSFORMED

Not surprisingly, this latter portion of the enquiry, entitled Malaria in

the Duars, was left unpublished until its tabling as an unheralded one-off
document in 1911. Its conclusions however would thoroughly inform the
‘Human Factor’ paper presented at the Bombay Congress in February 1909.
There, the two investigators articulated a more general relationship between
economic hardship and malaria lethality, pointing to endemic destitution
among indentured workers in labour camps and industrial sites across much
of the subcontinent, also expressed in an intense (‘exalted’) form of malaria.
The politically incriminating questions raised in Bombay by the second
Duars report, and by the ‘fulminant’ malaria epidemic in Punjab in the
autumn of 1908, would form the backdrop eight months later to the Impe-
rial Malaria Conference at Simla in October 1909. The six-day conference
attended by leading medical, sanitary, military, and administrative officials
was framed by Christophers’s findings that identified harvest failure and
‘scarcity’ (famine-level foodgrain prices) as underlying the 1908 epidemic’s
severe lethality.11 Together, the two enquiry reports directly implicated not
just epidemic destitution (‘famine’), but endemic immiseration in British
India as well, conditions related in no small part to indentured labour legis-
lation dating from the mid-nineteenth century. The goal of the Simla confer-
ence was to produce consensus on where government priorities should lie:
the directing of public effort and resources preferentially to areas of ‘intense’
malaria, and to their underlying causes, rather than to malaria transmission
per se. ‘If we could prevent the mortality from epidemic fulminant malaria,’
Christophers urged, ‘we should have removed the most urgent and distress-
ing effects of this disease and those manifestations which the people them-
selves are most impressed by.’12
Formal acknowledgement at Simla of the role of acute hunger in the
malaria mortality burden, and subsequent publication of the Punjab enquiry
report in late 1911, appear to have succeeded to some considerable extent in
quelling public calls by members of the sanitary administration and Indian
Medical Service for large-scale expenditure on mosquito control.13 It also
opened up permissible space to voice concern over the larger economic
dimensions underlying the malaria mortality problem in the subcontinent.

The ‘Human Factor’ within colonial

malaria discourse
In the years immediately following the official release of Christophers’s
Punjab report in late 1911, hunger overtly framed public health analysis of
the malaria problem at many levels. In his annual report as Special Malaria
Officer for Punjab, C.A. Gill in 1914 would describe conditions in the canal
colonies as ‘unfavourable to malaria, in so far as the people are well fed and
have consequently a high resisting power. A well-nourished man may con-
tract malaria, but he very rarely dies of it.’14 Attention to the human ‘host’ in

20
 THE ‘HUMAN FACTOR’ TRANSFORMED

predicting malaria lethality patterns took practical expression as well in the

routines of provincial public health administrations. Through the final dec-
ades of the colonial period Punjab officials continued to track weekly rainfall
and foodgrain prices to predict autumn epidemic potential in the province,
predictions upon which food and quinine distribution efforts were based.15
Attention to the ‘Human Factor’ in malaria lethality during these years
extended to the formal academic literature as well. ‘Christophers has shown
very clearly,’ a prominent tropical medicine text would point out in 1922,
‘[that] in malarious localities people of low social status suffer more than
the well-to-do and has called attention to the direct and indirect action of
various economic factors which influence the spread and intensity of the
disease.’16 Similar views found echo that same year in the Indian Medical
Gazette (IMG) in a special issue devoted to the ‘Economic Factor in Tropi-
cal Diseases.’17 Where ‘many millions of the poorer population live on a
minimum of food in India,’ the lead editorial urged, the medical commu-
nity needed to take into account ‘the play of economic factors in inducing
endemic and epidemic disease,’ including malaria. ‘[P]revalence of anophe-
line carriers is but one factor in the origin of such terrible epidemics [as that
in 1908]. . . . Food prices are just as important. A lowered and impoverished
diet diminishes body resistance.’18 Here, as at Simla earlier, concern for hun-
ger extended beyond famine, to endemic ‘semi-starvation.’ ‘Dr. Bentley’s
statistics for malaria in Bengal,’ the editorial pointed out, ‘find a parallel
in Colonel Christophers’ important work on epidemic malaria in the Pun-
jab (1911).’ Nor, the IMG editorial insisted, was the importance of hunger
limited to its effect on malaria. Poverty and economic conditions were now
being seen to be of ‘immense importance’ to a range of infectious diseases.19
Timing of the 1922 editorial may well have been prompted by a recently
completed study of lathyrism by a senior pathologist at the Calcutta Medi-
cal College. A summary of H.W. Acton’s findings was published in the same
September issue of the Indian Medical Gazette and illustrated the stark eco-
nomic dimensions to the disease: the desperation of labourers forced by
destitution to accept wages paid in kesari dal, a legume well known to cause
permanent neuro-paralysis.20 In his research into the syndrome, Acton had
identified the triggering agent as a specific neurotoxin. But he concluded
that the underlying cause was economic, and suggested that the solution to
lathyrism had to be ‘a sociological one,’ starting with abolition of the rural
debt-slavery that forced workers to accept kesari dal as their wages. His
second recommendation was directed to more effective famine relief ‘during
the years of a bad monsoon, as well as controlling the price of wheat, rice,
and dal, so that the poor can afford to buy these articles of food.’21
Other papers in the September 1922 special issue of the Indian Medical
Gazette addressed economic factors at a broader level. A detailed report
by Bentley on ‘Economic Aspects of Bengal Malaria’ critiqued land ten-
ure policy in the province and urged government economic development

21
 THE ‘HUMAN FACTOR’ TRANSFORMED

(agricultural ‘bonification’).22 Citing parallels with Christophers’s Punjab

conclusions, the IMG editorial argued that ‘the study of economics should
be part of the medical curriculum, at least in India.’23
The first major colonial textbook on malaria, published in India in 1910,
also pointed unequivocally to ‘impoverishment’ as an important ‘personal pre-
disposing cause’ of malaria mortality. ‘There is no doubt,’ Patrick Hehir would
write, ‘that persons in good health are capable of throwing off a mild infection
of malaria, . . . [whereas] all conditions enfeebling the body increase the sus-
ceptibility to malarial infection.’24 As with Christophers and Bentley, Hehir’s
concern was also grounded in economic pragmatism: residual infection among
the impoverished in mass labour camps led to wider dissemination of the dis-
ease and increased labour costs. Much of Hehir’s malaria textbook dealt with
anti-mosquito and anti-larval techniques for interrupting transmission and
malaria chemotherapeutics. But adequate remedies, he clearly also was say-
ing, lay not just in medical and entomological measures but in the legislative
sphere as well. Malaria control policy ought to extend to economic measures
that ensured ‘a sufficient quantity of wholesome food’ such as ‘enforcement of
a minimum wage for all labourers on all contractors and other employers of
coolie labour . . . [a policy] deserving all possible attention.’25
This level of frankness in public discussion of hunger in British India was
unprecedented. The phrase the ‘Human Factor’ itself was of course a euphe-
mism. Nonetheless, the Simla proceedings had endowed the subject with legit-
imacy both as a medical diagnosis and as a leading public health issue. Two
decades later, the second edition of Patrick Hehir’s Prophylaxis of Malaria in
India continued to point to ‘impoverishment’ as a key factor underlying sever-
ity of malarial infection, if such references were now tucked amidst the vastly
expanded microbiological and entomological sections of updated research.
Indeed, in the final pages of the 490-page 1927 edition, Hehir returned, with
some ‘melancholy,’ to the subject of socio-economic conditions. ‘Effective
dealing with malaria is not simply a matter of doing away with collections of
water, filling up or draining borrow-pits and distributing a limited amount of
quinine,’ he urged. ‘A progressive anti-malaria policy in rural areas would . . .
attach the greatest importance to the economic and social factor.’26
What also distinguished this period was the clarity with which medical
figures stressed the distinction between infection and disease (mortality). In
its same September editorial, the 1922 Indian Medical Gazette stressed that
‘[w]hat may be merely hookworm infection in a well nourished individual
passes into hookworm disease in states of malnutrition.’27 It was a distinc-
tion articulated a decade earlier by Bentley at the Third Meeting of the Gen-
eral Malaria Committee in November 1912 in relation to the ‘moribund’
river tracts of lower Bengal:

the occurrence of epidemics of malarial disease among the usu-

ally tolerant or partially tolerant races, indigenous to malarious

22
 THE ‘HUMAN FACTOR’ TRANSFORMED

country, signifies something beyond the mere presence of infection

and anopheles, . . . and it is just that ‘something’ which requires to
be investigated by malariologists in India.28

‘[A]lthough the brilliant discoveries of Laveran and Ross have extended our
knowledge of the parasitology of malaria,’ he continued,

we are still ignorant of many of the factors responsible for the

occurrence of malaria disease, more especially when it appears
in epidemic form. . . . [T]he infection index of a population may
remain almost stationary although at one time disease might be
prevalent and another time almost absent. Unfortunately the sig-
nificance of these observations has been largely overlooked and the
word ‘malaria’ is almost invariably applied to describe both the
conditions of infection and the state of disease which may be associ-
ated with it.29

By calling attention to this distinction, Bentley was not suggesting the sea-
sonal appearance of malarial fever was innocuous, but highlighting instead
the profound contrast in morbid consequence under conditions of economic
hardship.
The impetus at this point behind such transparency clearly lay beyond
the medical realm, in the strategic need to counter the arguments of those
within the sanitary administration advocating ‘mosquito extirpation’ as a
general sanitary policy. But the stimulus had broader origins as well. In the
wake of the Boer War–era scandal of physical ‘degeneracy’ amongst British
recruits, medical and public attention in Britain too had returned to poverty
to account for the continuing high prevalence of tuberculosis and nutri-
tional stunting among the poorer classes. There was growing recognition
of the insufficiency of sanitationist public health interventions in remedying
such conditions, which at their root lay in poverty. As delegates were gather-
ing at Simla in October 1909, for example, James Niven, Medical Officer of
Health for Manchester, was preparing his Presidential Address, ‘Poverty and
Disease,’ for presentation to the Epidemiological Section of the Royal Soci-
ety of Medicine in London. In his talk he urged that economic insecurity –
irregular employment, livelihood, and time available to women for the feeding
and care of children – still determined much of the excess mortality amongst
the poor in Britain, and that tuberculosis remained ‘the most convenient
mirror of [this] poverty.’30
It was this period as well in Britain that saw the emergence of signifi-
cant ‘social welfare’ policies, measures in no small part adopted in response
to testimony of medical officials who explicitly linked disease and physi-
cal degeneracy. Such legislation included a Workmen’s Compensation Act,
provision of school meals in 1906, and two years later, a Mines Act and

23
 THE ‘HUMAN FACTOR’ TRANSFORMED

initiation of old age pensions. Growing pressure in the international sphere

for further labour reforms culminated in 1919 in the formation of the Inter-
national Labour Organization (ILO) with the aim that all states should
have standard labour legislation to ensure ‘there was no unfair competition’
amongst industrialized countries.31 Though yet modest in scope, legislation
on conditions and hours of work held major implications for bare subsist-
ence precarity. The emergence of the ILO itself was an expression of grow-
ing political pressure – in Britain with the emergence of trade unions and the
Labour Party – to address the economic determinants of health.
In India, this period corresponds to a beginning move away from the
expendability of labour (‘using up coolies’32) with legislation that began
the process of ultimately dismantling indentured labour laws. Changes
to the Labour Code date, hardly coincidentally, from the 1908 Malaria in
the Duars enquiry, amendments that would see planters’ power of ‘private
arrest’ abolished.33 Final abolition of the Indentured Labour Act would not
come for another twelve years, with the colonial government in 1920 facing
increasing international opprobrium after India joined the newly instituted
International Labour Organization.34 Indentured labour contracts were
phased out over the following five years, although penal convictions contin-
ued to be registered under the old Act for some years.35 Abolition in 1920
nonetheless marked the beginning of rudimentary public oversight over con-
ditions of work on the tea estates. A 1922 Enquiry Committee for the first
time sought to investigate levels of food consumption and individual and
family budgets of tea plantation labour on some estates.36

Malaria as a ‘Social Disease’: the League of

Nations Malaria Commission
Alongside its industrial-scale military slaughter, the 1914–1918 war would
offer an equally stark demonstration of the relationship between hunger and
epidemic disease. By the end of the war, mass destitution in Russia and east-
ern Europe had spawned widespread and highly lethal typhus and malaria
epidemics, a mortality toll that helped spur the creation in 1922 of a Health
Organisation within the newly formed League of Nations. Its initial man-
date was global epidemiological surveillance, and here the recently created
Rockefeller Foundation responded immediately as a major financial contrib-
utor.37 Interest soon expanded however to the investigation of broader socio-
economic conditions underlying epidemic mortality patterns. With respect
to malaria, S.P. James, an earlier research colleague of Christophers in the
Indian Medical Service, recounted that at this point ‘[f]aith in the efficacy of
every prophylactic and therapeutic measure had fallen almost to zero.’

Everyone who had actually taken part in efforts to deal with malaria
in different parts of the world during the War came home with the

24
 THE ‘HUMAN FACTOR’ TRANSFORMED

uncomfortable feeling that we know much less about the disease

than we thought we did. . . . Malaria was everywhere prevalent
and severe . . . [raising] the old question whether malaria among
poor illiterate people should be dealt with as an isolated problem
separate from the general medical and public health problems of
the country concerned.38

Researchers in Europe were arriving at similar economic conclusions to

those of Bentley in Bengal a continent away, concluding that agricultural
development and prosperity were a pre-condition for solving the malaria
problem.
By 1924, a specially dedicated Malaria Commission (LNMC) had been
established within the League of Nations Health Organisation. Within its
first year it had embarked upon a series of study tours undertaken in the still
malarious regions of eastern and southern Europe and the southern United
States, to observe and collate the varying experience of control efforts. One
of the first countries included was Italy where intensive malaria control
work had been going on since the turn of the century under the energetic
guidance of Angelo Celli. Although Italian scientists had been at the fore-
front of efforts to unravel the microbiological and entomological intricacies
underlying malaria transmission, anti-malaria policies had not been directed
primarily to vector control but rather to ensuring access to treatment (qui-
nine) and promoting agricultural improvement. The approach, referred to
as ‘bonificazione,’39 involved land reclamation that made possible intensive
agricultural production on previously waste or abandoned land, with per-
manent settlement of the labourers who were guaranteed a portion of the
produce.
Such efforts, Celli explained in a 1912 address, were not limited to drain-
age. ‘We are now directing our attention to new laws to make those lands
remunerative . . . [by providing] loans to labourers in addition to land-
owners, inexpensive credit with interest redirected back into farms.’40 The
goal, the Malaria Commission would later observe, was one of changing ‘a
swampy region with a poor, scattered, often semi-nomadic population into
a settled well-to-do one. . . . Now that villages have been formed, the poor
law can come into action; sick-clubs are formed to bring medical assistance
to those unable to pay for it.’41 Malaria deaths in the country over this
initial period of Celli’s efforts had declined dramatically, from an estimated
16,000 per year, a rate of 0.49 per 1,000 in 1900, to 2,045 in 1914 (0.057
per 1,000).42
In its 1924 overview of anti-malarial measures in Europe, the Malaria
Commission pointed out that land reclamation efforts in malarious tracts
of Europe likewise often had had little impact on rates of malaria trans-
mission.43 Improved economic conditions however, N.H. Swellengrebel
concluded in an appended report on malaria in Italy, meant ‘the disease,

25
 THE ‘HUMAN FACTOR’ TRANSFORMED

although still present, had lost much of its terrors.’44 Land reclamation in
Italy, he stressed,

has been closely connected with anti-malarial measures [n]ot

because these ‘bonifications’ were supposed to have any immediate
beneficial effect in reducing the incidence of malaria, even when
complete, but because they were rightly supposed to enrich the pop-
ulation, the enhanced well-being reflecting favourably on the resist-
ance of the population against various diseases and against malaria
in particular. The argument in favour of encouraging ‘bonifications’
was an economic one: to gain sanitary ends by economic means.45

Coming from a researcher highly regarded for his work on ‘species sanita-
tion’ (the targeting of anti-mosquito operations specifically to those anophe-
line species responsible for transmission in a region), Swellengrebel could
hardly be accused of being biased against mosquito control.46
Three years later, in a report on ‘Antimalarial Measures in Europe,’ the
Malaria Commission acknowledged that despite many experimental pro-
grams in Malaria Commission member countries directed at vector ‘sanita-
tion,’ there were in fact few examples of successful rural control of malaria
transmission.47 It concluded that the painstaking and costly work of anti-
mosquito measures as a general approach to malaria control was unafford-
able even in Europe; their costs, moreover, put at risk adequate funding of
agricultural improvements.48 Though not ruling out the importance of local
anti-larval measures where financially and technically feasible, the Commis-
sion urged that the benefits of such programs had to be assessed in relation
to their financial costs, and not undertaken at the expense of economic and
therapeutic measures. ‘Since the advent of the new knowledge of the trans-
mission of malaria by mosquitoes,’ it warned, ‘there has been a tendency to
forget that there are many methods of dealing with the disease.’49 As Bentley
had done two decades earlier in Bengal, the Commission urged that ‘a sharp
distinction should be made between reduction of mortality and morbidity,
two results of antimalarial activity which need by no means run a parallel
course.’50

The Malaria Commission’s study tour in India

It would be to India that the Commission turned in 1929 for extensive
experience of ‘malaria among poor illiterate people . . . in the tropics.’51
The four-month India tour led by W.A.C. Schüffner, Director of the Section
of Tropical Hygiene of the Royal Colonial Institute, Amsterdam,52 stud-
ied malaria conditions and control efforts in three major malarial regions
of the subcontinent: Bengal, Punjab, and the hyperendemic hill tracts in
the Himalayan foothills and the Deccan peninsula. For all three regions

26
 THE ‘HUMAN FACTOR’ TRANSFORMED

the study group ultimately came to concur with local malaria researchers
regarding the centrality of underlying economic conditions in determining
the illness and mortality burden of the disease. Several Commission mem-
bers had expressed initial scepticism over Bentley’s interpretation of the
malaria problem in the ‘dying river’ tracts of lower Bengal, in the 1860s
and 1870s referred to as ‘Burdwan fever,’ views which ‘were so contrary to
all our own experiences.’53 However by the close of the eight-day tour of
Bengal, Schüffner had come to agree with Bentley: what was needed in Ben-
gal was more irrigation, not less. Re-establishing inundation irrigation and
agricultural prosperity, it concluded, was the key to the malaria problem in
the ‘unhealthy’ dying-rivers districts of Bengal.

No special anti-larval measures are needed: merely the re-

establishment of the old system of irrigation by dredging the canals
and improving embankments, roads, railways and bridges, so that
they no longer obstruct the free flow of water. It is an economic and
agricultural measure, which will not prevent anopheles breeding,
but which will render them harmless.54

The Malaria Commission’s report went further, pointing to broader politi-

cal conditions of land tenure in Bengal under colonial rule as instrumental
in undermining agricultural productivity. At the time of the 1793 Permanent
Settlement Act,55 it noted, special local taxes used to maintain the canals for
irrigation had been abolished, thus depriving the traditional irrigation sys-
tem of its financial base. In a scarcely disguised reference to the zamindari
system of absentee landlords established under East India Company rule,
the Commission pointed out, the Permanent Settlement compounded the
problem by ‘prevent[ing] the deterioration of the soil being noticed, except
by the actual tiller of the soil.’56 The malaria problems in Bengal bore obvi-
ous parallels to conditions of intense malaria in the Italian latifundia and
demonstrated equally the limitations of anti-larval work in isolation from
such larger determinants.
With respect to Punjab, the Malaria Commission concurred with Christo-
phers’s conclusions as to the key role of economic conditions underlying the
phenomenon of fulminant epidemics in the province:

Excessive rainfall, causing adverse economic conditions by flood-

ing and water-logging, especially if these conditions were already
bad owing to a number of dry years, predicts the advent of an
epidemic outbreak of malaria. . . . The duty of the public health
officer is . . . what Colonel Gill is doing. . . ‘[taking] measures to
assure prompt treatment . . . and to improve, by supplying food,
clothing, housing and other means, the physical conditions of the
population.’57

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 THE ‘HUMAN FACTOR’ TRANSFORMED

In major industrial mining, rail and plantation enclave regions, efforts

directed to vector control had been employed with some success, the report
detailed. Criticism, however, was directed to urban vector control efforts,
where ‘much still remain[ed] to be done’ in Bombay and Delhi.58 In the
Bombay municipality, vector control was considered both technically pos-
sible and financially feasible, involving anti-larval measures of public and
private cisterns and wells, the chief sites of An. stephensi breeding.59 But the
municipal Malaria Department had been disbanded in 1918 and malaria
reappeared episodically in Bombay thereafter. Elsewhere, however, the
Study Tour report noted approvingly that malaria control activities had
been directed primarily to broader economic measures rather than vector
control, and to improved quinine access. Even in the Rohilkand Terai –
the poorly drained sub-Himalayan hill tract of the United Provinces where
highly anthropophilic malaria vectors and plantation in-migration made for
intensive transmission rates – the report concurred that ‘[c]onditions greatly
improve if the immigrant population is well-housed, well-fed, well-cared
for medically and sanitarily, even without any special anti-malarial precau-
tions.’60 These observations closely mirrored those from the earlier Malaria
Commission study tours in Europe.
Well into the 1930s, then, a role for human destitution in malaria epide-
miology and lethality was documented and taken seriously by public health
officials and malaria researchers within India and internationally, a view
that informed malaria control policy at a number of levels. Where then did
this understanding go?

Hunger eclipsed
Within South Asian malaria literature, it is difficult to identify a discrete
moment or debate where the role of human destitution in the mortality bur-
den of malaria was questioned. Instead, a role for hunger in malaria lethality
seems simply to have been set aside. A range of factors contributed. Among
them was the decline after 1908 in the fulminant form of malaria itself, cer-
tainly in Punjab, with the control of famine. In the wake of the two ‘great’
famines at the turn of the twentieth century, famine relief policy was trans-
formed over the ensuing two decades from palliative relief of ‘established’
famine to early, pre-emptive support of the agricultural economy before frank
famine ‘had declared itself.’ This support included, but was not limited to,
agriculture taxation (land revenue) relief. In Punjab, relief measures after 1920
also began to be sanctioned for crop losses due to flooding; and ultimately, on
the basis of ‘scarcity’ (foodgrain prices more than 40 per cent above normal
levels) alone, without famine ever being declared.61 Moreover, drought relief
after 1908 increasingly became a policy of routine application in response to
local harvest shortfall, in contrast to the 1880 policy which restricted relief
to years of widespread, severe harvest failure. These changes held major

28
 THE ‘HUMAN FACTOR’ TRANSFORMED

implications for human survival across periods of acute harvest failure. And
as overt famine increasingly was brought under control after 1908, so too
were the most dramatic examples of the link between starvation and epidemic
malaria mortality. Thus with each new cohort of younger malaria researchers,
fewer among them had direct experience of the phenomenon of fulminant
malaria.
Meanwhile, public health administrators in the post-famine era would
find it increasingly difficult to incorporate economic conditions into practi-
cal ways of measuring such stress. Gill’s efforts, for example, to take price
data into account in his annual predictions of expected autumn epidemic
severity were frustrated by the fact that price swings after the first decade
of the twentieth century were determined less by local harvest conditions
and more by international events: two world wars and the global Depres-
sion. Without a statistical vehicle for measuring local economic conditions,
malaria research by default shifted to measures that could be readily meas-
ured: human spleen and parasite rates, and infected mosquitoes, viz., meas-
ures of malaria transmission (infection).
Even so, malaria would reappear in fulminant form in 1934–1935 in
South Asia in concert with famine in neighbouring Ceylon (Sri Lanka), and
again a decade later both in Bengal and in 1942 Punjab,62 each a stark
reminder of the powerful relationship between epidemic starvation and epi-
demic malaria mortality. Clearly then, there were factors other than lack of
examples of ‘fulminant’ malaria conditions at play in the fading visibility of
the ‘Human Factor’ in academic epidemic analysis.
Among them, microbiologic advances in the emerging medical subdisci-
plines of medical entomology and immunology in the early decades of the
twentieth century were accentuating a narrow focus on disease transmis-
sion, offering competing hypotheses of epidemic patterns. Already, there
was intense interest within the Indian Medical Service in immunological
approaches to the control of infective diseases with the development of vac-
cines against cholera, plague, and typhoid fever, as well as rabies antivenin,
many produced locally in the early twentieth century at Pasteur institutes
in India.63 Developments in the field of immunology held particular sway
in malaria analysis with what came to be referred to as the ‘theory of non-
immunes.’ The significance of acquired immunity had long been apparent
to imperial administrations in relation to holoendemic malaria conditions
in West Africa, a region where differences in susceptibility to clinical illness
between newcomers to an endemic area and the indigenous population were
marked.64 Differences in malaria susceptibility were apparent also in rela-
tion to the hyperendemic hill tracts of South Asia, and assumed by the early
twentieth century to be related to acquired immunity. Such interest in the
protective effect of malaria-specific immunity soon took more systematic
form, spurred in part by observations on spleen rate patterns in Punjab in
the wake of the 1908 epidemic.

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 THE ‘HUMAN FACTOR’ TRANSFORMED

Punjab and the theory of non-immunes

In 1914, immunological interpretation of malaria epidemicity received a
fillip in the writing of E.L. Perry, an IMS officer then on special duty investi-
gating malaria in the hyperendemic Jeypore hills of the Madras Presidency.
In July of that year, Perry read a paper before the Punjab Branch of the
British Medical Association in which he reported ‘startling’ observations
on spleen rates in the Gujrat district of Punjab province in the years follow-
ing the 1908 epidemic.65 The spleen rate, a measure of spleen enlargement
prevalence in a population, was considered a general indicator of malaria
transmission in a population.66 Surveys he had conducted in Khatala village
showed continuing high child spleen rates of 75 per cent in 1909 and 1910.
By 1912 however the rate had fallen to 21 per cent.67 Perry was struck by
the ‘enormous degree of fluctuation’ in spleen rate, contrasting this with
conditions in the Jeypore hills, a hyperendemic region where spleen rates
were high but not subject to major variation year to year, nor apparently
to severe epidemics.68 He went on in his paper to infer a causal relationship
between fluctuating levels of acquired immunity (as reflected by spleen rate
levels) in Punjab and the region’s vulnerability to ‘fulminant’ malaria.
To medical scientists already intrigued by ongoing developments in the
emerging field of immunology, the 1914 Perry paper appeared to offer the
compelling prospect of being able to predict epidemic patterns.69 That same
year provincial public health authorities instituted province-wide biannual
spleen surveys of young school children, a program recommended by Perry
and initiated under C.A. Gill as special malaria officer in the province. In an
article published in the Indian Journal of Medical Research earlier that year,
Gill himself had proposed that ‘when a period of low immunity is associated
with a sudden great increase in the amount of infection, the unprotected
population will suffer from a severe epidemic.’70
In subsequent years Gill pursued the waning-immunity hypothesis further,
attempting to test the thesis in Punjab by employing Christophers’s rain-price
epidemic model to analyze malaria mortality patterns in the city of Amritsar for
the period 1870–1913.71 Gill’s choice of Amritsar city as test locality is puzzling.
In a major urban setting, grain prices would be expected to reflect less closely
economic stress than for the rural areas where both employment livelihood and
foodgrain price levels were directly determined by harvest conditions. But it
was curious also because only two of the city’s four major epidemic years over
the 43-year period had been preceded by drought and thus held the possibility
of testing decline in acquired immunity as a factor in epidemic etiology.72 Nev-
ertheless, employing similar quantitative measures as in Christophers’s 1911
study, he calculated a correlation coefficient of 0.57 between fever mortality,
rainfall, and foodgrain prices. Viewing his statistical results as ‘still incomplete,’
he went on to postulate – with no empirical data on spleen rate levels avail-
able – the ‘missing’ variable to be acquired immunity.73

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 THE ‘HUMAN FACTOR’ TRANSFORMED

Gill’s hypothesis was questionable in many respects, making application

of the waning-immunity thesis of malaria epidemicity to Punjab province
manifestly premature. But Perry’s observations had also been premature,
limited to only three years’ observations in a single village area.74 Rainfall
levels in Gujrat district in 1911 had been in marked deficit, and in 1912
were also below normal, conditions that likely contributed to the marked
fall in spleen rate in the study village.75 Yet fulminant malaria did not fol-
low in 1913 with the return of good rains,76 the autumn fever death rate
recorded as 5.3 deaths per 1,000 for the district compared to 27.0 per 1,000
in 1908. In other words, there was little empirical evidence that supported
Perry’s hypothesis of a link between fluctuating acquired immunity levels
and fulminant malaria mortality.
To be clear, in pursuing a role for acquired immunity in malaria epidemicity in
the province, neither Gill nor Perry was rejecting Christophers’s economic 1911
conclusions: both emphasized ‘scarcity’ and ‘disastrous floods’ as ‘predisposing’
factors in the 1908 epidemic. Nevertheless, the Perry paper would come to be
cited in subsequent malaria literature in support of the waning-immunity thesis
of Punjab malaria epidemicity.77 It would take three more decades before district
spleen rate data were analyzed by Punjab public health officials. M. Yacob and
S. Swaroop would find no significant correlation between June spleen rates and
subsequent autumn malaria mortality for the period 1914–1943, analysis that
suggested little empirical support for the thesis.78 Well before, however, malaria
researchers in the province had begun to modify the non-immune thesis, based
in part on the results of a study by Christophers of hyperendemic malaria con-
ditions in the iron mine labour camps of Singhbhum district, southwest Bengal
(what is now western Bihar state).

Singhbhum
The Singhbhum study, conducted in 1923, was one of the first field studies in
India to provide extensive data on malaria infection rates over time among
an entire population.79 The study confirmed what Christophers earlier had
observed in Sierra Leone under conditions of extremely high malaria trans-
mission rates:80 that gametocyte levels, the sexual form of the malaria para-
site transmitted from infected humans to the anopheline vector during the
mosquito’s blood meal,81 were highest among very young children undergo-
ing initial ‘acute [malaria] infestation.’82 Through meticulous observations
on parasite rates and gametocyte counts, Christophers estimated that over
two-thirds of the gametocyte ‘load’ of the labour camp population occurred
among children under 2 years of age. Near-continuous re-infection through
much of the year (hyperendemicity) induced rapid development of acquired
immunity in all but the youngest children, a state termed ‘premunity’ where
clinical symptoms are negligible and parasite levels, including gametocytes,
are low despite high re-infection rates.

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 THE ‘HUMAN FACTOR’ TRANSFORMED

Christophers’s findings confirmed the key role of young, non-immune,

children in the chain of malaria transmission in hyperendemic populations.
Malaria workers began to ask to what extent fluctuations in numbers of
non-immune infants in Punjab province might account for epidemicity
there, a region where rainfall and malaria transmission was highly variable
from year to year. A single year of drought and negligible transmission, it
was suggested, could add an entire additional year’s cohort of newborns to
the non-immune child population.83

The Karnal Research Station, 1929–1936

Through the late 1920s and 1930s intensive epidemiological studies were
conducted in six villages in the southeastern district of Karnal to explore
‘the mechanism of the production of epidemics of malaria in the Punjab.’
In 1931, a 28-year-old George Macdonald and colleague, J. Abdul Majid,
published the results of two years’ observations that included extensive
entomological data on vectors, breeding sites, seasonal profile of vivax and
falciparum parasite rates, and spleen rates, data that would contribute to
subsequent theoretical modelling of malaria transmission.84 Unfortunately
for the investigative purposes of the study, the two consecutive study years
(1929–1930) were marked by below normal rainfall, which meant there
was little opportunity to observe malaria under epidemic conditions.
Despite the deficit in precipitation however, little decline was observed in
spleen rate levels. Those villages subject to more severe epidemic malaria
conditions in the recent past continued to show higher rates of transmis-
sion, even when rainfall was low.85 Further, they observed, villages worst
affected in recent severe epidemics were those most vulnerable to higher
fever mortality during the study years. Evidently the persistence of higher
endemic levels of malaria transmission in the study villages overrode any
protective effect of acquired immunity in the population derived from previ-
ous epidemic conditions. These observations were generally consistent with
what Christophers had recorded two decades earlier for the province more
broadly. The northern submontane districts with generally higher endemic
levels of transmission, he showed, were at least as prone to fulminant epi-
demics as the north-central and southeast districts.86
Macdonald offered the hypothesis that in regions of what he termed ‘unsta-
ble’ malaria such as Punjab, where active transmission was highly variable year
to year, epidemicity did not depend primarily upon waning levels of acquired
immunity levels among the general population,87 but instead upon fluctuations
in numbers of non-immune infants born since the previous severe epidemic,
among whom gametocytes rates could be expected to be much higher.

[T]he fact that we are able to demonstrate marked signs of immu-

nity in the older children in Karnal, even after four successive years

32
 THE ‘HUMAN FACTOR’ TRANSFORMED

of deficient rainfall, makes us believe that the effect of a series of

years of low rainfall is not so much to lessen the immunity of the
general population as to allow of the growth of an infant popula-
tion, the larger part of which has never been infected with malaria
and is consequently non-immune.88

In closing remarks, however, he went further to suggest that ‘[i]f the period
of transmission is sufficiently long, and there is a suitable non-immune
infant population, this will culminate in a fulminant epidemic at the end of
the malaria season.’89 The assumption here, if not articulated precisely, was
that episodic low-transmission years and corresponding rise in non-immune
young children underlay a population’s vulnerability to epidemic malaria
conditions.
Yet the study period did not encompass an epidemic in the sense of ‘ful-
minancy’ as addressed in Christophers’s 1911 study. With monsoon rainfall
for the two study years (1929–1930) well below average levels, there had
been little opportunity to actually test the non-immune hypothesis of epi-
demicity. Nor had the study investigated mortality rates. It appears, then,
that the investigators’s closing statement linking non-immune infants and
fulminant malaria was offered rather as a tentative hypothesis, in anticipa-
tion of ongoing research.
Research did continue at the Karnal research station for another five
years. Conducted now by E.P. Hicks and J. Abdul Majid, these later efforts
included tracking gametocyte and spleen rates by year of age among village
children in relation to rainfall, conditions of atmospheric humidity, and in
addition, accompanying malaria mortality rates through the pre-monsoon
and malarial seasons. Unlike in the hyperendemic regions of Singhbhum,
however, infectivity of children at Karnal (in terms of numbers of game-
tocytes) was found to decline much later in childhood than observed at
Singhbhum, children above the age of five years showing high levels of
gametocytes.90 This much wider age group of heavy gametocyte carriers
appeared to suggest that adding one year’s cohort of non-immune infants
(induced by a preceding year of drought and low transmission) was unlikely
to be a factor in explaining epidemicity.
The single factor that was observed to influence malaria transmission rates
year to year was continuity of monsoon rainfall. Fluctuations in levels of
malaria infection between 1932 and 1935 were found to be ‘almost entirely’
due to variation in amount of rainfall and its even distribution across the
monsoon period. Adequate atmospheric humidity, where levels were con-
tinuously above 60 per cent, was key to vector longevity, Hicks and Majid
concluded.91 It ensured that those adult anopheline mosquitoes, infected at
the beginning of the transmission season from the few gametocyte carriers
left in the population from the previous year, survived long enough to trans-
mit infection in each subsequent 30-day round of vector-host transmission.

33
 THE ‘HUMAN FACTOR’ TRANSFORMED

In 1933 and 1935, both years of above average rainfall, July–September

atmospheric humidity never fell below 60 per cent and falciparum parasite
rates were observed to increase from very low (6 to 7 per cent) to levels
above 40 per cent, a level considered to indicate near-universal infection
prevalence in the population.92 Hicks and Majid concluded that

fluctuations in the malaria of the Karnal district are almost entirely

due to fluctuations in the dose of infection, and that the dose of
infection is determined chiefly by the length of the period of low
saturation deficiency [viz. high atmospheric humidity]. The latter
depends rather on an even distribution of rainfall than on the total
amount of rain.93

The observed importance of continuous adequate humidity helped, in turn,

to explain the epidemic-facilitating impact of flooding.
Here, the investigators’ use of the term ‘dose’ of infection was as a meas-
ure of malaria transmission in a population: the percentage of gametocyte
carriers among children under 10 years multiplied by the mean number of
An. culicifacies identified in sample sites for each month of July, August,
September. This was a different meaning to the term than that explored
by Christophers in his earlier sparrow experiments, where ‘dose’ was con-
sidered the number of sporozoites injected by an infected mosquito with
each blood meal.94 But Hicks and Majid were employing a different mean-
ing to the term ‘epidemic’ as well, one based on levels of infection in the
village community, rather than malaria mortality as had framed Christo-
phers’s 1911 study. Though a central purpose to the study as set out in the
1937 paper’s introduction was ostensibly one of investigating the ‘severe
epidemic[s]’ of Punjab95 – severity measured by malaria mortality – most of
the analysis presented was directed instead to levels of malaria transmission.
Did geometric increase in malaria infection rates (incidence) in itself
explain fulminancy, viz., soaring malaria death rates? The Hicks and
Majid study did record autumn child mortality (< 10 yrs of age) across the
1929–1935 study period, converting autumn fever deaths into ‘epidemic
figures,’ as employed by Christophers in 1911.96 Here, autumn death rates
(Sept.–Dec.) were found to correspond to levels of malaria transmission: the
years 1933 and 1935 showing the highest Epidemic Figures, 2.21 and 1.99,
respectively. Yet these levels of mortality were hardly representative of the
epidemics of the pre-1909 period. By comparison, the 1908 epidemic had
seen entire thanas (100 or more villages) with Epidemic Figures of 11, some
as high as 30: autumn mortality reaching 30 times that of non-epidemic
years.97 By contrast, the highest mortality recorded in the study villages in
1933 and 1935 were at a level Christophers had considered to be the ‘nor-
mal’ endemic autumnal increase in the province – an Epidemic Figure of 1.0
indicating no autumn rise in fever deaths above the April–July rate. In other

34
 THE ‘HUMAN FACTOR’ TRANSFORMED

words, favourable atmospheric humidity conditions could explain year-to-

year fluctuation in malaria transmission, but not the soaring mortality wit-
nessed in ‘fulminant’ epidemics such as that in 1908.
One final comment on the Karnal Research Station results relates to a
‘missing’ epidemic. Though not remarked upon in either of the major scien-
tific papers coming out of the 1929–1935 Karnal research period, the two
initial study years (1929–1930), as years of drought, presented the investi-
gators in effect with a non-immune ‘scenario.’ Third-quarter rainfall was
nine inches in 1929 compared to a mean for the district of 20 inches, with
‘extremely few cases of “fever’’’ that year. The year 1930 was also one of
relative drought, with monsoon rainfall at 13.8 inches. Presumably these
conditions produced several years’ cohorts of lesser- or non-exposed (non-
immune) infants. Yet malaria conditions did not take on epidemic propor-
tions with the return of good rains in 1931 (at 23.6 inches, slightly above
normal level). The recorded Epidemic Figure in the study villages was 1.34,
again a tiny fraction of that recorded in epidemic tracts in 1908.98
In sum, extremely valuable observations had come out of these years
of field research at the Karnal Research Station between 1929 and 1935.
But the work offered little support for the thesis that an expanded cohort
of never-exposed infants was a key factor underlying variation in malaria
transmission year to year, let alone an explanation of fulminancy (greatly
heightened malaria lethality). Efforts to explain malaria epidemicity in terms
of waning acquired immunity appeared to be at an impasse.

Acquired immunity and immune

capacity conflated
In the meantime, another development relating to the non-immune the-
sis of malaria epidemicity had emerged. In his 1928 Genesis of Epidemics
text – an ambitious overview of existing epidemiological understanding of
major epidemic diseases including malaria – Gill would propose the term
‘communal immunity’ to encompass both spleen rate and economic con-
ditions together as an index of a population’s vulnerability, or resistance,
to epidemic malaria.99 Though offered perhaps as a shorthand in annual
epidemic forecasting discussion, the combining of the two phenomena argu-
ably helped set the stage for the conflation of the two concepts of immune
capacity and acquired immunity.100
The distinction between the two concepts was of course a central one.
The former reflected immunological potential, the human host’s physiologi-
cal ability to mount an adequate immunological response to future infec-
tion. Acquired immunity, on the other hand, referred to specific antibodies
already present, stimulated by previous infection. The contrast was current
immune-competence versus past exposure, the former encompassing Chris-
tophers’s ‘Human Factor’ and representing the host side of the epidemic

35
 THE ‘HUMAN FACTOR’ TRANSFORMED

equation; the latter, a function of prevailing levels of malaria transmission,

the germ side of the epidemic equation. Though fundamentally different, in
the heady enthusiasm for immunological developments of this period, it was
a distinction that would inadvertently come to be blurred with Gill’s term,
‘communal immunity.’
Despite the unpromising findings of the Karnal research regarding the
influence of ‘non-immunity’ in malaria epidemicity, medical interest in
immunological factors as contributing to epidemic malaria behaviour con-
tinued, with the concept of ‘communal immunity’ framing academic malaria
discussion through the 1930s. The phrase increasingly would be employed,
however, not in Gill’s original sense of combined immune capacity and
acquired immunity, but to the effective exclusion of the former, and with
it conditions of the human host.101 In the meantime, too, the meaning of
‘epidemic,’ itself, was also becoming blurred, as malaria infection (transmis-
sion) was increasingly conflated with malaria mortality.
It was in the final years of the Karnal field research work that genuinely
‘fulminant’ malaria conditions re-appeared in South Asia – not in Punjab,
but in an opposite corner of the region, also under British colonial rule.
The Ceylon epidemic of 1934–1935 would be one of the last highly lethal
regional malaria epidemics to occur in South Asia (save for the war-time
epidemics of 1942 and 1943). Because of its timing in the 1930s, it attracted
exceptional attention from the now-burgeoning community of Western
malariologists, and in its wake, numerous academic articles appeared offer-
ing unofficial commentary and analysis. These accounts largely interpreted
the epidemic in entomological and related immunological terms, a view
that has predominated through to the post-colonial period.102 In effect, the
1934–1935 Ceylon epidemic marked the final stage in the demise of the
‘Human Factor’ as a central concept in understanding malaria lethality his-
torically as articulated in Christophers’s 1911 Punjab study – an epidemic
to which we now turn.

Notes
1 S.R. Christophers, ‘Malaria in the Punjab,’ Scientific Memoirs by Officers of the
Medical and Sanitary Departments of the Government of India (New Series),
No. 46 (Calcutta: Superintendent Govt Printing, 1911).
2 W.E. Jennings, ed., Transactions of the Bombay Medical Congress, 1909 (Bom-
bay: Bennett, Coleman & Co., 1910) [hereafter, Trans. Bombay Congress].
3 S.R. Christophers, and C.A. Bentley, ‘The Human Factor: An Extension of our
Knowledge regarding the Epidemiology of Malarial Disease,’ in Jennings, ed.,
Trans. Bombay Congress, 78–83; S.R. Christophers, and C.A. Bentley, Malaria
in the Duars. Being the Second Report to the Advisory Committee Appointed
by the Government of India to Conduct an Enquiry Regarding Blackwater
and Other Fevers Prevalent in the Duars (Simla: Government Monotype Press,
1909).

36
 THE ‘HUMAN FACTOR’ TRANSFORMED

4 GOI, Proceedings of the Imperial Malaria Conference held at Simla in Octo-

ber 1909 (Simla: Government Central Branch Press, 1910) [hereafter, Simla
Conf.].
5 Christophers, ‘Malaria in the Punjab,’ 127, 133.
6 S.P. James, ‘Malaria in Mian Mir,’ in Jennings, ed., Trans. Bombay Congress,
84–93.
7 Christophers and Bentley, ‘The Human Factor.’
8 S.R. Christophers, and C.A. Bentley, ‘Black-water Fever: Being the First Report
to the Advisory Committee Appointed by the Government of India to Conduct
an Enquiry Regarding Black-Water and Other Fevers Prevalent in the Duars,’
Sci. Mem. Med. Sanit. Dep., no. 35, 1908.
9 Christophers and Bentley, ‘Malaria in the Duars, 5.
10 Christophers and Bentley, ‘The Human Factor,’ 83; Christophers and Bentley,
Malaria in the Duars, 5.
11 S.R. Christophers, ‘On Malaria in the Punjab,’ Simla Conf., 29–47.
12 Ibid., 43.
13 S. Zurbrigg, Epidemic Malaria and Hunger in Colonial Punjab (London: Rout-
ledge, 2019), ch. 8.
14 Report on Malaria in the Punjab During the Year 1914 (Lahore: Punjab Medical
Dept), 2.
15 For details, see Zurbrigg, Epidemic Malaria and Hunger, ch. 9.
16 S.P. James, and S.R. Christophers, ‘Malaria. General Etiology,’ in W. Byam, and
R.G. Archibald, eds., The Practice of Medicine in the Tropics (London: Henry
Frowde and Hodder and Stoughton, 1922), vol. 2, 1509–1515, at 1514.
17 Editorial, ‘The Economic Factor in Tropical Disease,’ Indian Medical Gazette,
57, Sept. 1922, 341–343 [hereafter IMG].
18 Ibid.
19 Ibid. In an article entitled ‘Malnutrition and Malaria,’ the August 1921 issue
of The Modern Review (Calcutta) also highlighted Bentley’s Bengal findings,
suggesting that ‘the conditions which produce malarial fever are the self-same
conditions which produce poverty by causing agricultural deterioration’; 266.
20 H.W. Acton, ‘An Investigation into the Causation of Lathyrism in Man,’ IMG,
July 1922, 241–247.
21 Ibid., 247.
22 C.A Bentley, ‘Some Economic Aspects of Bengal Malaria,’ IMG, Sept. 1922,
321–326.
23 Editorial, ‘The Economic Factor,’ 343.
24 P. Hehir, Prophylaxis of Malaria in India (Allahabad: Pioneer Press, 1910),
33, 30.
25 Ibid., 31, 33.
26 P. Hehir, Malaria in India (Bombay: Humphrey Milford, 1927), 434–435. See
also C.A. Gill, The Genesis of Epidemics (London: Bailliere, Tindall and Cox,
1928), 208–210.
27 Editorial, ‘The Economic Factor,’ 343 [emphasis added].
28 C.A. Bentley, ‘A New Conception Regarding Malaria,’ Proceedings, 3rd Meeting
of the General Malaria Committee, Nov. 18–20, 1912, held at Madras (Simla:
Govt. Monotype Press, 1913), 61–84, at 62 [emphasis in the original].
29 Ibid., 61.
30 J. Niven, ‘Poverty and Disease,’ Presidential Address, Epidemiology Section, Oct.
22, 1909, Proceedings of the Royal Society of Medicine, 3, 1910, 1–44, at 11.
31 P. Weindling, ‘Social Medicine at the League of Nations Health Organisation and
the International Labour Office compared,’ in P. Weindling, ed., International

37
 THE ‘HUMAN FACTOR’ TRANSFORMED

Health Organisations and Movements, 1918–1939 (New York: Cambridge Uni-

versity Press, 1995), 134–153, at 138.
32 R. Senior White, Studies in Malaria as It Affect Indian Railways, Indian Research
Fund Association, Technical Paper, 258 (Calcutta: Central Publications Branch,
1928), 7, 1.
33 R.P. Behal, and P. Mohapatra, ‘Tea and Money Versus Human Life: The Rise and
Fall of the Indenture System in the Assam Tea Plantations 1840–1908,’ Journal
of Peasant Studies, 19, 3/4, 1992, 142–172, at 167. Whether draft amendments
to the Labour Act were already in process during the course of the Duars enquiry
is unclear. It is perhaps safe to assume by the scope of the study that its conclu-
sions were scarcely in doubt from its earliest stages.
34 M. Anderson, ‘India, 1858–1930: The Illusion of Free Labour,’ in D. Hay, and
P. Craven, eds., Masters, Servants and Magistrates in Britain and the Empire,
1562–1955 (Chapel Hill/London: University of North Carolina Press, 2004),
433–454, at 448. In part this reflected a change in politics in the metropole,
where the momentum of the labour movement in the wake of the 1901 Taff Vale
decision heightened political and social attention to labour conditions; ibid., 447.
In India, growing labour militancy and more organised forms of labour resist-
ance emerged after 1920; R.P. Behal, ‘Power Structure, Discipline, and Labour in
Assam Tea Plantations under Colonial Rule,’ International Review of Social His-
tory, 51, 2006, Supplement, 143–172, at 168–169; P. Mohapatra, ‘Assam and
the West Indies, 1860–1920: Immobilizing Plantation Labour,’ in D. Hay and P.
Craven, Masters, Servants, 455–480, at 478. For treatment of post-war labour
reforms motivated by fears of Russian Bolshevism, see D. Chakrabarty, ‘Condi-
tions for Knowledge of Working-Class Conditions: Employers, Government and
the Jute Workers of Calcutta, 1890–1940,’ in R. Guha, ed. Subaltern Studies II,
Writings on South Asian History and Society (Delhi: Oxford University Press,
1983), 259–310, at 266.
35 ‘The penal legislation may have been abolished, but the huge unrelenting appa-
ratus of surveillance and detention, carefully crafted since 1860, remained,’ what
Mohapatra refers to as ‘the power behind the shadow’; ‘Assam and the West
Indies,’ 478–480.
36 Report of the Assam Labour Enquiry Committee, 1921–22, 35; cited in R.P.
Behal, Wage Structure and Labour: Assam valley tea plantations, 1900–1947
(New Delhi: V.V. Giri National Labour Institute, 2003).
37 Through the 1920s, the Foundation contributed over one-third of the finances of
the League of Nation’s Health Organisation; P. Weindling, ‘American Foundations
and the Internationalizing of Public Health,’ in S.G. Solomon, L. Murard, and P.
Zylberman, eds., Shifting Boundaries of Public Health: Europe in the Twentieth
Century (Rochester: University of Rochester Press, 2008), 63–85, at 75.
38 S.P. James, ‘Advances in Knowledge of Malaria Since the War,’ Transactions
of the Royal Society of Tropical Medicine and Hygiene, 31, 1937, 263–280, at
268–269.
39 A. Celli, ‘The Restriction of Malaria in Italy,’ in Transactions of the Fifteenth
International Congress on Hygiene and Demography, Washington, Septem-
ber 23–28, 1912 (Washington: Govt Publ. Off., 1913) 516–531, at 530. ‘Land
reclamations’ appear to have begun as early as 1901, possibly even before qui-
nine distribution increased in 1904; J.A. Nájera, ‘ “Malaria Control” Achieve-
ments, Problems and Strategies,’ Parassitologia, 43, 2001, 1–89, at 12.
40 Celli, ‘The Restriction of Malaria in Italy,’ 530.
41 League of Nations Malaria Commission, Principles and Methods of Antima-
larial Measures in Europe (Geneva: League of Nations, 1927), 87 [hereafter
LNMC].

38
 THE ‘HUMAN FACTOR’ TRANSFORMED

42 F.L. Snowdon, The Conquest of Malaria: Italy, 1900–1962 (New Haven: Yale
University Press, 2006), 89.
43 LNMC, Report on its Tour of Investigation in Certain European Countries in
1924 (Geneva: League of Nations, 1925), 59.
44 N.H. Swellengrebel, ‘Some Aspects of the Malaria Problem in Italy,’ in Investiga-
tion in Certain European Countries, Annex 11, 168–171, at 171.
45 Ibid., 168–169.
46 S. Litsios, The Tomorrow of Malaria (Wellington, NZ: Pacific Press, 1996), 63,
48–49. Similar conclusions would be reached by J.A. Sinton in Spain investigat-
ing intense malaria associated with extension of rice cultivation, under condi-
tions of aggregation of migrant labour; ‘Rice cultivation in Spain, with special
reference to the conditions in the delta of the River Ebro,’ Records of the Malaria
Survey of India, 3, 3, June 1933, 495–506 [hereafter, RMSI].
47 The report cited two exceptions, regions in which anti-larval measures had been
carried out on a considerable scale ‘with definitely successful results’: the first
was in the Karst Mountains of Dalmatia, ‘bare, dry, waterless hills’; and in Pal-
estine where the ‘mountains are dry, the valleys easy to drain . . . [and] rainfall is
negligible during the malaria season’; LNMC, Principles and Methods of Anti-
malarial Measures in Europe (Geneva: League of Nations, 1927), 81–82.
48 Ibid., 31, 89.
49 Ibid., 13.
50 Ibid., 86.
51 James, ‘Advances in Knowledge of Malaria Since the War,’ 264.
52 LNMC, Report of the Malaria Commission on its Study Tour of India (Geneva:
League of Nations, Aug. 1930), [hereafter, LNMC, India Report] Other study
tour members included M. Ciuca, secretary of the Malaria Commission, Prof.,
Faculty of Medicine in the University of Jassy, Roumania; N.H. Swellengrebel,
Chief of Laboratory of the Section of Tropical Hygiene of the Royal Colonial
Institute, Amsterdam; Louis Williams, Head of the Anti-Malaria Service, U.S.
Public Health Service; Dr S. de Buen, Professor of Parasitology, Institute of
Health Madrid; Major M. Peltier, Prof. of Social Hygiene, School of Sanitary
Service of Colonial Troops, Marseilles.
53 W. Schüffner, ‘Notes on the Indian Tour of the Malaria Commission of the
League of Nations,’ RMSI, 11, 3, Sept. 1931, 337–347, at 340.
54 LNMC, India Report, 43; Schüffner, ‘Notes on the Indian Tour,’ 340.
55 Under the Permanent Settlement, state demand was fixed at 89 per cent of the
rent, with 11 per cent retained by the Zamindars.
56 LNMC, India Report, 42–43. Recent analysis of Burdwan fever has taken varied
perspectives: cultural, literary, eco-entomological, science-decolonising, in addi-
tion to imperial critique. See, e.g., A. Samanta, Malaria Fever in Colonial Ben-
gal, 1820–1939: Social History of an Epidemic, (Kolkata: Firma KLM, 2002);
I. Kazi, Historical Study of Malaria in Bengal, 1860–1920 (Dhaka: Pip Inter-
national Publishers, 2004); R. Deb Roy, Malarial Subjects: Empire, Medicine
and Nonhumans in British India, 1820–1909 (Cambridge: Cambridge Univer-
sity Press, 2017); P.B. Mukharji, ‘Verncularizing Political Medicine: Locating
the Medical betwixt the Literal and the Literary in Two Texts on the Burdwan
Fever, Bengal c. 1870s,’ in R. Deb Roy, and G.N.A. Attewell, eds., Locating the
Medical: Explorations in South Asian History (New Delhi: Oxford University
Press, 2018), 235–263. In this work, rural immiseration consequent on interrup-
tion of irrigation flows is generally acknowledged, including within a ‘political
medicine’ and ‘psychic injuries’ critique (Mukharji). The profound implications
of abrupt cropping decline on human survival and attendant rending of social
relations has perhaps been less explored. For discussion of these immiserating

39
 THE ‘HUMAN FACTOR’ TRANSFORMED

consequences, see Zurbrigg, Epidemic Malaria and Hunger, 274–276, 229–230;

also, A. Biswas, ‘The Decay of Irrigation and Cropping in West Bengal, 1850–
1925,’ in B. Chattopadhyay, and P. Spitz, eds., Food Systems and Society in East-
ern India (Geneva: United Nations Research Institute for Social Development,
1987), 85–131; R. Mukherjee, Changing Face of Bengal: A Study in Riverine
Economy (Calcutta: University of Calcutta, 1938).
57 LNMC, India Report, 38–39.
58 Ibid., 60–61.
59 C.A. Bentley, Report of an Investigation into the Causes of Malaria in Bombay
(Bombay: Miscellaneous Official Publications, 1911).
60 LNMC, India Report, 45.
61 For details of these policy changes and discussion of their potential impact,
see Zurbrigg, Epidemic Malaria and Hunger, chs. 10–11; A. Maharatna, ‘The
Regional Variation in the Demographic Consequences of Famines in the Late
Nineteenth Century,’ Economic and Political Weekly, 29, 23, 1994, 1399–1410;
A. Maharatna, The Demography of Famines (Delhi: Oxford University Press,
1996).
62 For details, see Zurbrigg, Epidemic Malaria and Hunger, ch. 12. Also, ch. 2,
below.
63 P. Chakrabarti, Bacteriology in British India Laboratory Medicine and the Trop-
ics (New York: University of Rochester Press, 2012); M. Worboys, Spreading
Germs: Disease Theories and Medical Practice in Britain, 1865–1900 (Cam-
bridge: Cambridge University Press, 2000), 43. For an account of the intense
interest in immunology at the Tenth International Congress of Medicine at Ber-
lin in 1890, see P.M.H. Mazumdar, ‘Immunity in 1890,’ Journal of the History
of Medicine and Allied Sciences, 27, 3, 1972, 312–324.
64 P. Curtin, ‘Malaria Immunities in Nineteenth-Century West Africa and the Car-
ibbean,’ Parassitologia, 36, 1994, 69–92.
65 E.L. Perry, Recent Additions to Our Knowledge of Malaria in the Punjab.
A paper read before the Punjab Branch of the British Medical Association at
Simla, on July 17, 1914 (Simla: Thacker, Spink & Co, 1914), 11.
66 As the principal organ that breaks down malaria parasite–damaged red blood
cells, the spleen typically enlarges following malaria infection to be palpable
below the left rib cage: the ‘spleen rate’ is generally defined as the per cent of
children under the age of 10 years with an enlarged (palpable) spleen.
67 Ibid., 7. The paper provided a graph but no actual rates. Gill, in an earlier paper,
did provide numerical rates in a graph that also included data for December 1913;
C.A. Gill, ‘Epidemic or Fulminant Malaria Together with a Preliminary Study of
the Part Played by Immunity in Malaria,’ Indian Journal of Medical Research, 2,
2, 1, July 1914, 268–314, Chart II, 294 [hereafter, IJMR].
68 Perry, ‘Recent Additions,’ 12.
69 Randall Packard documents a similar tendency in this period for colonial officials
in Swaziland to interpret malaria epidemicity in entomological terms related to
rainfall patterns, despite limited empirical evidence; ‘Maize, Cattle and Mos-
quitoes: The Political Economy of Malaria Epidemic in Colonial Swaziland,’
Journal of African History, 25, 1984, 189–212, at 193–194.
70 Gill, ‘Epidemic or Fulminant Malaria,’ 297.
71 C.A. Gill, Report on Malaria in Amritsar, Together with a Study of Endemic and
Epidemic Malaria and an Account of the Measures Necessary to Their Control
(Lahore: Punjab Govt, 1917).
72 Between 1870 and 1913 the town experienced four severe epidemics. Of these,
two were preceded by drought, 1908 and 1881; Zurbrigg, Epidemic Malaria

40
 THE ‘HUMAN FACTOR’ TRANSFORMED

and Hunger, ch. 5. The 1876 and 1887 epidemics however were not, though
both were associated with marked economic stress: export-triggered soaring
foodgrain prices in 1887, and severe flood-related crop failure in 1875 preceding
the 1876 epidemic.
73 C.A. Gill, ‘The Relationship of Malaria and Rainfall, IJMR, 7, 3, 1920, 618–
632, at 628–629.
74 Perry, ‘Recent Additions,’ 7.
75 Provincial 1911 third-quarter rain was 6.8 inches compared to a mean of 13.9;
for Gujrat district, 8.3 versus 16.4 inches; 1909 and 1910 Gujrat district rain
was 21.9 and 19.1 inches, respectively.
76 Perry did not include actual spleen rate data in his July 1914 paper, simply a
chart; Perry, ‘Recent Additions,’ 7. Data appear however in an article published
by Gill earlier in the year; ‘Epidemic or Fulminant Malaria,’ 294.
77 Lewis Hackett, prominent malaria worker with the Rockefeller Foundation,
would cite Perry’s 1914 paper as support for the waning-immunity thesis, the
observed spleen rate decline showing that the study village was ‘then ready for
an epidemic’; Malaria in Europe: An Ecological Study (London: Oxford Univer-
sity Press, 1937), 228–229.
78 M. Yacob, and S. Swaroop, ‘Malaria and Spleen Rate in the Punjab,’ Indian
Journal of Malariology, 1, 4, Dec. 1947, 469–489, at 479. The routine spleen
surveys involved male school children under the age of 10 years, among whom
prevalence of splenic enlargement was considerably lower than rates recorded by
Perry. The discrepancy is likely attributable to the older age group of children,
cumulative acquired immunity resulting in gradual reduction in spleen size with
increasing age. As well, as Yacob and Swaroop pointed out, children attending
school were largely from ‘well-to-do’ classes, whereas spleen rates were notably
higher among the poor; ibid., 469.
79 S.R. Christophers, Enquiry on Malaria, Blackwater-fever and Ankylostomiasis
in Singhbhum. Report No. 1 (Govt Publ. Behar and Orissa, 1923), 363–407.
80 J.W.W. Stephens, and S.R. Christophers, ‘The Malaria Infection in Native Chil-
dren,’ in Reports of the Malaria Committee of the Royal Society, 3rd series
(London: Harrison and Sons, 1900).
81 For an overview of the microbiological life cycle of the malaria parasite, its dif-
ferent forms and species, and conditions of transmission in the Punjab plains, see
Appendix I.
82 S. Christophers, ‘The Mechanism of Immunity against Malaria in Communities
Living under Hyper-Endemic Conditions,’ IJMR, 12, 2, Oct. 1924, 273–294.
83 Growing interest in immunological explanations of epidemic behaviour across
this period was reflected in Gill’s 1928 text, The Genesis of Epidemics.
84 G. Macdonald, and J. Abdul Majid, ‘Report on an Intensive Malaria Survey in
the Karnal District, Punjab,’ RMSI, 2, 3, Sep. 1931, 423–477.
85 ‘This,’ the investigators surmised, ‘is presumably due to the greater number of
gametocyte carriers in the village providing a ready means of infection for the
reduced numbers of dangerous anophelines than in the neighbouring villages’;
ibid., 435.
86 Christophers, ‘Malaria in the Punjab,’ 71, 73, 131; Simla Conf., 38. On this, see
Zurbrigg, Epidemic Malaria and Hunger, ch. 2.
87 For an overview of the early twentieth-century emergence of the concept of ‘herd
immunity,’ see M. Worboys, ‘Before McKeown: Explaining the Decline in Tuber-
culosis in Britain, 1880–1930,’ in F. Condrau and M. Worboys, eds., Tuber-
culosis Then and Now: Perspectives on the History of an Infectious Disease
(Montreal: McGill-Queen's University Press, 2010), 148–170 at 159–160.

41
 THE ‘HUMAN FACTOR’ TRANSFORMED

88 Macdonald and Majid, ‘Report on an Intensive Malaria Survey,’ 466.

89 Ibid., 468.
90 ‘We have found little evidence of any change in the immunity of the population
in the period under review. If the size of the average enlarged spleen is accepted
as a valid measurement of immunity, it shows that if there has been any change,
it has been unimportant’; E.P. Hicks, and J. Abdul Majid, ‘A Study of the Epi-
demiology of Malaria in a Punjab District,’ RMSI, 7, 1, Mar. 1937, 1–43, at 33.
91 Rather than atmospheric humidity, the investigators used ‘saturation defi-
ciency,’ a measure that takes into account additional factors such as tempera-
ture affecting the rate of loss of water from insects; Hicks and Majid, ‘Malaria
in a Punjab district,’ 23. See also P.A. Buxton, ‘The Effect of Climatic Condi-
tions upon Population of Insects,’ Transactions of the Royal Society of Tropical
Medicine and Hygiene, 28, 4, 1933, 325–256.
92 Given the intermittent nature of malarial parasitemia, a parasite rate of 50 per
cent generally was considered to indicate near-universal infection in a popula-
tion; Hicks and Majid, ‘Malaria in a Punjab District,’ 40, Appendix 3, 31.
93 Ibid., 34.
94 Zurbrigg, Epidemic Malaria and Hunger, 78–82.
95 Ibid., 2, 29.
96 For the purposes of mapping comparative levels of epidemic intensity in 1908,
Christophers devised a ratio measure of autumn malaria mortality. For each
thana he calculated what he termed an ‘Epidemic Figure,’ derived by divid-
ing the number of deaths recorded in October by the average non-epidemic
monthly death rate. The latter was calculated as the previous five-year aver-
age of June and July deaths, ‘avoiding those years in which plague or cholera
disturbed the figures’; Christophers, ‘Malaria in the Punjab,’ 19. See also, Zur-
brigg, Epidemic Malaria and Hunger, 66. For discussion of the limitations of
the Epidemic Figure, see, ibid., 103.
97 Christophers, ‘Malaria in the Punjab,’ 21.
98 Hicks and Majid, ‘Malaria in a Punjab District,’ 7. The epidemic figure
employed by Hicks and Majid represents malaria deaths in children less than
10 years whereas Christophers’s 1908 figures included all age groups; however,
given that the measure is a ratio of non-malaria to malaria deaths, and the fact
that malaria mortality affected predominately young children, the two figures
can be considered roughly comparable.
99 Gill, Genesis of Epidemics, 191.
100 A 1924 report by the newly formed Malaria Commission of the LNHO
included an entire section on ‘The Human Factor,’ considered under three sep-
arate headings: ‘Immunity,’ meaning acquired immunity; ‘Increase of Popula-
tion’; and ‘Economic Changes’; N.H. Swellengrebel, Malaria in the Kingdom of
the Netherlands (Geneva: League of Nations, 1924), 15–17.
101 See, e.g., G. Harrison, Mosquitoes, Malaria and Man: A History of the Hostili-
ties since 1880 (New York: E.P. Dutton, 1978), 203.
102 Among many examples, see A.T.A. Learmonth, ‘Some Contrasts in the Regional
Geography of Malaria in India and Pakistan,’ Transactions and Papers (Insti-
tute of British Geographers), 23, 1957, 37–59, at 48.

42
 2
THE 1934–1935 CEYLON
EPIDEMIC AND ITS EPISTEMIC
AFTERMATH

The necessity for ensuring that the population of the affected

area has sufficient food is of primary importance as an anti-
malarial measure.
—– R. Briercliffe, The Ceylon Malaria Epidemic,
1934–35. Report by the Director of Medical and
Sanitary Service (Colombo: Ceylon Govt Press,
Sept. 1935), 73

Though important insights into malaria transmission had come out of the
field research conducted in Karnal district, this work had not succeeded in
explaining fulminant malaria in immunological terms. As the researchers
were completing the second phase of their epidemiological studies, a major
malaria epidemic, coincidentally, was unfolding on the neighbouring island
of Sri Lanka (colonial Ceylon), one that would soon come to be interpreted
as offering the entomo-immunological ‘test-case’ that Karnal had not. ‘The
great epidemic of 1934–35 was the result of the failure of the South-West
Monsoon of 1934,’ C.L. Dunn, a former provincial Director of Public Health
in India, concluded in a prominent 1936 monograph, conditions that ‘caused
a great extension in the favourite breeding grounds of the insect carrier (An.
culicifacies)’ in drying river beds, amongst ‘a “susceptible” population due
to four years of waning immunity.’1 That same year, researchers with the
Malaria Survey of India compared the 1934–1935 Ceylon epidemic to that in
1929 in the western province of Sind (now southern Pakistan) and concluded
in similar terms that ‘the origin of both these epidemics may be adequately
explained by the sudden production of conditions unusually favourable to
the propagation, longevity and activity of An. culicifacies in an area inhab-
ited by a population in whom the communal immunity is at a low level.’2
Interpretation of the 1934–1935 Ceylon epidemic has many other links
to the malaria research community in India, in the methodological tools and
concepts employed to analyze it and in the investigators directly involved.
C.A. Gill, recently retired from the Indian Medical Service and returning to

43
 THE 1934–1935 CEYLON EPIDEMIC

Britain from Burma, on hearing of the epidemic, chose to detour to Cey-

lon and volunteer his services for the official investigation already under-
way. His study, conducted in the final months of the epidemic, would be
published as a Ceylon Sessional Paper alongside the colonial government’s
report.3 S.R. Christophers, now based in London, would also figure in the
professional deliberations on the epidemic in a 1936 meeting of the Royal
Society of Tropical Medicine and Hygiene.4 In that role, he would offer
key, if characteristically epigrammatic, commentary on the significance of
prevailing economic conditions leading up to the epidemic, as he had done
a quarter-century earlier in relation to epidemic malaria in Punjab5 – and as
concluded in the official investigation by R. Briercliffe, Director of Medical
and Sanitary Services for Ceylon, some months before.6
Alongside enhanced malaria transmission, triggered in the case of Ceylon
by drought, failure of the 1934 southwest monsoon had brought record
crop failure to over half of the country’s major districts.7 Harvest failure
however was only the final phase of a period of severe economic hardship,
set against a backdrop of four years of plummeting tea and rubber exports
triggered by the global Depression. Thus amongst local health officials,
widespread destitution was seen as both triggering and fuelling a vicious
circle of starvation and disease. Indeed, throughout the epidemic, food and
employment provision had been accorded as much prominence as medical
treatment (quinine) in government relief efforts.
In subsequent Western malaria literature, however, an entomo-
immunological reading of the 1934–1935 epidemic would prevail, one
deemed to have become ‘classic in malariology’ among historians as resolv-
ing the larger ‘riddle’ of malaria epidemicity. ‘It now seems so obvious,’ Gor-
don Harrison, concluded in 1978, ‘how with a large number of man-biting
mosquitoes, a mighty epidemic could grow rapidly from so few carriers . . .
[and] spread rapidly among non-immunes.’8 In epistemic terms, the Sri Lan-
kan malaria epidemic of 1934–1935 can thus also be seen as marking the
final stage in the transformation of the ‘Human Factor’ from a concept of
‘physiological poverty’ (hunger) to one of microbe transmission. In a very
concrete sense, the two epidemics, that in Punjab in 1908 and in Sri Lanka
in 1934–1935, represent book-ends to an era of remarkable epidemiologi-
cal research on malaria mortality bounded on each side, before and after,
by a marked narrowing in epidemiological thought. These links to Punjab
malaria history, together with its paradigmatic significance in malaria his-
toriography, warrant consideration of the Ceylon epidemic in some detail.

Sri Lankan malaria endemiology

Malaria in Sri Lanka, as in Punjab and much of the plains of the Indian
subcontinent, is transmitted primarily by the mosquito vector, Anopheles

44
 THE 1934–1935 CEYLON EPIDEMIC

culicifacies. But despite a common vector, the specific conditions condu-

cive to transmission and epidemicity in Ceylon were generally viewed in
the late colonial malaria literature as the inverse of those in the Punjab
plains. Where excess rainfall and consequent flooding was the key trigger
of severe epidemics in northwest India, many contemporary entomologists
considered the prime trigger in Ceylon to be drought: the still, clear pools
of drying river beds or irrigation channels acting as major anopheline
breeding sites.9
This emphasis on river pools derived from well-recognized differences in
malaria prevalence rates across the island. In the dryer plains region of the
north and northeast, hyperendemic malaria generally prevailed, in contrast
to conditions in the hills and mountains of the central and southwest ‘wet’
zones where malaria prevalence rates were low or negligible. Marked dif-
ferences in regional rain catchment and topography accounted for this con-
trast, presenting two distinct ecological zones. The southwest quadrant of
the island receives the benefit of both the southwest (May to September) and
northeast (October to January) monsoons, with an annual rainfall ranging
between 100 to 200 inches, compared to 50 to 75 inches in the northern and
eastern regions where rainfall is limited principally to the later northeast
monsoon (Figure 2.1).10
In the hills and mountains of the southwest and central ‘wet zone,’ riv-
ers generally were full and fast flowing, the more regular rains tending to
wash clear potential riverine An. culicifacies breeding sites, and doing so
also in the western tracts downstream from the hills.11 Vector numbers and
malaria incidence were considered to vary from low to moderate. By con-
trast, in the plains of the northern dry zone, rainfall was highly seasonal and
malaria transmission was endemic, reflected in much higher spleen rates
(Figure 2.2).12
Regional contrasts in rainfall predicted large economic differences across
the island as well. Except for the coastal areas, agriculture in the northern
zone was precarious, with only a single, highly variable period of annual
rainfall, and limited irrigation infrastructure. Death rates often exceeded
birth rates and the sparse population was maintained only through immi-
gration.13 In the southwest region of the island with its generous rainfall,
agriculture was more secure, double-cropping common, and population
density high.
These two major ecological regions were separated by a narrow ‘inter-
mediate zone’ of malaria prevalence in the central and south-central hills
(Figure 2.1), the site of rubber, tea, and coconut plantations dating from
the later nineteenth century. By the early twentieth century the planta-
tion estates numbered over 1,400 and were worked primarily by Tamil
labourers recruited from southern India. Like the wet zone, the interme-
diate zone was densely populated, with the majority non-estate Sinhalese

45
 THE 1934–1935 CEYLON EPIDEMIC

Figure 2.1 Mean annual rainfall (inches), Ceylon

Source: T.W. Tyssul Jones, ‘Deforestation and epidemic malaria in the wet and intermediate
zones of Ceylon’, Indian Journal of Malariology, 5, 1, Mar. 1951, 135–161, Map 2, p. 140;
reproduced from K.J. Rustomjee, ‘Observations on the epidemiology of malaria in Ceylon,’
Sessional Paper XXIV, 1944, Ceylon Government Press.

population involved in rice cultivation and small-scale rubber and coco-

nut production. By virtue of its dual economy the intermediate region also
enjoyed relative economic insulation from the vagaries of the monsoon.
However, in years of poor rains, the upper reaches of the streams and
rivers tended to dry and form river-bed pools particularly conducive to

46
 THE 1934–1935 CEYLON EPIDEMIC

Figure 2.2 Spleen rate (per cent), Ceylon, 1922–1923

Source: R. Briercliffe, The Ceylon Malaria Epidemic, 1934–35 (Colombo: Ceylon Govt Press,
Sept. 1935). Supplement to the Sessional Paper XXII – 1935, Map 2.

mosquito breeding, a phenomenon likely enhanced by the deforestation

that accompanied establishment of the plantation economy.14 As in Pun-
jab, however, effective malaria transmission awaited rising atmospheric
humidity and increased mosquito lifespan with return of the October
monsoon rains.

47
 THE 1934–1935 CEYLON EPIDEMIC

Portrait of the 1934–1935 malaria epidemic

Record drought conditions on the island in 1934 were broken by heavy
rains beginning on October 6, followed by the sudden outbreak of malarial
fever amongst all age-groups on October 27.15 Dispensary attendance and
hospital admissions rose simultaneously across much of the island in the
early weeks of November, rising exponentially in the early weeks of Decem-
ber. Between November 1934 and April 1935 attendances at government
hospitals and dispensaries rose by an estimated 3 million above levels in pre-
epidemic years in a total population of 5.5 million.16 The earliest increase
occurred in the plantation-region districts of Kegalle, Kurunegala, and Rat-
napura, where mortality, in absolute numbers, ultimately was heaviest.17
The focal centre of the 1934–1935 epidemic involved Kurunegala dis-
trict straddling the intermediate and dry zones, and Kegalla and Kandy dis-
tricts in the wet and intermediate zones. By January 1935 the spleen rate
in Kurunegala district had risen to 71.9 per cent from a pre-epidemic aver-
age of 40–60 per cent, whereas the rate in the western coastal district of
Colombo rose only to 8.8 per cent.18 Entomological surveys conducted dur-
ing the course of the epidemic documented increased numbers of An. culici-
facies in the river basins of the intermediate zone where river and stream
water levels had been reduced to standing pools.19 The Briercliffe report
concluded that many of the severely affected villages bordered rivers, but
also noted that ‘the breeding places of An. culicifacies . . . were by no means
confined to pools in the river beds.’20
A total of 69,615 excess deaths were recorded for the island as a whole
between November 1934 and March 1935, the crude death rate increasing
from a preceding quinquennial mean of 23.1 to 36.6 in 1935.21 Of these
deaths, 54.6 per cent were recorded in children under 5 years of age.22
Deaths among children 5–10 years accounted for a further 7.9 per cent
of excess mortality. No systematic surveys of malaria species prevalence
were undertaken during the epidemic, but among severe cases admitted to
hospital, falciparum infection was as high as 43 per cent at the peak of the
epidemic in January 1935. Thus an increase in prevalence of falciparum
infection may have been a factor underlying epidemic intensity in the later
stages of the epidemic. However, the high prevalence of vivax infection,
a species not normally lethal, among severe cases also suggests that spe-
cies of parasite likely was not the main factor contributing to lethality of
infection.23
Of the total excess deaths, the large majority (59,144) were recorded in
the nine districts encompassing the watershed regions of the four major west-
draining rivers of the intermediate and wet zones.24 Assuming a key etiological
role for the drying river-beds of this region, Briercliffe designated this nine-
district watershed tract as ‘the epidemic area,’ indicated on his maps with
a black boundary line and there termed the ‘epidemic zone’ (Figure 2.3).25

48
 THE 1934–1935 CEYLON EPIDEMIC

Figure 2.3 Nov.–Apr. death rate per 1,000, Ceylon, 1934–1935

Source: R. Briercliffe, The Ceylon Malaria Epidemic, 1934–35 (Colombo: Ceylon Govt Press,
Sept. 1935). Supplement to the Sessional Paper XXII – 1935, Map 18.
Note: The four-river watershed ‘epidemic area /zone’ is designated by a solid black line.

In the worst affected divisions of Kegalla and Kurunegala districts, mor-

tality rates appear to have reached 5 per cent or more of the population.26
Encompassing much of the intermediate zone and neighbouring wet zone
plantation districts, the ‘epidemic area /zone’ extended southwest to include
Colombo as well, together encompassing well over half the entire 5.5 million

49
 THE 1934–1935 CEYLON EPIDEMIC

population of the island. Excess deaths ‘outside the epidemic area,’ by con-
trast, numbered 10,471.27
Initial mapping of mortality for the epidemic period of November 1934 to
April 1935 showed extremely high death rates in much of the northern dry zone
in addition to the plantation districts of the intermediate and wet zones (Figure
2.3).28 Recognizing the dry zone’s ‘normally excessive’ mortality levels, Briercliffe
chose an additional measure to convey relative epidemic severity across the island
in 1934–1935, calculating for each division (subunits of a district) the per cent
increase in mortality over non-epidemic year levels (Figure 2.4).29
The resulting map indicated that the ‘epicentre’ of the malaria epi-
demic – those divisions where mortality increased 400 per cent or more in
1934–1935 – lay in the three intermediate zone and peri-intermediate zone
districts of Kegalla, Kurunegala, and Kandy. But it also showed that while
the greatest relative increase in mortality occurred within the watershed-
defined ‘epidemic area /zone,’ markedly heightened death rates extended
into the northern dry zone districts of Anuradhapura and Puttalam well
beyond the catchment area of major intermediate zone rivers.30
Briercliffe pointed out this lack of complete congruence between epidemic
intensity and the watershed-defined epidemic area/zone, acknowledging
that the boundaries of the ‘epidemic area’ were ‘fixed rather arbitrarily and
are to some extent artificial.’31 Nevertheless, he framed much of his mortal-
ity analysis on the basis of the ‘epidemic area’ categorization, presenting
and comparing data in the nine districts of the ‘epidemic area’ versus those
districts ‘outside the epidemic area.’
Briercliffe’s attention perhaps understandably was directed to those dis-
tricts where excess deaths were geographically concentrated. In the context
of near universal malaria infection and plummeting access to basic subsist-
ence, the administrative demands entailed in providing famine relief along-
side medical treatment to much of the population were enormous.32 Deaths
in absolute numbers in the sparsely populated dry zone northern districts by
comparison were far fewer. Nonetheless, the report’s focus on the ‘epidemic
zone’ was problematic interpretatively, conveying a sense of the primacy of
dry river beds and lack of previously acquired specific immunity, viz., ento-
mological conditions, underlying epidemic intensity.
However, there also were interpretative problems associated with Brier-
cliffe’s proportionate (per cent increase) mortality measure of epidemic
intensity. In northern districts, the ‘normal’ death rate was in the range of
35–40 per 1,000, compared to 20 per 1,000 or less in the intermediate and
wet zone districts.33 Mean infant mortality for the previous decade in Anu-
radhapura district, for example, was 309 per 1,000 live births; in Puttalam
district, 342 per 1,000 live births. With infant deaths a leading component
of malaria mortality, such high rates allowed little statistical ‘room’ for
a four-fold increase in overall mortality, as was observed during the epi-
demic in the normally lower-mortality tracts.34 A proportionate measure

50
 THE 1934–1935 CEYLON EPIDEMIC

Figure 2.4 Per cent increase in total mortality, by division, Ceylon, Nov. 1934 to
Apr. 1935
Source: R. Briercliffe, The Ceylon Malaria Epidemic, 1934–35 (Colombo: Ceylon Govt Press,
Sept. 1935). Supplement to the Sessional Paper XXII – 1935, Map 19.
Note: The four-river watershed ‘epidemic area /zone’ is designated by a solid black line.

of epidemic intensity thus tended to underestimate epidemic severity in

those regions of the island where death rates were endemically very high
before the epidemic.
An alternative measure of epidemic intensity Briercliffe might have used
was simply the absolute increase in death rate per mille. Had such figures

51
 THE 1934–1935 CEYLON EPIDEMIC

been used, the northern district of Anuradhapura, for example, would have
stood out as one where the epidemic rise approximated that for many of the
severely affected districts in the ‘epidemic area/zone’ (Table 2.1). In other
non-‘epidemic-area’ northern districts also, the ‘excess’ death rate was mod-
erately severe.
Despite the methodological limitations of Briercliffe’s proportionate
measure of epidemic intensity, his mapping did provide important epidemio-
logical insights. It suggested that considerable malaria endemicity as judged
by 1920s spleen rates did not necessarily offer protection against epidemic
mortality in 1934–1935 (Figs. 2.2 and 2.4).35 In much of Kurunegala dis-
trict, where mortality increase was greatest, endemic malaria transmission
levels in the decade preceding the epidemic appear to have been relatively
high, with a spleen rate ranging between 40 and 60 per cent. Moreover,
death rates soared in neighbouring dry zone districts like Anuradhapura
despite prevailing hyperendemic malaria conditions but where drought-
triggered harvest failure had also been severe. Famine relief efforts were in
fact already in progress in the dry zone when the malaria epidemic struck in
the final months of 1934.36 Even in the ‘intermediate’ zone of greatest rela-
tive epidemic severity, malaria endemicity likely was not inconsiderable, if
spleen rate levels (20–40 per cent) observed in the 1920s can be assumed to
have prevailed into the 1930s.
But it also suggests that a purely vector-driven explanation of epidemic-
ity was questionable as well: it is difficult to interpret the epidemic increase
in mortality in the northern highly endemic district of Anuradhapura in
entomological terms of drying riverbeds when such conditions character-
ized the region even in non-epidemic years. Entomological factors alone, in
other words, appear insufficient to explain why the epidemic in 1934–1935
assumed, in Eric Meyer’s terms, ‘une forme virulente.’37 Further, Briercliffe’s
mortality mapping left unclear was how the entomological effects of drought
in the watersheds could be distinguished from the economic consequences.
Briercliffe himself was fully aware of the larger economic backdrop to the
epidemic. In a separate section on ‘economic factors’ he detailed the scale
of the impact of the economic recession triggered by the global Depres-
sion. Between 1929 and 1933, exports had plummeted, the value of rubber,
tea, and coconut exports falling 60 per cent.38 With 42.1 per cent of the
island’s GDP based on the export of these products, the impact on liveli-
hood had been severe.39 H.E. Newnham, Commissioner for Relief during
the epidemic, described the consequences:

The export of tea and rubber was restricted in an endeavour to

raise the price of those commodities, and this restriction had caused
the closing down of an appreciable acreage of estates, particularly,
among the smaller holdings. . . . The effect of the general depres-
sion was . . . felt in the villages of the wet zone where most of the

52
Table 2.1 Crude death rate (per 1,000 population), infant mortality rate (per 1,000 live births), Nov. 1934–Apr. 1935, extent harvest
failure, by district, Ceylon [Sri Lanka]

District Crude death rate Infant mortality Estimated extent of

rate 1934 crop loss
‘Expected’ (previous 4-yr. Actual Excess
mean)

Districts ‘affected by the epidemic’ (“epidemic area”)*

Kurunegala 13.4 62.3 48.9 799.9 ‘greatest degree’
Matale 12.8 46.0 33.2 497.1 ‘limited areas’
Kegalla 8.3 41.2 32.9 452.2 ‘greatest degree’
Kandy 10.4 28.6 18.2 310.4 ‘limited areas’
Chilaw 9.0 22.6 13.7 311.2 ‘very limited areas’
Negombo 8.5 20.9 12.4 269.5 n.a.
Ratnapura 10.4 22.6 12.2 232.8 ‘limited areas’
Colombo 10.2 17.2 7.0 196.4 ‘limited areas’
Kalutara 9.2 12.1 2.9 128.9 ‘very limited areas’
Districts ‘outside the “epidemic area” ’*
North-Central:
Anuradhapura 20.7 48.2 27.5 613.0 ‘greatest degree’
Puttalam 18.6 33.3 14.7 512.3 ‘very limited areas’
Mullaittivu 20.4 32.6 12.2 474.3 ‘greatest degree’
Mannar 19.9 27.6 7.6 434.0 ‘greatest degree’
Hambantota 16.2 30.9 14.7 310.8 ‘limited areas’
Trincomalee 15.1 25.3 10.2 285.1 ‘very limited areas’
Badulla 12.5 17.6 5.0 204.2 ‘limited areas’
Matara 10.5 14.9 4.4 142.3 ‘very limited areas’
Nuwara Eliya 9.9 13.1 3.1 195.0 ‘very limited areas’
Galle 10.7 12.9 2.1 136.1 ‘limited areas’
Batticaloa 14.4 15.3 0.9 209.7 ‘limited areas’
Jaffna 14.2 14.8 0.5 222.9 ‘limited areas’
Source: R. Briercliffe, The Ceylon Malaria Epidemic, 1934–45. Report by the Director of Medical and Sanitary Services, Sessional Paper XXII, (Colombo:
Ceylon Govt Press, Sept. 1935), pp. 40, 44, 27.
* For definitions, see text at pages 48–50.
 THE 1934–1935 CEYLON EPIDEMIC

tea, rubber, and coconut plantations are situated. . . . The estates

no longer needed the same amount of causal labour for weeding,
tapping, and plucking. Contractors no longer needed their services
on public and private works. Their coconuts ceased to add to the
family income. But in almost every village there are rice fields . . .
which provide some degree of insurance against a slump in com-
mercial products.40

Superimposed upon four years’ economic depression however was the

severe 1934 drought, ‘the greatest drought on record’ for the island.41
‘[W]ith failure of the summer rains,’ Newnham continued,

a rice shortage emerged by the second half of 1934, the autumn

harvest amounting to ‘about a quarter of the normal crop. . . . The
peasants of the wet zone, who were formerly better off had lost
many of their usual chances of maintaining their higher standard,
and had begun to sink towards the level of those in the dry zone.42

Data on acreage of failed crops by district apparently were not available

to Newnham, but he categorized the 21 districts of the island into three lev-
els of harvest failure severity, detailed in the Briercliffe report.43 Those dis-
tricts hardest affected by the drought overlapped both the intermediate zone
and the northern dry zone. Only in the southern two districts of Galle and
Matara and the northern tip of the Jaffna peninsula had 1934 rainfall been
at normal levels, and these districts did not suffer from epidemic malaria.44
In other words, there were two major sources of economic hardship
leading up to the epidemic in late 1934, each varying in their impact geo-
graphically across the island and accounting for quite marked differences
in economic stress among regions. Where harvest failure and the effects of
the global Depression overlapped in the three hill districts in and bordering
the intermediate zone, epidemic intensity was greatest: precisely that area
where dependence on the plantation export economy was highest and crop
failure most severe. Patterns of economic hardship, then, can be seen to
have predicted epidemic severity (increase in death rate) at least as closely as
entomological conditions and considerably more closely than low immunity
(spleen rate).
It appears that the dry zone districts that experienced heightened malaria
mortality in 1934–1935 were not considered part of ‘the epidemic area’
because such increases occurred often, endemically. As Briercliffe explained,

[i]n most parts of the dry zone, increased prevalence of malaria was
not considered to be in the nature of an epidemic. In the North-
Central Province [in 1934–35] . . . there was an abnormal increase
both in the morbidity and mortality due to malaria, but as malaria

54
 THE 1934–1935 CEYLON EPIDEMIC

in this province is hyper-endemic the increase was attributed to a

worse malaria season than usual. If there had been no epidemic else-
where conditions in the North-Central Province would have called
for little comment since ‘bad malaria years’ are frequent there.45

In effect, as Newnham observed, combined drought- and Depression-

unemployment appear to have pushed up destitution (acute hunger) levels in
export-dependent districts to those in the dry zone, a ‘catching-up’ of sorts
to conditions normally endemic in the north-central districts.
But there was a further limitation to Briercliffe’s mapping of epidemic
relative intensity, minor by comparison, but one also with important inter-
pretative consequences. Although he employed four categories of mortality
severity, the highest level (400 per cent or more above non-epidemic levels)
itself included a wide range of severity levels, from ‘severe’ to extreme. C.A.
Gill, working apparently with the same subdistrict (divisional) data, also
mapped epidemic intensity patterns. But in doing so, he included an even
higher category, 7–12 times ‘normal,’ a categorization that allowed even
greater spatial discernment of epidemic mortality patterns across the island.
The significance becomes apparent in comparing Briercliffe’s epidemic inten-
sity map (Figure 2.4) with that prepared by Gill (Figure 2.5).46
As a ratio of epidemic to previous years’ mortality, Gill’s mapping of his
‘Epidemic Figures’ also tended to underestimate intensity in the higher mor-
tality northern dry zone, as did Briercliffe’s. Nonetheless, his mapping sug-
gests more clearly than do the Briercliffe maps a broad focal character to
epidemic mortality in 1934–1935, a pattern reminiscent of Christophers’s
maps of epidemic mortality in Punjab three decades earlier: that is to say,
one of regular mortality increase as the centre of the epidemic region is
approached.47 Thus it suggested a similar ‘general determining influence’
unlikely to be explained by local entomological factors. Indeed, Christo-
phers himself would later describe the Ceylon epidemic of 1934–1935 as
‘show[ing] the same focal character which was so conspicuous in the Punjab
epidemics,’48 and which he had concluded in the latter case to be a function
of agricultural hardship: harvest failure and associated famishment (acute
hunger).

Mortality differentials within epidemic tracts

The impact of economic conditions (destitution) on malaria lethality was
supported as well by mortality differentials observed within the epidemic
tracts, differentials that were not readily explained by differences in expo-
sure to malarial infection. The increase in death rate amongst the general
population, for example, was recorded to be almost three times greater
than that observed for the estate population.49 Mortality in the plantation
population rose from 21.1 per 1,000 in the 1924–1933 period, to 26.7 per

55
 THE 1934–1935 CEYLON EPIDEMIC

Figure 2.5 ‘Epidemic Figure’* map of 1934–1935 Ceylon malaria epidemic

Source: C.A. Gill, Report on the Malaria Epidemic in Ceylon in 1934–35 (Colombo: Ceylon
Govt Press, Sept. 1935), Map IV. Sessional Paper XXIII – 1935.
*Calculated by C.A. Gill as the number of times the Nov. 1934–Mar. 1935 mortality rate
exceeded that of the same period for the preceding year. See note 46.

1,000 in 1935, an increase of 21 per cent; for Ceylon as a whole, from 23.1
to 36.6 per 1,000, a 58 per cent increase. Direct comparison is somewhat
problematic because these rates are not age-adjusted. However, similar dif-
ferentials are apparent for infant mortality rates, where this is not a con-
cern. In Kegalla district, for example, infant mortality levels in estate and

56
 THE 1934–1935 CEYLON EPIDEMIC

non-estate sectors were at similar levels before 1935, but rose 315 percent in
the non-estate population in 1935, from approximately 125 deaths to 515
per 1,000 live births, compared to a 116 percent in the estate population, to
251 deaths per 1,000 live births (Table 2.2).50
It seems unlikely these mortality differentials reflected major differences
in malaria exposure. ‘Looking for an explanation in natural causes,’ Meyer
notes, ‘medical authorities . . . asserted that severity was proportionate to
proximity to the rivers.’ But there were many settlements, he suggests, citing
Village Expansion Schemes within Kegalle and Kurunegala districts, seri-
ously affected by the epidemic that were situated far from water courses.51
The Kegalla district, Meegama has pointed out,

can broadly be divided into two sectors, the estate sector with a
settled Indian labour force, and in between them a rural peasant
sector dependent on paddy cultivation. The drought of 1934–35 led
to a failure of crops in the peasant sector where there were famine
and distress on an unprecedented scale. The estates, on the other
hand, . . . cultivated a perennial like rubber which, in the short
term, was not affected by a drought. Thus the estate labourer . . .
had stable employment and he lived on imported food [hence] his
level of nutrition was unaffected by the drought.52

Meegama’s observations can be qualified somewhat. Estate labour may

have had relatively ‘stable employment’ for those left on the plantations in
1934–1935. But according to Meyer, as prices and export demand plum-
meted during the Depression years of 1931–1934, considerable emigration
from some estates had taken place.53 Some labourers no doubt repatriated
to India in advance of the epidemic, though under Depression conditions

Infant mortality rate, estate and non-estate sectors, Kegalla district,

Table 2.2 
Ceylon [Sri Lanka], 1930–1940

Year Estate sector Non-estate sector

1930 136 133
1931 127 126
1932 128 114
1933 112 123
1934 116 136
1935 251 515
1936 103 132
1937 109 118
1938 137 124
1939 141 159
1940 117 113
Source: S.A. Meegama, ‘Malaria Eradication and its Effect on Mortality Levels’, Population
Studies, 21, 3, Nov. 1967, p. 230.

57
 THE 1934–1935 CEYLON EPIDEMIC

there was perhaps little incentive to do so. Others may well have added
to the numbers of destitute labourers in the surrounding non-estate areas,
further amplifying estate/non-estate differentials in destitution, and in turn
epidemic mortality levels in 1934–1935. Even on the estates, livelihood ‘sta-
bility’ was also relative. In the context of a dramatic fall in estate production,
labour households likely accepted having fewer members in employment,
and lower wage levels, before abandoning the estates altogether in search
of livelihood off the plantation. If relatively protected from the effects of
harvest failure, many estate households, in other words, probably were also
under considerable economic stress leading up to the epidemic.
At the same time, only a small portion of the population in the ‘estate
districts’ was employed on the estates.54 Most households were non-estate
Sinhalese small peasants, dependent on subsistence rice cultivation and
small-scale cash crop cultivation of rubber and coconut. In the economic
circumstances of 1934, these non-estate small peasant producers were hit
doubly hard: first by the Depression-induced loss of cash crop income since
as small independent producers their access to international export mar-
kets likely was even more limited than on the estates; and then by crop
failure.55
Other indicators of a major role for economic hardship in epidemic
severity are anecdotal accounts of class and caste differentials within the
non-estate village population. Colonial officials were struck by the evident
severity of the epidemic amongst the poorest. ‘In almost adjacent wasa-
mas [groups of villages], one finds surprising differences in the change of
the death rate during this year,’ Meyer notes, adding that ‘the areas most
affected were not of the [higher] Goyigama caste.’56 The 1935 administra-
tive report also noted that ‘[t]he most affected localities were the poorest
and the most depressed.’57
The importance of underlying emaciation is suggested in clinical obser-
vations as well. Medical officers documented ‘a large number’ of cases of
oedema among malarial patients, particularly among children. Variously
attributed to malaria-induced anaemia and hookworm infection, Briercliffe
questioned this interpretation, recounting in some detail the findings of a
study of 19 severe malaria cases. Vivax malaria (a species generally associ-
ated with lower parasite levels) was as common as falciparum malaria, and
less than a third were found to have hookworm infection. Among those
with anemia there appeared to be ‘no correspondence between the degree
of anaemia and the severity of the oedema.’ Briercliffe’s ‘personal opinion’
was that these were cases of starvation oedema ‘of the same category as . . .
famine oedema’ or ‘war oedema,’ adding that ‘the one feature common
to all . . . was repeated attacks of fever.’ Good food, enforced rest, and
treatment provided in hospital, he noted, effected ‘a rapid and striking
improvement,’ though the overall death rate among young children was
45 per cent.58

58
 THE 1934–1935 CEYLON EPIDEMIC

There was of course a third economic dimension to the epidemic, also

dramatically apparent in narrative accounts: that of starvation secondary to
malaria debility. ‘[W]ith whole communities laid low with fever,’ local offi-
cials observed, ‘there was no one to work the chenas (village fields) . . . peo-
ple, weakened by disease and unable to work, were under threat of death
through starvation.’ In one house

everyone was down with fever with the exception of a small child
eighteen months old. She was sprawling about, howling for food
which her mother, in a state of delirium, was unable to give. . . .
[F]ew, if any, villagers could provide for themselves or had sufficient
food to maintain a livelihood. It was obvious therefore that steps
had to be taken to provide not only medical comforts but the ordi-
nary necessities of life.59

This level of distress was officially recognized on December 6, a month into

the epidemic, and relief was initiated that included school feeding. It was
clear to administrators that breaking the circle required food.
Still, the question remained as to how the vicious circle came to be estab-
lished. Without preceding starvation, would the downward cycle have begun
in the first place? Or at least would it have been amenable to interruption?
It was a question that Briercliffe also felt compelled to address in the official
report on the Ceylon epidemic. ‘Even if the masses had been well fed and
prosperous,’ he concluded, ‘there would have been an epidemic of malaria,
but the vicious circle of malaria and destitution acting and reacting on one
another would not have been established.’60

The non-immune thesis resurgent

Despite the many references to extreme economic hardship in Briercliffe’s
official report,61 subsequent writing by Western malaria workers on epi-
demic causation would focus almost exclusively, as we have seen, on aspects
of malaria transmission: a sudden increase in malaria transmission amongst
a population with only limited previously acquired specific immunity.62
These later accounts share several features. First, there is little discussion of
the maps that indicated spatial distribution of epidemic mortality, in par-
ticular, Gill’s ‘Epidemic Figure’ map. Second, even in those accounts that
made reference to economic hardship, such conditions generally were left
unexplored and failed to appear in the writers’ conclusions.63
A further characteristic of the later ‘off-shore’ accounts is a paucity of
historical context. Meyer remarks on the tendency of subsequent analysts to
view the 1934–1935 epidemic as exceptional, ‘sans précédent.’64 A largely
ahistorical analysis, Meyer suggests, allows the convenience of a man-
ageable, clearly delineated and dramatic epidemic ‘story,’ the designation

59
 THE 1934–1935 CEYLON EPIDEMIC

‘unprecedented’ suggesting that exploration of broader dimensions and pat-

terns is unnecessary.
Curiously also, in a paper on the 1934–1935 epidemic presented to
the Royal Society of Medicine in November 1935, Briercliffe and his co-
contributor, W. Dalrymple-Champneys, made no mention of famine condi-
tions leading up to the epidemic.65 Gill, in a presentation to the Royal Society
of Tropical Medicine and Hygiene two months later, also dealt solely with
microbiological aspects of malaria transmission across the epidemic period,66
despite having referred to famine ‘as an important predisposing cause’ of
regional epidemics in his initial 1935 report. Indeed, he went on to propose
a purely speculative explanation as epidemic ‘trigger’ – a biologically deter-
mined periodic reactivation (‘relapse’) of the malaria parasite.67 It would be
left up to Dalrymple-Champneys, the Deputy Chief Medical Officer of Health
of Ceylon, also in attendance at the January 1936 Royal Society meeting, to
remind Gill of ‘the important fact that these [Sri Lankan] people were under-
nourished, very many of them grossly so, owing to the partial failure of the
paddy crop.’68 It was as if an implicit obligation existed to direct analysis for
a scientific audience solely to microbiological considerations.
Certainly, increasing political sensitivity would have been a factor in the
downplaying or setting aside of the role of starvation in the 1934–1935
epidemic. In the final years of the colonial period, growing anti-colonial
movements in South Asia left even less political ‘space’ for highlighting hun-
ger in published documents in the metropole.69 At the same time, attraction
to entomo-immunological explanations of the Ceylon epidemic reflected
burgeoning medical anticipation of tools to predict epidemic events in the
microbiologic realm, a pursuit expressed earlier in Gill’s efforts to forecast
epidemic occurrence in Punjab province. It was an interest that can be traced
back to Ross’s early efforts at mathematical modelling of malaria transmis-
sion in India,70 work later pursued more intently by G. Macdonald.71 Math-
ematical precision conferred an aura of analytic certitude and competency,
whereas acknowledgement of social determinants seemed to take control of
epidemic malaria out of the hands of the medical profession.
But the retreat from economic dimensions in epidemic causality can be
seen to reflect a larger dichotomy in views of epidemic malaria causation in
the 1930s. That fault-line had been etched a decade earlier in heated debates
within the League of Nations Malaria Commission, with members largely
divided between those with extended ‘field’ experience of malaria – and
direct responsibility for its toll, such as Bentley – and those whose expertise
lay in vector-control work. In the case of Ceylon, H.E. Newnham, Special
Commissioner for the Relief of Distress in 1934–1935 Ceylon, represented
the former, who urged – in terms starkly reminiscent of the 1924 and 1927
Malaria Commission reports – a program of complete ‘rural reconstruction’
to address the ‘near starvation of the peasantry’ as the only realistic solution
to future epidemics.72

60
 THE 1934–1935 CEYLON EPIDEMIC

Yet it would be the entomo-immunological explanations of the Ceylon

epidemic that prevailed in subsequent medical literature. ‘In Ceylon,’ Paul
Russell wrote in 1952, ‘deficiency in the . . . monsoon rains will result in cer-
tain rivers drying to the point where they become series of countless pools
of the type favoured by culicifacies. In each case an epidemic of fulminant
proportions has resulted.’73 That same year Macdonald again asserted that
‘the disastrous Ceylon epidemic of 1934 and 1935 was shown, like the 1908
Punjab epidemic, to be . . . [the result of] the general interplay of inter-
rupted transmission and varying immunity.’74 Analysis was marked by a
‘narrow environmental determinism’ that continues to influence, Silva sug-
gests, modern interpretation of malaria history.75
Within modern malaria historiography, where economic hardship is rec-
ognized in the case of major South Asian epidemics, generally it is so only
in passing, the compelling quantifiable micro-dynamics overshadowing
conditions of the human host. In his 1978 Mosquitoes, Man, and Malaria,
Harrison would acknowledge the possibility of ‘other conditions’ contribut-
ing to the 1934–1935 epidemic, including ‘general physical well-being.’ But
attracted, it seems, by the mathematic models of malaria transmission, he
concluded that

[t]he events in Ceylon could be precisely accounted for, Mac-

Donald calculated, by an increase of 5.3 times in the numbers of
culicifacies or equally by a slight increase in longevity. . . . Briefly
what happened in 1934–35 was that [following] an extraordinary
drought . . . the resultant epidemic swept devastatingly through a
non-immune population.76

The contribution of prevailing economic hardship, in turn, was deemed

‘coincidence,’ at best ‘suggestive,’ unlike the role attributed to factors of
transmission: ‘[t]he coincidence that the people of Ceylon, like those of Sind
and Punjab, met their enemy somewhat debilitated by hard times was sug-
gestive if not conclusive that a lowering of general physical resistance played
some part.’77

Christophers’s query
There is a serious loss here. Harrison was hardly at fault in his reading
of the post-1935 secondary literature on the Ceylon epidemic in such terms.
The privileging in this period of microbiologic factors in explaining epi-
demic malaria to the virtual exclusion of conditions of the human host had
left the central question of malaria historiography unaddressed: what fac-
tors underlay the immense range in historical malaria mortality? A further
glimpse into this question appears in brief commentary by Christophers,
also in attendance at the January 1936 meeting of the Royal Society of

61
 THE 1934–1935 CEYLON EPIDEMIC

Tropical Medicine devoted to the Ceylon malaria epidemic. As in his ear-

lier work, the question of malaria intensity was clearly on Christophers’s
mind, though he would raise the issue in characteristically oblique fashion.
It would appear in his response to the relapse hypothesis offered by Gill
to explain the initial two-week phase of mild cases documented in Octo-
ber 1934. ‘[E]vidence of such [initial] mildness,’ Christophers observed,
‘does not necessarily prove the relapse theory since the mildness of the cases
in the beginning might be a result of numerically poor infections in the
anophelines.’78
Here, by inference, Christophers appears to have been addressing the
question of dose of infection, and in turn the possibility of heavy, ‘intense’
infections arising among subsequent cases. What was significant, he
was suggesting, was not the mildness of the early cases, which might be
expected in the initial cycle of infections transmitted from those in the
population still harbouring sparse gametocytes from the previous year’s
transmission season. Rather, what was exceptional was the exponential
rise in fever death rate (lethality) thereafter. As in Malaria in the Punjab,
Christophers appears to have interpreted the rapid rise in malaria mortal-
ity as suggesting heightened vulnerability among the famished, but possi-
bly also an increased dose of infection being transmitted, by virtue of this
famishment.79
Interestingly, too, Christophers went on to query the emerging view that
the conditions underlying the fulminant form of the malaria in Ceylon were
the inverse to those in northern India.

Emphasis has been laid on the fact that the [Ceylon] epidemic
was one occasioned by unusual drought, i.e., conditions quite the
opposite to those in North India. It is well, however, to note that
a preceding period of drought is also seen in the northern epidem-
ics [in India], and the heavy rainfall in October occurring after the
drought may have been the actual cause of unusual prevalence of
A. culicifacies.80

The Ceylon epidemic, he emphasized, was preceded by ‘the greatest drought

on record,’ inferring that appreciation of the severity of prevailing economic
stress was essential for understanding why the 1934–1935 epidemic assumed
such severe proportions. And to press the point, he had come prepared.
Presenting his earlier mortality maps of the 1908 and 1892 Punjab epi-
demics alongside Gill’s Ceylon ‘Epidemic Figure’ map (Figure 2.5), Christo-
phers indicated the spatial similarities in mortality patterns. That a ‘general
determining influence’ was at work in the Ceylon epidemic was suggested,
as in earlier Punjab epidemics, by the broad focal pattern to mortality, one of
regular increase as the epicentre of the epidemic is approached. Such a pat-
tern was more likely the result of generalized harvest failure than ecological

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 THE 1934–1935 CEYLON EPIDEMIC

particularities of dry river-bed catchment areas. ‘No one looking at these

[Punjab] maps,’ he continued,

or that prepared by Colonel Gill of the Ceylon epidemic, can fail,

I think, to be struck by the resemblance to maps of meteorologi-
cal phenomena. They are, one feels instinctively, maps of ‘malaria
cyclones.’ This resemblance is not merely superficial, but is due
to the fact that the fundamental causation of these epidemics is
meteorological.81

In his ‘meteorological’ phrasing, was Christophers referring to entomo-

logical conditions as the general determining influence? Or related immuno-
logical consequences of preceding drought? Or instead the economic impact
of preceding drought patterns, as in 1908 Punjab? Or perhaps all three?
True to form, he doesn’t tell his audience explicitly. Yet in his cartographi-
cal comparison of the Ceylon malaria epidemic to fulminant epidemics in
Punjab, the intended meaning seems evident – if perhaps clearer to those in
attendance already familiar with his 1911 Punjab study.82
The distinction between malaria transmission and malaria mortality was
crucial in understanding the epidemic of deaths in 1934–1935. Nor was it a
new insight, forming the core of the earlier Duars and Punjab analyses. It lay
also at the centre of many of the League of Nations Malaria Commission’s
1920s study-tour observations, as seen above in Chapter 1. Destitution
and starvation (‘physiological poverty’) triggered and fed the vicious circle
between illness, unemployment, and prolonged parasitemia rates (‘residual
infection’), undermining previously acquired specific immunity and in turn
‘profoundly influencing the incidence of malaria.’83
The two sides of the epidemic equation – germ transmission and host
response – were not mutually exclusive. Yet in medical interpretation after
1935 they had become so. Under the gaze of a new generation of Western
malaria researchers the Ceylon epidemic came to be interpreted exclusively
in terms of malaria transmission: enhanced transmission in the epidemic
year itself, and ‘insufficient’ transmission levels in the period preceding the
epidemic, leaving a non-immune (‘little salted’) population particularly
vulnerable.84
But the narrowed framework post-1935 also held a larger significance.
For many of the malaria researchers whose work focused primarily on
malaria transmission control, the Ceylon epidemic marked a shedding of
the so-called pessimistic view that malaria, like tuberculosis, was a ‘social
disease’ requiring broad economic development. An immuno-entomological
reading of the 1934–1935 Ceylon epidemic arguably allowed a final jetti-
soning, in the academic literature that followed, of the brake to the sanita-
tionist (vector control) approach. There was, of course, a deep irony to this
‘shedding.’ For the 1934–1935 epidemic had also brought open recognition

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 THE 1934–1935 CEYLON EPIDEMIC

among colonial medical officers of the technical difficulties of controlling

malaria transmission on the island under conditions of drought. From the
earliest weeks of the epidemic, the public health department had attempted
extensive anti-larval measures to control river-bed anopheline larval
development – oiling pools, flushing river beds – to little avail. In the after-
math of the epidemic, all involved acknowledged that anti-larval efforts could
not hope to alter drought-triggered vector breeding that triggered such epi-
demics on the island.85 V.B. Wigglesworth, lecturer at the London School of
Hygiene and Tropical Medicine, . . . would conclude that ‘[f]or the moment,
efficient treatment of the disease is all that can be offered to the villager.’86 In
effect, the ‘mere-palliation’ ghost of Mian Mir had arisen once again.
At the theoretical level, however, interpretation of the 1934–1935 epi-
demic in entomo-immunological terms rekindled the ‘optimistic’ view that
malaria ‘control’ need not await economic development, viz., ‘control’ of
destitution. It lay in identifying and altering the weakest link in the fragile
chain of vector transmission,87 in turn pushing malaria analysis even further
in the direction of theoretical modelling.

Post-1935 mathematical modelling

In the aftermath of the 1934–1935 Ceylon epidemic, the ‘Human Factor’ in
its original meaning, as applied to Punjab regional epidemics, largely disap-
peared from literature on South Asian malaria. Macdonald would go on
to formulate mathematical models of malaria transmission, work which
helped lay the theoretical basis for malaria eradication programs in the post-
WW2 period. At the same time, fiscal retrenchment in India further intensi-
fied in all spheres of British colonial governance including public health. To
the extent that malaria research continued on the subcontinent, increasingly
it was undertaken by malaria workers funded by the International Health
Division of the Rockefeller Foundation and the Ross Institute in London,
and was directed to anti-vector experimental work and circumscribed con-
trol programs in industrial and plantation estates. With European political
tensions rising, little in the way of field research into epidemicity contin-
ued at the Karnal malaria research station, and British and U.S. malaria
researchers were soon reassigned to WW2 military priorities.
In the early post-war period Punjab became the site of residual insec-
ticide (DDT) trials, which brought an end to field research work on the
mechanisms of malaria mortality epidemicity. Academic interest in malaria
immunity now shifted to another form, channelled into intense debate over
the wisdom of extending DDT programs in holoendemic regions of Africa
and the possible risks associated with reducing levels of protective immunity
in populations.88 By this time, Yacob and Swaroop had revisited the ques-
tion of epidemicity and immunity in Punjab by analyzing the almost three
decades of spleen rate data collected in the province.89 Their conclusion that

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 THE 1934–1935 CEYLON EPIDEMIC

spleen rates failed to predict epidemicity was overshadowed, however, by

the immunological view now prevailing in the international literature on
South Asian regional (‘fulminant’) epidemics.90
It was in this period that Macdonald would reach back briefly to Chris-
tophers’s 1911 Punjab study, interpreting its conclusions regarding the
region’s ‘fulminant’ epidemics, as we have seen, in terms of ‘certain rainfall
characteristics and an inadequate immunity in the local population.’91 Given
the context, by ‘inadequate immunity’ Macdonald almost certainly was
referring to acquired (malaria-induced) immunity.92 Here, the conceptual
blurring of general immune capacity and acquired immunity under Gill’s
term ‘communal immunity’ had given way to a complete supplanting. In
effect, acquired immunity, a function of malaria transmission, had come to
be accorded the full mantle of the ‘Human Factor’ in malaria.
The most important question left unanswered by the theory of non-
immunes was explaining the post-1920 decline in South Asian malaria epi-
demics. Episodic drought continued to afflict Punjab after 1908, as before,
with presumably year-to-year fluctuation in the proportion of non-immune
infants in the population. Yet fulminant malaria epidemics did not.93 Writ-
ing in the 1920s, at a point when this decline in epidemicity was not yet
definitive, Gill’s attraction to the non-immunes thesis is perhaps understand-
able. But by mid-century, with three decades essentially free of ‘fulminant’
epidemics, commitment to the thesis is more puzzling.94
More curious still, in his quantitative modelling of malaria epidemicity,
Macdonald never directly incorporated a non-immune factor.95 Indeed, at
one point he would express doubts about the adequacy of the theoretical
models for explaining fulminant malaria in South Asia. ‘Personal work
in two of the great epidemic areas – the Punjab and Ceylon,’ he openly
acknowledged in the same 1952 paper,

has left [me] satisfied that the accepted explanation of periodic

epidemics is an entirely satisfactory statement of what happens,
but completely unsatisfying as a statement of why it happens. . . .
[I]t is not clear why small changes in climate should produce such
dramatic changes in the amount of transmission.96

What Macdonald appears to have been puzzled about was not ‘dramatic’
changes in levels of malaria transmission – the proportion of a population
infected – but rather changes in its lethality. The mathematical models could
explain how rates of infection could rise rapidly from low to near-universal
levels in a given year, but not why soaring malaria lethality was seen in some
years of universal infection such as 1908 and not in others. It was as if, Mac-
donald was suggesting, a key variable was still missing.
Despite offering his mathematical modelling as potentially a ‘complete’
representation of malaria transmission and epidemicity,97 in fact a number

65
 THE 1934–1935 CEYLON EPIDEMIC

of factors relating to the human host and ‘physiological poverty’ were miss-
ing from them, which potentially could be important for influencing rates of
transmission. Dose of infection was one, and the range of possible factors
influencing effective dose. Recovery rate was another, the time required for a
person with malaria to throw off infection, or to succumb to it. Any length-
ening of the period that gametocytes remained patent in the human host,
for example, could potentially amplify the man-mosquito cycle of transmis-
sion. In the early years of malaria research in India, such questions relating
to ‘residual infection’ and recovery rate had been assumed to be central
for understanding epidemiological patterns of malaria transmission. ‘All
the circumstances . . . which tend to delay recovery, or to lessen the resist-
ing power of individuals,’ a tropical medicine text in 1922 had stressed,
‘enhance the prevalence and severity.’98 Interestingly, at one point Macdon-
ald himself would acknowledge the possibility of variation in recovery rate.
But as a factor in the practical workings of his epidemic malaria model, he
considered that it was ‘not liable to abrupt change . . . and its significance
in this context is therefore slight.’99 In the process, the question as to what
could cause variation in recovery rate also was left unaddressed.
The ‘great epidemics’ of Punjab were, above all, epidemics of death. What
appears to have been perplexing Macdonald was the enormous variation in
mortality from year to year: how ‘small changes in rainfall’ could explain
10- or 20-fold increases in mortality as seen throughout the first half of the
colonial period. But he does not pose the question in these terms; his refer-
ence is solely to ‘amount of transmission,’ in a seeming conflation of the
two issues. The analytic difficulties stemming from the conflation appear
obvious. But at the time, the transformation in meaning of ‘epidemic’ –
from one of mortality to one of infection (transmission) – appears to have
been anything but. What had intervened in the interim was the emergence,
unarticulated, of a very different concept of ‘epidemic.’ No longer viewed
as ‘epidemics of death,’ the term by the 1930s had come to mean primarily
increased rates of infection. This narrowed meaning can be seen in the Cey-
lon colonial literature as well. Briercliffe’s designation of ‘epidemic zone’
was an entomological definition, delineated by watershed boundaries in
terms of drying river-bed pools: malaria transmission. The equating of ‘epi-
demic’ to infection (transmission) would be articulated even more explicitly
in Wigglesworth’s assessment of 1934–1935 Ceylon mortality patterns, one
in which he excludes the dry-zone northern districts from his analysis on the
basis that ‘the people are so saturated with the disease that true “epidem-
ics” of malaria [there] are impossible.’100 Dunn similarly would explain that

[a]s this [northern dry zone] is the hyperendemic area, a rise of this
nature, while noteworthy, may be considered to be in the nature of
a minor ‘localised epidemic’ of the kind which often occurs owing
to the failure or partial failure of the North-East Monsoon without

66
 THE 1934–1935 CEYLON EPIDEMIC

any important connection with the chief epidemic, mostly confined

to the non-endemic area.101

The point here is that this reading was possible because an immunological
explanation of epidemicity was already assumed, seemingly internalized, in
epidemiological thought: drought and dry river beds may have been wide-
spread across much of the island in the lead-up to the 1934–1935 epidemic,
but malaria mortality was presumed to have soared primarily where specific
(acquired) immunity was low, despite spleen rate data to the contrary in the
case of the northern epidemic areas and much of Kurunegala district.102
Of course, one can recognize reasons for attention to specific immu-
nity. Acquired immunity could and did offer relative protection in hyper-
and holoendemic regions of the world, including in some areas in South
Asia. Indeed, recent epidemiological reports suggest that some degree of
‘acquired’ protection (immunity) among adults can follow even a limited
number of episodes of falciparum malaria infection.103 What was problem-
atic was preoccupation with the concept in analytic circumstances where a
different set of questions – patterns of relative mortality risk – required to
be addressed.104 With epidemicity equated to infection (transmission), other
issues previously recognized as key to epidemicity such as recovery rate,
dose of infection, and case fatality rate would fade in importance and in
investigative attention in turn.

Epistemic aftermath
This brief sketch of South Asian malaria research through the second half
of the colonial period suggests that understanding of the ‘Human Factor’ in
malaria epidemicity dropped out of sight not through empirical refutation,
but instead by default. Earlier socio-economic observations, rather than
being integrated with new developments in microbiology, immunology, and
entomology, were in effect superseded by them.
The supersession, however, was not universal. Christophers would
retire from the Indian Medical Service and the Directorship of the Cen-
tral Research Institute at Kasauli in 1932, and was appointed Professor of
Malaria Studies of London University at the London School of Hygiene and
Tropical Medicine, a post he held until 1938. In this subsequent work atten-
tion to hunger remained peripheral to his continuing entomological writing
and research into anti-malarial drugs and their modes of action. But where
economic questions arose his analysis remained as meticulous as for para-
site and vector investigation. In his 1928 League of Nations Malaria Com-
mission report on ‘How to do a malaria survey,’ for example, one section
included the ‘study of the economic, immigration and other human condi-
tions.’ Under the heading of ‘Food conditions – price of food stuffs [and]
wages,’ he advised assiduous analysis of ‘[d]ietary as ascertained by actual

67
 THE 1934–1935 CEYLON EPIDEMIC

observation and weighment.’105 As a scientist, in other words, Christophers

had not forgotten the subsistence circumstances of the human host, taking
into account hunger as meticulously as entomological, microbiological, and
biochemical aspects. There is thus little to suggest that he himself had come
to reconsider his earlier conclusions.
True to character he never openly queried the non-immune thesis, respect-
fully acknowledging the views of colleagues, though in his own 1911 anal-
ysis of fulminant epidemics in Punjab he had stressed that more highly
endemic tracts in the province were equally vulnerable to fulminant epidem-
ics.106 Indeed, in all his writing and literature reviews Christophers scrupu-
lously reported the views of his colleagues: quoting verbatim, for example,
Macdonald, Gill, and Perry’s non-immune conclusions.107 Yet in addressing
specific epidemics he never failed to insert, if undemonstrably, economic
dimensions. In 1949, in a chapter on malaria epidemiology and endemiol-
ogy in M.F. Boyd’s Malariology: A Comprehensive Survey, the first major
compendium of malaria science, he cited once again the statistical results
of his 1911 study, Malaria in the Punjab, complete with reproductions of
his original epidemic maps.108 He also described Bentley’s work on intense
malaria in lower Bengal in relation to agricultural decline and ‘decay in
human prosperity’: ‘physical changes in the land’ that had transformed once
‘prosperous communities . . . [into] decayed and poverty stricken’ regions;109
elsewhere lauding Bentley’s ‘bonification’ efforts.110 Addressing the signifi-
cance of ‘tropical aggregation of labour,’ he highlighted – in addition to the
potential mixture of non-immunes with those already infected – the likeli-
hood of ‘much private hardship’ in labour camps, ‘especially when sickness
breaks out and families become broken up.’111
Nor had his earlier studies been forgotten among Indian Medical Service
colleagues. In his 1926 testimony to the Royal Commission on Agricul-
ture in India, J.D. Graham, Public Health Commission for the GOI, would
cite Christophers and Bentley’s Malaria in the Duars as a ‘very interesting
[report] . . . work[ing] out . . . the economic side of the labour wage’ by
addressing ‘questions of food, housing, social conditions and standards of
comfort of labour in this intensely malarious area.’112 Christophers’s 1911
economic conclusions continued to be cited in scientific papers through-
out the 1930s.113 Yet despite continuing acknowledgement, and apparent
regard, few papers actually attempted to incorporate economic factors in
interpreting the results of their own studies. The earlier ‘Human Factor’
research remained in full view as historical documents, but as an investiga-
tive subject it did not.114
The non-immune thesis, in Gill’s hands, did not start off as a rival theory
of fulminant malaria. But it quickly became so. By the 1930s, the focus in
research and theoretical interest now lay elsewhere, and Christophers’s ear-
lier research came to be read through very different conceptual lenses. In a
highly laudatory 12-page bibliographic memoir of Christophers’s scientific

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 THE 1934–1935 CEYLON EPIDEMIC

accomplishments following his death in 1977, both the Punjab and Duars
malaria studies were cited among his 215 published scientific papers,
reports, and texts. Yet Punjab epidemic causality would be interpreted solely
in terms of disease transmission: flooding and ‘practically absent immunity.’
More puzzling still, Malaria in the Duars would be grouped among a num-
ber of studies of hyperendemic malaria in ‘population[s] saturated with
infection, [where] pathogenicity was low.’115
Beyond absorption with immunological theory, however, there was an
additional source of conceptual loss at play in the demise of the ‘Human
Factor’ within academic malaria thought through the final years of the colo-
nial period. Already by the 1930s, practical comprehension of ‘predispo-
sition’ to disease rapidly was fading as the subject of hunger came to be
reformulated under the influence of another new medical subdiscipline, that
of nutritional science. In place of hunger, qualitative ‘dietary’ issues increas-
ingly would come to dominate medical discussion, overshadowing quantita-
tive issues of not enough of any food to eat.
The analytic impact of this parallel development can be glimpsed in
a 1941 address delivered to the Rotary Club of the Nilgiris in southern
India by Paul F. Russell on deputation from the Rockefeller Foundation’s
International Health Division for experimental mosquito control meas-
ures in southern India. We will meet up with Russell again in his central
role in post-WW2 malaria eradication policy. Here, however, his 1941
talk sheds light on the conceptual shift already well underway in medi-
cal understanding of human hunger. In the epidemiology of malaria in
the Indian subcontinent, Russell argued, there was ‘not the slightest evi-
dence that better food will help either to prevent infection or to produce a
milder attack. Well fed soldiers in perfect physical condition go down with
malaria as rapidly and as seriously, with as high a death rate as average
villagers.’116
In this dismissal of nutritional factors in South Asian malaria lethality
Russell was probably correct, if in relation to ‘better’ food he had in mind
issues of micronutrient deficiency: there was little evidence that a qualita-
tively ‘better’ diet offered protection from fulminant malaria.117 But here he
would have been speaking to a very different meaning of ‘nutrition’ than
that expressed in the term the ‘Human Factor’ in earlier malaria literature:
the latter denoting acute hunger (semi- and frank starvation). In interpreting
past epidemic experience in India, malaria workers by mid-twentieth cen-
tury, in other words, were working with concepts of hunger fundamentally
different than those addressed by researchers and public health officials in
colonial service a generation earlier. That Russell’s dismissal of hunger in
relation to malaria mortality stood uncontested in 1941 speaks to a funda-
mental transformation in understanding of human subsistence which had
taken place in the intervening decades since publication of Malaria in the
Punjab.

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 THE 1934–1935 CEYLON EPIDEMIC

However anodyne the term ‘Human Factor’ had been in the earlier malaria
literature, the designation nevertheless had conferred scientific prominence
and legitimacy, if fleetingly, on the issue of human hunger within the emerg-
ing discipline of malaria studies. Now stripped of its formal designation,
acute hunger (semi-/frank starvation) as a causal agent in malaria epidemic-
ity no longer belonged within medical discourse. The demise of hunger as a
medical category in epidemic history is a central question for health histo-
riography. In the chapter that follows, one key stage in this loss is explored
in the emergence of nutritional science as it took disciplinary shape in early
twentieth-century colonial India.

Notes
1 C.L. Dunn, Malaria in Ceylon: An Enquiry into its Causes (London: Bailliere,
Tindall and Cox, 1936), 54.
2 G. Covell, and J.D. Baily, ‘Further Observations on a Regional Epidemic of
malaria in Northern Sind,’ Records of the Malaria Survey of India, 6, 3, Sept.
1936, 411–437, at 426.
3 C.A. Gill, Report on the Malaria Epidemic in Ceylon in 1934–35 (Colombo:
Ceylon Govt Press, 1935).
4 S.R. Christophers, ‘Commentary,’ in C.A. Gill, ‘Some Points in the Epidemiol-
ogy of Malaria Arising out of the Study of the Malaria Epidemic in Ceylon in
1934–35,’ Transactions of the Royal Society of Tropical Medicine and Hygiene,
29, 5, Feb. 1936, 427–480, at 466–469.
5 S.R. Christophers, ‘Malaria in the Punjab,’ Scientific Memoirs by Officers of the
Medical and Sanitary Departments of the Government of India (New Series),
No. 46 (Calcutta: Superintendent Govt Printing, 1911).
6 R. Briercliffe, The Ceylon Malaria Epidemic, 1934–35. Report by the Director
of Medical and Sanitary Services (Colombo: Ceylon Govt Press, 1935), 26–27.
Briercliffe’s maps and charts were published separately as a Supplement to his
main 1935 report.
7 Ibid., 27.
8 G. Harrison, Mosquitoes, Malaria and Man: A History of the Hostilities since
1880 (New York: E.P. Dutton, 1978), 203.
9 V.B. Wigglesworth, ‘Malaria in Ceylon,’ Asiatic Review, 32, 1936, 611–619, at
613; Dunn, Malaria in Ceylon, 5; Harrison, Mosquitoes, Malaria and Man, 205.
10 T.W. Tyssul Jones, ‘Deforestation and Epidemic Malaria in the Wet and Interme-
diate Zones of Ceylon,’ Indian Journal of Malariology, 5, 1, Mar. 1951, 135–
161, Map 2 at 140 [hereafter, IJM].
11 S. Rajendram, and S.H. Jayewickreme, ‘Malaria in Ceylon,’ IJM, 5, 1, Pt. 1,
Mar. 1951, 1–73.
12 For the definition of spleen rate, see ch. 1, note 66.
13 Agricultural impoverishment was not inevitable in the dry zone; historically, the
northern half of Ceylon supported a vibrant canal irrigation rural economy;
T.W. Tyssul Jones, ‘Malaria and the Ancient Cities of Ceylon,’ IJM, 5, 1, Mar.
1951, 125–133; Briercliffe, The Ceylon Malaria Epidemic, 43.
14 Tyssul Jones, ‘Deforestation and Epidemic Malaria; Briercliffe, The Ceylon
Malaria Epidemic, 23–26; H.F. Carter, and W.P. Jacocks, ‘Observations on the
Transmission of Malaria by Anopheline Mosquitoes in Ceylon,’ Ceylon Journal
of Science, Section D, Pt. 2, 1929, 67–86.

70
 THE 1934–1935 CEYLON EPIDEMIC

15 Gill, Report on the Malaria Epidemic in Ceylon, 19. Dunn reports ‘11.3 inches
of rain between October 6 and October 30. . . rain [that] partially flushed the
river breeding grounds of the mosquito . . . but the relative humidity rose from
51 per cent before the rain to 72 per cent after’; Malaria in Ceylon, 22.
16 Briercliffe, The Ceylon Malaria Epidemic, 35.
17 Ibid., 28, 41–42, Chart 7.
18 Gill, Report on the Malaria Epidemic in Ceylon, 17.
19 Ibid., 16.
20 Briercliffe, The Ceylon Malaria Epidemic, 26. Gill summarized earlier entomo-
logical findings by H.F. Carter as showing that ‘although An. culicifacies exhibits
a predilection for sun-lit pools in river beds, it also breeds freely and frequently
in many other situations, more especially in wells, . . . borrow pits, quarries,
drains, and pools and sheets of water formed during the rains’; Gill, Report on the
Malaria Epidemic in Ceylon, 15; H.F. Carter, ‘Report on Malaria and Anopheline
Mosquitoes in Ceylon.’ Sessional Paper VII. (Colombo: Ceylon Govt Press, 1927);
H.F. Carter, and W.P. Jacocks, ‘Observations on the Transmission of Malaria by
Anopheline Mosquitoes in Ceylon,’ Ceylon Journal of Science, 2, Pt. 4, 1930.
21 Briercliffe, The Ceylon Malaria Epidemic, 39; S. Rajendram and Jayewickreme,
‘Malaria in Ceylon,’ 54.
22 Briercliffe, The Ceylon Malaria Epidemic, 44–46. Deaths recorded among chil-
dren under 5 years of age in 1908 Punjab ranged from 47 per cent in Amritsar
city to 60–80 per cent in smaller rural towns where age distribution was less
likely affected by adult male migration; S. Zurbrigg, Epidemic Malaria and Hun-
ger in Colonial Punjab: ‘Weakened by Want’ (London and New Delhi: Rout-
ledge, 2019), 62.
23 The proportion of falciparum infections increased over the course of the epi-
demic, from 24.7 per cent in November to 43.7 per cent in January; Briercliffe,
The Ceylon Malaria Epidemic, 46–48.
24 Ibid., 39.
25 Ibid., Map 18. Rather confusingly, Briercliffe uses the term ‘epidemic zone’ on
a contour map (Map 6) and in a subheading (p. 21); otherwise, he refers to the
‘epidemic area’ (or ‘districts affected by the epidemic’) throughout the text, in
contrast to districts ‘outside the epidemic area.’ The demarcating line based on
the four-river watershed is referred to on Maps 18 and 19 as the ‘Boundary of
Epidemic 1934–35.’
26 Ibid., 40.
27 Ibid., 39.
28 Briercliffe, The Ceylon Malaria Epidemic, 43, Map 18.
29 Ibid., Map 19.
30 Ibid., 40, 43.
31 Ibid., 18.
32 Ibid., 21, Table 9; R.M. Dickson, ‘The Malaria Epidemic in Ceylon, 1934–35,’
Journal of the Royal Army Medical Corps, 1935, 85–90.
33 Briercliffe, The Ceylon Malaria Epidemic, 46, Table 24(b).
34 Ibid., 44.
35 The highest ‘Epidemic Figure’ area (7–12 times ‘normal’) appears to have
extended beyond the ‘intermediate zone’ of 20–40 per cent spleen rates to
slightly overlap the neighbouring dry zone divisions of 40–60 per cent spleen
rate; the second highest ‘Epidemic Figure’ area (4–7) extended well into the
northern 40–60 per cent region.
36 Briercliffe, The Ceylon Malaria Epidemic, 43. In a 1929 report, Carter described
‘great hardships’ for the dry north-central population, ‘the people are in a

71
 THE 1934–1935 CEYLON EPIDEMIC

continual state of ill-health through malarial infections and lack of food. . . . [I]t
is scarcely surprising that many of the villages in the interior of the dry zone are
poverty stricken, that malaria and other disease are prevalent’; Carter, ‘Report
on Malaria and Anopheline Mosquitoes in Ceylon,’ 8, as cited in Briercliffe, The
Ceylon Malaria Epidemic, 43.
37 E. Meyer, ‘L’Épidémie de malaria de 1934–1935 à Sri-Lanka: fluctuations
économiques et fluctuations climatiques,’ Cultures et Développement, 14, 2–3,
1982, 183–226, at 186; ibid., 14, 4, 589–638.
38 Briercliffe, The Ceylon Malaria Epidemic, Supplement, Chart 3.
39 World Bank, The Economic Development of Ceylon (Baltimore: Johns Hopkins
Press, 1952), 12.
40 H.E. Newnham, Report on the Relief of Distress due to Sickness and Shortage of
Food, September 1934 to December 1935 (Colombo: Ceylon Government Press,
1936), 6–7.
41 Ibid., 7; S.R. Christophers, ‘Endemic and Epidemic Prevalence,’ in M.F. Boyd,
ed., Malariology (Philadelphia: W.B. Saunders, 1949), 698–721, at 712.
42 Newnham, Report on the Relief of Distress, 7.
43 Briercliffe, The Ceylon Malaria Epidemic, 27. Briercliffe mapped 1934 South-
West Monsoon (May–Sept.) deficit levels using absolute rainfall figures rather
than proportionate decline, the resulting map failing to convey relative severity
of the drought in the normally low-rainfall (dry) zone; Briercliffe, The Ceylon
Malaria Epidemic, Map 13; R. Briercliffe, and W. Dalrymple-Champneys, ‘Dis-
cussion on the Malaria Epidemic in Ceylon, 1934–35,’ Proceedings of the Royal
Society of Medicine, 29, 1936, 543, Fig. 5.
44 Briercliffe, The Ceylon Malaria Epidemic, 27, 68.
45 Ibid., 20.
46 Gill employed subdistrict (division) mortality data from 130 registration circles,
as had Christophers with Punjab thana-level data, to map epidemic intensity spa-
tially across the island. His ‘normal’ comparative rate, however, was the mean
Nov. 1933–Mar. 1934 death rate rather than a quinquennial mean ‘because the
statistical data for a longer period could not be obtained without undue delay’;
Report on the Malaria Epidemic in Ceylon, 11–12, Map IV.
47 Christophers, Malaria in the Punjab, Maps 1 and 3; reproduced in Zurbrigg,
Epidemic Malaria and Hunger, 67, 69.
48 Christophers, ‘Endemic and Epidemic Prevalence,’ 712. On the etiological sig-
nificance of the focal mortality pattern, see Zurbrigg, Epidemic Malaria and
Hunger, 68–69.
49 Ceylon, Administrative Report, Commissioner of Labour, 1935, 24; as cited in
Meyer, ‘L’Épidémie de malaria,’ 195; S.A. Meegama, ‘Malaria Eradication and its
Effect on Mortality Levels,’ Population Studies, 21, 3, Nov. 1967, 207–237, at 230.
50 Meegama, ‘Malaria Eradication,’ 230.
51 Meyer, ‘L’Épidémie de malaria,’ 194.
52 Meegama, ‘Malaria Eradication,’ 229.
53 Meyer, ‘L’Épidémie de malaria,’ 194. Meyer questions the strict ‘enclave’ notion
of the estate economy, suggesting considerable interflow; ‘ “Enclave” Planta-
tions, “Hemmed-In” Villages and Dualistic Representations in Colonial Ceylon,’
Journal of Peasant Studies, 19, 3/4, 1992, 199–228, at 194.
54 Dunn’s figures suggest one-eighth of the population of the estate districts consti-
tuted estate labour households; Malaria in Ceylon, Graph 2.
55 Meyer, ‘L’Épidémie de malaria,’ 213.
56 ‘[I]l existe une corrélation spatiale précise entre la localisation de l’épicentre du
fléau et celle de nombreuses communautés non-Goyigama’; Meyer, ‘L’Épidémie
de malaria,’ 198–199.

72
 THE 1934–1935 CEYLON EPIDEMIC

57 Administrative Report, Western Province (Colombo, Kalutara), 1935, A5;

Administrative Report, Sabaragamuwa Province (Ratnapura, Kegalle), 14; as
cited in Meyer, ‘L’Épidémie de malaria,’ 194, 198–200.
58 Briercliffe, The Ceylon Malaria Epidemic, 51.
59 Newnham, Report on the Relief of Distress, 45–46; cited in Meegama, ‘Malaria
Eradication,’ 230.
60 Briercliffe, The Ceylon Malaria Epidemic, 27.
61 In his review of earlier epidemics, Briercliffe pointed to co-existing conditions
of famine or aggregation of migrant labour. An 1894 epidemic was ‘attributed
to “the opening of tea estates on new land in the district aggravated by scarcity
of food and bad water from long continued drought.”. . . . The following year,
1895, fever was . . . attributed to the disturbance of the soil when cutting the rail-
way from Galle to Matara.’ A major epidemic in 1906 occurred in ‘those parts
of the country where large tracts of land were being cleared for the extension of
rubber cultivation, there the fever was most virulent and widely prevalent’; The
Ceylon Malaria Epidemic, 66. On the heightened malaria lethality related to
‘aggregation of tropical labour’ in British India, see Zurbrigg, Epidemic Malaria
and Hunger, 228–231.
62 Dunn, Malaria in Ceylon, 54l; Wigglesworth, ‘Malaria in Ceylon,’ 617.
63 Dunn, Malaria in Ceylon, Appendix, ‘Graph 2.’ Dunn, too, noted large mor-
tality differentials within the epicentre districts – indeed, went to the trouble
of graphing death rate differentials between the estate and non-estate (general)
population for each of the six estate districts. But these apparent anomalies were
set aside in his conclusions, leaving the impression that local differences in trans-
mission and non-immunes were sufficient to explain the epidemic of deaths.
64 He describes ‘un intéressant phénomène d’amnésie collective, chacune des épi-
démies qui se sont succédées depuis le milieu du XIXème siécle ont été quali-
fiées par les contemporains de sans précédent’; Meyer, ‘L’Épidémie de malaria,’
205 [emphasis added]; as noted in R. Briercliffe, and W. Dalrymple-Champneys,
‘Discussion on the malaria epidemic in Ceylon, 1934–35,’ Proceedings of the
Royal Society of Medicine, 29, 1936, 537–562, at 547.
65 Briercliffe and Dalrymple-Champneys, ‘Discussion on the Malaria Epidemic.’
66 Gill, ‘Some Points in the Epidemiology of Malaria,’ 458.
67 Ibid., 460–465.
68 Ibid., 477.
69 In their account of the Ceylon epidemic to the Royal Society of Medicine three
months earlier in November 1935, Briercliffe and Dalrymple-Champneys pref-
aced their presentation by pointing to ‘the misleading and inaccurate accounts
[of the epidemic] in the lay press of many countries . . . render[ing] it particularly
desirable that a clear account of the chief events and circumstances should be
given to the medical profession’; Briercliffe and Dalrymple, ‘Discussion on the
Malaria Epidemic,’ 537.
70 Ross, in admonishing Christophers and colleagues in 1904 for the ‘failure’ of
malaria control at Mian Mir, Punjab, had faulted them for inadequate quanti-
tative assessment of vector numbers, and urged analysis ‘prefaced by a math-
ematical inquiry’; R. Ross, ‘The Anti-Malarial Experiment at Mian Mir, Punjab,
India,’ Journal of Tropical Medicine, Aug. 15, 1904, 255.
71 L. Bruce-Chwatt, and V.J. Glanville, eds., Dynamics of Tropical Diseases: The
Late George Macdonald (London: Oxford University Press, 1973).
72 Interestingly, it would be Newnham, a non-medical official, who cited the socio-
economic conclusions of the earlier League of Nations Malaria Commission
reports; Newnham, Report on the Relief of Distress, 42, as noted by M. Jones
in her overview of the 1934–1935 epidemic and relief measures; Health Policy

73
 THE 1934–1935 CEYLON EPIDEMIC

in Britain’s Model Colony, Ceylon (1900–1948) (New Delhi: Orient Longman,

2004), 187–203.
73 P.F. Russell, Malaria: Basic Principles Briefly Stated (Oxford: Blackwell Scientific
Publs, 1952), 100.
74 G. Macdonald, ‘The Analysis of Equilibrium in Malaria,’ in Bruce-Chwatt and
Glanville, eds., Dynamics of Tropical Diseases, 132 [emphasis added].
75 K.T. Silva, ‘Malaria Eradication as a Legacy of Colonial Discourse: The Case of
Sri Lanka,’ Parassitologia, 36, 1994, 149–163.
76 Harrison, Mosquitoes, Malaria and Man, 202–206. For continuing focus on
acquired immunity in contemporary epidemic malaria analysis, see M.J. Bouma,
and H. van der Kaay, ‘The El Niño Southern Oscillation and the Historical
Malaria Epidemics on the Indian Subcontinent and Sri Lanka: An Early Warning
System for Future Epidemics?,’ Tropical Medicine and International Health, 1,
1, Feb. 1996, 86–96. For a critique of mathematical modelling in malaria work,
see J.A. Nájera, ‘A Critical Review of the Field Application of a Mathematical
Model of Malaria Eradication,’ Bulletin of the World Health Organization, 50,
1974, 449–457.
77 Harrison, Mosquitoes, Malaria and Man, 205.
78 Christophers, ‘Commentary,’ in Gill, ‘Some Points in the Epidemiology of
Malaria,’ 469.
79 Harrison notices Christophers’s attention to dose of infection. But he appears
to interpret increased dose simply as a function of exponential increase in trans-
mission and infection prevalence, assuming that a ‘snowballing’ in human and/
or vector infection rate (prevalence) is accompanied necessarily by a parallel
increase in the amount of infection (numbers of sporozoites) inoculated per
infected mosquito bite; Mosquitoes, Malaria and Man, 207.
80 Christophers, ‘Endemic and Epidemic Prevalence,’ 712.
81 Christophers, ‘Commentary,’ in Gill, ‘Some Points in the Epidemiology of
Malaria,’ 467–469.
82 Christophers, Malaria in the Punjab.
83 S.R Christophers, and C.A. Bentley, Malaria in the Duars: Being the second
report to the Advisory Committee Appointed by the Government of India to
Conduct an Enquiry Regarding Black-water and Other Fevers Prevalent in the
Duars (Simla: Government Monotype Press, 1911), 7, 51.
84 Russell, Malaria: Basic Principles Briefly Stated, 100; Macdonald, ‘Analysis of
Equilibrium in Malaria,’ 132; W. Dalrymple-Champneys, ‘Commentary,’ in Gill,
‘Some Points in the Epidemiology of Malaria,’ 477.
85 Briercliffe, The Ceylon Malaria Epidemic, 64; Rajendram and Jayewickreme,
‘Malaria in Ceylon,’ 21.
86 Wigglesworth, ‘Malaria in Ceylon,’ 619.
87 Packard and Gadelha also suggest that in the wake of the LNMC’s emphasis
on malaria as a ‘social disease,’ the highly publicized Rockefeller campaign to
eradicate An. gambiae (recently identified as An. arabiensis) in northwest Brazil
was key to the ‘resuscitation of the vector centred approach’ in the late 1930s;
‘A Land Filled with Mosquitoes: Fred L. Soper, the Rockefeller Foundation, and
the Anopheles Gambiae Invasion of Brazil,’ Medical Anthropology, 17, 1997,
215–238.
88 M.J. Dobson, M. Malowany, and R.W. Snow, ‘Malaria Control in East Africa:
The Kampala Conference and the Pare-Taveta Scheme: A Meeting of Common
and High Ground,’ Parassitologia, 42, 2000, 149–166. See below, ch. 6.
89 M. Yacob, and S. Swaroop, ‘Malaria and Spleen Rate in the Punjab,’ IJM, 1, 4,
Dec. 1947, 469–489.

74
 THE 1934–1935 CEYLON EPIDEMIC

90 A.T.A. Learmonth, ‘Some Contrasts in the Regional Geography of Malaria

in India and Pakistan,’ Transactions and Papers (Institute of British Geogra-
phers), 23, 1957, 37–59, at 48, 38.
91 Macdonald, ‘Analysis of Equilibrium in Malaria,’ 132; P. Russell, L.S. West,
R.D. Manwell, and G. Macdonald, Practical Malariology (London: Oxford
University Press, 1963), 473.
92 Macdonald’s remark appears in discussion of ‘constant transmission build[ing]
up a firm immunity which prevented epidemic happenings, whereas interrupted
transmission permitted a fall of immunity, followed by an epidemic’; ‘Analysis
of Equilibrium in Malaria,’ 132.
93 The one exception was the year 1942 with war-time hyperinflation, poor har-
vests, and absence of standard relief measures. On this, see Zurbrigg, Epidemic
Malaria and Hunger, ch. 12.
94 Christophers, for example, was aware of epidemic decline, in his 80s ponder-
ing the contribution of flood control; S.R. Christophers, ‘Policy in Relation to
Malaria Control,’ IJM, 9, 4, 1955, 297–303, at 301.
95 In hyperendemic areas ‘the infective reservoir is almost exclusively in new
entrants, either newborn children or immigrants. . . . This type of governing
mechanism is susceptible of mathematical analysis . . . but such an analysis
is not attempted here’; G. Macdonald, ‘Community Aspects of Immunity to
Malaria,’ in Bruce-Chwatt and Glanville, eds., Dynamics of Tropical Dis-
ease, at 82.
96 Macdonald, ‘Analysis of Equilibrium in Malaria,’ 133 [emphasis added].
97 G. Macdonald, ‘On the Scientific Basis of Tropical Hygiene,’ Presidential
address, Transactions of the Royal Society of Tropical Medicine and Hygiene,
59, 1965, 622–630, in Bruce-Chwatt and Glanville, eds., Dynamics of Tropi-
cal Disease, 26. J.A. Nájera remarks that ‘the idea that the epidemiology of
malaria could be unified in a single theoretical model gave a major impulse to
the concept that all malaria situations could be controlled by a single method’;
‘ “Malaria Control” Achievements, Problems and Strategies,’ Parassitologia,
43, 2001, 1–89, at 42.
98 W. Byam, and R.G. Archibald, eds., The Practice of Medicine in the Tropics
(London: Henry Frowde, Hodder, and Stoughton, 1922), vol. 2, 1514. Spleen
rates, Christophers once again stressed in 1949, were commonly observed to
be much higher among the poor, a pattern attributed not primarily to greater
exposure to infection among the poor but to reduced capacity to throw off
infection; ‘Endemic and Epidemic Prevalence,’ 704.
99 Macdonald, ‘Analysis of Equilibrium in Malaria,’ 135, 145.
100 Wigglesworth, ‘Malaria in Ceylon,’ 612.
101 Dunn, Malaria in Ceylon, 16, 11.
102 See also Meegama, ‘Malaria Eradication,’ 209.
103 D.L. Doolan, C. Dobaño, and J.K. Baird, ‘Acquired Immunity to Malaria,’
Clinical Microbiology Review, 22, 1, Jan. 2009, 13–36; H. Krisin, et al.,
‘Malaria in a Cohort of Javanese Migrants to Indonesian Papua,’ Annals of
Tropical Medicine and Parasitology, 97, 6, Sep. 2003, 543–556; J.K. Baird,
et al., ‘Adult Javanese Migrants to Indonesian Papua at High Risk of Severe
Disease Caused by Malaria,’ Epidemiology and Infection, 131, 1, Aug. 2003,
791–797.
104 With the exception of holo- or hyperendemic conditions where re-inoculation
is continuous, the protective effect of a single infective exposure was limited,
due to high levels of pleomorphism, multiple ‘antigenically distinct races or
strains between which [immunological] cross-protection is incomplete’; I.A.

75
 THE 1934–1935 CEYLON EPIDEMIC

McGregor, and R.J.M. Wilson, ‘Specific Immunity: Acquired in Man,’ in W.H.

Wernsdorfer, and I.A. McGregor, eds., Malaria: Principles and Practice of
Malariology (Edinburgh: Churchill Livingstone, 1988), 559–619, at 571.
105 S.R. Christophers, J.A. Sinton, and G. Covell, ‘How to Do a Malaria Survey,’
Health Bulletin, No. 14 (Calcutta: GOI, 1931), 110 [emphasis added].
106 Christophers, ‘Malaria in the Punjab,’ 73; Christophers, ‘Endemic and Epi-
demic Prevalence,’ 712. On this, see Zurbrigg, Epidemic Malaria and Hun-
ger, 82.
107 Christophers’s obituarist described him as a person without rancor, ‘impos-
sible to quarrel with,’ who ‘inspired respect, admiration and affection in all
those who worked with him’; M.W. Service, ‘Obituary. Sir Rickard Christo-
phers: A Tribute,’ Transactions of the Royal Society of Tropical Medicine and
Hygiene, 72, 1997, 678–680. This degree of collegial respect however could at
times leave it difficult to distinguish colleagues’ views from his own.
108 Christophers, ‘Endemic and Epidemic Prevalence,’ 709–710. It has been sug-
gested that with the 1930s’ identification of differing anopheline ‘sibling’ spe-
cies based on differential feeding habits (animal or human), Christophers came
to de-emphasize economic factors in his malaria analysis; H. Evans, ‘European
Malaria Policy in the 1920s and 1930s: The Epidemiology of Minutiae,’ ISIS,
80, 1989, 40–59, at 58–59. Yet such a shift is not evident in his later writing:
Christophers, ‘Endemic and Epidemic Prevalence’; Christophers, ‘Measures for
the Control of Malaria in India,’ Journal of the Royal Society of Arts, Apr. 30,
1943, 285–296, at 290.
109 Christophers, ‘Endemic and Epidemic Prevalence,’ 717–718.
110 Christophers, ‘Measures for the Control of Malaria in India,’ 289.
111 Christophers, ‘Endemic and Epidemic Prevalence,’ 715.
112 Great Britain, Report of the Royal Commission on Agriculture in India (Lon-
don: HMSO, 1928), vol. 1, Pt. 1, 145.
113 Macdonald, and Majid, ‘Report on an Intensive Malaria Survey,’ 466; G. Cov-
ell, ‘Method of forecasting and mitigating malaria epidemic in India,’ LNMC.
mimeograph document, C.H./Malaria/257–258, Geneva, Mar. 31, 1938.
114 In his 1957 overview of the Indian malaria literature Learmonth notes ear-
lier discussion of economic factors, but concludes that ‘[r]ecent work makes
one cautious about this nutritional factor,’ steering discussion to non-immune
young children; ‘Some contrasts in the regional geography of malaria,’ 48, 38.
A recent exception to the sidelining of hunger-induced malaria fulminancy
appears in the work of J.A. Nàjera; ‘ “Malaria control” achievements, prob-
lems and strategies,’ 23.
115 H.E. Shortt, and P.C.C. Garnham, Biographical Memoirs of Fellows of the
Royal Society, 25, 1979, 178–207, at 188, doi: 30928. Six years earlier, on the
occasion of his birth centenary, Christophers’s Punjab study was singled out
for praise for ‘introduc[ing] the method of mapping the incidence of malaria
and the possibility of predicting its occurrence on the basis of rainfall records.
Control measures by water management were suggested and applied with some
success’; L. Bruce-Chwatt, ‘Sir Rickard Christophers: The First 100 Years,’
Transactions of the Royal Society of Tropical Medicine and Hygiene, 67, 5,
1973, 729–730 [emphasis added].
116 P. Russell, ‘Some Aspects of Malaria in India,’ July 5, 1941, Rockefeller Archive
Centre, RG.1.1. S.464 B.11 f.87; as cited in J. Farley, To Cast Out Disease:
A History of the International Health Division of the Rockefeller Founda-
tion (1913–1951) (Oxford: Oxford University Press, 2004), 123. In another
inversion, Russell elsewhere would describe the ‘social obstacles’ to malaria

76
 THE 1934–1935 CEYLON EPIDEMIC

control to be ‘absence of educated’ public opinion, insufficient technical per-

sonnel, ‘lack of cognizance by public officials as to the cost of malaria’ and a
‘widespread ineptness in applying . . . the results of research in malariology’;
‘Malaria and its Influence on World Health,’ Bulletin of the New York Acad-
emy of Medicine, Sept. 1943, 597–630.
117 Recent research linking increased malaria morbidity and zinc deficiency may be
an exception.

77
 3
HUNGER ECLIPSED
Nutritional science in colonial South Asia

Alongside the dramatic medical science developments in entomology and

immunology in the early years of the twentieth century, the 1920s were a
period of rapid advances in understanding of the micronutrient constituents
of food, a research field initially termed ‘chemical hygiene.’1 In recent years,
much scholarship has been directed to the emergence of the ‘new science
of nutrition,’ exploring its powerful influence on Western dietary practices
and the rise of commercial food industries.2 Rather less attention, by com-
parison, has focused on what was left behind in the process. Within the new
medical subdiscipline of nutritional science, earlier concern for quantita-
tive hunger rapidly was overshadowed by that for food quality, seen largely
in terms of micronutrient deficiencies. In Western industrialized countries
this shift in nutritional focus took place at a time when hunger as a wide-
spread social reality, if not vanquished, was in considerable retreat through
a beginning rise in wage levels, and labour and social security legislation.
Elsewhere, however, the new dietary science came to compete with, and
largely supplant, attention to ‘macronutrient’ deficiency in societies where
both acute and chronic hunger still remained pervasive realities.3
The overshadowing of hunger as a medical category and as a central his-
toriographical subject is a question of much broader dimensions and sig-
nificance for health and demographic history than can be addressed here.
In this chapter, we consider simply two aspects of this transformation as
it unfolded in colonial India: first, its epistemic impact as one additional
strand contributing to the demise in understanding of hunger as a central
factor in South Asian malaria mortality history; and second, the principled
efforts of a handful of scientists, nascent trade unions, and members of the
Indian public who questioned and sought to resist the reductive character
and consequences of the new dietary science.
Colonial interest in micronutrient deficiency states in India grew rapidly
in the early years of the twentieth century, in no small part propelled by the
emergence of the syndrome of beriberi among naval and other institutional
populations in eastern and South Asia in the late nineteenth century. One of
the early consequences of modern food processing, beriberi in its epidemic

78
 HUNGER ECLIPSED

form was a paralytic syndrome that notably appeared with the rapid expan-
sion of machine-milling of staple grains, in particular rice. Early on, the
disease had been linked to diet, its sudden appearance in the Japanese navy
prompting a shift to more varied food rations, a measure that saw the inci-
dence of the syndrome plummet from 30 per cent to nil between 1882 and
1886. By the turn of the century Dutch scientists in Java had concluded
that beriberi was a deficiency disease caused by the absence of ‘protective’
substances in ‘polished’ rice, minute substances removed in the process of
industrial machine-milling. In the Malay peninsula, the syndrome was elimi-
nated following a 1911 government prohibition on highly polished rice sup-
plied to government institutions.4 The specific seed-coat substance removed
in milling would be identified in 1926 as thiamine, termed vitamin B1.5
In India, formal nutritional research began in the 1910s, undertaken by Colo-
nel R. McCay, a physiologist at Calcutta Medical College, work that initially
focused on protein and its relative content in the region’s staple foodgrains.6
With the identification of specific vitamins through the 1920s, interest rapidly
extended to micronutrient deficiencies as well, with a Beri-beri Enquiry initiated
in 1921 under Robert McCarrison at the Pasteur Institute at Coonoor in the
western hills of the Madras Presidency.7 Four years later, the institute’s man-
date broadened to ‘Deficiency Diseases’ in general, and in 1929, the Nutrition
Research Laboratories were formally established also at Coonoor.
As in much of the world, the paradigmatic power of the new science
of nutrition was immediate. Where in 1922 the Indian Medical Gazette
had described insufficient food (hunger) as the overwhelming nutritional
problem facing the country and interpreted micronutrient deficiency states
as largely problems of poverty (not enough of any food), by 1936 a special
nutritional issue of the same journal would be devoted exclusively to issues
of ‘dietary’ quality. Frank states of micronutrient deficiency diseases such
as beriberi were uncommon, medical advisors acknowledged, but ‘milder
forms’ were now considered a wide-spread form of ‘hidden hunger.’8
In the early nutritional literature, the term ‘malnutrition’ was used in its
etymological sense of dietary imbalance rather than insufficient food (under-
nourishment). McCarrison was at pains to emphasize the distinction, defining
malnutrition as ‘the impairment of the normal physiological processes of the
body consequent on the use of a food which is deficient in quality although it
may be abundant in quantity.’9 Although his interest included specific micro-
nutrient deficiencies such as iodine deficiency in relation to goitre in certain
Himalayan hill tracts, a major focus to McCarrison’s research was what he
considered to be macronutrient imbalance: insufficient dietary protein and
excess carbohydrate, a problem he considered particularly serious in southern
and eastern regions of India where rice was a common staple grain.10

The effect of imperfect food in causing a degree of physical inef-

ficiency, which may not be associated with any gross evidence of

79
 HUNGER ECLIPSED

disease, is exemplified in India as in few other countries in the

world. . . . Malnutrition is thus the most far-reaching of the causes
of disease in India. It is one of the greatest – if not the greatest –
problems with which the investigator of disease is faced.11

The concern with rice stemmed from what was seen as the grain’s low
protein content. It was believed that where diets were based primarily on
rice, the ‘bulk’ of such a diet made it difficult to consume quantities suf-
ficient to meet protein requirements. For Western scientists accustomed to
meat-based diets, the nature and content of protein in common foods was a
long-standing preoccupation.12 In the early twentieth century adult protein
requirement was considered to be above 100 grams per day, almost double
the level recognized as adequate in the 1980s.13
McCarrison’s views on protein deficiency were rapidly embraced in South
Asian medical circles. By the 1930s the Indian Medical Gazette can be seen cor-
respondingly urging, ‘[i]n the language of modern dietetics, . . . the ideal should
be to provide a ‘square meal’ . . . well balanced from the point of view of bulk
as well as flavour and in the approximately correct proportions of essential
constituents.’14 Here, concern with dietary ‘bulk’ no longer meant insufficient
food (staple grains) but rather its opposite, too much carbohydrate, too much
rice in particular. In 1938 a bacteriologist at the recently inaugurated All-India
Institute of Hygiene and Public Health was warning that the ‘great excess of
carbohydrates’ was ‘directly or indirectly responsible . . . for the most severe
ravages of this country by the various tropical diseases, such as malaria, kala-
azar, tuberculosis . . . etc.’15 Thus, in little more than a decade, medical percep-
tion of the ‘nutrition problem’ in India had largely shifted from one of hunger,
not enough food, as articulated so clearly in the 1922 pages of the Indian Medi-
cal Gazette, to instead the wrong kind of food – which, in turn, was interpreted
as a principal cause of economic backwardness and poverty.
These views were rapidly embraced by constituencies well beyond the medi-
cal profession. As a prominent witness invited to testify at the 1926–1927 pro-
ceedings of the Royal Commission on Agriculture in India (RCAI), McCarrison
urged that ‘defective’ and ‘faulty food’ was ‘the most far-reaching of the causes
of disease in India.’16 ‘Cholera, malaria, dysentery, tuberculosis and leprosy
kill their thousands every year; but malnutrition maims its millions, and is the
means whereby the soil of the human body is made ready for the rank growth
of the pathogenic agents of many of those diseases which afflict the Indian peo-
ple.’17 In the course of their proceedings, the Commissioners personally toured
McCarrison’s laboratory at Coonoor, where his experiments comparing growth
of laboratory rats fed a wheat- versus rice-based diet garnered intense interest.18
Commission members came away determined to

dispel the idea that malnutrition and starvation are the same. Actu-
ally, a person suffering from malnutrition may be consuming more

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 HUNGER ECLIPSED

than his system can utilise. . . . [L]ack of physique and vigour in

Bengal was most probably due to a deficiency of protein in the
diet . . . owing to the bulkiness of the rice diet.19

Deficiency diseases, they emphasized, were not primarily economic in origin.

They resulted from ‘the absence of some essential element in the diet. Their
occurrence is, therefore, no indication of poverty and consequent scarcity
of food.’20 The Commission went on to cite estimates prepared by the 1925
All-India Conference of Medical Research Workers that ‘loss of efficiency’
due to ‘preventable malnutrition and disease was not less than twenty per
cent,’ and concluded that malnutrition was a major cause of ‘physical inef-
ficiency and ill-health among the masses of India.’21

‘Nutrient imbalance’ questioned

The rapid embrace of dietary quality as the leading nutrition problem
in India did not go unopposed. Within the public health administration,
officials still attuned to field realities of hunger openly queried the sweep-
ing generalizations of ill-health being offered on the basis of the McCay-
McCarrison research. C.A. Bentley was one, whose testimony at the 1927
hearings of the Royal Commission on Agriculture demonstrates the concep-
tual gulf already at play within the administration. As Director of Public
Health for Bengal and leading analyst of agricultural decline in the Presi-
dency, Bentley was a key witness at the Bengal sessions of the Agriculture
enquiry. In his written submission to the Commission he had had a great deal
to say, not unexpectedly, about the relationship between agriculture, eco-
nomic prosperity, and health.22 Many of the questions directed to him in the
oral hearings, however, related not to agricultural decline, nor to its relation-
ship with malaria, but rather to nutritional deficiency disease in Bengal.23
Following brief enquiries about irrigation, hookworm, and school
latrines, the Commission’s Chairman turned to querying if Bentley attached
‘great importance to the problem of malnutrition in the Presidency,’ a ques-
tion which prompted the following exchange:

BENTLEY: In one sense, yes. There is a very large proportion of the popula-
tion that at certain times of the year or in certain districts does not get
enough nourishment at all.
CHAIR: That is starvation. I want to know whether the diet is badly bal-
anced or whether certain essential food-stuffs are absent? . . . Do they
take too much rice?
B: They take too little proteids [sic] The milk-supply is very poor. It is very
costly and a large number of people cannot buy milk; they cannot
take sufficient quantity of ghi also. Most of the people cannot take
even fish.24

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 HUNGER ECLIPSED

Unsatisfied, the Commission Chairman repeated the question. Was there

not an ‘excess of rice’ in the Bengali diet? ‘It is one of those things on which
we cannot have too much information,’ Bentley replied diplomatically, add-
ing, ‘[i]t is very difficult to say whether one would place this problem above
everything else in importance. But there is no doubt that it is exceedingly
important.’ Frustrated, a second commissioner reworded the question:

SIR THOMAS MIDDLETON: [I]s it not a most important thing for the public
health of the community . . . that steps should be taken to correct the
ill-balanced diet?
B: This is a thing in which I myself am very keen; I would like to see it. But
I should first like to see them get sufficient food. . . . That is really our
problem in Bengal. I have known cultivators when I was investigating
malaria in villages . . . who at certain times of the year had practically
nothing but the produce of their fruit trees.
M: That would apply only to 10 per cent of the population?
B: No; very much more than that. . . . [I]n certain areas of the Birbhum dis-
trict, a very large proportion of the population do not have enough to
eat, although it has not been considered bad enough to call it a famine.
Only a couple of years ago I visited in the Birbhum district in which
the bulk of the people had not enough food. I went in connection with
cholera, but I found that the people were starving.
M: That is quite likely. But taking the normal position, whereas your state-
ment would refer, one would hope, only to a small percentage. Colonel
McCay’s conclusion that the general diet is ill-balanced must refer to
something like 90 per cent of the population? . . . You are convinced as
a medical man that, generally speaking, it is true that the dietary of a
Bengali is badly balanced?25

To this, Bentley replied with a monosyllabic ‘Yes,’ a response which

prompted, in turn, suggestions for nutritional ‘education and propaganda’
schemes, as he perhaps had anticipated. ‘[W]e have not emphasized it so
much,’ Bentley explained, ‘because it is really not so obvious. If we were to
start emphasizing the question of diet at the present time, in the beginning
we should be looked upon by the bulk of the people as mad men.’ Under
still more urging, however, he ultimately conceded: ‘Yes; we want [dietary]
education in our schools; this is a matter which should be taken up.’26
What is remarkable in this exchange, aside from the seeming lack of
interest in what might be termed ‘ordinary’ (endemic) starvation, is how
thoroughly the idea of qualitative dietary imbalance had already absorbed
official attention, notwithstanding the virtual absence of epidemiological
evidence as to its significance. Enormous questions remained with respect
to the ‘great excess of carbohydrates’ thesis: among others, how applicable
laboratory-based research was to humans; and the degree to which

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laboratory conditions represented ‘native’ diets.27 Nor had any effort been
made to examine empirically the ‘too much rice’ thesis in relation to regional
differences in mortality levels, though general death rates were considerably
lower in the southern ‘rice-eating’ Madras Presidency than in the wheat-
based northwest.28
So compelling was the idea of dietary imbalance that the laboratory find-
ings of McCarrison would override direct epidemiological observation,
including that coming from Bentley, one of the most experienced colonial
Public Health officials in the country. Nor was he alone in questioning the
emphasis on dietary quality. In his testimony to the Commission, the Public
Health Commissioner with the Government of India, J.D. Graham, also
voiced caution in embracing McCarrison’s emphasis on protein deficiency.
Asked if he thought the ‘superior physique of the peoples of northern India’
was due to diet, Graham suggested that

the question is very much sub judice at the moment. Colonel McCay
went very strongly for the absence of the protein elements in the
diet as being the causation; but I showed [in written testimony]
how that had been questioned by Dr. Hindhede, a leading Danish
dietetic expert, and that is one of the reasons why I say we require
more inquiry in India on this particular subject.29

Bentley’s testimony on the degree and priority of the ‘quantitative’ nutri-

tion problem however remained unpursued within the RCAI proceedings.30
Referring back to the work of both McCarrison and McCay, the Com-
mission concluded that ‘diet is the all-important factor in determining the
degree of physical development and general well-being of the people, and
that with a low protein consumption, deficient stamina, mental and physi-
cal, must be expected.’ Echoing McCarrison, it recommended, in addition
to mass dietary education (‘propaganda’) campaigns, greater production ‘of
foodstuffs containing the nutrient substances which the staple food lacks.’31
As for the protein deficiency thesis itself, it remained just that. By the
early 1940s, following analysis of the nutritive value of a range of com-
mon Indian foods, it ultimately was recognized that, where staple foodgrain
consumption was adequate to meet caloric needs, protein requirement also
was generally met. In the case of greater protein requirement among young
children, protein content could be made up with very modest levels of tra-
ditional pulses (lentils).32 Staple foodgrain ‘bulk’ was an issue, but primarily
for its quantitative insufficiency: a problem of poverty.33 But by this point,
the concept and terminology of ‘malnutrition,’ and the thesis of dietary
imbalance, had already become broadly entrenched.
Serious micronutrient deficiency states did exist in the Indian subconti-
nent. These included iodine deficiency in the central sub-Himalayan hills,
and keratomalacia caused by severe vitamin A deficiency, a softening and

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ulceration of the cornea leading to blindness, the latter seen particularly

among young children in the end-stages of severe emaciation. It appeared
also in relation to famine relief camps along with outbreaks of scurvy (vita-
min C deficiency)34 in situations where access to traditional ‘famine foods’
(leafy greens, rich in vitamins A and C) was also severely compromised.
Non-famine consumption of leafy greens was generally more common
amongst the very poor because of their minimal cost as a low status famine
food.35
Severe thiamine deficiency (beriberi) also was a serious medical condi-
tion. But as a phenomenon largely triggered by modern techniques of food
processing, its relationship to poverty was somewhat more complex. As we
have seen, major beriberi outbreaks had appeared abruptly in the late nine-
teenth century amongst naval troops, prisons, schools, and large industrial
undertakings. These were institutions in which large numbers were fully
dependent on centralized provisioning where industrially milled rice was
preferred for its greater resistance to spoilage.36 But ‘polished’ rice had
quickly also assumed a higher social status among the civilian population,
in a fashion similar to that for white bread in Europe a century before. By
the early twentieth century local outbreaks of clinical thiamine deficiency
began to appear as well amongst lower-middle classes in urban centres such
as Calcutta for whom machine-polished rice constituted nearly the sole food
source.37
As for rural prevalence, beriberi was largely localized to the northern
deltaic region of the Madras Presidency (now Andhra Pradesh), known as
the North Circars. Here the syndrome was overtly a disease of poverty, lim-
ited to the agricultural labourer households who produced, and consumed,
the rice now highly polished for export markets, and whose intense impov-
erishment proscribed even minimal consumption of pulses or vegetables.
Elsewhere in the southern rice region of the subcontinent, the traditional
practice of parboiling harvested paddy ensured that adequate thiamine con-
tent remained after milling.38

Micronutrient hunger and the shift of responsibility

What accounts for the ideological power of the new science of dietetics?
Historians of nutritional science in recent decades have traced the profes-
sional and commercial interests associated with modern nutritional theory
in industrialized countries,39 a critique that has been extended to colonial
societies as well in the work of C. Sathyamala, Michael Worboys, V.R.
Muraleedharan, and David Arnold, among others.40 Certainly in South Asia
the idea of ‘micronutrient hunger’ as an invisible menace captured the imagi-
nations of administrators and the educated Indian public as readily as it was
doing in other parts of the world. Presented as primarily a ‘hidden’ hunger,

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it was, by definition, virtually impossible to assess personal risk. Subclinical

degrees of deficiency could, in theory, affect anyone.41 In his position as the
director of the Coonoor Nutrition Research Laboratories, W.R. Aykroyd
(1899–1979) in 1935 ominously suggested in his popular writing that ‘[i]n
all probability, there are food deficiency diseases in India which have never
been observed or described.’42 Six years later, the highly respected Indian
scientist, Sir P.C. Ray, would warn that with respect to the ‘[e]lusive chemi-
cal substances called vitamins . . . there is a large “no man’s land” between
frank illness and optimum health, and it is possible to be well without being
as healthy as an optimum diet would have permitted.’43 Like microbial infec-
tion, hidden nutrient deficiency states increasingly were perceived as a con-
stant, covert threat.
Interest among medical professionals in South Asia probably was further
heightened by the fact that thiamine deficiency presented an epidemiological
profile in some ways different from that of most infective diseases in that
it was not exclusively associated with the rural poor, in Calcutta affect-
ing some urban lower-middle class groups as well. To this extent it offered
something of a moral oasis from the litany of ‘diseases of poverty’ which
otherwise surrounded them. But the idea of micronutrient ‘health’ also
offered many positive attractions. For the educated elite it was modern and
scientific, promising an open-ended possibility of ‘optimum’ health. At the
same time, for colonial administrations dietary therapy appeared to offer a
simple fix for the ill-health and disease of the poor, in theory accessible to
everyone. Like mosquito and malaria eradication, it therefore was attractive
for its seeming broad democratic appeal.
But the micronutrient diagnosis of ill-health also offered the possibility of
shifting responsibility away from the state to the individual. Malnutrition
was rapidly being recast as a problem of ignorance regarding choice of qual-
itatively nutritious foods, the solution to which lay in education. Already,
legislation to limit the high degree of rice ‘polishing’ had been rejected by
the government to assuage commercial grain interests.44 In his October 1926
testimony to the Royal Commission on Agriculture, J.D. Graham, GOI
Public Health Commissioner, highlighted the conclusions of a recent British
Medical Research Council report pointing to ‘maternal [in]efficiency’ as key
to the nutrition problem in Scotland.45 By 1931, the Punjab Public Health
department was citing ‘measures directed against dysgenic habits and cus-
toms,’ as one of its most important tasks: habits, it stressed, ‘that deprive
the body of essential food factors (vitamins), and thereby lower resistance to
infection or give rise to specific disease.’ This, even as the province’s annual
report continued to be prefaced with data on grain prices, harvest condi-
tions, and wage levels.46 The influence of the new dietary science in refram-
ing understanding of the nature of the hunger problem in India, in other
words, was quite profound.

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Dietetic momentum
Beyond scientific fascination, there was a larger momentum involved, how-
ever, similar to that faced by the Government of India in relation to malaria
and the related onus to embrace Anopheles mosquito eradication.47 The
professional imperative to apply ‘scientific’ microbiologic knowledge was
extremely difficult to resist, even for those with extensive professional expe-
rience and administrative authority. In their tenacious grilling of Bentley,
members of the Royal Commission on Agriculture were implicitly ques-
tioning his professional competence: that ‘as a medical man’ he ought to
appreciate the importance of ill-balanced dietaries. It was at this point in the
proceedings that even Bentley relented, agreeing to the educational priority
of balanced dietaries, a view which he clearly saw in the context of rural
Bengal as absurd.
As the former chief medical officer to the Empire of India and Ceylon
Tea Company, Bentley’s concern for hunger could hardly be seen as ideo-
logically driven. As was the case for Christophers and James as well, it was
based on extensive field experience and pragmatic common sense. What
he was describing to the Inquiry Commissioners was endemic acute hun-
ger: recurring, seasonal semi-starvation, superimposed upon general under-
nourishment (‘chronic’ hunger).48 The commissioners clearly did not share
either this experience, or apparently his concern. Presumably they would
have responded to conditions of frank ‘famine’ (epidemic starvation), for
which by this time there were clear administrative obligations. But endemic
hunger, acute and chronic, was not a responsibility of medical professionals,
unlike nutrient imbalance had now become.
Waning interest in, and indeed comprehension of, ‘ordinary’ (non-
famine) hunger on the part of 1926–1927 Agricultural Inquiry members
contrasted starkly with that expressed four decades earlier at the highest lev-
els of the administration in the 1888 Dufferin Inquiry into the condition of
the poorer classes. That earlier enquiry sought to assess both aspects of hun-
ger based upon a common understanding of human subsistence precarity,
one expressed in terms of prevalence of two, one, or zero meals per day.49
Undoubtedly, broader administrative interest in 1888 had been prompted by
a growing political imperative to avoid famines, and the need to know how
close to the edge of starvation the rural poor actually were in the various
regions of the subcontinent. Now, in the 1920s, with frank famine largely
controlled through major recent changes to the Famine Code,50 attention to
the less politically incriminating form of acute hunger – endemic in form –
amongst colonial administrators was fast receding. And so too was its sci-
entific and medical legitimacy as a public health issue.
The problem, of course, lay not in nutritional science itself. Micronutrient
deficiency states did exist and in specific cases could hold important epide-
miological consequences.51 Interpretation of their public health significance

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however was taking place in this period without adequate, indeed often with-
out any, epidemiological investigation. Scientific fascination with the phe-
nomena was outstripping the obligation to place the microbiologic insights
in context, and in turn overriding judgement. In the case of thiamine defi-
ciency, the specific menace was connoted to apply to ‘diet’ in general. Little
attention was paid in the professional literature to the central role of indus-
trial food processing in its etiology as a public health problem. Nor to ready
remedies: simple, minimal additions to staple foods of greens or pulses. The
uncritical presumption of scientific expertise left little room for inserting
commonplace experience, or for incorporating traditional understanding of
‘diet.’ As seen above, in many of the southern rice-growing regions, rural
understanding of thiamine deficiency historically had been evident in the
time- and labour-intensive traditional practice of parboiling rice before
milling. Yet one is hard-pressed to find appreciation of such understanding
reflected in nutritional tracts of the period. Key insights were thus forfeited,
and with them, essential epidemiological perspective. Research into micro-
nutrient disease was not incompatible with concern for macronutrient hun-
ger and its socio-economic dimensions. Nevertheless, as in Britain and other
industrial countries, concern for the former largely came to supplant, rather
than complement, that for quantitative deficiency.52
The academic sidelining of hunger can be seen to reflect a seductive ‘logic’
inherent to scientific discovery, one where new medical discoveries generally
lay in previously ‘hidden’ microbiologic domains. Any tension between the
earlier ‘macrobiologic’ understanding of hunger and the new microbiologic
insights clearly was an artificial one. Nevertheless, the cascading microbial
and micronutrient discoveries of the period provided powerful new areas of
medical expertise and, as Foucauldians would point out, channels of pro-
fessional and political control – a reductive momentum that few within the
South Asian medical community, or elsewhere, felt able publicly to question.
In that process of overshadowing, the visibility and legitimacy of hunger as
a medical and public health category was rapidly being undermined.
A further manifestation of this epistemic transformation can be seen in
the appropriation of language. The expression ‘two square meals a day,’
employed in the Dufferin Inquiry, colloquially meaning ‘enough to satisfy
hunger,’ was a quantitative concept from antiquity. In an unwitting sleight
of hand, a 1936 Indian Medical Gazette editorial on ‘dietary and nutritional
standards in India’ would employ the term instead, however, to convey the
new nutritional sense of ‘square’: ‘one which is well balanced from the point
of view of bulk as well as flavour and in the approximately correct pro-
portions of essential constituents.’53 Here, entirely different meanings were
being wrapped in an earlier language of hunger in a near-seamless supplant-
ing of quantitative issues by qualitative. Basic concepts were being shed and
the very language of hunger itself recast. In the process, the exclusivity of
the new ‘language of dietetics’ was removing access to discussion of hunger

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from the public domain, and corralling it instead within the sphere of medi-
cal specialists. These developments of course were not unique to British
India. Added momentum to the new specialty of nutritional science was
coming from outside India’s borders, in the work of the Health Organi-
sation of the League of Nations (LNHO). And here, also, W.R. Aykroyd
played a central role, in work that preceded his 1935 colonial appointment
to India.

The League of Nations and nutrition

By the early 1930s, the mandate of the League of Nations Health Organi-
sation had expanded to include nutrition alongside communicable disease
control, a concern heightened by the global effects of the economic Depres-
sion.54 In 1931, a nutrition committee was established under Aykroyd, then
a young British nutritionist with epidemiological experience investigating
beriberi in the late 1920s among isolated Newfoundland fishing communi-
ties dependent on highly refined (‘white’) wheat flour. In its earliest delib-
erations, nutrition committee delegates from African colonies and India
had stressed the economic dimensions to the nutrition problem: insufficient
income and food of any kind.55 Over time, however, the committee’s work
veered increasingly to issues of dietary quality, with a particular empha-
sis on milk protein, a shift evident in Aykroyd’s final League of Nations
report.56 Co-authored with Etienne Burnet, the 1935 ‘Nutrition and Public
Health’ report set out a rather different tone. ‘Thirty years ago,’ it began,

it was generally believed that the dietary requirements of human

beings are satisfied so long as they have enough to eat. . . . We now
know that the adequacy of a dietary depends on the presence of
a considerable number of factors and that mere quantitative suf-
ficiency may co-exist with a whole series of qualitative defects.57

Thus set out, the remainder of the report was informed largely by con-
cern for ‘qualitative defects.’ Of its 133 pages, fewer than four dealt with
‘nutrition and poverty.’ Even where raised, economic aspects generally were
qualified. Conclusions from a Czechoslovakian household budgets study at
one point were cited, with the comment that ‘it was irrational to recom-
mend a higher intake of “protective” foods to people who were only just
able to purchase sufficient Calories.’58 Yet this was followed immediately by
the citing of a 1926 British Medical Research Council report59 that stressed
‘maternal inefficiency’:

It is clear that a mere increase in wages or relief would not elimi-

nate all dietary deficiency associated with poverty; education is also
necessary. . . . [There was] no reason to doubt that valuable results

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can be obtained even among families with very small incomes, by

educational means.60

Here, once again, the economic dimension was minimized, indeed trivial-
ized, in this case, as ‘mere’ wages.
But beyond the class-ist and sexist assumptions of maternal ‘ineffi-
ciency,’61 the logic of the educational approach was questionable for another
reason. Dietary studies undertaken during this period, both colonial and
European, consistently showed that household consumption of ‘protective’
foods declined in tandem with lower levels of income – a predictable con-
sequence in light of their greater cost per calorie. A 1933 Swedish study
showed a close relationship, even within the working class, between house-
hold income and the price paid per 10,000 calories. In the Netherlands, ‘the
employed families spent . . . 1.71 [cents] per 100 calories, while the unem-
ployed spent only 1.07 cents.’62
What the inter-war nutrition surveys in fact were demonstrating was the
fundamental rationality of the poor in maximizing the priority caloric value
of the foods chosen in the face of often grossly inadequate income. Igno-
rance (of dietary principles) and income levels were manifestly not of equal
importance in explaining the ‘nutrition problem.’ The overriding barrier
was economic.63
The larger context for the 1935 Burnet-Aykroyd report, and the League
of Nations’ engagement in nutrition, was the Depression-aggravated crisis
in global agriculture and the broader world economy. The global ‘nutri-
tion problem’ was clearly linked to international trade structures and the
contradictory situation where hunger due to unemployment and lack of
purchasing power co-existed with enormous global foodgrain surpluses.
Those surpluses had prompted mass destruction of stocks in Western
countries as a means of supporting their rural constituencies by increas-
ing foodgrain prices.64 But by the mid-1930s prevailing economic doctrine
that had produced policies to ‘restrict production drastically, create scar-
city, and wait for prices to rise’65 was no longer politically tenable. In the
words of the Bengali academic and agricultural scientist Nagendranath
Gangulee, these policies addressed the dilemma of ‘poverty in the midst of
plenty by eliminating the plenty instead of the poverty.’66 Prominent Anglo-
Commonwealth figures at this point stepped in, urging, under the rubric
of ‘a marriage of health and agriculture,’ that the problem of global hun-
ger lay in inadequate extension of modern agro-technology, proposals that
would soon take shape in the post-war Food and Agricultural Organization
(FAO) and ‘green revolution’67 – if without addressing the structural issues
of access to food and to productive resources. In the meantime, however,
following publication of his 1935 ‘Nutrition and Public Health,’ Aykroyd
was appointed to succeed McCarrison as director of the nutrition labora-
tories at Coonoor in India.

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‘Nutrient imbalance’ challenged

Important research on the nutritive value of Indian foods followed under
Aykroyd’s directorship of the Nutrition Research Laboratories at Coonoor,68
work that led in 1938 to a re-evaluation of earlier assumptions regarding
protein deficiency as a priority nutrition concern in India, as we have seen.69
Research emphasis now was channelled into defending the protein ‘quality’
of the native Indian diet and to assessing the relative merits of vegetarian
and non-vegetarian diets. This significant work tended also, however, to
redirect attention to dietary quality aspects. Already, in the earliest months
of his Coonoor appointment, Aykroyd, in his non-academic writing con-
tinued to articulate his view of the ‘malnutrition problem in India’ as one
primarily of ‘faulty diet.’ Policy recommendations, as in many of the major
League of Nations reports, were directed to the production of more food
of ‘superior quality’ and mass education to remedy ‘ignorance and preju-
dice’ underlying such ‘defective diet[s].’70 For Aykroyd himself, this meant
repeated emphasis on the superior quality of milk.71
The academic focus on dietary quality however did not go unopposed.
From the early 1930s, emerging industrial trade unions in India had been
working to re-inject economic dimensions into discussion of the ‘nutrition
problem’ in the country. In their memorandum to the 1931 Royal Com-
mission on Labour, the Bombay Textile Labour Union, for example, sub-
mitted a detailed analysis of industrial wages that showed the cost of even
a very modest nutritionally balanced diet exceeded prevailing wage rates;
indeed, that their caloric purchasing value was lower even than that of
prison rations.72 Subsequent diet surveys of Madras city industrial workers
in 1935–1936 showed only 3 per cent of labourer households with food
budgets sufficient for a ‘well-balanced’ diet.73 For over one-third of house-
holds surveyed total food expenditure amounted to barely half the cost of
a minimally ‘balanced’ diet74 – this, among a group that represented ‘a rela-
tively highly paid class.’75 These data confirmed that the nutrition problem
lay overwhelmingly in the economic realm.
By the 1930s the International Labour Organization (ILO) also was urg-
ing greater attention to economic dimensions of the nutrition problem, as
the human effects of the global Depression continued to deepen. Beyond
basic advocacy, the ILO was circulating similar income survey protocols
internationally to facilitate such economic studies.76 Up to this point the
nutrition problem in South Asia was assumed to be most severe among
the urban labour population.77 But greater investigation of rural conditions
increasingly was being urged, and in 1936 Aykroyd, in collaboration with
colleague B.G. Krishnan, initiated a detailed rural household income and
dietary survey in the Madras Presidency.78 What the survey revealed was a
pattern similar to that of the European survey results, but much more pro-
nounced: amongst low- and lowest-income households, reliance upon the

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least expensive food sources, with negligible consumption in the latter case
of pulses – though only marginally less ‘cheap’ than cereals. Even at this,
daily food intake averaged less than 2,300 calories per consumption unit in
40 per cent of households.79 Among poor tenant households (one-quarter
of study families), food intake averaged 1,664 calories per consumption
unit a day; in 10 per cent of households, less than 1,600 calories.80 Such
levels of severe undernourishment meant that some kind of physiological
‘adjustment’ occurs, the authors observed: ‘basal metabolism is reduced, the
body functioning is at a lower level of vitality . . . the under-fed labourer is
lethargic and his output of work is small. [It is a] level of food intake which
permits only a languid existence.’81 Such households ‘may without exag-
geration be described as half-starved,’ the report concluded, adding that ‘the
problem of under- and malnutrition in South India is more serious than has
yet been realized.’82
Extremely low to nil expenditure on oils, milk, meat, pulses, and vegeta-
bles was documented as well in 1941 among Bihar industrial workers, with
the single partial exception of the cheapest ‘green leafy vegetables.’83 The
consistent nature of the relationship between household income and caloric
consumption level highlighted the overriding role of economics underlying
low consumption of ‘protective’ foods. Indeed, in the early 1950s, an esti-
mated 97 per cent of calories obtained by agricultural labourer households
in India came from cereals, the cheapest food sources available, and even
at this, between one-third and one-half did not meet bare minimum caloric
requirement.84
The stark economic dimensions to the ‘nutrition problem’ in India as
revealed in these studies would be taken up more comprehensively in 1939
by Nagendranath Gangulee, in a 336-page text, Health and Nutrition in
India. Gangulee was a soil biologist, not a nutritionist, who as Professor
of Agriculture, Animal Husbandry and Rural Economy at the University
of Calcutta, had been a member of the 1926–1927 Royal Commission on
Agriculture in India. In the years that followed, however, he had directed
his investigations increasingly to human nutrition. Concern over the grow-
ing tendency for qualitative issues of diet to supplant quantitative in the
nutrition literature had in turn prompted him to compile and analyze data
from available household income and dietary studies. Among them was a
diet survey of Assam tea plantation labourer households that revealed adult
consumption levels to be 15 ounces of staple foodgrains a day, amounting
to approximately 1,460 calories.85 Together, such figures made it clear, he
concluded, that ‘[t]he working class suffers from malnutrition, not because
it is ignorant but because it is poor.’ What was required was not ‘palliation,’
but ‘a profound modification in the economic structure of society.’86
Though at times he assumed the nutritionist division of foods into ‘energy-
producing’ and ‘protective,’ Gangulee did not waver from his insistence on
the primacy of the economic diagnosis. In his 1939 text neither the colonial

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government nor the Indian elite was spared. ‘Moneylenders, landlords, trad-
ers, priests and hosts of others take away the fruits of the labours [of the
poor].’ A solution to hunger required structural reforms that addressed the
‘enormous disparity in incomes which creates a tiny caste of plutocrats and
an immense group of the very poor. . . . [I]n the face of poverty, medi-
cal science is rendered impotent.’87 Structural economic reforms, he urged,
started with establishment and enforcement of a legal minimum wage, but
extended to land reform and overall taxation policies, quoting the Report
of the Indian Statutory Commission as describing British India as ‘a country
in which there are large accumulations of wealth on which the burden of
Government rests very lightly.’88
His most scathing critique was directed to the ‘backward state of agri-
culture’ as the root of the rural hunger problem, pointing out that the ‘land
could yield at least twice or three times as much human food as it does at
present,’ and outlining in the final chapters fundamental reforms required to
remedy agricultural impoverishment, low productivity, and endemic under-
nourishment.89 Here he was also sceptical of purely technological solutions
to agriculture productivity such as chemical fertilizers, arguing instead for
green and farmyard manuring, composting, crop rotation, and seed selec-
tion, practices that had produced far higher yields in eastern Asia, but which
required far greater re-investment of agricultural profits into production.
Above all, he urged effective credit extension to small producers. In his
critique of ‘the combined forces of feudalism and capitalism,’ Gangulee at
times could lapse into somewhat idealized notions of Indian rural society
and possibilities for voluntary self-help.90 Hunger, and its causes, never-
theless were starkly articulated as the overriding ‘nutrition problem,’ both
unnecessary and illegitimate.

Allure of the scientific

The key questions raised by the trade unions and figures like Gangulee in
the 1930s however would remain largely unaddressed within the nutritional
science discipline. Emphasis on the economic roots of ‘malnutrition’ was
unsustained in British India, a pattern common well beyond South Asia. At
one level, attraction to the narrow framework was a function, in part, of
the sweeping euphoria of the time for science and technology. In the context
of the immense failures faced by Western industrial societies – the demon-
strated bankruptcy of economic orthodoxy; the catastrophic consequences
of internecine warfare that enveloped their imperial domains; and imperial
decline itself – science offered a ready antidote to ebbing confidence and
optimism. Overarching faith in science could transcend political bounda-
ries, however, as seen in Soviet Russia as well.
In the medical arena, the career of Aykroyd serves as an example of the
professional search for progress through science, though there can be little

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doubt that he understood poverty to be the ‘basic cause of malnutrition.’ In

1940, for example, he signed his name as co-author to an astute analysis of
the economic ‘rationality’ of south Indian villagers in their rapid adoption
of power milling of rice. The study took into account the time and energy
burden required of women in the hand-milling of rice and the added con-
straints this work posed for their children’s nourishment, and their own.91
The 84-page monograph once again acknowledged that concerns over pro-
tein insufficiency had been ‘exaggerated by certain workers’ and questioned
the ‘myth’ of the supposed ‘indigestibility’ of ‘bulky’ rice diets.92
Yet in his popular writing and in his advisory roles, Aykroyd would con-
tinue to articulate a technical view of the ‘malnutrition problem’ in India.
Citing prospects for vitamin tablets, alongside education and ‘development
of agriculture,’ he insisted that ‘if the resources of science are brought to
bear on the problem, progress can be made, however formidable the obsta-
cles of poverty.’ Acknowledging that the ‘idea of giving malnourished school
children in India a daily capsule, at present seems rather outlandish,’ he
nevertheless urged that ‘science . . . usually has a few aces up her abundant
sleeve. Even in existing economic circumstances . . . much can be done.’93
Technology, in other words, could circumvent constraints of poverty and its
messy underlying socio-political determinants. In one of his last formal pub-
lications in India, he continued to urge the ‘spread of knowledge,’ school
feeding programs, and agricultural policies aimed at correcting ‘the defi-
ciencies in the diet of the population . . . [and] the diseases to which faulty
feeding gives rise.’94
C. Sathyamala highlights this deeply contradictory stance, noting that
‘[e]ven where brief reference was given to poverty or lack of income,’ Ayk-
royd ‘would often minimise their importance by adding additional factors
such as ignorance of food values etc as reasons for undernutrition.’95 In this,
however, he was hardly alone. A parallel shift from insufficient food to micro-
nutrient deficiencies was taking place as well in the Colonial Office. Michael
Worboys has documented the rewriting (‘emasculat[ion]’) of a draft report
submitted in 1936 to an enquiry on malnutrition in Africa which similarly
shifted focus from economics to ignorance in the final published version.96
As expert advisor, Aykroyd consistently gave in to the professional expec-
tation to come up with ‘interventions’ in the technical realm. It was, after
all, the mandate of the nutritional scientist to offer optimism that some-
thing could be done97 – though the option remained of speaking, as a sci-
entist, to both the economic and the biomedical, as Gangulee continued
to do. Instead, circumvention of the economic and political had become a
recurring pattern. Insufficient food, he suggested at one point, was an issue
separate from nutritional science, the former already being addressed by
the appropriate authorities: ‘These are questions of special interest to those
concerned with labour problems and they are at present being actively stud-
ied by the International Labour Office.’98 Nutritional scientists could quite

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legitimately focus on qualitative issues, he was suggesting, which, after all,

was their area of competence.
This compartmentalization of professional responsibilities was mirrored
in a new concept of food itself. Human sustenance had now been catego-
rized into two groups: ‘protective’ foods containing essential vitamins, min-
erals, and ‘first-class protein’ of animal origin, on the one hand, and ‘energy’
foods, on the other.99 By this definition, the diets of most of the world’s
population based on staple foodgrains were automatically ‘unbalanced,’
inherently so. Ignored in this formulation was the fact that most staple
foodgrains supplied a broad range of micronutrients, as well as protein, in
addition to complex carbohydrates. Nutritional science, in effect, was cast-
ing blanket disparagement on a fundamental aspect of colonized societies,
and in doing so, positing yet another realm of ‘native’ culture as requiring
Western enlightenment. In the process also, this binary conceptualization
misconstrued the very nature of food, with ‘protective’ foods, rather than
staple foodgrains, now those ‘most necessary for good health.’100 It was a
powerful recharacterization. Despite deep reservations for many of McCa-
rrison’s conclusions, even M.K. Gandhi would come to refer to polished
rice as ‘pure starch.’101 And it was one that would leave a legacy of misun-
derstanding of basic food needs long into the future. Only in the 1970s did
nutritionists distance themselves from what was the general thesis of protein
deficiency in the low-income world.102 In the meantime however, the new
nutritional science would come to inform two major reports in the dying
days of British rule.

Nutritionist expertise and the Bengal famine

Administrative concern over hunger would reappear starkly in the early
1940s with the Bengal famine bringing to a head the longstanding crisis in
food production in British India. Of any official document of this period, the
report by the Bengal Famine Commission tabled in 1945 might have been
expected to address hunger unequivocally and its relationship to mortality
from infective disease. This would hardly be the case however, as we will
consider below. First, by way of context, a brief overview is offered of the
famine itself.
Much has been written recently about the wartime famine in Bengal in
which over 2 million Bengalis perished in 1943–1944.103 In 1981, Amartya
Sen reclaimed key insights into its causes: most prominent among them was
the fact that starvation was triggered not by harvest failure (food availability
decline) but primarily by hyperinflation: the soaring cost of foodgrains.104
Numerous disastrous errors in foodgrain administration in the province fol-
lowed the 1942 Japanese occupation of Burma (Myanmar). Wartime hyper-
inflation and the British administration’s preoccupation with ensuring rice
supplies to the war-related industrial workforce in Calcutta, culminated in

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1943 in a 500 per cent increase in grain prices throughout Bengal. Despite
desperate pleas from district-levels officials, the government blocked imple-
mentation of the Famine Code, relief measures otherwise routinely applied
from the 1920s on when grain prices rose over 40 per cent above normal
levels.105 For a large portion of the landless poor, purchasing power was
reduced to a tiny fraction of its already bare-subsistence level, and epidemic
starvation ensued.
Sen’s study highlighted as well that the ‘gigantic’ rise in mortality across
the famine period mirrored the normal seasonal pattern of deaths in non-
famine years, ‘just linearly displaced severely upwards’ (Figure 3.1).106
Paramount among the excess deaths was post-monsoon malaria mortality,
though rainfall and environmental conditions were unchanged. In earlier
work, I have explored the central role of starvation underlying the dramatic
rise in malaria lethality in Bengal in 1943,107 and argued that the extremely

Figure 3.1 Mortality, by month, Bengal province, July 1943–June 1944

Source: Based on Famine Inquiry Commission, India. Report on Bengal, 1945, p. 113.

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close seasonal timing of mortality in 1943 relative to non-famine years

strongly suggests magnified lethality of endemic diseases rather than sub-
stantial change in exposure to microbes and malaria vectors. In this sense,
the Bengal famine is a particularly stark example of the power of hunger to
shift infection lethality.
If the Bengal famine is also an abject example of the consequences of
‘scarcity’ in the absence of the Famine Code, it is a demonstration as well of
how close to the edge of destitution much of the population in the final years
of British rule remained. At the close of the colonial period, calorie con-
sumption for the bottom 10 per cent of households in India was estimated
at bare basal metabolic requirement, levels suggesting endemic borderline
semi-starvation, with little capacity for regular work.108 In the absence of
fundamental structural reforms in agriculture, per capita foodgrain avail-
ability had declined steadily after 1920 with the control of famine (epi-
demic starvation).109 Colonial land tenure and lack of affordable credit for
the vast majority of smallholders and tenant cultivators continued to block
increased foodgrain production that otherwise ought to have accompanied
modest growth in population after 1920.110
It is notable, then, that the medical portion of 1945 Bengal Famine Com-
mission report111 largely failed to address the underlying context to the
famine: prevailing endemic hunger. The final report of the Famine Inquiry
Commission did acknowledge that

a well-balanced and satisfactory diet is beyond the means of a large

section of the population. The poor man is forced, in order to sat-
isfy hunger, to depend largely on the cheaper kinds of food. The
lack of purchasing power is thus a most important, perhaps the
most important cause of malnutrition.112

Yet even here, equivocation remains. It is conceivable that by ‘satisfac-

tory diet’ and ‘malnutrition’ the intended meaning was a quantitative one:
enough to eat. But with the terms employed there is no way really to know.
Clarity on the issue of hunger, in other words, even in a famine report, was
elusive with the use of the term ‘well-balanced.’
Moreover, the remark appears to imply that poverty (lack of purchasing
power) was a problem primarily in terms of food quality.113 But was this
actually the case? Did the cheaper staple foods of the poor necessarily place
them at risk of micronutrient deficiencies? The staple grains consumed by
much of the rural population were millets such as ragi (finger millet), jowar
(sorghum), or bajra (pearl millet), grains somewhat richer in micronutrients
and protein content typically than the more expensive grains such as rice.
Leafy greens were cheapest of all – food of the poor, as ‘famine foods’ –
and were an abundant source of vitamins and minerals.114 What does seem
clear is that with the lay language of hunger dispensed with, or in the case

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of ‘square’ meals per day appropriated, the imprecision of the new dietary
discourse made the shift from macro- to micronutrient deficiency that much
easier.
In the immediate aftermath of the 1943–1944 Bengal famine, far-reaching
measures of food rationing and price control measures were instituted, such
that by October 1946 over half the population of British India, more than
150 million people, were included in these policies.115 Accompanied by a
brief post-war economic boom, the modest, but real, shift in food secu-
rity through these distribution programs was associated with a pronounced
decline in mortality levels. In Punjab province, for example, the crude death
rate fell from 27.8 in 1944 to 19.8 in 1946.116 With the acute war-time food
crisis under relative control, however, perception of the nature of the food
problem rapidly narrowed once again to one of food availability rather than
food access. Addressing hunger was becoming primarily a macro-managerial
task directed to increasing overall production.
The question of food availability was not, of course, an unimportant one.
Food production in India in 1957 was still estimated at only 2,200 calo-
ries per adult.117 But in the post-war era, technological methods became a
pre-eminent focus, to the relative neglect of structural barriers to increased
productivity (land reform, tenancy, assured credit access for small produc-
ers). Issues of access to food – ‘underfeeding,’ wages, conditions of work for
women, and maldistribution of all resources – raised with such clarity in the
1930s – would once again recede into the background, and with it, medical
engagement with that vast domain of undernourishment and endemic star-
vation: ‘normal’ hunger.’118
With rapid expansion of Western technical assistance in the immediate
post-war and post-Independence periods, academic interpretation of the
nutrition problem in India reverted increasingly to the domain of nutritional
science and its overriding framework of dietary quality. In the place of wage
legislation and fundamental land reform, nutritional policy was directed to
production of the right kinds of foods and nutritional education.119 Admin-
istratively, this retreat from quantitative hunger would be formally reflected
in 1946 in the pages of the Report of the Health Survey and Development
Committee, chaired by Sir Joseph Bhore.

Hunger and the Bhore report

Commissioned in the final days of the colonial administration as a thorough
overhaul of the medical and public health care systems in India, the Bhore
report has been applauded, justly, for its emphasis on extension of primary
and preventive health care beyond the urban medical enclaves. In address-
ing the underlying ‘nutritional’ determinants of ill-health in India, however,
the Committee largely adopted the narrow framework and language of the
new nutritional science. ‘Faulty nutrition,’ the introductory paragraph to

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chapter 5 (‘The Nutrition of the People’) read, ‘is directly and indirectly
responsible for a large amount of ill-health in the community.’ Based upon a
report by the Nutrition Advisory Committee, the Bhore Committee’s nutri-
tion assessment and recommendations closely reflected those of Aykroyd
who headed the special committee. ‘Defective nutrition,’ it offered, ‘may
take two forms resulting either from an ill-balanced diet, which fails to pro-
vide the required constituents of food in their proper proportions, or from
the energy value of the food being insufficient to provide for all the activities
of the individual concerned.’120 Here, the quantitative dimensions of the
problem – not enough food – is mentioned, but in such terms that one might
be forgiven for failing to recognize the phrasing to mean hunger.
A single reference is made to Aykroyd’s earlier assessment that an esti-
mated 30 per cent of the population did not get enough to eat. But the
admission was followed in the same sentence by a description of Indian diets
as ‘almost invariably ill-balanced . . . in terms of food factors, a deficiency
in fats, vitamins, and proteins of high biological value.’121 Further on, ‘the
main defects of the average Indian diet’ are described as, first, ‘an insuffi-
ciency of proteins’ particularly ‘first class protein’ of animal origin; then, of
mineral salts and vitamins.122
It is puzzling why Aykroyd continued to stress protein deficiency in his
role as advisor to the Bhore committee when his earlier research indicated
otherwise.123 But equally so, why the central issue of ‘insufficient energy
value’ was not followed up with specific policy recommendations, aside from
education, in the 19 pages that detailed the nature of defective nutrition. In
all, only one example of the ‘Economic Aspect of the Problem’ appears in
the 25-page nutrition section of the Bhore report, injected abruptly, as if
the ghost of Nagendranath Gangulee were wafting by the committee room
door: passing reference to the Rs 15 per month wage of peons in the Gov-
ernment Secretariat, a wage level well below the cost of even a very modest
‘balanced’ diet for a family, estimated to be Rs 16–24. ‘These figures,’ the
text read, ‘give a striking illustration of the gulf that existed between the
expenditure necessary on food and that which large numbers of workers
could afford.’124
Yet with the exception of expanded training of nutrition specialists and
school feeding programs, policy measures aimed at addressing the economic
dimensions of the nutrition problem were absent. In their place were rec-
ommendations for fortification of foods (iodized salt), future distribution
of synthetic vitamin tablets, and ‘local nutrition committees . . . to teach
the people satisfactory dietary habits and spread knowledge of nutrition.’
As for poverty, ‘[a]n increase in the prosperity of the country, associated
with a rise in agricultural production,’ it was argued, ‘will . . . automati-
cally produce a general improvement in nutrition.’125 Curiously, the report
‘refrained from making any reference to the activities of the Food Depart-
ment of the GOI . . . confining our review . . . to the period ending with the

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year 1941.’126 Thus the monumental food ration distribution system enacted
across the country in the aftermath of the Bengal famine was left invisible,
and also any discussion of its continuation or its impact on the public’s
health.
Elsewhere, in a chapter on occupational health, the Bhore report did rec-
ommend wage levels to permit 3,000 calories per day for manual workers
in industrial work; also, limiting hours of work for women, and a statu-
tory obligation of industries employing more than 50 women to provide
crèches and free milk to children.127 These brief recommendations however
were largely lost within the 724 pages of the overall report. Moreover, to
the extent that poverty, hunger, and the conditions of work that under-
lay endemic hunger remained the domain of public health, they no longer
belonged within the ambit of ‘nutrition’ discussion. Hunger was no longer
the mandate of nutritional science, as Aykroyd had signalled earlier, but
belonged to the domain of economists or labour organizations. Indeed, the
very word by this point had slipped from view.128
How then did the sidelining of hunger in nutritional science analysis affect
understanding of malaria? We return to Paul Russell’s assertion in 1941 that
‘better food’ failed to offer protection from malaria and the academic cir-
cumstances that may have bolstered this claim, as an important example.129

Nutritional science and malaria

In 1940, researchers at the Nutrition Research laboratories at Coonoor
published the results of a study on the effect of diet on the course of malaria
infection.130 The study involved monkeys experimentally infected with
malaria and subsequently assessed for intensity of infection in terms of ensu-
ing blood parasite levels. Two groups of laboratory animals were tested:
one fed a wheat-based diet with ample milk, pulses, ghee, and vegetables;
the second group, an ‘ill-balanced’ diet limited largely to parboiled milled
rice, and ‘particularly deficient in vitamins C and A and calcium.’ The die-
tary framework employed for assessing ‘malnutrition’ impact was based, in
other words, on qualitative dietary factors rather than quantitative levels of
hunger. Average maximum parasite prevalence was found to be similar in
both groups, and the authors concluded that ‘[t]he course and severity of
primary attacks of malaria were unaffected by the difference in the state of
nutrition of the monkeys previous to infection.’131
In discussing their results, Passmore and Sommerville cited at some
length Christophers’s 1911 report, Malaria in the Punjab. In doing so,
however, they questioned his ‘scarcity’ conclusions, offering simply that the
scarcity-epidemic link could instead be explained on the basis of entomolog-
ical factors alone: drought-induced waning acquired immunity and vector
deviation (increased cattle mortality resulting in enhanced mosquito vector
feeding on humans). Suggesting that their own experimental findings put to

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question the earlier Punjab study conclusions, they went on to advise that
‘[t]he mere association of malnutrition and a high malaria mortality in such
circumstances cannot be taken as proof that malnutrition per se is an impor-
tant or essential factor in the causation of malaria epidemics.’132
It is difficult to see the paper as ideologically influenced, for Passmore was not
disinterested in the issue of hunger. A decade later, for example, he appealed, in
the pages of the Lancet, for less punitive conditions of famine relief and a ‘thor-
ough overhaul’ of policies, arguing that the Famine Codes ‘have neglected the
basic physiology of work.’133 All the more so, then, the Passmore-Sommerville
article reflects the profound conceptual shifts in disease and nutritional thought
that had taken place in the intervening three decades since publication of Chris-
tophers’s 1911 epidemic malaria report. Their conclusion – that severity of
malaria was ‘unaffected by the state of nutrition’ – rested upon a micronutri-
ent definition of ‘nutrition’ (qualitative malnutrition), and additionally, upon a
microbiologic measure of ‘severity’ (blood parasite levels).134 It thus addressed
questions bearing little resemblance to the questions Christophers had explored
in the earlier Punjab study – enhanced malaria lethality in relation to acute
hunger – nor those that Sri Lankan observers had sought to raise regarding the
1934–1935 malaria epidemic. Remarkably enough, such basic distinctions by
1940 had become so blurred as to be now unrecognizable.135
Despite such interpretative problems, and the manifest methodological
difficulties with the study itself,136 the Passmore-Sommerville conclusions
would figure prominently in subsequent malaria literature. Russell’s 1941
definitive claim that ‘[w]ell fed soldiers in perfect physical condition go
down with malaria as rapidly and as seriously, with as high a death rate as
average villagers’137 appears in an article he published in the Indian Medical
Gazette that same year.138 It was a claim repeated in his 1946 text, Practical
Malariology, and again in the text’s third edition in 1963.139 In each case the
single reference given was the 1940 Passmore-Sommerville paper, although
by the mid-1940s, more comprehensive experimental research on diet, both
quantitative and qualitative aspects, was suggesting quite different results.140
The influence of the Passmore-Sommerville article, however, extended
well beyond Russell’s writing. The 1940 paper would centrally inform
a brief discussion of the question of ‘nutritional status and malaria’ in
Boyd’s prominent 1949 compendium of malaria research.141 Epidemiologi-
cal studies such as Malaria in the Punjab and Malaria in the Duars, in con-
trast, were missing from the brief review. Possibly they were alluded to in
the acknowledgement that ‘[m]any writers have suggested that [malaria]
infection is of more severe character in ill-nourished populations.’ If so,
they appear to have been dismissed as unscientific with the follow-up
comment that ‘[u]ntil recently no experimental data on this subject were
available.’142 To qualify as scientific, a role for hunger now required experi-
mental (microbiologic) validation (and indeed, appears in this case to have
rested upon its impact on the malaria parasite) though immunological

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hypotheses, however uncorroborated by epidemiological experience, as

seen in the preceding two chapters, did not.143

Conclusion
In his overview of the emergence of nutritional science in India, Arnold
has observed that ‘[m]etropolitian [nutritional] science was reworked and
remoulded to meet local needs.’ And indeed, as he points out, the food pro-
duction crisis, which assumed acute form with the Bengal famine, was used
as a ‘critique of colonial neglect.’144 But it is less clear that this ‘reworking’
did in fact better address ‘local needs.’ Certainly, it held the potential of
such a critique. Yet in veering to dietary quality, it offered instead a reprieve,
arguably a diversion, from the reality of widespread undernourishment and
subsistence insecurity. Moreover, the focus on qualitative aspects of Indian
agriculture would serve in the post-colonial period to draw attention further
away from fundamental structural reforms and the underlying problems of
servitude and class.
Thus if the new science of nutrition was being remolded, it is unclear
to what extent those needs encompassed the priorities of the endemically
hungry. The ‘dietary critique’ which non-nutritionist voices had succeeded
momentarily in transforming into a critique of colonial agricultural poli-
cies was in fact already being edged off the stage. That critique did exist.
But it lay largely outside the professional domain of nutritional science.
Instead, hunger as a medical reality was quickly fading from public health
view. In its place was left a term, ‘malnutrition,’ which in its original use
was never intended to encompass hunger.145 McCarrison in all his writ-
ing had insisted on the distinction between qualitative ‘malnutrition’ and
quantitative ‘underfeeding’ – in modern terminology, ‘undernutrition’ – in
order to stress what he saw as the overriding public health importance of
the former. Like McCarrison, Nagendranath Gangulee also was scrupulous
in distinguishing the two, though for very different reasons. Recognizing
the growing confusion, he urged that the term ‘malnutrition’ ‘be avoided
as often as under feeding will do the work’: urging, in effect, ‘say what you
mean.’146
It was not to be. Increasing use of the term ‘malnutrition’ brought further
blurring of the two very different nutritional issues. In the process, both the
concept and the very term ‘hunger’ was being lost, and with it, other basic
language and concepts as well: scarcity, destitution, physiological poverty.
The consequences were profound. Margaret Pelling describes the ‘scientis-
ing of diet in the twentieth century,’ pointing to Shryock’s 1936 Develop-
ment of Modern Medicine,

in which the index entry for ‘diet’ . . . directs the reader first to ‘mal-
nutrition’ and secondly to ‘vitamins’, while an entry for ‘nutrition’

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refers simply to medical criticism of the feeding of babies, and to

nineteenth-century physiological chemistry. This is one reflection of
the scale of the physician’s abandonment of the broader interpreta-
tive aspects of nutrition.147

Pelling’s ‘broader nutrition,’ it would seem, encompasses daily subsist-

ence. Even where ‘malnutrition’ was employed to refer to hunger, the mean-
ing conveyed had become something rather different. Malnutrition was now
a medical syndrome, a clinical state, rather than a social and political con-
cern. As a medical diagnosis rather than the product of structural economic
conditions, the narrowed diagnostic framework lent itself in turn to equally
narrow solutions, those appropriate for the acute care health worker but
not for framing preventive policy. With underfeeding as both the condition
(diagnosis) and now also the cause (etiology), the solution (treatment) was
more feeding, thus less ignorance (on the part of poor women), a condi-
tion considered amenable to educational interventions: ‘spread of knowl-
edge’ about correct diet. Shorn of their economic and social dimensions,
the factors which brought about ‘undernutrition’ – wage levels, conditions
of women’s productive and reproductive work, and so on – were also being
allowed to fade from view. In this sense, the ‘discovery of colonial malnutri-
tion’ in 1920s South Asia is better understood as a supplanting of an earlier
understanding of hunger as quantitative insufficiency of food and precarity
of access, with qualitative issues of diet, maternal behaviour, and in the
1950s the term ‘protein-energy malnutrition’ (PEM) in turn. In the process,
a central reality that has shaped so much of human history had also come
to be set aside.
That consideration of the ‘Human Factor’ in malaria epidemicity could
be sidelined so casually from medical and intellectual discourse speaks to
the epistemological power of modern biomedical science, narrowly applied.
In this sense, the reshaping of the ‘Human Factor’ in South Asian malaria
history is a dual transformation: from non-specific to acquired immunity,
and from hunger to micronutrient imbalance, in an arena of conceptual and
linguistic abstraction and conflation that made the ‘uncoupling’ of disease
and destitution much more likely. It is a legacy that continues to bedevil his-
torical enquiry to the present day. Almost a half-century after the Passmore-
Sommerville article’s publication, a major review of the role of ‘nutrition’ in
malaria would also conclude, that

[w]hile there is some evidence that malaria can adversely influence

the nutritional status of humans, there is little which supports a
concept that malnutrition enhances the severity of malarial infec-
tions in man. Indeed, the balance of available evidence indicates
that malnutrition in humans is more commonly antagonistic to
malaria.148

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The role of acute hunger in malaria lethality, as documented in the South

Asian colonial malaria literature, was never refuted. In the preoccupation
with immunological and micronutrient developments in the final decades of
the colonial period, it simply came to be set aside.149 In a sense, the subdisci-
pline of ‘malariology’ could no longer ‘see’ what was missing because basic
concepts and indeed the very language with which to do so were gone as
well. But as recent historiography of Western public health suggests, the loss
of language and concepts of human hunger did not begin with the twentieth-
century disciplines of immunology and nutritional science. Set in larger his-
torical context, the demise of the ‘Human Factor’ in malaria understanding
was an expression of a much broader transformation in the conceptual-
ization of health and disease in Western medical thought, one that can be
seen more than a century earlier within the sanitary movements of western
Europe.
Moreover, among local public health officials in India, the sidelin-
ing of economic conditions from epidemic understanding did not go
unopposed. And here the voluminous pages of the colonial sanitary
records offer, in addition to their important vital registration data, a
fascinating window on the struggle by individual public health figures
who questioned the reductionist tide set in train by the sanitationist and
biomedical revolution, a chapter of the region’s health history to which
we now turn.

Notes
1 By 1934 there were over 2,700 members of the American Dietetic Association,
most ‘actually earning their living by nutrition work’; E. Burnet, and W.R. Ayk-
royd, ‘Nutrition and Public Health,’ Quarterly Bulletin of the Health Organi-
sation of the League of Nations, 4, 2, June 1935, 323–474, at 389 [hereafter,
QBHO].
2 For an overview of nutritional science development, see H. Kamminga, and
A. Cunningham, ‘Introduction,’ in H. Kamminga, and A. Cunningham, eds.,
The Science and Culture of Nutrition, 1840–1940 (Amsterdam: Rodopi, 1995),
1–14.
3 M. Worboys, ‘The Discovery of Colonial Malnutrition Between the Wars,’ in D.
Arnold, ed., Imperial Medicine and Indigenous Societies (Manchester: Manches-
ter University Press, 1988), 208–225.
4 W.R. Aykroyd, Conquest of Deficiency Diseases (Geneva: World Health Organi-
zation, 1970), 20; F. Dunn, ‘Beriberi,’ in K.F. Kiple, and K.C. Ornelas, eds.,
Cambridge World History of Food (Cambridge: Cambridge University Press,
2008), 914–919.
5 Aykroyd, The Conquest of Deficiency Diseases, 20–21.
6 D. McCay, Investigations on Bengal Jail Dietaries: With Some Observations on
the Influence of Dietary on the Physical Development and Well-Being of the
People of Bengal (Calcutta: Superintendent Govt. Print., 1910).
7 R. McCarrison, Studies in Deficiency Diseases (London: Henry Frowde, Hod-
der & Stoughton, 1921); J.A. Shorten, ‘The Role of Vitamins in Tropical Dis-
eases,’ Indian Medical Gazette, May 1922, 164–169 [hereafter, IMG].

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8 Editorial, ‘The Economic Factor in Tropical Disease,’ Indian Medical Gazette,

57, Sept. 1922, 341–343 [hereafter IMG]; Editorial, ‘Dietary and Nutritional
Standards in India,’ IMG, July 1936, 405–406.
9 R. McCarrison, ‘Memorandum on Malnutrition as a Cause of Physical Ineffi-
ciency and Ill-Health Among the Masses in India,’ in Great Britain, Report of the
Royal Commission on Agriculture in India (London: HMSO, 1928), vol. 1, Pt.
II, 100 [hereafter RCAI], republished in H.M. Sinclair, The Work of Sir Robert
McCarrison (London: Faber and Faber, 1953), 261–283.
10 R. McCarrison, ‘Problems of Nutrition in India,’ Nutrition Abstracts and
Reviews, 2, 1932, 1–2, as cited in The Work of Sir Robert McCarrison, 268–269.
11 McCarrison, ‘Memorandum on Malnutrition,’ 96–97.
12 K.J. Carpenter, Protein and Energy: A Study of Changing Ideas in Nutrition
(Cambridge: Cambridge University Press, 1994).
13 H.N. Munro, ‘Historical Perspective on Protein Requirement: Objectives for the
Future,’ in K. Blaxter, and J.C. Waterlow, eds., Nutritional Adaptation in Man
(London: John Libby, 1985), 155–168.
14 Editorial, ‘Dietary and Nutritional Standards in India.’
15 S.C. Seal, ‘Diet and the Incidence of Disease in India,’ IMG, May 1938, 291–
301, at 297, 300, 296.
16 McCarrison, ‘Memorandum on Malnutrition,’ 96–97.
17 Ibid., 95.
18 RCAI, vol. 1, Pt. I, 494.
19 Ibid., 493, 494.
20 Ibid., 495.
21 Ibid., 481–482, 494; Resolution of the All-India Conference of Medical Research
Workers held at Calcutta on 27th to 29th October 1924 and on 15th to 17th
December 1925; reproduced in RCAI, vol. I, Pt. I, 1928, Appendix III, 155.
22 RCAI, vol. IV, Bengal Evidence, 240–247.
23 Ibid., 248–271.
24 Ibid., 253.
25 Ibid., 259. [emphasis added]
26 Ibid., 260. Bentley’s frustration at one point prompted overt critique of imperial
fiscal policies: he argued that the Presidency was ‘treated so badly by the finan-
cial settlement . . . [that] of every 6 or 8 rupees of revenue raised in Bengal only
2 rupees remain in the Province, and it does not give us a fair chance’; ibid., 259.
27 For a comprehensive account of the absorbing focus on protein requirement
and its overestimation among European scientists, see Carpenter, Protein and
Energy; K.J. Carpenter, ‘A Short History of Nutritional Science: Part 4 (1945–
1985),’ Journal of Nutrition, 133, 2003, 3331–3342. C. Sathyamala points to the
remarkable absence of empirical investigation in human communities to support
the ‘too much rice’ thesis; ‘Nutrition as a Public Health Problem (1900–1947),’
International Institute of Social Studies, Working Paper No. 510, Dec. 2010.
28 Mean 1931–39 crude death rate figures: Punjab, 23.9; Bombay, 24.8; Central
Provinces and Berar, 32.8; Madras, 22.7; Bengal, 22.7; Stat. Abst.
29 RCAI, vol. I, 143, 163.
30 This, despite reference by Graham to ‘[t]he economic side of the labour wage in
so far as it affects malaria,’ a subject that ‘has been worked out in a very interest-
ing way in regard to the tea gardens in the Duars by Christophers and Bentley in
a report now fifteen years old’; RCAI, vol. I, 145.
31 RCAI, vol. IV, 493.
32 W.R. Aykroyd, Nutrition, Oxford Pamphlets on Indian Affairs, No. 21 (Bom-
bay: Humphrey Milford, Oxford University Press, 1944), 17.

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33 Poverty and livelihood precarity also meant overriding time constraints for
women in feeding young children sufficiently frequently through the day, as well
as negligible access to more costly, energy-dense cooking oils.
34 W.R. Aykroyd, and B.G. Krishnan, ‘Diets Surveys in South Indian villages,’
Indian Journal of Medical Research, 24, 3, Jan. 1937, 667–688, at 685 [hereaf-
ter, IJMR]; J.D. Graham, Public Health Commissioner with the GOI, ‘Replies to
the Questionnaire,’ RCAI, vol. I, 140–148, at 145.
35 Among Jamshedpur (Bihar) industrial labourers, for example, daily consump-
tion of leafy greens was observed to be higher among the poorest income group
than among the highest (1.2 ozs. compared to 0.1 oz); W.R. Aykroyd, ‘Economic
Aspects of the Problem of Nutrition in India, Indian Journal of Social Work, 2,
3, Dec. 1941, 269–282, at 278; W.R. Aykroyd, Diet Surveys in India (Cawn-
pore: The Job Press, 1948), 3. A sense of stigma associated with leafy greens as
a famine food perhaps explains a substantial prevalence of subclinical vitamin
A insufficiency in the general population.
36 Beriberi afflicted the Brazilian navy and workers engaged in constructing the
Panama Canal, and also British soldiers in 1916 subsisting on bread made from
refined wheat flour during the siege of Kut in Mesopotamia (Iraq); Aykroyd,
Conquest of Deficiency Diseases, 18.
37 RCAI, vol. IV, 253; Editorial, ‘The Economic Factor in Tropical Disease, IMG,
Sept. 1922, 341.
38 Referring to beriberi in the North Circars as ‘a poor man’s disease,’ McCarrison
noted that it commonly appeared ‘following attacks of some debilitating illness
(diarrhoea, dysentery) or in sufferers from some chronic debilitating malady’
and typically during or shortly following the winter monsoon rains, the season
of peak agricultural stress; R. McCarrison, and R.V. Norris, ‘The Relation of
Rice to Beri-beri in India,’ Indian Medical Research Memoir, No. 2 (Calcutta:
Thacker, Spink & Co, 1924), in Sinclair, Work of Sir Robert McCarrison, 238.
39 Among the substantial literature: S.M. Horrocks, ‘The Business of Vitamins:
Nutrition Science and the Food Industry in Inter-war Britain,’ in Kamminga and
Cunningham, eds., Science and Culture of Nutrition, 235–258; D.F. Smith, ed.,
Nutrition in Britain: Science, Scientists and Politics in the Twentieth Century
(London: Routledge, 1997), 219; H. Levenstein, Paradox of Plenty: A Social
History of Eating in Modern America (New York: Oxford University Press,
1993); J. Vernon, Hunger: A Modern History (Cambridge, MA: Belknap Press
of Harvard University Press, 2007); M. Nestle, Food Politics: How the Food
Industry Influences Nutrition, and Health (Berkeley: University of California
Press, 2007); I. Mosby, Food Will Win the War: The Politics, Culture, and Sci-
ence of Food on Canada’s Home Front (Vancouver: University of British Colum-
bia Press, 2014).
40 Sathyamala, ‘Nutrition as a Public Health Problem’; Worboys, ‘The Discovery of
Colonial Malnutrition’; V.R. Muraleedharan, ‘Diet, Disease and Death in Colo-
nial South India,’ Economic and Political Weekly, Jan. 1–8 1994, 55–63; D.
Arnold, ‘The “Discovery” of Malnutrition and Diet in Colonial India,’ Indian
Economic and Social History Review, 31, 1, 1994, 1–26; D. Arnold, ‘British
India and the “Beriberi Problem”, 1798–1942,' Medical History, 54, 2010,
295–314.
41 In 1941 the American Medical Association warned that ‘hidden hunger’ struck
those who ‘satiate[d] themselves with vast quantities of food’ but did not eat
enough essential nutrients; ‘National Nutrition,’ Journal of the American Medi-
cal Association, 116, Jun. 28, 1941, 2854, cited in Levenstein, Paradox of
Plenty, 23.

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42 W.R. Aykroyd, ‘The Problem of Malnutrition in India,’ Current Science, 4, 2,

Aug. 1935, 75–77.
43 Sir P.C. Ray, ‘The Problem of Nutrition in India,’ The Indian Review, 42, Apr.
1941, 209–212.
44 N. Gangulee, Health and Nutrition in India (London: Faber and Faber,
1939), 136.
45 RCAI, vol. I, 149; D.N. Paton, and L. Findlay, Child Life Investigations. Pov-
erty, Nutrition and Growth. Studies of Child Life in Cities and Rural Districts
in Scotland, Medical Research Council Special Report Series, no. 101 (1926);
as cited in D. Smith, and M. Nicolson, ‘Nutrition, Education, Ignorance and
Income: A Twentieth-Century Debate,’ in Kamminga and Cunningham, eds.,
Science and Culture of Nutrition, 288–318 at 294, note 2.
46 Report on the Public Health Administration of the Punjab, 1931, 8.
47 On this, see S. Zurbrigg, Epidemic Malaria and Hunger in Colonial Punjab:
‘Weakened by Want’ (London and New Delhi: Routledge, 2019), ch. 7, 264–266.
48 For discussion of categories of hunger in physical and epidemiological terms, see
Appendix II.
49 For references to meals-per-day, excerpted from the provincial reports submitted
to the confidential 1888 Dufferin Inquiry, see Government of Punjab, Report on
the Famine in the Punjab in 1896–97 (Lahore: Civil and Military Gazette Press,
1898), Appendix II. ‘Normal condition of the poorer classes,’ No. 263 S., dated
Simla, June 23, 1888, xxxvii–xlii at xlii, cited in Zurbrigg, Epidemic Malaria
and Hunger, 110. See also W. Digby, 'Prosperous' British India: A Revelation
from Official Records (London: T. Fisher Unwin, 1901), 472, 511; B.M. Bhatia,
Famines in India (Delhi: Asia Publishing House, 1963), 147–149.
50 Zurbrigg, Epidemic Malaria and Hunger, chs. 10–11.
51 Incidence of the infantile form of beriberi, for example, rose markedly in the
1950s in Burma and the Philippines with expansion of power-mills to rural areas;
M.S. Meade, ‘Beriberi,’ in F. Kiple, ed., Cambridge World History of Human
Disease (Cambridge: Cambridge University Press, 1993), 606–611, at 608.
52 Worboys, ‘The Discovery of Colonial Malnutrition,’ 221–222, 209. See also,
Smith and Nicolson, ‘Nutrition, Education, Ignorance’; C. Petty, ‘Food, Poverty
and Growth: The Application of Nutrition Science, 1918–1939,’ Bulletin of the
Society for the Social History of Medicine, 1987, 37–40.
53 Editorial, ‘Dietary and Nutritional Standards in India.’
54 League of Nations, ‘The Problem of Nutrition,’ vol. I, Interim Report of the
Mixed Committee on the Problem of Nutrition (Geneva: LNHO, 1936).
55 Medical representatives from both African colonies and India, for example,
urged that ‘[i]n an under-nourished population, especially if it is subjected to
periods of famine or semi-famine, the mere treatment of disease . . . will achieve
but negligible results. . . . [T]he first task before the administrations of predomi-
nantly native territories is the raising of the economic status of the population’;
‘Report on an International Conference of representatives of health services of
African Territories and British India,’ QBHO, II, 1933, 104, cited in Worboys,
‘Discovery of Colonial Malnutrition,’ 215.
56 Burnet and Aykroyd, ‘Nutrition and Public Health.’ ‘For practical public health
work, a standard of from 70 to 100 grams of protein may well be employed, and
the desirability that a reasonable proportion should be of animal origin may be
emphasized’; ibid., 347. This, despite serious questioning of the protein insuf-
ficiency thesis from within the League of Nations itself, as seen in the work of
E.F. Terroine; ‘Report on the Protein Component of the Human Diet,’ QBHO,
4, 1935. See also Gangulee, Health and Nutrition in India, 44.

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57 Burnet and Aykroyd, ‘Nutrition and Public Health,’ 327 [emphasis added].
58 Ibid., 385.
59 Paton and Findlay, ‘Poverty, Nutrition and Growth,’ 294.
60 Burnet and Aykroyd, ‘Nutrition and Public Health,’ 386.
61 W. Hannington, secretary of the Unemployed Workers Movement (UK)
responded: ‘I think the workers are entitled to be indignant at the patronising
insults of those who suggest that the ill-health of their families is due to the igno-
rance of the harassed housewife’; The Problem of the Distressed Areas, as cited
in Smith and Nicolson, ‘Nutrition, Education, Ignorance,’ 302.
62 League of Nations, Final Report of the Mixed Committee of the League of
Nations on The Relation of Nutrition to Health, Agriculture and Economic
Policy (Geneva: LNHO, 1937), 248–274, at 251, 274.
63 Micronutrient deficiencies, rather than macro-, were singled out as ‘paving the
way’ for infectious disease and physical inefficiency, and remedial emphasis was
on education; Burnet and Aykroyd, ‘Nutrition and Public Health,’ 327.
64 A.L.S. Staples, The Birth of Development: How the World Bank, Food and
Agriculture Organization, and World Health Organization Changed the World,
1945–1965 (Kent, OH: Kent State University Press, 2006), 71–76; T. Boon,
‘Agreement and Disagreement in the Making of World of Plenty,’ in Smith,
Nutrition in Britain, ch. 8.
65 W.R. Aykroyd, ‘International Health – A Retrospective Memoir,’ Perspectives in
Biology and Medicine, 11, 2, 1968, 273–285, at 279.
66 Gangulee, Health and Nutrition in India, 21.
67 J.H. Perkins, Geopolitics and the Green Revolution: Wheat, Genes, and the
Cold War (Oxford: Oxford University Press, 1999); Staples, Birth of Develop-
ment, 74.
68 Aykroyd, The Nutritive Value of Indian Foods.
69 Aykroyd in 1948 again observed that ‘intake of total protein is usually suffi-
cient when cereals form the bulk of the diet and calorie yield is adequate,’ and
repeated his 1937 observation that up to one-third of the rural population ‘does
not get enough to eat’; Diet Surveys in India, 4–5, 3. See also, Aykroyd, Nutri-
tion, Oxford Pamphlets, 3, 17.
70 See, e.g., Aykroyd, ‘The Problem of Malnutrition in India.’
71 W.R. Aykroyd, and B.G. Krishnan, ‘The Effect of Skimmed Milk, Soya Bean,
and Other Foods in Supplementing Typical Indian Diets,’ IJMR, 24, 1937,
1093–1115.
72 GOI, Report of the Royal Commission on Labour in India (Calcutta: GOI
Central Publication Branch, 1931), vol. I, Pt. I, 316–317. Here too, however,
the notion that cereal-based diets were ‘too bulky’ and unbalanced is evident;
ibid., 28.
73 N.K. Adyanthaya, Report on the Enquiry into the Family Budgets of Indus-
trial Workers in Madras City, 1935–1936 (Madras: Superintendent, Govt. Press,
1940), as estimated by Aykroyd in ‘Economic Aspects,’ 276, 275.
74 ‘The cost of a “well-balanced” diet was estimated at between Rs 4 to 6 per adult
monthly’; Aykroyd, ‘Economic Aspects,’ 271.
75 Ibid., 273. A detailed overview of the results of nutritional surveys is given in
Muraleedharan, ‘Diet, Disease and Death.’
76 P. Weindling, ‘The Role of International Organizations in Setting Nutritional
Standards in the 1920s and 1930s,’ in Kamminga and Cunningham, eds., Sci-
ence and Culture of Nutrition, 319–332, at 327–329.
77 Gangulee, Health and Nutrition in India, 27.
78 Aykroyd and Krishnan, ‘Diet Surveys in South Indian Villages.’

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79 The measure ‘calories per consumption unit per day’ takes into account differing
requirements by age and gender, thus making comparison between households
possible.
80 Aykroyd and Krishnan, ‘Diet Surveys in South Indian Villages,’ 674–675, Table
II, 688.
81 Half of the poorest households consumed regular, if small, amounts of green
leafy vegetables, a larger proportion than among the highest-income group; and
for all, hand-pounded parboiled rice and millets formed the staple grain. All
households were found to consume tamarind, a good source of thiamine and
limited amounts of vitamins C and A; ibid., 684.
82 Ibid., 687.
83 Aykroyd, ‘Economic Aspects,’ Table 3, 278.
84 India, Directorate of the National Malaria Eradication Programme. Agricul-
tural Labour in India, Intensive Family Survey (Delhi: Ministry of Labour, GOI,
1955), vol. I, 150–151, cited in R.P. Sinha, Food in India: An Analysis of the
Prospects for Self-sufficiency by 1975–76 (Bombay: Oxford University Press,
1961), 20. Corresponding percentages arrived at by the ICMR were 83.4 for
agriculturalists and 75.2 for industrial wage-earners; ibid.
85 Dr. Margaret Balfour, ‘Maternity conditions and anaemia in the Assam Tea-
gardens, Journal of the Association of Medical Women in India, vol. 24, 1936,
cited in Gangulee, Health and Nutrition in India, 230.
86 Ibid., 228, 234, 74, 112. In his research Gangulee may well have come across
Christophers’s Malaria in the Punjab, noting that ‘it has been demonstrated that
a direct relationship exists between the price of essential foodstuffs and the epi-
demic malaria’; ibid., 78.
87 Ibid., 81, 111, 212.
88 Ibid., 25–26, 225–226, 306.
89 Ibid., 225, 269, 277, 306.
90 Ibid., 277, 302.
91 W.R. Aykroyd, B.G. Krishnan, R. Passmore, and A.R. Sundarajan, ‘The Rice
Problem in India,’ The Indian Medical Research Memoirs, No. 32, Jan. 1940,
1–84, at 65, 61–71.
92 Ibid., 18, 13. See also, W.R. Aykroyd, ‘Nutrition, International and National,’
Current Science, Mar. 1936, 639–642, at 639. Earlier, Aykroyd had also
acknowledged that nutritional education ‘propaganda may easily become insult-
ing if it is directed at a population struggling to feed itself on a totally inadequate
wage or allowance’; W.R. Aykroyd, ‘Diet in Relation to Small Incomes,’ QBHO,
2, 1933, 130–153, at 150.
93 Aykroyd, ‘Economic Aspects,’ 280–282.
94 Aykroyd, Nutrition, Oxford Pamphlets, 32, 29, 15.
95 Sathyamala, ‘Nutrition as a public health problem,’ 19. In a small monograph
published in Britain in 1937, Aykroyd acknowledged that ‘to ascribe the ill-
feeding of the children of poor mothers to “maternal inefficiency” is heartless
and on the whole unjustifiable’; yet in the next sentence he urged that ‘the edu-
cation of young mothers on dietetics might produce useful results’; W.R. Ayk-
royd, Human Nutrition and Diet (London: Thorton Butterworth, 1937), 224. In
1948, poverty and ignorance would be conflated overtly: ‘Everybody knows that
the basic cause of malnutrition is poverty, and the illiteracy and ignorance which
accompany poverty’; W.R Aykroyd, Director, Nutrition Division, FAO, Proceed-
ings of the Fourth International Congress on Tropical Medicine and Malaria,
Washington, D.C., May 10–18, 1948, 1178.

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96 By the early 1940s, Worboys observes, malnutrition was reinterpreted as a

technical problem: ‘ignorance as to what to grow, how to grow it, what to eat
and how to cook it’; with the ‘growing tendency to “scientise” or “medicalise”
social problems,’ the nutrition problem became ‘depoliticised . . . chang[ing]
from one of inappropriate structures to one of inadequate knowledge,’ with
remedies increasingly ‘sought, not through structural changes, but by “techni-
cal fixes”: dietary supplements and nutritional education’; ‘The Discovery of
Colonial Malnutrition,’ 221–222, 209.
97 Aykroyd, Nutrition, Oxford Pamphlet, 27. ‘An incidental and no doubt
intended consequence of this change of emphasis,’ Worboys observes, ‘was to
shift the tone of the [Colonial Office] Report from one of pessimism to one of
optimism’; ‘Discovery of Colonial Malnutrition,’ 220.
98 Aykroyd, ‘Nutrition, International and National,’ 641.
99 This division had been formalized earlier at LNHO meetings held at the
LSHTM in November 1935 where two separate subcommittees were formed
on ‘ “energy-bearing” substances and protective foods’; Sathyamala, ‘Nutrition
as a Public Health Problem,’ 14.
100 United Nations Conference, ‘Final Act of the United Nations Conference on
Food and Agriculture, Hot Springs, Virginia, United States of America, 18th
May–3rd June 1943,’ reproduced in ‘United Nations Conference on Food and
Agriculture: Text of the Final Act,’ The American Journal of International
Law, 37, 4, Supplement: Official Documents (Oct. 1943), 159–192.
101 M.K. Gandhi, Diet and Diet Reform (Ahmedabad: Navajivan Publishing
House, 1949), 33–34.
102 See, e.g., J.C. Waterlow, and P.R. Payne, ‘The Protein Gap,’ Nature, 258, 113–
115; D. McLaren ‘The Great Protein Fiasco,’ Lancet, Jul. 13, 1974, 93–96. For
an overview of changing estimates of protein requirement, see H.N. Munro,
‘Historical Perspective on Protein Requirement: Objectives for the Future,’ in
K. Blaxter, and J.C. Waterlow, eds., Nutritional Adaption in Man (London:
John Libby, 1985), 155–168; also, Carpenter, Protein and Energy, 180–203.
103 T. Dyson, and A. Maharatna, ‘Excess Mortality During the Bengal Famine:
A Re-Evaluation,’ Indian Economic and Social History Review, 28, 3, 1991,
281–297.
104 A. Sen, Poverty and Famines: An Essay on Entitlement and Deprivation
(Oxford: Oxford University Press, 1981).
105 For an overview of early twentieth-century reforms in famine relief policy, see
Zurbrigg, Epidemic Malaria and Hunger, ch. 11.
106 Sen, Poverty and Famines, 216. As the Commission subsequently suggested,
‘the presence of famine accentuated the lethal effect of disease present in lesser
degrees in normal times’; Famine Inquiry Commission, Report on Bengal (New
Delhi: GOI, 1945), 112–113.
107 S. Zurbrigg, ‘Did Starvation Protect from Malaria? Distinguishing Between
Severity and Lethality of Infectious Disease in Colonial India,’ Social Science
History, 21, 1, 1997, 27–58.
108 GOI. Ministry of Labour, Agricultural Labour: How They Work and Live
(New Delhi: All-India Agricultural Labour Enquiry, 1952), cited in D. Narain,
Distribution of the Marketed Surplus of Agricultural Produce by Size-Level
of Holding in India (Bombay: Asia Publishers House, 1961), 36–37. An early
1940s rural Bengal survey found 10.7 per cent of ‘households living on Rs 100
a year or less, equivalent to daily grain consumption of 11 ounces per capita
(312.5 grams), amounting to 1,150 calories.’ Though encompassing both child

109
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and adult consumption levels, this figure nevertheless indicated severe caloric
insufficiency; R.B. Lal, and S.C. Seal, General Rural Health Survey, Singur
Health Centre, 1944 (Calcutta: GOI Press, 1949), 95. A similar finding has
been estimated for the bottom 10 per cent of the population in pre-Revolution-
ary France; R. Fogel, ‘Second Thoughts on the European Escape from Hunger:
Famines, Chronic Malnutrition, and Mortality Rates,’ in S.R. Osmani, ed.,
Nutrition and Poverty (Oxford: Clarendon Press, 1992), 243–280.
109 For an account of WW2-related famine conditions in southeastern Punjab in
1942, see Zurbrigg, Epidemic Malaria and Hunger, 371–372.
110 P. Mohapatra, ‘Coolies and Colliers: A Study of the Agrarian Context of
Labour Migration from Chotanagpur, 1880–1920,’ Studies in History, 1, 2,
n.s., 1985, 297–299; E. Boserup, The Conditions of Agricultural Growth (Chi-
cago: Aldine, 1965), 98–100; G. Omvedt, The Political Economy of Starvation:
Imperialism and the World Food Crisis (Bombay: Leela Bhosale, 1975), 27–35.
111 Report on Bengal, ch. II, ‘Causes of Disease and Mortality,’ 116–123.
112 Famine Inquiry Commission: Final Report (Delhi: Govt Press, 1945), 112.
113 Although the Famine Inquiry report did acknowledge that an estimated 30
per cent of the population ‘does not get enough to eat,’ most of its eight-page
chapter on ‘The Problem of Nutrition’ was directed to insufficient production
and consumption of ‘protective’ foods; ibid., 105–112.
114 Interestingly, Aykroyd in 1970 would attribute the decline of beriberi ‘to far-
reaching changes in economic circumstances and conditions of employment’ as
well as ‘scientific understanding of its cause’; Aykroyd, Conquest of Deficiency
Diseases, 25. Long before, however, the idea of beriberi had already established
a micronutrient prominence in nutritional science.
115 H.F. Knight, Food Administration in India, 1939–47 (Stanford: Stanford Uni-
versity Press, 1954), 189, 215, 307–8; Zurbrigg, Epidemic Malaria and Hun-
ger, ch. 12.
116 Zurbrigg, Epidemic Malaria and Hunger, ch. 12.
117 Ministry of Food and Agriculture. Department of Food, Report of the
Foodgrains Enquiry Committee (New Delhi: GOI, 1957), 40.
118 ‘As in Britain,’ Worboys observes, ‘the technical dimensions of the problem
allowed for this radicalism to be lost as the definition of the problem changed
from one of inappropriate structures to one of inadequate knowledge’; ‘Discov-
ery of Colonial Malnutrition,’ 222.
119 For a succinct account of the protein insufficiency thesis as informing the work
of FAO and broader UN agencies in the 1950s and 1960s, see Carpenter, ‘A
Short History of Nutritional Science,’ 3331–3342.
120 Famine Inquiry Commission, India, Report of the Health Survey and Develop-
ment Committee (New Delhi: GOI, 1946), vol. 1, 12, 54. For background to
the appointment of the Health Survey, see S. Amrith, Decolonizing Interna-
tional Health: India and Southeast Asia, 1930–65 (Basingstoke: Palgrave Mac-
millan, 2006), 57–63.
121 Famine Inquiry Commission, India, Health Survey and Development Commit-
tee, vol. 1, 57.
122 Ibid., vol. 2, 70.
123 See note 68.
124 Ibid., vol. 1, 56.
125 Ibid., vol. 2, 71.
126 Ibid., vol. 1, 58.
127 Ibid., vol. 2, 130.

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128 C. Sathyamala points to an alternative report by a health subcommittee headed

by Col. S.S. Sohkey, appointed in 1938 by the National Planning Committee of
the Indian National Congress [National Health. National Planning Committee
Series (Bombay: Vora & Co. Publishers, 1948)] that addressed the ‘root cause
of disease’ as ‘found in the poverty – almost destitution – of the people’ where
per capita income for many is ‘barely sufficient to provide one meal per day’;
‘Nutrition as a Public Health Problem,’ 23–24.
129 P. Russell, ‘Some Aspects of Malaria in India,’ Jul. 5, 1941, Rockefeller Archive
Centre, RG.1.1. S.464 B.11 f.87; cited in J. Farley. To Cast Out Disease: A His-
tory of the International Health Division of the Rockefeller Foundation (1913–
1951) (Oxford: Oxford University Press, 2004), 123.
130 R. Passmore, and T. Sommerville, ‘An Investigation of the Effect of Diet on the
Course of Experimental Malaria in Monkeys,’ Journal of the Malaria Institute
of India, 3, 4, Dec. 1940, 447–455.
131 Ibid., 455.
132 Ibid.
133 Ibid., 448.
134 Ibid., 455.
135 ‘By increasing metabolic demands, the code lowers the effectiveness of the
relief. . . . Clearly relief would be more effective if the large camps and works
could be abolished and the people helped in their own villages’; R. Passmore,
‘Famine in India,’ Lancet, Aug. 1951, 303–307.
136 Information on only 15 malaria-symptomatic animals is given: eight in the ‘ill-
balanced’ rice diet group, and seven in the ‘well-balanced’ diet group, making
the possibility of statistically significant conclusions unlikely. Moreover, half
of the animals in the ‘ill-balanced’ diet group lost weight during the pre-
inoculation period, two deaths occurring among those with greatest weight
loss, compared to one death among the ‘well-balanced’ diet group. Thus,
though the study’s intent was to look at qualitative malnutrition rather than
acute hunger, the monotonous ‘malnourished’ (rice) diet appears to have led
to moderate quantitative deficiency in some animals as well, further con-
founding results; Passmore and Sommerville, ‘An investigation of the effect
of diet.’
137 See ch. 2, above.
138 P.F. Russell, ‘Some Social Obstacles to Malaria Control,’ IMG, Nov. 1941,
681–690.
139 P. Russell, L.S. West, and R.D. Manwell, Practical Malariology (Philadelphia:
W.B. Saunders, 1946), 540–541. ‘The results clearly added weight to the view
that one may not hope to control malaria simply by combating malnutrition’;
Russell, West, Manwell, and Macdonald, Practical Malariology, 3rd ed.,
1963, 625.
140 M.M. Brooke, ‘Effect of Dietary Changes upon Avian Malaria,’ American
Journal of Hygiene, 41, 1945, 81–108.
141 J.D. Fulton, and B.G. Maegraith, ch. 38, ‘The Physiologic Pathology of Malaria,’
in M.F. Boyd, ed., Malariology: A Comprehensive Survey of All Aspects of This
Group of Diseases from a Global Standpoint (Philadelphia: W.B. Saunders,
1949), 904–934, at 915–916. Results of two other studies also were cited that
suggested thiamine and biotin deficiency states increased malaria severity; how-
ever, in both cases the extreme diets required to ensure absence of the specific
micronutrient appear to have confounded results; ibid.
142 Ibid.

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143 For discussion of experimental research on quantitative hunger and malaria

carried out by S.P. Ramakrishnan in the early 1950s, see S. Zurbrigg, ‘Did
Starvation Protect from Malaria?: Distinguishing Between Severity and Lethal-
ity of Infectious Disease in Colonial India,’ Social Science History, 21, 1, 1997,
27–58.
144 Arnold, ‘The “Discovery” of Malnutrition and Diet,’ 26.
145 See above, at note 9.
146 Gangulee, ‘Health and Nutrition in India,’ 81.
147 M. Pelling, The Common Lot: Sickness, Medical Occupations and the Urban
Poor in Early Modern England (London: Longman, 1998), 61.
148 I.A. McGregor, ‘Malaria and Nutrition,’ in W.H. Wernsdorfer, and I.A.
McGregor, eds., Malaria: Principles and Practice of Malariology (London:
Churchill Livingstone, 1988), 754–777, at 763. It is unclear the meaning of
‘malnutrition’ intended by McGregor here, but undernourishment seems
implied. Curiously, only 14 years earlier McGregor, after several decades of
malaria work in the Gambia, rued that ‘[w]e have tended to forget what the
very distinguished Italian school of malariologists taught us many years ago,
namely, that the real bulwarks against malaria lie in the progressive “bonifica-
tion” of a country, that is to say, in progressive improvement in the economic,
the educational, the agricultural, and . . . the health standards of a country’;
‘Darling Foundation Award,’ WHO Chronicle, 1974, 28, 356–358.
149 Hamlin similarly observes that ‘[t]he role of predisposition was not something
that could be disproved’ by Chadwick in his 1842 Sanitary Report, ‘but it
could be ignored’; C. Hamlin ‘Predisposing Causes and Public Health in Early
Nineteenth-Century Medical Thought,’ Society for the Social History of Medi-
cine, 5, 1, Apr. 1992, 43–70, at 70.

112
 4
THE LARGER SANITATIONIST
CONTEXT

[U]nless some better support both in Quantity and Quality of

provisions can be procured . . . some putrid epidemic disease
must be the Consequence.
—– Henry Legge to John King 13 May 1800;
cited in Douglas Hay, ‘War, Dearth and
Theft in the Eighteenth Century: The Record
of the English Courts,’ Past and Present,
95, 117–160, 129

The demise within medical discourse of hunger’s role in malaria mortal-

ity across the final years of the colonial period reflected a much broader
transformation taking place in concepts of infective disease and epidemic
causation in Western medical thought, a reductive trajectory apparent from
the early nineteenth century. Historians of public health in recent years have
extended analysis beyond narrowly framed institutional accounts of the
early modern sanitary movement in industrializing Europe to investigate
the far-reaching transformation in understanding of health and disease that
movement represented, and its consequences.1 Christopher Hamlin in par-
ticular has explored the ‘uncoupling of disease and destitution’2 in medical
theory that took shape in mid-nineteenth-century Britain under the mantle
of Edwin Chadwick’s 1842 Sanitary Report: how an earlier ‘predisposition-
ist’ understanding of epidemic causation that encompassed conditions of
hunger and physical debility in the human ‘host’ was set aside, leaving the
recurring ‘fever’ epidemics in the burgeoning industrial urban slums nar-
rowly attributed to atmospheric vapours emanating from ‘filth’ in the exter-
nal environment.3
A similar conceptual narrowing, if less complete, can be seen within the
Indian Medical Service in the later nineteenth century with the transfer
of the sanitationist epidemic paradigm – and soon laboratory and ‘tropi-
cal’ (primarily vector-based) medicine – to British India. In the case of
malaria, by the final years of colonial rule this epistemic shift had led to a

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fundamental redefinition of the nature of the ‘malaria problem’ in South

Asia, and in turn to a rapid reshaping of theoretical approaches to its con-
trol. It was to the earlier, pre-Chadwickian understanding of ‘predisposing’
factors in epidemic causation that Christophers was turning, in his 1911
epidemic malaria enquiry report, and attempting to reclaim. In tracking,
then, the ultimate demise of the ‘Human Factor’ in malaria epistemology
in the Indian subcontinent, this earlier experience in the British metropole
provides essential context.
This chapter briefly traces the sanitationist transformation in epidemic
thought in nineteenth-century Britain. It goes on to explore, in the pages of
the colonial sanitary records, how the narrowed doctrine of ‘miasmic filth’,
transported to South Asia, was perceived in Punjab by district-level sanitary
officers, and contested. In the process, it highlights the larger economic con-
tent implicit in earlier ‘climatist’ theories of epidemic disease: dimensions that
encompassed harvest and land drainage conditions, aspects often unrecog-
nized in modern critiques of pre-bacteriological epidemic thought. In doing
so, it reinterprets the ‘clash’ of epidemic paradigms encountered at the profes-
sional level within the Indian Medical Service to be, at the local administra-
tive level, instead a reasoned accommodation of both the so-called climatist
and new microbial understandings of epidemic disease – an accommodation
that would be increasingly challenged by the paradigmatic power of the rap-
idly emerging subspecialisms of modern laboratory-based medicine.

Context to the nineteenth-century sanitationist

epidemic model
The singular environmental focus of Edwin Chadwick’s 1842 Sanitary
Report in its etiological assessment of epidemic ‘fever’, primarily typhus,4 in
industrializing Britain had its roots, in part at least, in earlier climatist (often
referred to as ‘anticontagionist’) theories of epidemic disease causation.
Atmospheric conditions had long been considered conducive to noxious
vapours responsible for a range of fevers. Climatist theories however were
not generally exclusivist, but to varying extents took into account additional
co-existing factors underlying disease causation. Constitutionist theory, for
example, considered various disease diatheses, hereditary or induced, which
rendered an individual more vulnerable to a morbid or mortal disease out-
come. Related, but broader still, was a ‘predispositionist’ understanding of
disease, where physical exhaustion (‘physiologic poverty’) resulting from
hunger, mental anxieties, and debilitating conditions of work and living was
seen as a central underlying determinant of human vulnerability to disease
and to epidemic occurrence. The common endemic fevers such as typhus,
relapsing fever, and malaria, where direct human-to-human ‘contagion’ was
only irregularly evident, were thought to be triggered by miasmas (in the
latter case, ‘mal-aria’ or bad air) emanating from rotting organic waste or

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waterlogged soils and thus affected by climatic conditions. These miasmas,

however, in many cases were considered ‘exciting’ or proximate causes,
understood to require physical debility (‘predisposition’) among the afflicted
for their morbid expression to take form in epidemic mortality.5
The importance of predisposition was expressed most transparently per-
haps in the writing of Johann Frank in his late eighteenth-century text, The
People’s Misery: Mother of Diseases:6

The weaker the organism and the more exhausted from troubles the
human machine is, the sooner miasmas and contagions penetrate
it like a dry sponge. . . . Even a light infection, localized in a small
spot, soon develops into a deadly disease similar to jail or hospital
fever and spreads among relatives and friends who are exhausted
by misery and predisposed for it.

Recognition of a key role for human destitution underlying epidemic disease

also underlay Rudolf Virchow’s famed assessment of the cause of the major
typhus epidemic in the impoverished rural tracts of Upper Silesia in the late
1840s.7 ‘Physiological misery’ was recognized also as endemically at play
in recurring typhus epidemics in Britain and documented in the writing of
prominent medical figures such as William Pulteney Alison of Edinburgh,
as well as in the testimony of local Poor Law medical officers to the 1839
Sanitary Inquiry chaired by Chadwick.8 What distinguished the nineteenth-
century sanitationist view of epidemic causation articulated in the 1842
Sanitary Report was the singular focus on external filth to the exclusion of
conditions of the human host.
The neologism ‘sanitary,’ derived from the French term cordon sanitaire,
appears to have been first used as an English term in the mid-1820s, Mar-
garet Pelling has suggested, initially in a pejorative sense in referring to
quarantine laws.9 By the early 1830s, however, the term had been given a
‘positive, environmental connotation’ by the Benthamite sanitarians, associ-
ating it with water provision, waste removal (conservancy), and sewer infra-
structure. Simply through use, it quickly came to commandeer an authority
which pre-empted awkward definitional questions, Hamlin suggests, mak-
ing the exclusion of issues such as poverty and hunger possible.10
The reception accorded the narrowed Chadwickian-sanitationist model
of epidemic fever in Britain at one level can be understood in the context
of scientific developments of the period. From the early nineteenth century,
physico-chemical investigation of fermentation had led to greater specifica-
tion within miasma theory where diseases were considered to be caused
by specific poisons (ferments or ‘zymes’). William Farr employed the term
‘zymotic’ in his initial vital registration classification system in the late 1830s
to refer to fevers considered to be caused by broad atmospheric conditions
conducive to organic decay of environmental filth, thus diseases associated

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with particular regions or localities.11 With ongoing developments in pathol-

ogy that identified discreet anatomical lesions, medical attention turned
increasingly to specific miasmic agents and the differentiation of individual
disease entities (nosology). During these years, Hamlin observes, ‘an older
physiological conception of disease was giving way to an ontological one’;
in the process, as Michael Worboys also notes, making ‘diseases “things” or
entities that were separate from the patient.’12
At another level, the emergence of a narrowed miasmic theory of epi-
demic disease in Britain took place in the context of extremely rapid urbani-
zation, in a society unprepared infrastructurally and philosophically, with
the ascent of laissez-faire, to deal with the human consequences. Between
the late eighteenth century and 1900, the proportion of the population liv-
ing in urban areas in Britain grew from 15 to 85 per cent, with recurring
waves of Irish famine refugees adding fuel to the urban fires of epidemic
typhus. Municipal provision of minimal water supply and sewage disposal
was a reactive response to a profound crisis of unmet basic human needs,
but also to the fears and panic of the non-poor.13
Yet there was a larger context involved as well. As secretary to the Poor
Law Commission preceding his appointment to head the 1839 Sanitary
Inquiry, Chadwick was at the centre of 1832 reforms to the Elizabethan
Poor Laws, changes that reduced poor relief expenditure by half by restrict-
ing relief only to those willing to reside within the repellent (and often pes-
tiferous) confines of workhouses.14 Thus, though the promise of water and
sewers, achieved in the final decades of the nineteenth century, was unques-
tionably a ‘public good,’ it came at the expense of the earlier system of
parish relief, itself meagre, and with an undermining of notions of social
obligation. Epistemically, it came also with a redefinition of epidemic fever
causation. Environmental miasma, Chadwick now argued, was the princi-
pal cause of destitution (‘pauperism’) in industrializing Britain through the
debility and illness it triggered, rather than underlying hunger and condi-
tions of work. A number of leading medical observers disagreed.15 But their
testimony to the 1839 Sanitary Inquiry was largely omitted from the pages
of the 1842 Sanitary Report.16
Identification of specific microbes in the final decades of the nineteenth
century would further amplify the reductive trajectory. Much of the new
laboratory research was channelled into bacteriology’s twin discipline
of immunology: techniques to induce or bolster ‘acquired’ immunity to
specific microbes (vaccines and anti-toxins), spurred by the compelling,
if somewhat unrepresentative, example of smallpox (vaccinia) vaccina-
tion, and initial successes in animal husbandry in the case of an anthrax
vaccine. In the process, attention slipped further away from those condi-
tions of the human host that undermined general immune capacity, con-
ditions that underlay epidemics of typhus17 and as well the lethality of
very many other endemic infections such as tuberculosis, and common

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respiratory and diarrheal infections.18 Disease increasingly was equated to

infection and microbial transmission per se (‘invading germs’), with little
attention to the response of the human host to this infection, a response
mediated by the immune capacity of the individual. This conflation was
expressed linguistically in the growing prominence of the term ‘infectious
disease.’ By the late nineteenth century, the earlier ‘seed and soil’ under-
standing of disease saw ‘soil’ increasingly viewed principally in terms
of ‘acquired’ immunity, and a central goal of public health now that of
inducing specific immunity through vaccines19 – an approach that further
reinforced a focus on germ (infection) transmission and a movement away
from conditions of the human host conducing to morbid disease. Though
such an approach would prove invaluable for infections of major inher-
ent virulence such as tetanus, diphtheria, and whooping cough, ‘public
health’ by the early twentieth century, Galdston would observe, was

no longer humanist – but rather microbist . . . no longer concerned

with working conditions, hours, wages, literacy, child labor, in a
word, with man’s total environment. It is interested in germs, in
vaccines, in serums, in fumigation, sterilization, and quarantine.20

The sanitary paradigm transported to India

The epistemic shift taking place in disease theory in Europe was transported
to British India in the later decades of the nineteenth century, in this case as
‘tropical hygiene.’ Hamlin does not attempt to explore the broader impact
of the sanitationist paradigm transferred to the colonial context. Yet his
work sets the stage for such analysis by identifying the conceptual and lin-
guistic levers in Britain that first effected the demise of hunger as a public
health category there: among them, the removal of starvation as a medi-
cal cause of death from the mortality registers of mid-nineteenth-century
England.21 Such was the power of the sanitary paradigm in both concept
and terminology that hunger would be formally invisible in colonial Indian
vital registration ledgers as well – in a land where destitution as an engine
underlying epidemic disease was that much more manifest even than in the
proliferating slums of mid-nineteenth-century Britain.
South Asian public health historiography has yet to fully integrate the
conceptual implications of the nineteenth-century sanitarian movement
into the study of the colonial sanitary regime established in India. Recent
critiques of British Indian public health policy, including malaria control
policy, have been directed to its ‘enclavist’ character and reluctance on the
part of mid-nineteenth-century sanitary officials to immediately embrace
the new laboratory medicine.22 Much less attention has been directed to
the model itself. The story of public health policy under the British Raj, how-
ever, is considerably more complex. There were, for example, compelling

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epidemiological reasons for colonial sanitary officers’ reluctance to set aside

earlier pre-germ-theory understanding of epidemic disease causation. As in
Britain, there were those who questioned, and resisted, the view of epidemic
disease mortality as primarily ‘filth’ mediated.23 A major element to pre-
Chadwickian hygiene policy, in British India as in pre-industrial Europe,
was the prevention of a broad spectrum of diseases through ‘environmental’
changes relating to land drainage, if in the case of the former only rarely
applied.24 The deleterious effects of waterlogged soils on the health of an
agricultural population was explained in terms of miasmic vapours associ-
ated with moisture-induced organic fermentation. But an underlying con-
cern and purpose to land drainage was clearly understood as economic,
centred on productivity of the soil. In the case of the Jumna Canal inquiry
in 1840s eastern Punjab, for example, agricultural impoverishment due to
waterlogging was recognized as a key factor in predisposing to ‘intense’
malarial fever in the waterlogged tracts,25 and led ultimately to a realign-
ment of the Jumna and Lower Bari canals.
Such an understanding is apparent as well in the 1863 Report of the
Royal Commission of Inquiry into the Sanitary State of the Army in India.
Epidemics in the Indian subcontinent, the report noted, ‘appear, disappear
and reappear in different periods and at different degrees of intensity but
always occur among populations exposed to certain unhealthy conditions.’
Of the ‘unhealthy’ conditions listed, the first one cited by the Commission
related to agricultural drainage.

[I]ntermittent [malarial] fever disappeared from places which it

formerly ravaged after drainage of the soil and improved cultiva-
tion. . . . It is evident that when men are exposed to the operation
of very unhealthy places, many of the weak are cut off at once . . .
and others . . . so enfeebled that they rapidly succumb.26

Implicit in the concern with drainage, in other words, lay agricultural pros-
perity: an understanding that economic hardship underpinned the virulent
(epidemic) form of fevers.27
Within the British Indian army itself, there was of course less concern for
frank destitution, with troops insulated from the vicissitudes of harvests and
foodgrain markets. The physical debility that did exist in the army came
by virtue of class recruitment, indifferent attention to ration adequacy and
palatability, and above all the physical exhaustion of military campaigns.
In the wake of the 1857 Rebellion, the administration had been forced to
acknowledge, and better attend to, such physical exhaustion among both
British and Indian troops.28 The 1866 edition of the hygiene manual of
Edmund Parkes, the basic text for sanitation work in British India, devoted
several chapters to the effects of heat and physical debility associated with
campaigns, particularly among new recruits, and the need for rest, protected

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water supply, and improved quality of food. With regard to malaria specifi-
cally, the manual read,

it is well known in many diseases that two sets of causes are in

operation – one external, and one internal to the body (exciting,
and pre-disposing). . . . The internal disposition [to ‘the paroxysmal
fevers’] is greatly heightened by poor feeding, anaemia, and prob-
ably by scurvy. To remove the internal causes, our only means at
present are the administration of antiperiodics, especially quinine;
and good and generous living, . . . [with] warm clothing, warm cof-
fee, and a good meal before the time of exposure to the malaria.29

Radhika Ramasubban notes that after 1863, troop ‘vitality’ and efficiency
began to be remedied through greater attention to the palatability of food
rations and the physical demands made on troops. Morale, she suggests,
was managed less through unlimited supplies of liquor30 than through better
food and minimally humane conditions of military work and life.

Vital registration’s window

After 1863, greater attention of course was also directed to controlling the
environment in and around military populations through a system of rural
cantonments, and periodic stationing of British troops and administrative
staff in cooler hill stations.31 Still, the military could not be fully insulated
from the health conditions of the general population. This understanding
underlay establishment of a civilian vital registration system in the wake
of the 1863 report. In addition to mortality figures, information on harvest
conditions and prevailing foodgrain prices would be routinely recorded in
the annual provincial Sanitary Commission reports, data considered key to
anticipating epidemic patterns among the civilian population.
The significance of vital registration for imperial rule, however, very
quickly extended beyond that of an early warning system for the colonial
army. Lower-level (district) officials were soon confronting the magnitude
of fever mortality, pre-eminently malarial, as the leading non-enclave ‘public
health’ issue, and coming to appreciate the power of economic conditions
underlying its highly lethal form.32 The 1880 second edition of the Madras
Manual of Hygiene, for example, included as an Appendix, an exacting
analysis of epidemic mortality in relation to foodgrain price levels and star-
vation across the 1876–1877 South Indian famine prepared by the Madras
Sanitary Commission, W.R. Cornish.33 Thus within only a few years of its
establishment, a registration system set up to track the epidemic diseases of
priority to the government and imperial trade (cholera and smallpox) was
revealing malaria, and the destitution underlying its epidemic form, as the
leading ‘sanitary’ problem facing much of the subcontinent. In effect, the

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provincial sanitary ledgers were pulling back the miasmic curtain on price
starvation, and the human cost of the laissez-faire doctrines upon which the
imperial project rested.34 In Punjab, the same reports were also shedding
light on the locally disastrous economic consequences of interruption in sur-
face drainage, conditions often greatly exacerbated by extensive road and
rail infrastructure construction. Alongside climatist notions of the debilitat-
ing effects of heat and humidity on imperial forces, the overriding power of
economic hardship in determining epidemic mortality among the general
population was a reality rapidly permeating sanitary consciousness.
It was in this same period, of course, that the influence of sanitation-
ist and germ-based laboratory medicine was taking medical attention in
another direction. By the late nineteenth century, for example, the 1894
edition of the 433-page Indian (Madras) Manual of Hygiene no longer
included the Cornish appendix detailing epidemic mortality patterns in the
1876–1877 Madras famine.35 Attention to broader economic dimensions in
epidemic analysis was rapidly ebbing at the academic level with identifica-
tion of specific disease microbes in the final two decades of the nineteenth
century, if ‘on the ground’ the vital registration ledgers continued to throw
into sharp relief the impact of harvest and price conditions on death rates.
The development of immunological ‘interventions’ (vaccines, antitoxins)
and understanding of newly identified vectors was further shifting atten-
tion to microbe transmission,36 giving imperial medicine much finer tools
for protecting the colonial administrative populations in what quickly took
conceptual shape as ‘tropical medicine’ – although in practice most of the
rural population continued to be excluded.37 Pushing policies further to a
narrowed germ-transmission focus was the outbreak of plague in 1896, with
sanitary practice absorbed by the demands of anti-plague immunization and,
from 1907, vector (rat) extirpation, even if both measures in practice were
largely ineffective.38 Together, imperial economics, international trade obli-
gations, and the new laboratory medicine were pushing sanitary attention
at the administrative level in India to focus ever more narrowly on specific
disease interventions and to a wholly ‘contagionist’ (germ-transmission)
interpretation of epidemic causation.

Reinterpreting the ‘Clash’ of paradigms

In recent critiques of the colonial public health service in British India, his-
torians have highlighted the largely enclave framework to nineteenth-cen-
tury sanitary efforts that excluded most of the general population,39 as well
as the reluctance of many within the colonial sanitary service to abandon
‘anti-contagionist’ (climatist, miasmic) views of disease causation follow-
ing the identification of specific microbes and their modes of transmission.
Undoubtedly, a climatist theory of cholera epidemics, as Mark Harrison
suggests, was convenient for the British colonial regime, ‘a powerful tool

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against advocates of quarantine and those who pressed government to

intervene more directly in public health.’40 Yet while clearly congruent with
imperial trade interests, avoidance of quarantine measures was not the only
reason underlying the regime’s reluctance to embrace a ‘contagionist’ view
of epidemic disease. Miasmic theory in fact fit well with epidemiological
observation in much of the Indian subcontinent. In a region where fevers
(pre-eminently malarial) were manifestly associated with moisture, mon-
soon rainfall, and, in pernicious form, with waterlogged soils and human
destitution, a focus on broader determinants beyond simply contagion was
understandable. There were compelling empirical reasons, in other words, to
view the leading epidemic diseases, malaria and cholera, as climate related,
if the economic dimensions to climate fluctuations often went unarticulated.
Empirically, germ transmission (contagion theory) could not explain epide-
miological patterns of epidemic mortality on its own, even for cholera. John
Snow’s 1854 waterborne theory of cholera41 was considered dangerous by
many Indian Medical Service (IMS) officials not because it was wrong but
because it was insufficient to explain epidemic mortality patterns observed.
Contagion could explain local transmission in an outbreak, but neither the
timing nor the often vast extent of the major recurring epidemics.
Nonetheless, from the mid-1880s with the development of diphtheria
antitoxin, there was growing absorption with the specifics of microbe trans-
mission, enthusiasm further heightened with confirmation of mosquitoes
as vectors of diseases such as filariasis and malaria and the rapid emer-
gence of an institutional ‘tropical medicine’ at the turn of the century. These
were laboratory advances that appeared to hold out the promise of techni-
cal solutions to modify specific diseases, or to interrupt their transmission
altogether, what Paul Ehrlich (1854–1915), who developed the first effective
medicinal treatment (Salvarsan) for syphilis, would in 1906 term ‘magic
bullets.’42 Inevitably perhaps, the doctrinal collision between earlier clima-
tist theories of disease causation and a narrowly-applied germ-theory model
of disease triggered increasing policy debate within the senior ranks of the
Indian Medical Service.
These intra-professional tensions have been a major focus of recent South
Asian public health historiographic analysis. J.C. Hume importantly points
out that there were other sources of intra-professional conflict as well,
with the transformation to laboratory-based medicine. Among them were
deepening professional tensions arising from the Punjab administration’s
proposal to employ ‘traditional’ hakims as sanitary inspectors.43 Thus the
advent of scientific medicine was bringing into sharp relief an entire range
of questions as to who provided how much of what services (preventive or
curative) and for whom (enclave or public). The ensuing debate and dissen-
sion so prompted, Harrison has suggested, may well have allowed room for
continuing equivocation on the part of the Government of India, serving to
further postpone systematic public health policy.44

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These questions were, and remain, central to analysis of South Asian colo-
nial public health policy and practice. But the concerns they raise involve
largely intra-professional issues. They fail to convey how the paradigmatic
collision between pre-germ theory views and laboratory medicine played
out in sanitary practice at the local level. In terms of their practical applica-
tion, there was general accommodation between climatist (‘anticontagion-
ist’) theories that urged drainage, and contagionist views that focused on
‘germ’ transmission, though the underlying etiological theory differed.45 In
the practical policy domain of water supply, for example, little contradiction
existed between contagionists and climatists: a clear understanding existed
of water contamination, and the need for testing water supplies for organic
matter. For the miasmatist, the precise nature of the contamination (fer-
mentative ‘poisons’) differed from that identified by the later microbiolo-
gists. But the actual preventive measure or practice was similar. This was
the case as well for ‘conservancy,’ sewerage methods and policy. In practice,
both approaches were employed in India as well, certainly in the urban con-
text where some effort was made at improving and protecting water supply
beginning from the 1880s. At the level of practice, in other words, there was
less conflict than within academic halls of theoretical debate.46
Characterization of medical theory divisions of this period as a contest
between miasmatist ‘versus’ germ-theory views is problematic also, how-
ever, because it overlooks the deeper ‘tension’ faced by the British Raj in
regard to public health policy: the overarching economic (predisposition-
ist) dimensions to epidemic patterns. Deficiencies in the effectiveness of the
civilian sanitary service under the British Raj entailed more than grossly
inadequate funding, differences in theoretical underpinnings, or choices of
personnel ‘delivering’ sanitary interventions. A more fundamental prob-
lem lay in the insufficiency of both the ‘contagionist’ and ‘climatist’ disease
models where the latter was increasingly reduced in the later nineteenth
century to ‘sanitationist’ (filth) dimensions: that is, to factors external to the
human host. Neither offered the measures required for a civilian population
presenting a very different ‘soil’ than that of imperial military and admin-
istrative populations, one of widespread undernourishment and recurring
famine conditions, to a large extent unmitigated.47 In this sense, historio-
graphic focus on coverage or funding failures of the colonial public health
service arguably has left the limitations of the nineteenth-century sanitary
model itself unexamined. And with it, a dominant dimension to sanitary
deliberations of the period.

‘General Sanitation’: not a mere footnote

The 1911 All-India Sanitary Conference marked the moment of epistemic
truce in the epidemic causality debate, historians have noted. ‘No longer
was there thought to be any fundamental contradiction between the aims of

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research scientists and those who struggled on a day-to-day basis with prac-
tical sanitation.’48 At the level of public optics, this indeed appears to have
been the case. Yet the differences resolved at the Sanitary conference in
November 1911 did not lie primarily between contagionist (germ-theory)
and narrowly defined miasmatist views. What was being acknowledged in
the meeting’s Presidential address, and to a limited degree resolved, was a
broader economic content to the term ‘practical sanitation.’49 Only weeks
before, Christophers’s report, ‘Malaria in the Punjab,’ had finally been
tabled.50 In the wake of its official release, the accommodation arrived at in
Bombay involved a re-insertion of the ‘Human Factor’ (destitution) into the
epidemic equation. Tucked within the conference president’s linguistic enve-
lope of ‘practical sanitation’ was acknowledgement of the central impor-
tance of agricultural productivity and prosperity. In the case of Punjab this
was pre-eminently a matter of adequate surface drainage, as in the case of
the Jumna canal realignment; elsewhere, such as deltaic Bengal, restoration
of inundation irrigation flows. But nor was surface or inundation ‘drainage’
the only economic action authorities had in mind at this point in relation
to agricultural improvement. ‘Practical sanitation’ also encompassed fun-
damental changes in famine relief and foodgrain price policy, changes in
economic policy that would pre-empt mass destitution (‘famine’) and associ-
ated fulminant malaria conditions and begin to stem the recurring loss of
human and agricultural capital out of the rural economy triggered by recur-
ring famines.51
What the 1911 epistemic compromise represented in effect was a reinser-
tion of a broader ‘climatist’ perspective into epidemic causality, one where
climate was understood in terms of its specific subsistence consequences:
harvests, livelihood, and staple foodgrain access (prices). Christophers’s
spatial mapping of 1908 malaria epidemic mortality had confirmed what
already was suggested by the clinical and class profile of epidemic malaria
mortality: such patterns could not be understood merely on the basis of
malaria transmission. The broad geographic pattern to malaria epidemic-
ity distinguished the phenomenon from contagion alone, calling to mind
instead earlier ‘zymotic’ dimensions of fever epidemics, the nineteenth-
century European term employed to convey posited atmospheric conditions
conducive to fermentation as the causal agency at play. Christophers in sub-
sequent writing would alter the term to emphasize the specific economic
dimensions to the spatial mortality pattern, coining the neologism ‘zymonic’
for the purpose.

The word epidemic, applied as it is to outbreaks of disease on a

small scale, does not sufficiently characterise such vast exhibitions
of the power of zymotic disease, and I propose to call such phenom-
ena zymonic from their likeness in distribution to cyclonic distur-
bances in the atmosphere.’52

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As in his earlier ‘Malaria in the Punjab’ analysis, Christophers would refer

to the economic nature of that different causal agent with concerted deli-
cacy: in this instance, adding a single key sentence: ‘Almost coming under
the phase of zymones, were the famines that once decimated tracts in India’;
then adding that ‘[f]ortunately these no longer figure on our list as direct
causes of mortality.’53 Significantly, he also went on to suggest that ‘epidem-
ics of this magnitude . . . [were] by no means confined to malaria.’

Immense cholera epidemics have been of frequent occurrence. They

are ascribed to infection carried by pilgrims returning from the
pilgrim melas . . . but there must be something more at the back
of them than the mere fact of such dissemination, some condition
peculiarly favourable to the spread of cholera in such years.54

Here Christophers was bringing the microbiologic (contagionist) and pre-

dispositionist understandings together, under the rubric of ‘general sanita-
tion,’ the term he had used in his 1909 ‘Human Factor’ paper to refer to
measures that addressed human destitution.55
Part of the historiographical difficulty in interpreting theoretical debate and
policy developments taking place in British India in this period, one can suggest,
lies with the level of abstraction in colonial officials’ use of the term ‘general
sanitation.’ Hidden within the term could be almost any economic measure.
As with the nineteenth-century Jumna canal realignment, it included drainage
(waterlogging remediation) in which the paramount effect was understood as
economic. After 1908, ‘sanitary’ measures also extended to flood-, drought-,
and price-relief, and in time more systematic ‘bonification’ measures in Punjab
in the form of surface water drainage.56 In his 1917 report on malaria in Amrit-
sar, C.A. Gill explicitly employed the term ‘General Sanitation’ in referring to
measures directed to ameliorating those conditions that tend ‘to bring about
repeated relapses . . . [such as] poor and insufficient food, bad housing, excessive
exposure to climatic conditions.’ ‘All measures,’ he continued, ‘which promote
the well-being of the people and their powers of resistance to disease come indi-
rectly within the scope of anti-malarial measures.’57
Certainly for Christophers, his use of the term was as code for alleviating
destitution. Repeatedly in his published writing he employed the term ‘gen-
eral sanitary reforms’ in circumstances where the sole meaning could only
be economic. Thus he concluded the 1911 Punjab inquiry urging that ‘the
immediate removal or prevention of flood water, should be the first step in
the sanitation of a rural tract,’58 where the economic consequences of flood
conditions had been vividly articulated at the Simla malaria conference two
years earlier.59 To subsequent analysts, however, this larger content to the
term could easily be missed.60
In other words, the ‘compromise’ reached among top officials in the
Indian Medical Service in December 1911 was not a mere footnote to the

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competing medical theory debates and professional discord of the period.

Instead it involved acknowledgement of the primacy of hunger in the pub-
lic health burden of malaria in India, an issue that lay at the core of the
epistemic contest within the sanitary administration at this point, and
which was the pivot around which subsequent colonial public health policy,
and arguably the region’s health history, revolved. Yet if the ‘fundamen-
tal contradiction’ between public health figures seemingly was resolved in
formal declarations in 1911, deep dissension remained among individual
members of the Indian Medical Service regarding disease theory and policy
approaches,61 and views of the sanitarian’s task, as will be considered in
chapter five. But first we consider how the late nineteenth-century ‘collision’
of disease theories played out in the practical experience of sanitary officers
working ‘in the field,’ a rather different story from that taking place at the
level of academic debate.

Epidemic causation: view from the field

All three perspectives on epidemic causality – contagion, climate, and pre-
disposition (destitution) – are evident in the early sanitary records of Punjab
province, as are tensions arising in relation to them as succeeding provincial
sanitary commissioners responded to recurring epidemics and the dramatic
microbiologic developments of the later nineteenth century. Thus in addi-
tion to their important quantitative data, the annual sanitary reports offer a
vivid portrait of the response at the local level to the epistemological shifts
in health understanding taking place with the emergence of a germ-theory-
based medicine and sanitary practice, and correspondingly the vicissitudes
of predisposition as a concept within public health thought.
Debate over epidemic causation was most acute in relation to cholera,
the disease of paramount concern to the British Raj in much of the nine-
teenth century for its effects on imperial trade and the ever-present threat of
international quarantines. By virtue of geography, cholera was of additional
concern for the Punjab administration, the eastern portion of the province
having been the site where cholera had, for a period, compromised British
efforts to regain military control during the 1857–1858 Indian Rebellion.
But as well, major Indian army cantonments were located in the province
which bordered the northwest frontier region where military campaigns in
Afghanistan continued through the remainder of the nineteenth century.
Thus cholera statistics and theoretical discussion of cholera causation loom
large in the provincial records, far overshadowing those for fever (primarily
malaria). In this context, it is hardly surprising that the first provincial sani-
tary commissioner for Punjab would be an IMS officer ardently committed
to developing protected water supply systems.
Over the course of his 1867–1875 tenure, A.C.C. DeRenzy would become
increasingly adamant in urging modern water-supply infrastructure for the

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province, arguing that even ‘covered wells were a hazard.’62 At the central
level, in contrast, the post of Sanitary Commissioner to the Government
of India was filled by a ‘climatist,’ J.M. Cuningham, whose reluctance to
embrace a contagionist view of cholera would trigger increasing criticism
from more junior members of the sanitary service. Most prominent among
them was DeRenzy, whose ridicule of Cuningham’s ‘anti-contagionist’ views
in the pages of the Lancet ultimately led in 1875 to the former’s transfer to
a less prestigious posting in Assam.63
Emphasis on cholera continued, however, under DeRenzy’s successor, H.W.
Bellew. Fifty-one pages of the 1879 Punjab sanitary report, a year of famine in
the province, were devoted not to fever mortality, which was enormous, but
to cholera. Unlike DeRenzy however, Bellew’s views of cholera etiology were
distinctly climatist, directed more to ‘conditions of the climate’ and of the soil
in explaining patterns of the disease.64 Moreover, Bellew’s attention would
increasingly turn to the very much greater mortality burden being recorded
under the category of fever deaths, in his 1882 report describing fever as ‘the
most deadly and most baneful disease which we have to contend against in
this Province.’ Here, too, his perspective was climatist, noting that severe epi-
demics occurred ‘when seasons of unusual drought are followed by copious
rainfall,’ a view that broadened in time to encompass ‘defect[s] in food sup-
ply’ and ‘unusual exposure to fatigue [and] privations.’65 In this, Bellew had
the support of leading medical figures such as Joseph Fayrer, Surgeon-General
and President of the India Office Medical Board, who continued to advocate
a broader epidemiological and ‘natural history’ approach to understanding
epidemic behaviour in the subcontinent.66 As to remedial measures, however,
Bellew’s recommendations took an increasingly moralistic tone, urging vil-
lagers to adopt domestic cleanliness, to wear clothing ‘appropriate to the cli-
mate’ and to heat their homes through the night to avoid chills and sickness,
admonishments that revealed a level of behaviouralist naivété that in time
became difficult even for his superiors to ignore.67
It was in the middle of Bellew’s 1875–1885 tenure that the malaria plas-
modium was identified by Alphonse Laveran. Two years later in 1882,
Robert Koch identified the tuberculosis bacillus, and the following year, the
cholera vibrio. Already, however, the colonial government was itself begin-
ning to shift its ‘climatist’ views to accommodate the new microbiologic
research, inaugurating in 1880 the first scientific medical journal, Scientific
Memoirs by Medical Officers of the Army of India. Five years later Cuning-
ham was replaced as Sanitary Commissioner with the Government of India
by Surgeon-General B. Simpson, an ardent proponent of the new laboratory
medicine. That same year in Punjab, Bellew would be succeeded by A. Ste-
phen as provincial sanitary commissioner.
Stephen brought a much more rigorous analytic approach to his obser-
vations of epidemic mortality, in the case of cholera initiating a detailed
system of mapping outbreaks and mortality across the province. Like his

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predecessor, he also drew attention to the inordinately greater mortality

recorded under the category of fever, calculating fever deaths in 1887 to
be 51 times greater than cholera mortality; in 1889, 54 times greater than
smallpox deaths and 151 times greater than cholera.68 Like Bellew, Stephen
saw climatic conditions of rainfall and waterlogging as prime determinants
of local health conditions. But in his concern with locality and soils, Ste-
phen gave greater emphasis to the economic consequences of waterlogging
on autumnal fever mortality, pointing increasingly to rail, road, and canal
embankments as directly contributing to the problem.69
Under the more sympathetic vice-regency of Lord Dufferin (1884–1888),
Sanitary Boards were established in 1888 in each province and Stephen
enthusiastically oversaw beginning efforts at improving rural drainage,
supervising district-level surveys of areas where surface drainage was
blocked by infrastructure embankments. At the March 1891 Sanitary Board
meeting, he urged that ‘[e]fficient drainage [was] the only effectual means of
preventing outbreaks of malarial fevers and their sequellae.’70 Deputy Com-
missioners were instructed to

report on all areas . . . in which drainage has been intercepted by

railways, canals or other works carried out by Government. . . . Pro-
jects for the drainage of water-logged areas should be undertaken,
and sufficient water-way should always be provided when embank-
ments are raised in constructing railways, canals, and roads.71

At the same time, he took direct aim at the administration of the canal irri-
gation system, highlighting the ‘evil effect on health of excessive irrigation
by canal water.’

[U]nless special precautions are undertaken canals are not an

unmixed good. When canal water is allowed to flow over an almost
level country, unless arrangements are made to get rid of the sur-
plus, the subsoil gradually becomes water-logged, and malarial
fevers with enlargement of spleen become very prevalent.72

But along with drainage operations, Stephen also stressed the need for
immediate relief for flood-paralyzed villages:

[W]hile the country remains liable to such floods . . . sickness and

mortality will be excessive, and . . . the inhabitants will certainly
undergo physical deterioration unless they are speedily relieved. . . .
Were those suffering from malarial fevers among the general popu-
lation as carefully treated, fed and nursed as fever patients in Jails
and in the Native Army, the mortality from these causes would be
very much smaller than it is.73

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Though no doubt aware at this point of the malaria plasmodium, he contin-

ued to advance the ‘classical’ hygienic measures of surface drainage works,
and to articulate the pre-sanitationist distinction between triggering factors
in malaria epidemics and underlying factors. In his 1887 report he quoted
affirmatively a district-level Civil Surgeon’s assessment of the severe epi-
demic conditions that autumn who had described ‘the predisposing cause [of
the 1887 epidemic] as debility produced by scarcity of food and the exciting
cause as waterlogging of sub-soil from excessive rainfall and floods.’74
By the mid-1890s, however, drainage efforts by the provincial Irrigation
Department appear to have stalled over financing disputes between central
and local levels of government,75 an impasse perhaps reflecting a change in
viceregal leadership. In the meantime, major famines in the final years of the
nineteenth century and the outbreak of plague in 1897 further diverted atten-
tion and funds from surface drainage. Few accounts of major flood control
projects appear in the annual sanitary reports after 1895, until the 1920s.
Nonetheless, while Stephen was the first provincial sanitary official to
openly question the unalloyed benefits of canal irrigation, his annual reports
were surprisingly silent regarding the effects of soaring grain exports out
of the province – export earnings upon which the fiscal foundation of the
British Raj rested. It would be Land Revenue administration officials, rather
than members of the Sanitary Department, who in published form warned
of the effects of the booming export trade on public health. Certainly, Ste-
phen was aware of the severity of these epidemics, pointing to 1890 as the
first year on record that deaths in the province exceeded births, in that year
by 11.3 per mille, and acknowledging the effect of the high prices in ‘reduc-
ing the physical powers’ of the population. But elsewhere he would down-
play the recurring grain-price crises that marked his tenure, giving little hint
of the extraordinary shifts in food security taking place.76 ‘[N]o real scar-
city,’ existed in 1890, he reported, ‘and the health of the people was prob-
ably not appreciably affected by the slight [price] rise.’77 Blocked surface
drainage was considered to be remediable, but price behaviour apparently
was not. To the extent that he addressed the social distribution of mortality
in the province, attention was directed not to class differentials which were
large, but to politically safer differences among the major religious groups
and increasingly to sex differentials in infant mortality.78
It was under the 1894–1897 tenure of Stephen’s successor, W.A. Roe, a
microbiologist, that public health analysis would veer sharply to a reductive
framework. With 1895 rainfall ‘considerably below the average,’ Roe con-
cluded that ‘meteorological conditions were more favourable to health.’ The
offending cause of fever mortality was now reduced to ‘moisture,’ and its
absence equated to ‘health.’79 Roe’s tenure as Punjab Sanitary Commissioner
predated Ross’s confirmation of the role of mosquitoes in malaria transmis-
sion, yet already understanding of ‘health’ had come to be reduced to the
‘exciting’ or triggering factor in fulminant malaria: monsoon rainfall levels.

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The narrowness of Roe’s logic was too much, it seems, even for the Brit-
ish Raj to ignore. A GOI directive in early 1896 prodded provincial sani-
tary officials to be ‘considering, as far as may be possible, the influence of
weather and food prices on the death rate.’80 Yet conditions following a sec-
ond year of drought in 1896 would again be described by Roe as ‘remark-
ably dry and very healthy.’81 Absent was any hint of the economic livelihood
effects of two consecutive years of drought. Indeed, the famine year of 1897
would be described as ‘on the whole a healthy one,’ on the basis it seems
that though the monsoon rains had returned, they were slightly below aver-
age levels.82 Yet 1897 mortality rates in the province had risen by 50 per cent
against the previous decade average, itself a level already elevated by a series
of major price-related epidemics in the late 1880s and early 1890s.83 In his
annual report for that year Roe limited his narrative remarks to one-third of
a page, with no reference to the autumn malaria epidemic in the southeast-
ern region of the province.
The equating of ‘health’ in the province to below-normal rainfall contin-
ued under Roe’s successor, C. J. Bamber, the latter perhaps concerned lest
he court ridicule by adhering to ‘old school’ miasmatist theories of epidemic
disease in the wake of Ronald Ross’s confirmation in 1897 of the vector role
of mosquitoes in malaria transmission. Though monsoon rainfall in 1899
stood at record low levels, Bamber’s annual sanitary report for the year con-
tained no hint of the broader consequences of extreme drought once again
afflicting the countryside. Indeed, for the first time since initiation of vital
registration reporting in the province in 1867, no foodgrain price data were
included in the annual report, though the province was plunging headlong
into ‘the great famine’ of the century. In its aftermath Bamber acknowl-
edged that the province had suffered severely, but even here his admission
was remarkably sanguine. ‘[G]eneral scarcity and dearness of food,’ he con-
cluded, ‘does not appear to have affected the health of the population to any
material extent, except in Hissár and Karnal districts, where insufficient and
unwholesome food helped to raise the death-rate by decreasing the power
of the people to resist disease.’ In fact, crude death rates had risen to over
double non-famine levels in the majority of the province’s 24 plains districts,
much of the mortality occurring at the close of the famine with return of
normal monsoon rains and malaria transmission in their wake. In three dis-
tricts, 1900 mortality rates had tripled, with one-tenth of the entire popula-
tion succumbing. ‘With the exception of a few districts,’ Bamber observed in
a seemingly reassuring tone, ‘the dearness of food did not lead to a demand
for higher wages. On the other hand, . . . labourers and artisans . . . [were]
found willing to work for lower wages owing to increased competition from
famine.’84
One is tempted to interpret the reluctance of sanitary officials to discuss
the health implications of harvest failure as stemming from official pressures
to avoid the politically sensitive issue of starvation deaths. Certainly, the

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highest echelons of the administration a decade earlier had concertedly dis-

couraged criticism of grain exports and their impact on price levels.85 Yet by
the late 1890s the Government of India itself was urging provincial sanitary
officials to consider economic conditions in their annual reporting. In the
wake of the 1900 famine, the GOI issued another directive, this time insist-
ing on more details than casual rote data on harvests, foodgrain prices, and
wage levels.86 Mention of meteorological, crop, and foodgrain price condi-
tions would re-appear in the Punjab sanitary report in 1903. But the subse-
quent year’s report contained no information on harvests, though rainfall
and humidity conditions received several pages’ commentary. ‘Fortunately,’
the sanitary commissioner again concluded, ‘the rainfall in 1904 was below
the normal and this accounts for the moderate death rate recorded from
fevers.’87
A similar reading of drought as good fortune due to reduced malaria
transmission would appear in somewhat different form that same year with
the decision to eliminate all irrigation channels at the rural military can-
tonment at Mian Mir (Lahore) and environs in pursuit of anopheles extir-
pation, a policy that reduced the area to its former near-desert state.88 In
the meantime, initial trials of mosquito destruction had been initiated in
municipal areas of several Punjab districts in 1903.89

Reductionism respite
Marked reluctance on the part of Punjab sanitary officials to address eco-
nomic conditions at the turn of the twentieth century would be broken three
years later by Bamber’s successor. Despite preoccupation with plague mortal-
ity that continued to soar in the province, Major E. Wilkinson in his 1907
provincial sanitary report pointed with alarm also to poor monsoon rains,
‘short crops,’ and rising prices.90 A year later in the aftermath of the disas-
trous 1908 fever epidemic, malaria lethality would be linked explicitly to
prevailing scarcity and harvest failure along with widespread destruction and
economic paralysis triggered by flooding.91 The 1908 sanitary report went
further, pointing to the epidemics of 1892 and 1900 as similar examples of
the association of malaria mortality with conditions of ‘scarcity’ (famine-level
prices). Three years later in 1911 the centrality of food security to mortality
in the province would formally be acknowledged with official publication
of Christophers’s ‘Malaria in the Punjab’ report. Much, of course, had tran-
spired in the preceding two-decade interval – including publication of the
1901 Famine Commission Report in which starvation unambiguously was
named as the key agent transforming endemic malaria in the country into
its disastrously lethal epidemic form.92 Deputed to conduct an enquiry into
the 1908 Punjab malaria epidemic, Christophers had begun by seeking out
the experience of earlier provincial sanitary commissioners. From the annual
reports of Bellew and Stephen he would have come across their graphs of

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annual fever mortality and rainfall data painstakingly and cumulatively

charted year by year. Impressed, it seems, by Stephen’s mapping of cholera
mortality during his tenure, Christophers employed similar techniques to
delineate 1908 autumn malaria mortality across the province, using what
appears to be the same district- and thana-level maps.93 He then went on to
devise statistical techniques to quantify the relationship between rainfall and
prices on malaria mortality, stimulated perhaps by this earlier work.
Beginning in 1908, the annual provincial sanitary reports would include
more detailed reviews of monsoon and harvests conditions, in addition to
price and wage trends, as economic preamble. And for the remainder of the
colonial period two voices, one microbiologic, the other overtly economic,
would frame analysis contained in the annual reports.94 The 1927 provin-
cial report, for example, highlighted ‘the profound influence upon the state
of the public health [of] . . . meteorological conditions, and more particu-
larly abnormal seasons . . . where health and to a large extent prosperity,
is a gamble in rain.’95 The following year the Public Health Commissioner
with the Government of India prefaced his own annual report with seven
pages detailing all-India rainfall, agricultural, and economic conditions.96
And in the early days of the global Depression, the Punjab Director of Public
Health (formerly provincial ‘Sanitary Commissioner’) described infant mor-
tality rates as ‘a delicate test of economic stress.’97 Six years later the 1937
annual report for the GOI advised that ‘public health cannot be regarded
as an entity distinct from the general, social and economic life of the com-
munity,’ and called for

further legislation which will undoubtedly have far-reaching effects

on the economic life and general well-being of the people. Agricul-
tural indebtedness, land tenure and industrial problems, to cite a
few examples, are all receiving serious attention and . . . mention is
made of these wider aspects of community life in order to empha-
sise the necessity of viewing health problems from the widest pos-
sible angle.98

It was of course this ‘widest possible angle’ that had been sought in the
enquiry into the 1908 Punjab malaria epidemic almost three decades earlier,
and cogently argued in the 1922 pages of the Indian Medical Gazette.99 In
other words, whatever theoretical disagreement had existed at the academic
level at the turn of the twentieth century regarding epidemic disease causa-
tion, little gulf remained in the 1910s and early 1920s at the level of the pub-
lic health administration between the microbiological dimensions of disease
transmission and economic determinants of disease lethality. If public health
officials could do little in the way of directly addressing these key economic
conditions, their advocacy in this regard nonetheless had become prominent
and unambiguous.

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A different kind of tension

Yet despite the seeming accommodation of the two perspectives – economic
and microbiological – a tension of another kind permeated the pages of the
Punjab public health reports through the final decades of colonial rule. From
the mid-1920s on, one can trace a sense of growing professional frustration
with the limited level of funding made available, in practice, for surface
drainage and flood control, and the limits to then-standard public health
technical interventions.100 Quinine distribution efforts were ‘merely pallia-
tive,’ W.H.C. Forster lamented in his 1923 public health report, urging that
‘schemes for land drainage must be regarded as the most effective method
of mitigating or preventing the occurrence of these disastrous epidemics.’101
Further fiscal retrenchment in the early 1920s prompted Gill, appointed
the following year as officiating Punjab Public Health director, to utter the
ultimate sanitationist blasphemy: that rural surface drainage schemes were
a far greater priority than conservancy work (sewage disposal) and drainage
inside rural villages.

[T]he execution of water supply and drainage projects in small vil-

lages is not a sound proposition from the economic point of view,
nor . . . [of] urgent importance from the view of public health. Here
land drainage schemes designated to prevent floods . . . are pecu-
liarly calculated to benefit the rural population.102

Such questioning of prevailing ‘germ-intervention’ orthodoxy would be

voiced even more openly a decade later, the Public Health Commissioner
for the GOI openly contesting exclusive attention to many standard public
health measures:

Abundant supplies of quinine, and the multiplication of tuberculo-

sis hospitals, sanatoria, leprosy colonies, and maternity and child
welfare centres are no doubt desirable, if not essential, but none of
these go to the root of the matter. The first essentials for the preven-
tion of disease are a higher standard of health, a better physique,
and a greater power of resistance to infection.103

This hardly amounted to a rejection of specific public health ‘interventions,’

but rather acknowledgement of their deep insufficiency.
As additional context to this growing frustration within the public health
service was the ever-expanding number of preventive techniques becoming
available, and corresponding work demands placed on staff. Through the
final years of the nineteenth century, the new laboratory-based medicine pre-
sented ever more avenues for micro-‘intervention’ measures: techniques for
containment of disease transmission, or in the case of cholera and plague,

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vaccines for inducing specific immunity. Most were poorly tested and many
would later be considered to be of questionable efficacy.104 Even before the
outbreak of plague in 1896, the demands on provincial public health staff
already were enormous. Provincial sanitary commissioners were expected
to be constantly on tour (until the 1930s, still largely non-motorized) across
a province of over 100,000 square miles of territory, in 50,000 scattered
villages, inspecting the sanitary condition of the country and investigating
both village and urban outbreaks of cholera, fever (malaria), and a grow-
ing number of diseases identified as important such as typhus and relapsing
fever in the hill regions, in addition to plague from the final years of the
nineteenth century. Touring was in addition to statistical reporting respon-
sibilities. These duties – identifying plague and cholera cases, ‘extirpating’
rats, then mosquitoes and intestinal hookworms – Forster would describe
in 1924 as ‘exceptionally onerous.’105 In the face of continuing outbreaks of
plague in the province through the 1910s and 1920s, it is hardly surprising
that sanitary officials ‘on the front lines’ were desperate for certitude, and
simultaneously lured to, and frustrated by, promises of simple fixes. In the
deluge, the central historical question of what turned endemic ‘common’
infections into highly lethal pestilential epidemics would quietly recede into
the background.
For others, the mounting preventive and containment duties were seen
increasingly as obscuring and pre-empting attention to the economic issues
underlying epidemic conditions. In his 1924 public health report, Gill would
quote a recent statement by Sir George Newman, Chief Medical Officer of
the British Ministry of Health, that ‘summarised the relationship of preven-
tive medicine to the body politic’:

Public Health is purchasable, but only in the long run, and only on
a true understanding of scientific facts. Merely to send post-haste
a Medical Inspector to visit on a preventive mission an area suf-
fering from an acute and exceptional prevalence of disease is to
shut the stable door when the horse has escaped, . . . It is neither
State-craft nor science. . . . In public health work this means sanita-
tion, nutrition, the establishment of immunity, and what Dr John
Simon called ‘the necessaries of health. . . . [I]t must be said quite
plainly that the prompt attack . . . to chlorinate the water, disinfect
the drains, boil the milk, provide a temporary hospital, or get vac-
cinated . . . has become so insistent, central and locally, that its
tendency has been to absorb attention. . . . What is needed for the
health of a community is that which is needed for the health of an
individual, a wholesome and resistent [sic] constitution.106

Perhaps the greatest frustration for public health officials in British India
of this period stemmed from being professionally sidelined from such

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broader economic policies. As late as 1927, Gill ruefully recorded that

‘[t]he Public Health Department is not directly in touch with the Water-
logging Committee’ regarding the several land drainage schemes undertaken
during the year.107 In Punjab few details of either drought or flood relief
measures, military food lifts, or surface drainage operations appear in the
annual public health records.108 That information, as in the 1890s, was pub-
lished primarily in the Land Revenue Administration records because it was
land revenue officials who were responsible for most relief activities at dis-
trict level. Clearly, this jurisdictional separation of economic measures from
public health duties was a source of intense personal frustration on the part
of provincial public health officials like Gill and Forster, seen as reinforcing
the reductive trajectory of public health as a discipline.
But there was yet another source for disquiet on the part of public health
officials in the immediate post-war period, one that came from within the
medical professional itself. Despite concerted efforts at reconciliation at
the 1911 Sanitary conference in Bombay, the dispute that had erupted at
the Medical Congress in the same city two years earlier between malaria
‘eradicationists’ (vector sanitation) and ‘ameliorationists’ (‘quininists’)
had not in fact receded. The 1914 Indian Sanitary Policy Resolution109
had given formal recognition to anti-mosquito strategies in malaria con-
trol policy. But vector extirpation programs had not been pursued beyond
trial projects in urban settings such as Saharanpur. Aspirations for anti-
mosquito programs on the part of proponents of ‘vector sanitation’ thus
had not been satiated. As we will consider in chapter five, advocates of
mosquito extirpation were increasingly turning to more inflated arguments
for action on malaria transmission control, the disease now framed as
a primary ‘block’ to economic development in the subcontinent,110 what
in contemporary public health analysis has come to be referred to as the
malaria-blocks-development (MBD) thesis.111 And in this they would be
joined by prominent medical luminaries such as William Osler who had
recently come to describe malaria as ‘the greatest single destroyer of the
human race.’112
Such was the force of this advocacy that Forster as Punjab Sanitary (Pub-
lic Health) Commissioner felt compelled in 1921 to dispute publicly in the
pages of his annual report the surging rhetoric that attributed the subcon-
tinent’s economic stagnation to malaria. ‘I am not one of those,’ he wrote,
referring evidently to W.H.S. Jones’s recent text, Malaria: A Neglected Fac-
tor in the History of Greece and Rome,113

who believes that malaria, qua malaria, is capable of extinguish-

ing an Empire. Remove the stimulus of gain, then malaria might
quite well do what is claimed of it, but the stimulus must first be
removed. . . . [Regarding] the unhealthiness of Gurgaon [district],
the fundamental cause . . . is loss of the economic stimulus. The soil

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is poor, the water saline, and the agricultural conditions generally

unfavourable. . . . the “Bunds” [have] ceased to function.114

Four years later, Forster would even more pointedly ‘repudiate the doctrine
that malaria per se is capable of destroying empires.’115
But the impetus for a narrowed and unidirectional reading of malaria as
the cause of the subcontinent’s poverty was now coming from a different
direction, one even more powerful perhaps than the personal advocacy of
Ross: that of fiscal retrenchment. Deep budgetary cutbacks were fanning
aspirations among public health workers for sources of alternate funding
from beyond India’s shores, creating an opening for the involvement of pri-
vate philanthropic institutions where momentum was fast growing for the
inverted doctrine of malaria as a cause of global underdevelopment.

Notes
1 Foucauldian analysis has explored consequences of late- and post-eighteenth-
century state engagement with health, disease, and medical care in relation to
institutional and political powers of social control; M. Foucault, and C. Gor-
don, Power/Knowledge: Selected Interviews and Other Writings, 1972–1977
(Brighton: Harvester Press, 1980). A further dimension to public ‘control’
related to food and hunger, and societal norms and obligations regarding human
destitution, though less directly addressed in analysis of shifts in socio-political
power resulting from the sanitationist redefinition of illness and disease. On this,
see D. Smith, and M. Nicolson, ‘Nutrition, Education, Ignorance and Income:
A Twentieth-Century Debate,’ in H. Kamminga, and A. Cunningham, eds., The
Science and Culture of Nutrition, 1840–1940 (Amsterdam: Rodopi, 1995),
288–318.
2 D. Brunton, Review of C. Hamlin, ‘Public Health and Social Justice,’ Journal of
the Society of the Social History of Medicine, 13, 1, Apr. 2000, 173–174.
3 C. Hamlin, Public Health and Social Justice in the Age of Chadwick (Cam-
bridge: Cambridge University Press, 1998); C. Hamlin, ‘William Pulteney Ali-
son, the Scottish Philosophy, and the Making of a Political Medicine,’ Journal
of the History of Medicine and Allied Sciences, 62, 2, 2006, 144–186. See also
D. Porter, Health, Civilization and the State: A History of Public Health from
Ancient to Modern Times (London: Routledge, 1999), 86; M.W. Flinn, ‘Intro-
duction,’ Report on the Sanitary Condition of the Labouring Population of Gt.
Britain (Edinburgh: Edinburgh University Press, 1965), at 63–64.
4 Typhus is caused by a rickettsial bacterium (R. prowazekii) transmitted inad-
vertently by the human louse, and endemically present historically in temperate
region populations, characteristically taking epidemic form under conditions of
destitution, related crowding, and incapacity for elemental hygiene, variously
termed famine fever, goal distemper (neurological symptoms), ship or camp
fever. Following initial infection, latent organisms can reactivate years later
under conditions of physical stress and immune suppression. In 1934 Zinsser
correctly hypothesized that Brill’s disease was a recrudescent form of typhus,
a view confirmed in the 1950s, the disease renamed Brill-Zinsser disease; V.A.
Harden, ‘Typhus, Epidemic,’ in K.F. Kiple, ed., Cambridge World History of
Disease (Cambridge: Cambridge University Press, 1993), 1080–1084.

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5 For an insightful overview of ‘pre-germ theory’ predispositionist understanding

of ‘infectious’ and epidemic disease, and its demise under nineteenth-century
‘sanitationism,’ see C. Hamlin, ‘Predisposing Causes and Public Health in Early
Nineteenth-Century Medical Thought,’ Society for the Social History of Medi-
cine, 5, 1, Apr. 1992, 43–70; J.V. Pickstone, ‘Death, Dirt and Fever Epidemics:
Rewriting the History of British “Public Health”, 1780–1850,’ in T. Ranger,
and P. Slack, eds., Epidemics and Ideas: Essays on the Historical Perception of
Pestilence (Cambridge: Cambridge University Press, 1992), 125–148.
6 Johann Peter Frank, Academic Address on The People’s Misery: Mother of Dis-
eases, An Address, delivered May 5, 1790 at the University of Pavia. Translated
from the Latin, with an Introduction by H.E. Sigerist, Bulletin of the History of
Medicine, 9, 1941, 81–100, at 98.
7 For an overview of Virchow’s analysis, see R. Taylor, and A. Rieger, ‘Rudolf
Virchow on the Typhus Epidemic in Upper Silesia: An Introduction and Transla-
tion,’ Sociology of Health and Illness, 6, 2, 1984, 201–217; G. Rosen, ‘What is
Social Medicine?,’ Bulletin of the History of Medicine, 21, 1947, 674–685.
8 W.P. Alison, Observations on the Management of the Poor in Scotland, and Its
Effects on the Health of Great Towns, 2nd ed. (Edinburgh: Blackwood, 1840),
10–11; R.B. Howard, ‘On the Prevalence of Diseases Arising from Contagion,
Malaria, and Certain Other Physical Causes amongst the Labouring Classes
in Manchester,’ in Sanitary Condition of the Labouring Population of Great
Britain. Local Reports for England and Wales, Parliamentary Papers (House
of Lords, 1842), 317, as cited in Hamlin, Public Health and Social Justice, 197.
See also Hamlin, ‘Public Health and Social Justice, 54–61, 188–201; Hamlin,
‘Predisposing Causes and Public Health,’ 43–70.
9 M. Pelling, Cholera, Fever and English Medicine 1825–1865 (Oxford: Oxford
University Press, 1978), 30–31.
10 Hamlin, Public Health and Social Justice, 101–102.
11 M. Worboys, Spreading Germs: Disease Theories and Medical Practice in Britain
(Cambridge: Cambridge University Press, 2000), 39–42; Hamlin, ‘Predisposing
Causes’; M. Harrison, Public Health in British India: Anglo-Indian Preventive
Medicine 1859–1914 (Cambridge: Cambridge University Press, 1994), 52.
12 C. Hamlin, ‘Could You Starve to Death in England in 1839? The Chadwick-Farr
Controversy and the Loss of the “Social” in Public Health,’ American Journal of
Public Health, 85, 6, Jun.1995, 856–66 at 859; Worboys, Spreading Germs, 5.
13 A. Hardy, The Epidemic Streets: Infectious Disease and the Rise of Preventive
Medicine, 1856–1900 (Oxford: Clarendon Press, 1993), 1. John Duffy suggests
that in the urban United States the germ theory ‘awakened the upper classes to
the realization that bacteria were no respecters of economic or social position,’
giving impetus to both public health and antipoverty programs; ‘Social Impact
of Disease in the Late Nineteenth Century,’ Bulletin of the New York Academy
of Medicine, 47, 1971, 797–811, at 809.
14 S. Szreter, ‘Rapid Economic Growth and “the Four Ds” of Disruption, Depri-
vation, Disease and Death,’ Tropical Medicine and International Health, 4, 2,
Feb. 1999, 146–152, at 148. Hamlin traces shifting notions of social obligation
through the eighteenth and early nineteenth century; ‘State Medicine in Great
Britain,’ in D. Arnold, ed., Warm Climates in Western Medicine: The Emergence
of Tropical Medicine, 1500–1900 (Amsterdam: Rodopi, 1996), 132–164. Doug-
las Hay describes the British State’s judicial abandonment of prohibitions on
‘engrossing and forestalling’ at the turn of the nineteenth century and thus any
normative role in food security; ‘The State and the Market: Lord Kenyon and
Mr Waddington,’ Past and Present, 162, Feb. 1999, 101–162.

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15 Alison, Observations on the Management of the Poor, 10–11; W.P. Alison,

Observations on the Famine of 1846–7 in the Highlands of Scotland or Ireland
(Edinburgh: Blackwood & Sons, 1847). For a detailed account of Alison’s work,
see Hamlin, ‘William Pulteney Alison.’
16 Hamlin, Public Health and Social Justice, 153–154. None of the testimony by
the Manchester Poor Law medical officer, R.B. Howard, on the powerful role
of poverty and destitution in typhus epidemicity appeared in the 1842 Sanitary
Report; ‘On the Prevalence of Diseases Arising from Contagion,’ 317, as cited in
Hamlin, Public Health and Social Justice,197.
17 See above, note 4.
18 The HIV-AIDS virus is anomalous historically speaking in targeting directly
the immune system itself; and in turn, exceptional in its potential to undermine
economies directly, in particular low-income populations where there are as yet
limited social support and public health networks.
19 Worboys, Spreading Germs, 6, 278–289.
20 I. Galdston, ‘Humanism and Public Health,’ Bulletin of the History of Medicine,
8, Jan. 1940, 1032–1039.
21 Hamlin, ‘Could You Starve to Death in England?’
22 J.C. Hume, ‘Colonialism and Sanitary Medicine: The Development of Preventive
Health Policy in the Punjab, 1860 to 1900,’ Modern Asian Studies, 20, 4, 1986,
703–724; S. Watts, ‘British Development Policies and Malaria in India 1897-
c.1929,’ Past and Present, 165, 1999, 141–181.
23 M. Harrison, Climates and Constitutions: Health, Race, Environment and Brit-
ish Imperialism in India, 1600–1850 (New Delhi: Oxford University Press,
1999), 170–177.
24 M. Worboys, ‘Germs, Malaria and the Invention of Mansonian Tropical Medi-
cine: From “Diseases in the Tropics” to “Tropical Disease”,’ in David Arnold,
ed., Warm Climates in Western Medicine, 196.
25 W.E. Baker, T.E. Dempster, and H. Yule, The Prevalence of Organic Disease of
the Spleen as a Test for Detecting Malarious Locality in Hot Climates (Calcutta:
Govt. Printing, 1848), reprinted in Records of the Malaria Survey of India, 1, 2,
Mar. 1930, 69–85 [hereafter, RMSI]; W.E. Baker, T.E. Dempster, and H. Yule,
‘Report of a committee assembled to report on the causes of the unhealthiness
which has existed at Kurnaul, and other portions of the country along the lane
of the Delhie canal, with Appendices on Malaria by Surgeon T.E. Dempster,’
1847; reprinted in RMSI, 1, 2, Mar. 1930, 1–68. On this, see S. Zurbrigg, Epi-
demic Malaria and Hunger in Colonial Punjab: ‘Weakened by Want’ (London
and New Delhi: Routledge, 2019), ch. 7.
26 Report of the Commissioners Appointed to Inquire into the Sanitary State of
the Army in India, Parliamentary Papers (London: HMSO, 1863), vol. I, 58
[emphasis added]. See also, E.A. Parkes, A Manual of Practical Hygiene, Pre-
pared Especially for Use in the Medical Service of the Army (London: John
Churchill, 1866), as cited in Harrison, Public Health in British India, 52. In
her overview of the development of imperial sanitary policy in British India,
Ramasubban notes it was ‘well-known’ early on that ‘intensity and frequency
of disease’ in the army depended upon the health of surrounding populations;
‘Imperial Health British India, 1857–1900,’ in R. MacLeod, and M. Lewis, Dis-
ease, Medicine and Empire (London: Routledge, 1988), 38–60, at 40.
27 Parkes, Manual of Practical Hygiene, 52.
28 In the latter case, debility also was addressed simply through discharge from the
army.
29 Parkes, Manual of Practical Hygiene, 444–45 [emphasis added].

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30 Ramasubban, ‘Imperial Health British India, 1857–1900,’ 41. Arnold notes that
annual death rates among both British and Indian troops in the 1860s were cut
in half by the late 1880s, to approximately 15 per 1,000, and reduced further
to 4.4 deaths per 1,000 by 1914; Colonizing the Body: State Medicine and Epi-
demic Disease in Nineteenth-Century India (Berkeley: University of California
Press, 1993), 75.
31 R. Ramasubban, Public Health and Medical Research in India: Their Origins
under the Impact of British Colonial Policy (Stockholm: SIDA, 1982), 15; Har-
rison, Public Health in British India, 101.
32 W.R. Cornish, Report of the Sanitary Commissioner for Madras for 1877
(Madras: Govt Press, 1878), 11, 142, xxviii. See Zurbrigg, Epidemic Malaria
and Hunger, 187.
33 Surgeon-Major H. King, The Madras Manual of Hygiene, 2nd ed. (Madras: E.
Keys, Govt Press, 1880), Appendix I, 371–383.
34 For details, see Zurbrigg, Epidemic Malaria and Hunger, ch. 5.
35 Surgeon-Captain H.E. Grant, The Indian Manual of Hygiene being King’s
Madras Manual, rev. ed. (Madras: Higginbotham & Co., 1894), 326. For dis-
cussion of early nineteenth-century colonial miasma theories, see K.T. Silva,
‘Malaria Eradication as a Legacy of Colonial Discourse: The Case of Sri Lanka,’
Parassitologia, 36, 1994, 149–163, at 154.
36 The first paragraphs of Patrick Manson’s classic 1898 tropical medicine text
read, ‘The malaria parasite . . . is by far the most important disease agency
in tropical pathology. . . . it undermines the health of millions; predisposing
them to other disease . . . impairing their powers of resistance and repair; and
otherwise unfitting them for the active business and enjoyment of life. Directly
and indirectly it is the principal cause of morbidity and death in the tropics and
sub-tropics’; Tropical Diseases: A Manual of the Diseases of Warm Climates
(London: Cassell and Co., 1898), 1.
37 ‘Tropical medicine was given marching orders – to secure the safety and improve
the productivity of the British Empire,’ MacLeod colourfully articulates. ‘The
French, Belgians, and Germans soon joined the fray. From the 1880s, the prac-
tice of medicine in the empire became a history of techniques and policies – of
education, epidemiology, and quarantine – the discovery of pathogens and vec-
tors and the segregation of races. Simultaneously, tropical medicine became a
history of mentalités, shaped by the Pasteurian revolution, which lent a con-
ceptual strategy to complement Europe’s political mission’; ‘Introduction,’ in R.
MacLeod, and M. Lewis, eds., Disease, Medicine and Empire, 1–18, at 7. It was
a sanitary model, he observes, that increasingly ‘obscure[d] the relationship of
disease to social structure.’
38 R. Chandavarkar, ‘Plague Panic and Epidemic Politics in India, 1896–1914,’ in
T. Ranger, and P. Slack, eds., Epidemics and Ideas (Cambridge: Cambridge Uni-
versity Press, 1992), 203–240; I. Catanach, ‘Plague and the Tensions of Empire:
India, 1896–1918,’ in D. Arnold, ed., Imperial Medicine and Indigenous Soci-
eties (Manchester: Manchester University Press, 1988), 149–171; F. Norman
White, Twenty Years of Plague in India with Special Reference to the Outbreak
of 1917–1918 (Simla: Government Central Branch Press, 1929).
39 R. Ramasubban, ‘Imperial Health British India, 1857–1900,’ 38–60; J.C. Hume,
‘Colonialism and Sanitary Medicine,’ 721–722; Harrison, Public Health in Brit-
ish India, 57; Harrison, Climates and Constitutions; D. Arnold, ‘Crisis and Con-
tradictions in India’s Public Health,’ in D. Porter, ed., The History of Public
Health and the Modern State (Amsterdam: Rodopi, 1994), 335–355.
40 Harrison, Public Health in British India, 102.

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41 Snow, considered one of the founders of modern epidemiology, famously identi-

fied the Broad Street pump in Soho as the common domestic water source for a
cholera epidemic in London.
42 In 1908, Ehrlich received the Nobel Prize in Physiology or Medicine for his con-
tributions to immunology.
43 Hakims were practitioners of yunN-I-tibb, or Greek medicine, the medical system
associated with Indian Muslims; Hume, ‘Colonialism and Sanitary Medicine.’
44 Harrison, Public Health in British India, 116; D. Arnold, “Introduction: Dis-
ease, Medicine and Empire,’ in Arnold, ed., Imperial Medicine and Indigenous
Societies, 1–26, at 20.
45 For articulation of the contagionist-anticontagionist framework, see E. Ack-
erknecht, ‘Anticontagionism Between 1821 and 1867,’ Bulletin of the His-
tory of Medicine, 22, 1948, 562–593. For critique of the framework, see C.
Hamlin, ‘Commentary: Ackerknecht and Anticontagionism: A Tale of Two
Dichotomies,’ International Journal of Epidemiology, 38, 1, 2009, 22–27;
Pelling, Cholera, Fever and English Medicine, 109. On the mid- to late
nineteenth-century evolution of medical concepts of malaria etiology, see M.
Worboys, ‘From Miasmas to Germs: Malaria 1850–1879,’ Parassitologia, 36,
Aug. 1994, 61–68.
46 Worboys argues this was often the case in European experience as well; Spread-
ing Germs.
47 Zurbrigg, Epidemic Malaria and Hunger, chs. 5, 10.
48 Harrison, Public Health in British India, 115.
49 Despite laudatory words offered to Ronald Ross (in absentia) and IMS Dir-Gen
Lukis, the conference president in his opening address reaffirmed, in words quin-
tessentially those of Christophers, that ‘the forefront of a sanitary programme
[in India] must be a reasoned account of the conditions and circumstances which
affect mortality and the increase and decrease of populations,’ requiring ‘the
study of the relative effects of . . . social and economic conditions’; Progs. All-
India Sanitary Conference, held at Bombay on 13th and 14th November 1911
(Calcutta: Superintendent Govt. Print., 1912), 1–2.
50 S.R. Christophers, ‘Malaria in the Punjab,’ Scientific Memoirs by Officers of the
Medical and Sanitary Departments of the Government of India (New Series),
No. 46 (Calcutta: Superintendent Govt Printing, GOI, 1911), 107 [hereafter, Sci.
Mem. Off. Med. San. Dep.]
51 For analysis of early twentieth-century changes in famine relief policies, see Zur-
brigg, Epidemic Malaria and Hunger, chs. 11–12.
52 S.R. Christophers, ‘What disease costs India: A statement of the problem before
medical research in India,’ Indian Medical Gazette, Apr. 1924, 196–200; Chris-
tophers, ‘Malaria in the Punjab,’ 24, 26. On this, see also Zurbrigg, Epidemic
Malaria and Hunger, 69–74.
53 Christophers, ‘What Disease Costs India,’ 199. Writing in 1924, Christophers at
this point, it seems, felt some confidence in the famine prevention measures being
enacted in the wake of the 1908 epidemic, allowing him to finally utter the term
‘famine’ in his published writing.
54 Ibid., 197 [emphasis added]. It perhaps is this understanding that helps explain
the marked decline in cholera research in twentieth-century colonial India that
Pratik Chakrabarti notes; in Bacteriology in British India: Laboratory Medicine
and the Tropics (Rochester: University of Rochester Press, 2012), 190–192.
55 S.R. Christophers and C.A. Bentley, ‘The Human Factor,’ in W.E. Jennings, ed.,
Transactions of the Bombay Medical Congress, 1909 (Bombay: Bennett, Cole-
man & Co., 1910), 78–83, at 83.

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56 Zurbrigg, Epidemic Malaria and Hunger, 344–45.

57 C.A. Gill, Report on Malaria in Amritsar, Together with a Study of Endemic and
Epidemic Malaria and an Account of the Measures Necessary to their Control
(Lahore: Miscellaneous Official Publications [Punjab], 1917), 90–91.
58 Christophers, ‘Malaria in the Punjab,’ 132 [emphasis in original]. Perhaps the
most overt use of the term ‘sanitary’ in relation to acute hunger appears in a
1878 account of Burdwan fever in lower Bengal. ‘The most dreadful fever we
have ever had in India,’ Sir Arthur Cotton recounted, ‘is that which has deso-
lated the country around Calcutta, solely from want of water. This is entirely
unirrigated and undrained. When the Engineer, and the Medical Officer were
ordered to enquire into this, they both reported that the first cause of this fatal
fever was the shocking state of the people in respect of even food, that they
were so dreadfully underfed that they had no stamina, but succumbed at once
to fever, that they might have otherwise thrown off with ease. . . . Nothing can
be more certain than that for one death caused by fever from Irrigation, a hun-
dred are prevented by all the sanitary effects of regulated water. And what shall
we say to the deaths caused by Famine?’; Sir Arthur Cotton, letter to Editor of
the Illustrated News, June 29, 1877, in anon., The Great Lesson of the Indian
Famine; with Appendix; Containing Letters from Sir A. Cotton (London, 1877)
[emphasis added].
59 GOI, Proceedings of the Imperial Malaria Conference held at Simla in October 1909
(Simla: Government Central Branch Press, 1910), 5 [hereafter, Simla Conf.].
60 Already in 1904, Christophers’s recommendation for ‘well-directed sanitary
reforms’ as an alternate approach to malaria mortality control in light of the
‘extreme difficulties’ of eradicating mosquito breeding at the Mian Mir canton-
ment would be derisively interpreted by Ronald Ross as provision of ‘night soil
buckets’; S.R. Christophers, ‘Second Report of the Anti-malarial Operations in
Mian Mir, 1901–1903,’ Sci. Mem. Off. Med. San. Dep., No. 9, 1904; R. Ross,
‘The Anti-malarial Experiment at Mian Mir,’ Annual Meeting of the British
Medical Association, July 1904: Proceedings of Section of Tropical Diseases,
British Medical Journal, Sep. 17, 1904, 632–635.
61 On this, see Zurbrigg, Epidemic Malaria and Hunger, ch. 8.
62 Hume, ‘Colonialism and Sanitary Medicine,’ 716–717.
63 Lancet, Jan. 14, 1871, 52; cited in Harrison, Public Health in British India, 110.
64 Report on the Sanitary Administration of the Punjab, 1882, 12 [hereafter,
PSCR].
65 PSCR 1882, 12, 18; PSCR 1878, 29.
66 Sir Joseph Fayrer, On the Climate and Fevers of India, Croonian Lecture, Mar.
1882, (London: J&A Churchill, 1882).
67 PSCR 1885, 15. See also Hume, ‘Colonialism and Sanitary Medicine,’ 720.
68 PSCR 1887, 33; PLGP, in PSCR 1889, 5.
69 PSCR 1887, 37; PSCR 1891, 17.
70 PSCR 1892, 18; ‘When this extensive flooding occurs while the temperature is
high, it is invariably followed in the Punjab by a severe outbreak of malarial
fever’; PSCR 1892, 18.
71 PSCR 1890, 17.
72 Ibid.
73 PSCR 1887, 36 [emphasis added]; PSCR 1890, 16.
74 PSCR 1887, 36.
75 Hume, ‘Colonialism and Sanitary Medicine,’ 723.
76 For details, see Zurbrigg, Epidemic Malaria and Hunger, 167–174.
77 PSCR 1891, 5 [emphasis added]; also, PSCR 1892, 5, 16.

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78 Zurbrigg, Epidemic Malaria and Hunger, 189–190.

79 PSCR 1895, 3.
80 PLGP, in PSCR 1895, 2. In its review of the 1895 PSCR, the provincial gov-
ernment would upbraid the Sanitary Commissioner for rote parroting of price
and rain data with no discussion of their implications upon the health of the
population, suggesting that ‘[a]n undigested statement of weather conditions
and a table of prices does not help us . . . [in the absence of analysis] pointing
out what particular effect the climatic conditions . . . had on the health of the
people’; ibid.
81 PSCR 1896, 14.
82 PLGP, in PSCR 1897, 1. The provincial CDR rose to 45 per mille against a
previous 10-year average of 30 per 1,000.
83 Zurbrigg, Epidemic Malaria and Hunger, ch. 5.
84 PSCR 1900, 3.
85 Zurbrigg, Epidemic Malaria and Hunger, ch. 5.
86 PLGP, in PSCR 1901, 1.
87 PSCR 1904, 12.
88 Zurbrigg, Epidemic Malaria and Hunger, ch. 7.
89 PSCR 1903, 13.
90 PSCR 1907, 1.
91 Simla Conf., 5.
92 Report of the Indian Famine Commission 1901 (London: HMSO, 1901),
61–62.
93 PSCR 1893, opp. page 14.
94 In 1921, the title of the sanitary service was changed to ‘public health’: at the
central level, Public Health Commissioner with the GOI; at the provincial level,
‘Directors of Public Health.’ The corresponding reports became: Annual Report
of the Public Health Commissioner with the Government of India (GOI-PHC),
and Report of the Public Health Administration of the Punjab (PPHA).
95 PPHA 1927, 1.
96 GOI-PHC 1928, Section I: ‘On the State of the Public Health in British India,’
The ‘key principle’ of public health work was the ‘study of the character and
incidence of disease, its causes and predisposing conditions, its mode of spread,
its social factors which increase or reduce it’; ibid., 2.
97 PPHA 1931, 3.
98 GOI-PHC 1937, 2.
99 Editorial, ‘The Economic Factor in Tropical Disease,’ Indian Medical Gazette,
57, Sept. 1922, 341–343.
100 Zurbrigg, Epidemic Malaria and Hunger, ch. 9.
101 PPHA 1923, 18.
102 PPHA 1924, 20–21.
103 GOI-PHC 1935, 2–3.
104 See David Arnold’s discussion of the limited effectiveness of cholera vaccines
in the late colonial period; ‘Cholera Mortality in British India, 1817–1947,’ in
T. Dyson, ed., India's Historical Demography: Studies in Famine, Disease and
Society (London: Curzon, 1989), 261–284, at 276); also C. Hamlin, Cholera:
The Biography (Oxford: Oxford University Press, 2009), 284–285.
105 PPHA, 1924, 24.
106 Ibid., 25.
107 PPHA 1927, 21. For a similar separation of poverty and public health policy
in Edwardian Britain and the existential dilemma it posed for public health
professionals, see J. Lewis, ‘The Origins and Development of Public Health in

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the UK,’ in R. Daetels, et al., eds., Third Oxford Text Book of Public Health
(Oxford: Oxford University Press, 1997), vol. 2, 27. As ‘the issue of poverty
shifted to social welfare – national insurance and old-age pensions,’ Lewis
observes, ‘their role became increasingly one of technicians, applying the spe-
cific interventions that germ research threw up . . . which were to earn the
MOH [Medical Officer of Health] the derogatory title of “drains doctor”, and
subsequently, “mother-craft” educators’; ibid.
108 A partial exception is famine relief activities during the 1939–1940 Hissar dis-
trict famine.
109 Indian Sanitary Policy. Being a Resolution issued by the Governor General in
Council on the 23rd May 1914 (Calcutta: Office of the Superintendent, Govt
Printing, 1914).
110 A. Balfour, and H. Scott, Health Problems of the Empire (London: W. Collins
Sons & Co., 1924).
111 P.J. Brown, ‘Malaria, Miseria, and Underpopulation in Sardinia: The “Malaria
Blocks Development” Cultural Model,’ Medical Anthropology, 17, 3,
May 1997, 239–254.
112 W. Osler, The Evolution of Modern Medicine: A Series of lectures delivered at
Yale University on the Silliman Foundation in April 1913 (New Haven: Yale
University Press, 1921), 223.
113 W.H.S. Jones, Malaria: A Neglected Factor in the History of Greece and Rome
(London: Macmillan, 1907).
114 PPHA 1921, 3.
115 PPHA 1925, 12.

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COLONIAL RETRENCHMENT
AND ‘SELLING’ VECTOR
CONTROL

Forster’s unease: ‘Malaria as Block to Development’

What explains Forster’s ‘repudiation’ of the doctrine of malaria as ‘destroyer
of empires’? What worried him in 1925? One immediate concern no doubt
was a practical one: advocacy for mosquito extirpation in colonial India was
now seen to be in direct competition for increasingly scarce public health
funds, a concern heightened in 1923 by the Inchcape Commission’s pre-
scription for yet further fiscal retrenchment. That consternation could only
have intensified with the 1924 publication of Balfour and Scott’s Health
Problems of Empire, where ‘everyday malaria’ would be described as ‘the
truly “Imperial” disease, the chronic relapsing malaria which saps life and
energy, alters mentality and leads to invalidism and poverty.’1 As director
of the newly expanded London School of Hygiene and Tropical Medicine,
and fresh from his Gorgas-esque vector-extirpation anti-malaria triumph in
Khartoum, Andrew Balfour’s prominence no doubt would have seemed vir-
tually unchallengeable. In the climate of extreme financial stringency, it was
perhaps inevitable that those public health officials in India who continu-
ally struggled for enhanced quinine supplies and funding for agricultural
‘bonification’ measures would see advocacy for expanded anti-larval con-
trol programs as a dangerous distraction. Yet from the ardency of Forster’s
words, one senses a deeper concern as well: it suggests a more general alarm
over an impending demise in understanding of the broader socio-economic
conditions underlying human health. For by the mid-1920s, disease as the
primary cause of India’s poverty had emerged as rhetorical argument at the
highest levels of the public health administration. Despite his later skepti-
cism regarding the protein deficiency thesis, J.D. Graham had argued in his
1924 report as GOI Public Health Commissioner that the prevention of
malaria’s ‘almost incalculable and disastrous results . . . [was] fundamental
in the growth of India into a strong nation.’2
Forster was hardly alone in his consternation over the hegemonic power
of the germ-centred model of health, if perhaps one of the earlier public
health workers in colonial South Asia to express such reservations in official

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documents. The reductive direction in modern disease theory was also by

this time becoming a central concern for a handful of Euro-U.S. public
health analysts, evident in the writing of Galdston and Ackerknecht3 and
the emergence of the concept of ‘social medicine.’ But it seems that the con-
cern for Forster was particularly acute in the case of malaria. Beyond the
immediate funding contest, it appears he had begun to gauge the full ideo-
logical force of the microbiological model of (ill-)health rapidly re-shaping
colonial public health debate: sensing the myriad conveniences, professional
and political, that were nourishing a narrowed view of the malaria problem
in India, and their potential consequences.
Here in this chapter, the inter-war exclusionary trajectory is explored
as it played out in colonial South Asia over the final decades of colonial
rule. This period offers a key portal for tracking the intersection of medical
subspecialisms, Western corporate philanthropy, professional interests, and
imperial exigencies that allowed malaria to become a key vehicle post-WW2
through which socio-economic understanding of the global infective disease
burden would be shed.

The 1925 Conference of Medical

Research Workers
The disease-as-cause-of-poverty thesis would be articulated formally in
1925 in the proceedings of the All-India Conference of Medical Research
Workers at Calcutta: ‘the greatest cause of poverty and financial stringency
in India is loss of efficiency resulting from preventable disease.’4 In a manner
presaging present-day ‘disability-adjusted life year’ (DALY) calculations,5
‘loss of efficiency . . . from preventable malnutrition and disease’ was esti-
mated as ‘not less than twenty per cent’ of the country’s economic output,
costing India ‘several hundreds of crores of rupees each year.’ Deemed ‘a
grave emergency,’ the Conference called for a ‘thorough enquiry into the
wastage of life and the economic depression in India.’6
Admirable in its acknowledgement of the extent of ill-health in the coun-
try, the Conference’s causal framework nevertheless turned upside down the
view of ‘the economic factor in tropical disease’ articulated so frankly in
the Indian Medical Gazette scarcely three years earlier.7 Proceedings from
the 1925 conference, unfortunately, do not appear to have been circulated:
unlike for the earlier pre-war Sanitary Congresses, transactions from the
annual Medical Research Workers conferences, initiated in 1923, were not
made public. However, brief accounts of resolutions adopted at the confer-
ence appear episodically in subsequent publications: in particular, in the
October 1927 issue of the Indian Medical Gazette.8 The journal’s eight-page
conference commentary suggests the proceedings may have been framed
around a 1924 paper by W.G. King in which the cost to India exacted
by malaria was estimated to reach ₤20 million annually in lost lives and

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labour.9 Long-retired from posts as provincial sanitary commissioner, King

had been greatly frustrated with Christophers’s analysis of epidemic malaria
in Punjab at the Simla malaria conference 15 years earlier, conclusions that
laid the basis for subsequent policy to be directed to the control of malaria’s
mortality burden rather than its vector-transmission.10 Through his 1924
paper it appears King was channelling that disaffection into deliberations
at the Medical Research Workers conference planned for the following year.
The unidirectional ‘disease-as-cause-of-poverty’ argument was not, of
course, a new one. The doctrine was already central to the tropical medicine
subspecialism of ‘malariology’ that emerged at the turn of the twentieth
century and held a key place in the writing of Ronald Ross.11 Continents
away, the general thesis had reached perhaps its most frank expression
within the Rockefeller Foundation’s Sanitary Commission, established in
1913, and its global mission of public health training and education, epito-
mized in the Foundation’s reputed creed that saw ‘disease . . . [as] the main
source of almost all other human ills – poverty, crime, ignorance, vice, ineffi-
ciency, hereditary taint, and many other evils.’12 But the thesis had an earlier
pedigree in the nineteenth-century sanitationist reformulation of epidemic
theory, with filth-engendered disease deemed the primary cause of urban
industrial pauperism.
Such theses, of course, contain an element of truth. In the case of malaria
as a ‘block to development,’ the view undoubtedly derived from Euro-
pean imperial experience with malaria in West Africa where conditions of
extremely intense (holoendemic) transmission had long delayed extensive
European settlement and economic exploitation along ‘the gold coast.’13
Malaria affected imperial balance-sheets in South Asia as well. Hyperen-
demic malarial conditions had rendered rail construction in specific hill tracts
difficult and particularly costly.14 Malaria also raised the labour recruitment
costs of the plantation industry on the northeastern tea estates. In the latter
case, however, it did so largely in the context of broader factors – conditions
of human destitution associated with specific indentured labour practices.
Indeed, in their 1909 Malaria in the Duars report, Christophers and Bentley
had openly challenged the thesis.

In a warm country like India there is perhaps every a priori reason

to expect malaria to be both prevalent and intense; but if by such
intensity we mean the condition so characteristic of the African
coast we shall have to modify our conception. . . . [L]arge tracts of
India are not particularly malarious in the sense that many tropical
countries are. . . . [T]his disease does not prevent the prosperity and
natural increase of the population.15

The characterization of malaria in much of India as ‘prevalent’ but ‘not

particularly malarious’ was a pointed rejection of the argument articulated

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by W.H.S. Jones two years earlier in his Malaria: A Neglected Factor in the
History of Greece and Rome, a work for which Ross had contributed the
introductory chapter.16 Yet the thesis of malaria as a central cause of pov-
erty prevailed. Extrapolated to malaria in general, it increasingly coloured
malaria and general public health debate in India, notwithstanding the
Indian Medical Gazette’s explicit 1922 editorial statement to the contrary.17

‘What malaria costs India’: the

Sinton monograph
Not surprisingly perhaps, the view of malaria as the cause of India’s
underdevelopment found a receptive audience within the broader colonial
administration. ‘Malaria,’ the 1928 Royal Commission on Agriculture in
India (RCAI) report asserted, ‘slays its thousands and lowers the economic
efficiency of hundreds of thousands.’ Extending the argument further to
hookworm disease and kala-azar as well,18 the RCAI commissioners urged
authorities to ‘[r]elease from the strangle-hold of disease . . . large areas
of the country,’ action that promised to ‘enormously enhance its general
prosperity.’19 A decade later the thesis was argued much more prominently
by J.A. Sinton in a monograph entitled ‘What Malaria Costs India.’20 At
the end of his tenure as Director of the Malaria Survey of India, Sinton
was determined to see malaria control efforts extended beyond the isolated
economic enclaves of tea estates, military cantonments, and railway estab-
lishments, and openly rued the fact that malaria ‘in ordinary times, excites
comparatively little comment among the lay public . . . [or] in the Indian
Legislature.’21 But in a fiscal climate of retrenchment, malaria transmission
control programs required raising taxes, and that meant convincing those
footing the bill that the cost of doing nothing was even greater. Government
and local provincial authorities, in other words, were unlikely to be per-
suaded unless economic productivity, and tax (land) revenues in particular,
were considered in jeopardy. In this vein, Sinton cited a 1919 U.S. Public
Health service editorial describing malaria as leaving a population ‘gener-
ally subnormal physically, mentally and economically.’22
What was the case for malaria undermining the colonial economy, most
of which was based on rural agriculture? For advocates of general anti-
mosquito measures it was difficult to point to examples of land going out of
production because of malaria. Certainly, there were localized tracts where
agricultural productivity had been thwarted by conditions of particularly
intense malaria transmission. This could be argued for the sub-Himalayan
Terai hill tracts of the United Provinces, and in the northern ‘dry zone’ of
Sri Lanka. However, even in these regions, settlement failed for reasons of
inadequate economic support for workers and immigrants to tide over the
period of extreme physical demands entailed in initial land clearing and
preparation. In the Terai, ‘swampy’ conditions required extensive and costly

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drainage operations before soil conditions could permit successful harvests.

Sinton himself understood this larger economic context to settlement fail-
ures, having officially investigated and documented such questions in his
1931 study of malaria in Spain.23 As for northern Sri Lanka, the region
historically had once supported a thriving Indic civilization;24 but sufficient
investment required to return the land to prosperous cultivation had not
been forthcoming under colonial rule.
Such areas moreover represented only a very small portion of the malari-
ous regions of the subcontinent.25 Where land was being lost it was generally
due to water-logging, often related to neglect of surface drainage in relation
to canal and transportation development, and here debilitating malaria was
a secondary effect to human impoverishment. In this case effective remedial
action was not anti-larval measures but improved drainage or flood control.
Indeed, it was well known that canal irrigation, though it often increased
malaria transmission levels, generally brought greater prosperity and food
production, and declining mortality levels in turn. The argument, in other
words, that malaria per se was the cause of agricultural impoverishment
generally across India was a very hard sell. It clearly required a monumental
promotional campaign. Sinton’s 194-page literature review, ‘What Malaria
Costs India,’ can be seen in this light,26 the monograph transparently offered
as a resource for ‘those workers who have to represent to the financial
authorities the necessity, the urgency and the economic importance of anti-
malaria measures.’27
To be fair, a role for underlying ‘economic stress’ in malaria’s toll was not
excluded from the Sinton monograph. Christophers and Bentley’s work on
the ‘Human Factor’ in malaria was briefly cited. Economic hardship had
a ‘marked influence,’ Sinton acknowledged, not only on the prevalence of
malaria, but also on ‘the case mortality among those afflicted.’28 Yet the
monograph’s overriding emphasis lay elsewhere. Bengal would be cited as
illustrating the ‘effects of malaria in causing a decline of agricultural pros-
perity,’ an inversion of the relationship documented painstakingly by Bent-
ley over the preceding several decades.29 In the monograph’s final pages all
reference to the role of underlying economic factors was omitted, Sinton
concluding in rhetorical style to rival the so-called Rockefeller creed that
malaria was ‘probably the greatest obstacle’ to India’s development, ‘engen-
dering poverty, diminishing the quantity and the quality of the food supply,
lowering the physical and intellectual standard of the nation, and hamper-
ing increased prosperity and economic progress in every way.’30
What explains the Sinton monograph’s stunning turnaround in disease
theory from that expressed in the Indian Medical Gazette 13 years earlier?31
Answers involve considerable conjecture, but among them, some are inevi-
tably political. For the colonial government, faced with a growing nation-
alist movement in the early decades of the twentieth century, the thesis of
malaria as a major cause of poverty – a postulate referred to in modern

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historiography as ‘malaria as a block to development’ (MBD)32 – offered a

near-irresistible alternative explanation (as opposed to colonial misrule) for
continuing endemic poverty in British India.33 For members of the Indian
Medical Service facing drastic research and program funding cutbacks post-
Inchcape, the temptation to ‘sell’ the public health costs of malaria transmis-
sion in unidirectional economic terms no doubt was equally compelling.34 But
fiscal retrenchment also brought with it another dynamic, setting the stage
for beginning reliance on external sources of funding for new ‘intervention-
ist’ public health programs, including that of malaria transmission control.
And as elsewhere in Western imperial domains, the Rockefeller Foundation
with its germ-eradication pedagogical framework was there to oblige.

Rockefeller in India
To what extent did Rockefeller Foundation engagement in India contribute
to the reversal in disease paradigms evident by the mid-1920s? Certainly, a
narrowed view of the detrimental impact of malaria on colonial economies
was already prominent among many malaria workers and sanitarians in
India in the lead-up to the 1909 Simla malaria conference. But the abrupt
epistemic turnaround in disease causation doctrine in the mid-1920s cor-
responds temporally with the Foundation’s growing presence and influence
in the country. By the later 1910s, the Rockefeller Foundation’s Interna-
tional Health Board (IHB)35 had already established a South Asian presence,
with prominent anti-hookworm schemes in the tea plantations of Ceylon
(Sri Lanka) and southern India.36 The timing, moreover, of the MBD-esque
resolutions at the 1925 Conference of Medical Research Workers coincides
with formal initiatives by Indian Medical Service officials to elicit Rockefel-
ler Foundation funding for disease control programs. A funding request by
the Director of the newly opened Calcutta School of Tropical Medicine, for
example, had already been submitted in 1922 – and turned down – by the
IHB, as were several other high-level requests.37 Thus it was clear that Rock-
efeller Foundation funding would be forthcoming only for projects closely
aligned with Foundation principles and largely under its direction.
Those principles were clear from IHB-funded anti-hookworm work in the
1910s on the Darjeeling and Madras tea plantations, projects that were pri-
marily educational in purpose, geared to demonstrate the economic value of
parasite eradication. There had been little IHB funding, by contrast, chan-
nelled to existing medical research facilities in India. Research was con-
sidered unnecessary apparently, for the answers were already at hand. In
the case of ankylostomiasis (hookworm), simple field surveys clearly dem-
onstrated widespread fecal presence of hookworm eggs. The Foundation’s
central goal instead was the training of a cadre of public health specialists
dedicated to eradicating specific microbes and ‘creat[ing] demand for pro-
tection against disease.’38

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Despite initial proposal rejections, prospects for Rockefeller funding in

India in the early 1920s must still have seemed promising, with the Founda-
tion’s public health philanthropy rapidly expanding on other continents.
Its global institution-building had begun in 1915 with the Peking Union
Medical College, and other projects had rapidly followed, with schools of
hygiene and public health in London and Prague in 1921, Warsaw in 1923;
Budapest, Zagreb, and Toronto in 1925; Rome, 1930; and Tokyo in 1933.
It was the school in London, however, that was of particular importance for
the Foundation’s pedagogical aspirations by virtue of the British empire’s
global reach – envisaged by Wycliffe Rose, Director of the International
Health Board, to be ‘a great dynamo that would vitalise and inspire pub-
lic health work, not only in the country, but throughout the world.’ The
$2 million facility would incorporate the existing London School of Tropi-
cal Medicine but refashion it to fully embrace ‘hygiene’ both in name and
programmatic commitment.39 Approval of the London School of Hygiene
and Tropical Medicine proposal by the British Cabinet had prompted acco-
lades in the British medical press, the Lancet describing the decision as ‘a
tremendous compliment to our Empire,’

convey[ing] . . . definite recognition by the United States that the

constructive side of British Imperialism can be used to the advan-
tage of the whole world . . . to serve the common needs of the medi-
cal services of the Foreign Office, the colonies, the India Office, the
combatant forces, and the Ministry of Health, and also those of
students, duly accredited from the medical centres of the world.40

The effusive 1923 Lancet editorial was followed, in stark contrast, by

a scathing British Medical Journal critique of public health and research
cutbacks in India that decried the country’s ‘rather evil reputation as a res-
ervoir for great epidemic diseases such as cholera and plague,’41 a rebuke
that undoubtedly reverberated throughout the IMS. Several months later, a
lead editorial in the Indian Medical Gazette compiled a list of Rockefeller
Foundation funding elsewhere in the colonial world, including a $10.5 mil-
lion grant directed to the Peking Union Medical College. These were ‘fig-
ures,’ the editor commented, ‘which make the mouth water and show the
possibilities for medical education in India.’42 The prospect of Rockefeller
funds filling some of the Inchcape gap in medical funding in India thus had
emerged enticingly on the horizon. By December of 1924, the All India Con-
ference of Medical Research Workers had passed a resolution urging the
Government of India to issue an invitation to the Rockefeller Foundation
to make a survey of medical education and research in India: an initiative
that would be embraced by the IHB as a prelude to Rockefeller funding of
a new separate training institution, what would become the All-India Insti-
tute of Hygiene and Public Health (AIIHPH) in Calcutta.43 Accounts of the

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Foundation’s global activities continued to appear regularly in the pages

of the Indian Medical Gazette through the 1920s, along with enthusiastic
updates of the Gorgas campaign in Panama which had led to completion of
the canal in 1914.
It seems likely, then, that the groundswell of interest in Rockefeller Foun-
dation funding was, in part, what Forster was reacting against in his Punjab
public health reports of 1921 and 1925. In the bleak climate of Inchcape
retrenchment, many in the beleaguered Indian medical research community
would have been ripe for almost any argument offering prospects of fund-
ing, and willing to voice support for the MBD premise, and its broader
sweep of disease theory.44 At the very least, the climate of expectant philan-
thropy made it that much more difficult for those IMS researchers, hopeful
of Rockefeller institutional beneficence, to question the reductive paradigm.
Nonetheless, provincial public health officers during these years still
continued to report prices, harvest conditions, and wages in the preamble
to their annual reports. In Punjab, Gill repeatedly stressed the distinction
between immediate triggers of epidemic malaria mortality and their under-
lying economic causes. ‘Famine,’ he wrote in his 1928 Genesis of Epidemics,
‘is a predisposing cause. Excess monsoon rainfall is the precipitating cause
of regional [malaria] epidemics.’45 Christophers, too, in this period of epis-
temological contestation would come to express his own unease with what
he saw as an increasingly divisive reliance on external medical expertise. In
the concluding remarks of his 1924 critique of funding cutbacks, he urged
the maintaining of an indigenous medical research establishment, arguing
‘[i]t is no question of applying such knowledge only as we now have, nor of
purchasing the necessary knowledge from Europe. Europe cannot help, for
her problems are different and she knows nothing of India’s requirements.’46
Characteristically oblique in wording, it seems quite possible the new Lon-
don School of Hygiene and Tropical Medicine was being alluded to within
his appellation of ‘Europe.’47

Hookworm eradication questioned

The reservations expressly publicly by Forster and Christophers over outside
‘expertise’ were all the more apt in light of the actual practical results of
the International Health Board’s work in India at this point. The Board’s
consultants had had in fact very limited success in galvanizing an hygienic
‘revolution’ against hookworm in South Asia in the 1920s. There were few
examples of project replication of its flagship campaign, even on the tea
estates where infection levels were highest and ‘pay-back,’ in theory, most
likely. Instead, many projects lay unreplicated or abandoned.48 With IHB fail-
ure to interest plantation and provincial government authorities in preventive
campaigns of latrine construction, India had become instead, some argue,
primarily a site for Rockefeller experimental testing of anti-hookworm drugs

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on ‘controlled communities’ of human populations (jail populations and tea

estate labour lines).49 By 1927, a ‘million’ treatments had been given, with
carbon tetrachloride considered the least toxic of the chemicals employed.50
The choice of hookworm as a public health campaign, as in the earlier Rock-
efeller campaign in the southern U.S., had been based from the beginning not
upon its priority as a cause of ill-health, but rather for its instrumental value
as a demonstration of rapid interventions and presumed mass instructional
impact. As a means of getting ‘knowledge into the minds of the people,’ J.D.
Rockefeller Sr had exhorted early on, ‘[h]ookworm seemed the best way.’51
‘Hookworm was a means to an end,’ Farley has observed, ‘a way to educate
the public, physicians, and politicians in public health with the hope that
professionally-run public health services would develop.’52
Then, in 1928, the results were released of a major epidemiological study
into hookworm infection in the country undertaken by the Calcutta School
of Tropical Medicine, findings that raised fundamental questions with
respect to the central premise underlying the anti-hookworm campaign.
Summarizing the study’s conclusions, the Indian Medical Gazette noted
that ‘although throughout India hookworm infestation is excessively com-
mon, yet heavy infections are rare, and hookworm disease – as apart from
infestation – is uncommon.’ The study also showed that ‘treatment only tem-
porarily reduced the worm load in the body,’ re-infection occurring rapidly
in the absence of regular use of footwear. Moreover, ‘a dry season of from 6
to 8 months ha[d] practically the same effect as mass treatment would have
on the population.’ ‘We have been accustomed for many years to think of
hookworm infection as being one of the chief scourges of India,’ Asa Chan-
dler, author of the report observed. ‘Actually, it is apparently a relatively
unimportant cause of disease in this country – except in certain specified
areas.’ Those areas were primarily the industrial plantations – the tea estates
of the Duars and Assam. Elsewhere, ‘hookworm disease is practically non-
existent in most places,’ he concluded, adding that ‘[o]f course, the vitality
and degree of resistance of the patient are important factors in determining
whether light infections may give rise to anaemia.’53 The study questioned
in turn policies promoting enclosed latrines, noting their rapid befoulment
in the absence of ready water supply. It urged greater hygienic benefit from
the rural practice of open areas ‘exposed to direct sunlight’ and traditional
conservancy practices in Bengal employing raised bamboo canes.54
Such basic questions had long been evident to many. Rama Rao, a promi-
nent physician in Madras city and member of the provincial legislature,
had raised similar concerns seven years earlier,55 frustrated by the drain of
resources and effort directed to an infection of limited significance relative
to tuberculosis, and the need instead for access to clean water and anti-
malarials. The Chandler findings, in other words, amounted to a clear
rebuke of the central Rockefeller paradigm: the assertion that infection per
se necessarily was the problem.

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Rural malaria vector-control trials

There was another deeply ironic dimension to the IHB anti-hookworm cam-
paign. Of any infection, it was malaria that the Rockefeller Foundation con-
sidered the greatest global health burden, not hookworm. Early on it had
judged malaria to be ‘probably the number one obstacle to the welfare and
economic efficiency of the human race.’56 Yet malaria received negligible
attention through the first two decades of Rockefeller involvement in South
Asia. Funding requests from the Malaria Survey of India, for example, had
consistently been rejected.57 Not until the mid-1930s did malaria become
a focus for the IHB, renamed in 1927 as the International Health Divi-
sion (IHD), and here funding was directed solely to experimental methods
of vector control, with anti-malarial drug research eschewed.58 In Novem-
ber 1934, Paul Russell, then on Rockefeller assignment in the Philippines,
was deputed by the IHD to work with the King Institute of Preventive Medi-
cine in Madras to assess rural malaria prevalence and initiate demonstration
control trials.59
Preliminary surveys soon led Russell to acknowledge that little scope
existed for rural malaria transmission control through existing anti-larval
methods, a conclusion not unfamiliar to Indian malaria workers. ‘Certainly
larval control by oil, Paris green, or drainage is out of the question in most
of rural India,’ he observed. ‘Deaths can be lessened and the duration of
malarial attacks shortened by better distribution of drugs. But at present
only amelioration and not prophylaxis seems economically possible.’60 Rus-
sell refrained, however, from acknowledging the earlier three decades of
studies which formed the basis for such conclusions. With respect to Bengal
he concluded ‘[i]t is likely there will be no real prevention of malaria in Ben-
gal until it is possible to institute a vast scheme of bonification which will
include regulation of surface waters and improved agriculture,’ again leav-
ing Bentley’s published studies uncited. As for Punjab malaria, he offered no
comment at all, for lack of ‘time and space.’61
Russell went on to investigate the problems of ‘untidy irrigation’ in
relation to the Mettur-Cauvery irrigation project, a canal system opened
in 1933 in the Tanjore district of Madras province. Excessive water usage
appeared to be the primary source of heightened malaria transmission, and
here he urged greater attention to the anti-malariogenic principles drawn
up years before for the irrigation department but left largely ignored.62 His
critique was scathing, highlighting the enormous revenue sums garnered
annually by the irrigation administration, and pointing out that ‘not a sin-
gle anna (penny)’ from the enormous irrigation revenues had ‘ever been
used for malaria research.’63 He went on to devise methods of intermittent
irrigation of paddy fields, a technique which appeared to offer ‘the only
cheap method of [malaria transmission] control.’ When it became clear that
local authorities were reluctant to promote such methods, however,64 he

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turned to a more geographically limited anti-larval project in Pattukottai

Town and the neighbouring village of Ennore. Here, too, he met with local
resistance for reasons of cost, and in 1939 the IHD transferred its malaria
headquarters and laboratory from the King Institute in Madras city to the
Pasteur Institute of southern India at Coonoor in Mysore State. There, Rus-
sell began investigating hyperendemic malaria in the neighbouring hills of
the western Ghats, a region seen to offer increasing potential for plantation
development. The choice of these later project sites, however, meant return-
ing to essentially an enclave framework, activities feasible financially only in
a limited rural industrial setting.65
In his final years of work in India Russell pursued economic arguments for
control of rural malaria transmission, initiating in 1939–1940 a ‘malario-
economic’ survey to assess the cost of malarial infection to rural communi-
ties. Undertaken in three villages in Pattukkottai taluk neighbouring the
recently opened Mettur-Cauvery canal, the study sought to measure the
costs of malarial fever in terms of medical care and lost wages. In a com-
munity where annual income averaged Rs 36–13–0, the cost of ‘fever’ illness
was estimated to be between Rs 2–2–0 to Rs 3–14–0 per capita annually.
The cost of ‘[s]pray killing’ (pyrethrum), by comparison, was estimated at
one-half to one rupee per capita annually. More thorough anti-mosquito
measures – cleaning and oiling ditches, irrigation channels, and standing
water collections – were estimated to cost ‘over two rupees’ per annum.
He concluded that ‘these villages could spend at least Re.1–0–0 per capita
per year for malaria control and if the control measures succeeded, they
would be financially better off.’ Ultimately, however, he acknowledged that
the prospects of raising such funds by direct taxation were ‘practically nil,’
calling instead for government funding of such work through revenues from
irrigation tax revenues.66
Published in 1942, Russell’s malario-economic study is important as one
of the first attempts in South Asia to estimate the economic costs to a rural
population of a major endemic disease. But its importance lies also as an
illustration of the analytic limitations flowing from a narrow microbiologic
focus to such calculations. Left unexplored were alternative approaches to
addressing the economic costs of seasonal malaria debility. Assured access to
quinine treatment could have substantially reduced the extent of lost wages
in addition to saving lives, and at a much smaller cost. Indeed, it could
be argued the study demonstrated instead the key importance of reliable
and affordable quinine access. Moreover, as a study ostensibly concerned
with agricultural development, one might also have expected at least pass-
ing attention to the comparative costs of malaria transmission control in
relation to other factors holding back agricultural productivity, constraints
such as lack of affordable credit and security of tenure. For in addition to
illness costs of malarial infection, the study also found that interest pay-
ments on debt, land rent, and taxes averaged Rs 8–1–0 per capita annually,

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or between 15 and 30 per cent of total household income.67 With the study
constructed narrowly as a problem of plasmodia, other sources of ‘wages
lost’ were invisible, including recurring seasonal un- and under-employment,
and thus also other causes of, and solutions to, agricultural underdevelop-
ment. Finally, as a public health study, it is puzzling that no discussion was
directed to the mortality data collected over the course of the study. In two
of the three malarious study villages, infant mortality and crude death rates
were considerably lower than in the two non-malarial study villages in a
neighbouring deltaic taluk. These data however failed to warrant comment.
This critique of the ‘malario-economic’ study’s conclusions is not to
ignore the human costs of endemic malaria infection, nor to dismiss the
potential value of enviro-entomological techniques of transmission control.
Rather, it highlights the limitations of health analysis framed narrowly with
a singular focus on infection transmission, and at that, on a single infection.
But it highlights, as well, the highly tenuous character of the MBD argument
that would be advanced several years later in post-WW2 deliberations on
the economic benefits of malaria eradication – a thesis argued in no small
part, it appears, on the basis of Russell’s 1942 study, as we will consider in
chapter six. The Pattukkottai study, in this sense, encapsulates many of the
concerns of public health officials such as Forster over the limitations of
the narrow sanitationist model that increasingly dominated deliberations
within the Indian Medical Service.

The germ-transmission paradigm ascendant

In a recent overview of the activities of the International Health Division in
India, Kavadi concludes that the tutelary ‘model’ of hygiene promoted by
Rockefeller Foundation activities had ‘only a marginal impact’ on colonial
government policy and program.68 This was the case, he suggests, even in
regard to the All-India Institute of Hygiene and Public Health (AIIHPH).69
More problematic, arguably, was the Foundation’s approach to public
health ‘modelling.’ Amrith notes the proliferation of demonstration projects
that only rarely expanded beyond the ‘pilot’ stage – a practice, he observes,
of ‘making “policy” out of myriad isolated “pilot projects” and “demon-
strations”, a model which the WHO [later] took to India, and elsewhere in
Southeast Asia, as a first step in reorienting the discourse and practice of
public health.’70 Kavadi notes that of the seven demonstration units initiated
under the IHD, only one was even moderately successful.71 To at least some
within the existing public health administration, the pursuit of disease con-
trol programs through ‘education,’ in isolation from basic curative health
services and broader subsistence security, was transparently unrealistic.72
Indeed, failure was privately acknowledged within the Rockefeller Foun-
dation itself. In internal reports to the New York office, IHD consultants

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referred to work in India as ‘a big disappointment. . . . [T]here is not a single

good example of [disease] control work to be demonstrated,’ one official
concluded.73 Responsibility for the failures was directed unsurprisingly not
to the Foundation itself, but laid at the feet of the Government of India, and
to disinterest and incompetence among provincial public health officials. It
is a view that has tended to colour modern historiographic analysis as well,
with colonial government recalcitrance (‘unwilling[ness] to learn’) inter-
preted in terms of official ‘defeatism’ or purely cynical ‘profit motivated’
jettisoning of health responsibility.74
Undoubtedly, there were elements of both. But there was a great deal
more lying behind medical and governmental unresponsiveness to the IHB/
IHD model projects. In the case of the hookworm campaign, as we have
seen, there were good reasons for scepticism. As for malaria, reluctance on
the part of the Government of India with respect to IHD programs is hardly
comprehensible without taking into account the larger context of pre-1920
British Indian experience and research into malaria mortality. That body
of epidemiological research on Punjab and Bengal malaria provided deep
insights into practical remedial measures and, crucially, where priorities
should lie. This earlier experience would be largely ignored however in the
activities of the IHD consultants. As to ‘native apathy,’ the record of local
rural response to malaria control initiatives was also clear: where programs
addressed economic conditions such as surface water drainage operations
and land reclamation, they generally were embraced with alacrity by rural
cultivators in Punjab. Assumptions of ‘native apathy,’ in other words, merit
considerably closer scrutiny as well.
One area of IHD achievement widely cited in post-Independence public
health literature lay in the 1946 Report of the Health Survey and Develop-
ment Committee (popularly referred to as the Bhore Committee Report),
a document that, as we have seen in chapter three, laid the groundwork
for post-Independence rural health care organization.75 A leading figure
behind the Bhore report was John Black Grant, a Rockefeller consultant
deputed to take over the directorship of the troubled AIIHPH in 1939
following his nearly two decades of work at the Peking Union Medical
College in China. Arguably, however, the need for basic rural health infra-
structure was already self-evident to the post-colonial government. More-
over, in prioritizing primary health care (viz. basic curative care along with
preventive), the Bhore report was itself quite unrepresentative of most pre-
vious Rockefeller policy. At the same time, in the absence of strong advo-
cacy for fundamental agricultural reforms, the report largely steered shy
of concrete economic recommendations that could begin to address the
deep poverty underlying much ill-health, or for that matter the political
conditions necessary to ensure accountability of the rural health services
recommended.76

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Epistemic success
One is tempted, from this history, to dismiss the Rockefeller Foundation’s
impact in South Asia as largely inconsequential, not least because what it
offered institutionally in terms of paramedical training was to a certain extent
already in place through smallpox vaccinators and ‘field’ Sanitary Inspec-
tors. Nevertheless, its pedagogic influence was real. In the immediate term,
it helped nourish within sectors of the Indian Medical Service a technologi-
cal view of health both in medical thought and broader public programs. In
Madras province IHB officials as early as 1925 were reminding government
officials that their ‘province was the main source of [hookworm] infection
spreading to foreign lands . . . [and] that they had an international obliga-
tion to control it.’77 At the central government level, Rockefeller influence
was evident in a Government of India directive to provincial public health
departments for anti-hookworm educational and treatment programs, with
special medical officers appointed to supervise mass carbon tetrachloride
‘preventive’ treatment camps.78 Despite questions of treatment risk, and far
greater priorities, Punjab officials obliged, though it was manifestly evident
to many in the field that, without latrines, there was little prospect of pre-
venting re-infection.79
With respect to malaria, one can wonder how the credibility of the
‘malaria-blocks-development’ thesis was sustained through this period. That
it was, however, is evident in the pages of the 1945 Bengal Famine Commis-
sion Report. At a time when famine had just claimed 2 million lives – the
largest proportion of deaths triggered by malaria primed by starvation –
the Famine Commission pointed to Russell’s 1941 Indian Medical Gazette
analysis of the obstacle to malaria prevention in India as primarily ‘a social
as much as a technical problem.’80 Yet the ‘social’ dimensions detailed in
the Russell article pertained not to economics and hunger, but rather to the
‘absence of a sufficient weight of public opinion’ in favour of vector control,
a situation where ‘[t]he average individual in India . . . has not the remotest
feeling of social responsibility for the control of the disease.’ Characterizing
malaria as an ‘insidious enemy, producing . . . lethargy and destroying initia-
tive and ambition,’ the 1945 Famine Commissioners’ report urged a ‘most
vigorous attack on both urban and rural malaria . . . after the war,’ conclud-
ing that ‘[m]alaria control . . . is essential to the satisfactory development of
the country’s agricultural resources.’81 In other words, the Rockefeller Foun-
dation’s influence on perception of the malaria problem in India appears to
have been substantial at the highest levels of the colonial administration.
Certainly Russell’s technical skills in malaria transmission control were
innovative, his anti-larval field work painstaking, and his recommenda-
tions on ‘untidy’ irrigation welcome, if directed to entomological concerns
rather than economic. Yet in all his South Asian writing, save his initial
1936 overview, socio-economic dimensions of the malaria problem in India

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were scrupulously set aside – a bias manifest, as we have seen, in his 1941
assertion that ‘well fed soldiers in perfect physical condition go down with
malaria as rapidly and as seriously, with as high a death rate as average vil-
lagers.’82 Five years later these same words would re-appear in a prominent
malaria text, Practical Malariology, with Russell as primary author.83
In the medical climate of 1946, Paul Russell’s dismissal of the role of hun-
ger in South Asia’s malaria burden went seemingly without remark within
the malaria research community. This, though it contradicted the entire
body of research on malaria linking much of the malaria lethality in the
subcontinent to human destitution, epidemiological experience which in the
early post-WW1 days had led the League of Nations’ Malaria Commission
(LNMC) to the shores of the Indian subcontinent. Here we return briefly to
that parallel perspective on India’s ‘malaria problem’ as documented by the
League’s Malaria Commission less than two decades earlier.

The League of Nations Malaria

Commission circumvented
As seen in chapter one, an alternate view of the malaria problem, one con-
trary to the MBD paradigm, was clearly evident internationally in the early
work of the League of Nations Malaria Commission in the 1920s. The Com-
mission’s frank articulation of broader determinants underlying the malaria
problem in Europe, however, had only fanned disagreement amongst West-
ern malaria workers, discord that the Commission had been established, in
part, to moderate. Packard describes the divide thus: one group, ‘influenced
by American and British scientists,’

view[ed] malaria narrowly as a problem of vector control. The

other group, following the lead of Celli in Italy (and influenced by
Virchow’s social medicine in Germany), [saw] malaria as a problem
of social uplift and thus intimately tied to social and economic con-
ditions like rural housing, nutrition, and agricultural production.84

Frustrations would erupt publicly in 1930, in Malcolm Watson’s response

to an address by S.P James to the Royal Society of Medicine a year earlier.
A prominent member of the League’s Malaria Commission, James had sug-
gested in his talk that malaria, like tuberculosis, was largely a disease of
poverty. Where ‘the level of wages is low, work is scarce,’ measures directed
to socio-economic improvement offered the primary route to control, he
had argued.

The sources of malaria are not eradicated by these [bonification]

schemes, but as the people live in better houses, have more and
better food and are within easy reach of medical aid, they are not

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infected so frequently, and the disease, when it occurs, is quickly

and effectively treated and overcome. Thus severe and fatal cases
become rare and, after a time, the disease ceases to be of great
importance as a cause of sickness and death.85

Watson, who had worked to reduce malaria transmission on the Malaysian

rubber plantations through drainage and jungle clearing, countered that
the designation of malaria as a ‘social disease’ was a defeatist stance, ‘in
effect, ‘amount[ing] to waiting until people acquire an active immunity to
malaria, . . . [which is] not likely to arise for thousands of years.’ ‘Was it
right,’ he asked, revisiting the acrimonious Mian Mir debate two decades
earlier, ‘that, on such flimsy evidence one of the most illuminating and revo-
lutionary discoveries in medicine should have been condemned and thrown
on the scrap-heap as useless to humanity?’86
For Watson, acknowledgement of economic dimensions to the malaria
problem appeared to threaten progress on vector control efforts. But the
‘social disease’ designation likely was also read as a slight on the technical
skills themselves, a professional affront. If so, Watson was hardly alone.
Earlier in 1929 an even more heated refutation of the Malaria Commission’s
‘social’ perspective on the world malaria problem had come from septua-
genarian Ronald Ross, in a letter to the editor of the Journal of Tropical
Medicine and Hygiene.

An absurd notion has been ventilated in the lay press to the effect
that the way to prevent malaria fever is to feed the natives more
copiously. We should all like to see them better fed, but doubt
much whether they will acquire malaria any less in consequence
than before. . . . The present propaganda . . . [can] be seen to be
sufficiently ridiculous when we remember that the Europeans and
soldiers in the tropics acquire much malaria in spite of being very
well fed as a rule. One wonders how such notions obtain any entry
into the British Press at all. The cost of a ‘free breakfast table’ for
all the natives in any colony would probably exceed the cost of any
anti-mosquito campaign a hundred times.87

By the late 1920s, in other words, the two streams of malaria workers were
at loggerheads, and as in India two decades earlier, disagreement was now
also spilling over into the public domain.88 Once again, the analytic fault
line lay in the definition of the malaria ‘problem’ – infection (transmission)
versus ‘pernicious’ malaria morbidity – a line that generally distinguished
those workers with years of experience in colonial service who were respon-
sible for malaria policy in large administrative areas ‘for the long haul’ and
required a broad epidemiological approach, and those who held roles as
short-term technical advisors on specifically limited assignments.89

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Inevitably perhaps, the Malaria Commission reports would be criticized

by vector control researchers as biased against anti-mosquito programs.90
The charge, however, was open to question. In the case of the 1930 report
on malaria in India, for example, the Malaria Commission had unequivo-
cally recommended anti-larval programs in areas where considered techni-
cally and financially feasible: in urban areas and industrial sites. Indeed, its
one area of pointed criticism of malaria control efforts in India had been
directed to insufficient funding for larval-control programs in the major
urban centres of the country, citing the failure of the anti-An. stephensi cam-
paign in municipal Bombay.91 Vector control clearly was not being ignored,
but nor were observations on the significance of economic conditions.
Working in an institutional setting where diplomatic consensus was
imperative, however, meant that members of the Malaria Commission were
reluctant to allow economic conclusions, deemed by critics as ‘political,’ to
jeopardize the ongoing functioning of the League of Nations Health Organi-
sation (LNHO), and above all its largest single source of funding, the Rock-
efeller Foundation.92 Subsequent reference to economic dimensions of the
malaria burden would be expressed in ever more nuanced ways, now within
the more abstract rubric of ‘social medicine.’93 At the same time, those very
voices increasingly were being replaced by younger cohorts from newly
established institutions of hygiene and tropical medicine but often without
extended rural epidemiological experience. Work within the Malaria Com-
mission itself through the 1930s was directed largely to the not unimportant
field of anti-malarial drug research. Moreover, by the later 1930s, the Ital-
ian approach of ‘bonaficazione,’ Litsios suggests, came to be ‘ “classified”
as fascist and, thus an inappropriate model,’94 a taint which overlooked the
fact that the dramatic decline in malaria death rates in much of the country
associated with quinine distribution and economic reclamation work under
Celli had predated Mussolini’s statist drainage of the Pontine marshes south
of Rome.95 Meanwhile, the umbrella Health Organisation of the League of
Nations had turned its attention through the Depression years to questions
of dietary quality, as we have seen, and away from issues of quantitative
hunger. By 1949 the first comprehensive malaria textbook, Malariology,
edited by M.F. Boyd, contained only two passing references to the exist-
ence of the League of Nations Malaria Commission. In neither case were its
study tour reports mentioned, nor any aspect of their content.96 Among the
compendium’s 1,500 pages, only a single contributor sought to bring the
historical experience of ‘fulminant’ malaria into analytic view, in a chapter
contributed by Christophers himself.97
Curiously, the work of the League of Nations Malaria Commission has
continued to receive little historiographic attention, despite the professional
prominence and extensive field experience of many of its study tours’ par-
ticipants.98 The Malaria Commission is remembered instead largely in terms
of the professional divisions between malaria workers on different sides of

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the Atlantic, rather than the epidemiological content of its study tour obser-
vations from which those differing opinions arose. Moreover, its assessment
of malaria work in India remains virtually invisible historiographically, a
reflection perhaps of how little attention in general has yet been directed to
the South Asian colonial malaria literature99 – and to malaria mortality his-
tory more generally.100
As for the malaria-blocks-development thesis itself, it would rise again
phoenix-like from the ashes of WW2 destruction and into the halls of the
emergent World Health Organization, now freed of the ‘social medicine’
constraints of an abandoned League of Nations Health Organisation. Ironi-
cally enough, in this resurgence, Russell’s brief malaria work in India in the
later 1930s would come to play a pre-eminent role, despite the limited track
record of Rockefeller malaria control work in India. More ironically still, it
would be Russell himself who carried, for reasons of timing and war-time
geopolitical circumstance, the mantle of South Asian malaria experience,
now MBD-transformed, into the WHO’s Expert Committee on Malaria, an
account of which is traced in the chapter that follows.

Notes
1 A. Balfour, and H.H. Scott, Health Problems of the Empire: Past, Present and
Future (New York: Henry Holt, 1924), 195, 232.
2 Annual Report of the Public Health Commissioner with the Government of
India, 1924, 99, 102.
3 I. Galdston, ‘Humanism and Public Health,’ Bulletin of the History of Medicine,
8, Jan. 1940, 1032–1039; E. Ackerknecht, ‘Hygiene in France, 1815–1848,’ Bul-
letin of the History of Medicine, 22, 1948, 117–155.
4 Anon. [‘from a special correspondent’], ‘The Need for a Public Health Policy for
India,’ Indian Medical Gazette, Oct. 1927, 575–582, at 575 [hereafter, IMG].
5 The disability-adjusted life year is a measure of overall disease burden, an esti-
mate of years lost due to ill-health, disability, or early death. See, e.g., the 1993
World Development Report; World Bank, Investing in Health (New York:
Oxford University Press, 1993) for application of DALY methodology. For cri-
tique of underlying assumptions of the measure, see, e.g., M. Rao, Disinvesting
in Health: The World Bank's Prescriptions for Health (Delhi: Sage, 1999).
6 Anon., ‘The Need for a Public Health Policy,’ 575.
7 Editorial, ‘The Economic Factor in Tropical Disease,’ IMG, 57, Sept. 1922, 341–
343. See above, ch. 1, at note 17.
8 Anon. ‘The Need for a Public Health Policy.’
9 W. King, ‘Sanitation in Politics,’ Science Progress [in the Twentieth Century], 18
(1923/24), 113–125, at 123–124.
10 S. Zurbrigg, Epidemic Malaria and Hunger in Colonial Punjab (London and
New Delhi: Routledge, 2019), ch. 8.
11 R. Ross, The Prevention of Malaria, 2nd ed. (London: John Murray, 1911).
12 The doctrine, according to later Rockefeller Foundation president Raymond
Fosdick, was articulated by Frederick Gates, principal administrative aide to
the Foundation; R. Fosdick, History of the Rockefeller Foundation (New York:
Harper Bros., 1952), 23.

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13 Regarding the exceptional entomologic conditions giving rise to holoendemic

malarial transmission in areas of sub-Saharan Africa, see J.L.A. Webb, Human-
ity’s Burden: A Global History of Malaria (New York: Cambridge University
Press, 2009), 27–41.
14 R. Senior White, ‘Studies in malaria as it affects Indian railways,’ Indian Research
Fund Association, Technical Paper, No. 258 (Calcutta: GOI, Central Publication
Branch, 1928).
15 S.R. Christophers, and C.A. Bentley, Malaria in the Duars. Being the Second
Report to the Advisory Committee Appointed by the Government of India to
Conduct an Enquiry Regarding Blackwater and Other Fevers Prevalent in the
Duars (Simla: Government Monotype Press, 1909), 12. The measure of ‘pros-
perity’ intended here of course was one belonging to a pre-modern era where the
definitional bar was set low: conditions where birth rates exceeded death rates.
It did not mean there was no mortality attributable directly to malaria.
16 W.H.S. Jones, Malaria: A Neglected Factor in the History of Greece and Rome
(London: Macmillan, 1907). Baron and Hamlin highlight overt racial dimen-
sions to Western analysis of the ‘great malaria problem’; C. Baron, and C. Ham-
lin, ‘Malaria and the Decline of Ancient Greece: Revisiting the Jones Hypothesis
in an Era of Interdisciplinarity,’ Minerva, 52, 2015, 327–358, at 331.
17 See ch. 1, note 17.
18 Great Britain, Report of the Royal Commission on Agriculture in India (Lon-
don: HMSO, 1928), 481–482; Appendix III, 155[hereafter RCAI].
19 RCAI, 492–493.
20 J.A. Sinton, ‘What Malaria Costs India, Nationally, Socially and Economically,’
Records of the Malaria Survey of India, 5, 3, Sept. 1935, 223–264 [hereafter,
RMSI]; Sinton, RMSI, 5, 4, Dec. 1935, 413–489; Sinton, RMSI, 6, 1, Mar. 1936,
92–169.
21 Sinton, ‘What Malaria Costs India,’ RMSI, Sept. 1935, 225.
22 Sinton, ‘What Malaria Costs India,’ RMSI, Dec. 1935, 424.
23 J.A. Sinton, League of Nations. Health Organisation, 1932. Document No. CH./
Mal.202; reprinted in ‘Rice Cultivation in Spain, with Special Reference to the
Conditions in the Delta of the River Ebro,’ RMSI, 3, 3, June 1933, 495–506.
Sinton’s 194-page ‘What Malaria Costs India’ monograph includes three pages
on anti-malarial ‘bonification’ work; RMSI, Mar. 1936, 131–133.
24 ‘Malaria is very intense in the Terai, which is the belt of low, swampy, forest
ground at the foot of the Himalaya mountains . . . [with] silted-up beds and
debouchures of rivers . . . land in which watercourses have been obstructed’;
Sir Joseph Fayrer, On the Climate and Fevers of India (London: J&A Churchill,
1882), 23, 41; T.W. Tyssul Jones, ‘Malaria and the Ancient Cities of Ceylon,’
Indian Journal of Malariology, 5, 1, Mar. 1951, 125–134.
25 In 1961, Indian officials enthusiastically pointed to an additional 130,562 acres
brought under agricultural production in Punjab following initiation of the DDT
malaria eradication program, an area of 14 miles square representing 0.2 per
cent of the plains of pre-Partition Punjab; Malaria Eradication in India (New
Delhi: Indian Central Health Education Bureau, GOI Press, 1961), 15, as cited
in A.L.S. Staples, The Birth of Development: How the World Bank, Food and
Agriculture Organization, and World Health Organization Changed the World,
1945–1965 (Kent, OH: Kent State University Press, 2006), 172.
26 Soper employed a similar strategy, R. Packard and P. Gadelha suggest, by rep-
resenting the arrival of An. gambiae in Brazil as a threat to all of the Ameri-
cas, a claim subsequently disputed by leading Brazilian entomologist Dr.
Leonidas Deane; ‘A Land Filled with Mosquitoes: Fred L. Soper, the Rockefeller

161
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Foundation, and the Anopheles gambiae Invasion of Brazil,’ Parassitologia, 36,

1–2, 1994, 197–213.
27 Sinton, ‘What Malaria Costs India,’ RMSI, Sept. 1935, 224.
28 Ibid., 252–255.
29 J.A. Sinton, ‘What malaria costs India,’ RMSI, Dec. 1935, 457, 459–460
[emphasis added]. Curiously, Sinton cites his Spain study only once, in relation
to problems of quinine cost but not to his key insights into migrant labour con-
ditions and need for economic support for workers during extension of cultiva-
tion; ‘Rice Cultivation in Spain,’ 142.
30 J.A. Sinton, ‘What Malaria Costs India,’ RMSI, 6, 1, Mar. 1936, 91–169, at 159.
31 Editorial, ‘The Economic Factor in Tropical Disease.’ A 1924 IMG editorial
hints at the shift in process. Listing malaria as the leading ‘scourge of India,’ it
concluded that ‘[t]hough it is true that poverty begets disease, and that disease
again begets further poverty, yet the general economic condition of the masses
in India is to-day distinctly in advance of what it was fifteen years ago’; ‘On the
Seven Scourges of India,’ IMG, July 1924, 351–355.
32 P.J. Brown, ‘Malaria, Miseria, and Underpopulation in Sardinia: The “Malaria
Blocks Development” Cultural Model,’ Medical Anthropology, 17, 3, May 1997,
239–254.
33 King’s 1924 treatise on malaria as key obstacle to India’s economic development
was phrased explicitly in terms of the ‘drain upon India’; ‘Sanitation in Politics.’
His critique offered the British Raj a more convenient explanation of the ‘drain’
on India’s economy, a ‘natural’ one of vectors and ecology, rather than the fis-
cal drain of revenues [tribute] back to London stressed in earlier anti-imperial
tracts such as Dadabhai Naoroji’s Poverty and Un-British Rule in India (Lon-
don: Swan Sonnenschein & Co, 1901); Romesh Chunder Dutt, The Economic
History of India under Early British Rule (London: Kegan Paul & Co., 1906).
34 David Rieff describes a similar dynamic in modern-day humanitarianism: ‘the
contest for limited resources and contracts feeds the imperative to “trumpet” . . .
worst-case scenarios . . . for acquiring a substantial “market share” of each
humanitarian crisis’; A Bed for the Night: Humanitarianism in Crisis (New
York: Simon & Schuster, 2003), 228.
35 Rockefeller Foundation international public health work was undertaken by
the International Health Commission (1913–1916), renamed the International
Health Board (IHB) in 1916 and the International Health Division (IHD) in
1927.
36 S.N. Kavadi, The Rockefeller Foundation and Public Health in Colonial India,
1916–1945, A Narrative History (Pune and Mumbai: Foundation for Research
in Community Health, 1999).
37 Kavadi’s detailed account of the Rockefeller Foundation’s involvement in British
India notes IHB rejection of an official Bengal funding request for anti-malarial
activities by the Central Cooperative Anti-Malarial Society of Calcutta. In 1926,
Christophers’s request for assistance in locating malaria personnel to join the
Central Research Institute for malaria work in India was also rejected; Kavadi,
Rockefeller Foundation and Public Health, 76–78. See also J. Farley, To Cast
Out Disease: A History of the International Health Division of the Rockefeller
Foundation, 1913–1951, (New York: Oxford University Press, 2004).
38 Kavadi, Rockefeller Foundation and Public Health, 16, 18–50, 53.
39 D. Fisher, ‘Rockefeller Philanthropy and the British Empire: The Creation of the
London School of Hygiene and Tropical Medicine,’ History of Education, 7, 2,
1978, 129–143, at 129, 130, 136, 142, 143. By 1937, the LSHTM was provid-
ing teaching or research facilities for 422 students from 27 countries. In this way,

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Fisher observes, ‘the Foundation helped preserve both life and capital in Britain
and her Empire and laid the ground for the increasing investment of American
capital in the underdeveloped world’; ibid., 129, 142–143.
40 Editorial, ‘An Imperial School of Hygiene,’ The Lancet, Mar. 4, 1922, 441. The
appointment of Andrew Balfour as the new school’s first director was a perfect
match: malaria, he pronounced in 1924 was ‘sapping life and energy’ from colo-
nial populations; Balfour, Health Problems of the Empire, 232. His admiration
for the Foundation’s anti-hookworm campaigns was unabashed:
Even when it began to dawn upon the medical world that hookworm
disease was a foe to be fought upon a large scale, the various British
Governments did next to nothing, and it was left to the Americans to
conceive the idea of a world campaign against the insidious enemy,
and, furnished with the sinews of war by John Rockefeller, to embark
upon one of the most remarkable enterprises recorded in the history of
hygiene; ibid., 195.
The text was written, Harrison suggests, ‘largely to convince British and
colonial administrations of the economic utility of medical intervention’; M.
Harrison, Public Health in British India: Anglo-Indian Preventive Medicine
1859–1914 (Cambridge: Cambridge University Press, 1994), 3.
41 Editorial, ‘Public Health and Medical Research in India,’ British Medical Jour-
nal, Apr. 14, 1923, 640.
42 ‘We need not humble ourselves and go hat in hand as beggars, all that is needed
is to invite the Foundation to send a commission to enquire into the needs of
India. . . . the conditions attached to the gifts are such that countries like England
have not hesitated to take full advantage of the benefactions of the Foundation’;
Editorial, IMG, Apr. 1924, 195–196.
43 Kavadi, Rockefeller Foundation and Public Health, 94.
44 See note 32, above.
45 C.A. Gill, The Genesis of Epidemics and the Natural History of Disease (Lon-
don: Bailliere & Co, 1928), 93 [emphasis in original].
46 S.R. Christophers, ‘What Disease Costs India’ – Being the presidential address
at the Medical Research Section of the Fifth Indian Science Congress, IMG, Apr.
1924, 196–201, at 200.
47 Ramasubban highlights the impact of the post-WW1 fiscal predicament in shift-
ing medical research back to tropical medicine institutes in Britain, a legacy
which continues with the ‘tendency . . . to rely on foreign and international
agencies’; R. Ramasubban, Public Health and Medical Research in India: Their
Origins under the Impact of British Colonial Policy (Stockholm: SIDA, 1982),
42–43.
48 Kavadi, Rockefeller Foundation and Public Health, 32; S. Hewa, ‘The Hook-
worm Epidemic on the Plantations in Colonial Sri Lanka,’ Medical History, 38,
1994, 73–90, at 84–87.
49 Kavadi observes ‘a carbon tetrachloride-chenopodium mixture was known to
be efficient but it was not known to be safe’; Rockefeller Foundation and Public
Health, 47, 136; S.N. Kavadi, ‘ “Wolves Come to Take Care of the Lamb”: The
Rockefeller Foundation Hookworm Campaign in the Madras Presidency, 1920–
29,’ in E. Rodríguez-Ocaña, ed., The Politics of the Healthy Life: An Interna-
tional Perspective (Sheffield: European Association for the History of Medicine
and Health, 2002), 89–111.
50 Kavadi, Rockefeller Foundation and Public Health, 50.

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51 V. Heiser, in A Doctor’s Odyssey: Adventures in Forty-five Countries (London:

Jonathan Cape, 1937), as quoted in Kavadi, Rockefeller Foundation and Public
Health, 16.
52 Farley, To Cast Out Disease, 27.
53 Editorial, ‘Hookworm in India,’ IMG, May 1928, 261–265, at 261–262; Asa
Chandler, ‘The Prevalence and Epidemiology of Hookworm and Other Helminth
Infection in India, Indian Journal of Medical Research, 15, Pt. XII, 1928, 695–743.
54 Editorial, ‘Hookworm in India,’ 264–265.
55 Kavadi, Rockefeller Foundation and Public Health, 40. For parallel critique of
the Rockefeller Foundation hookworm and malaria campaigns in Latin Amer-
ica, see Marcos Cueto, ‘The Cycles of Eradication: The Rockefeller Foundation
and Latin American Public Health, 1918–1940,’ in Paul Weindling, Interna-
tional Health Organisations and Movements, 1918–1939 (Cambridge: Cam-
bridge University Press, 1995), 222–243, at 228; M. Cueto, Cold War, Deadly
Fevers: Malaria Eradication in Mexico, 1955–1975 (Baltimore: Johns Hopkins
University Press, 2007); M. Cueto, and S. Palmer, Medicine and Public Health
in Latin America: A History (New York: Cambridge University Press, 2015).
A larger goal, Rockefeller officials acknowledged, was convincing the public
‘that the government has a real interest in [their] welfare, health and happi-
ness. Tuberculosis control, on the other hand, was routinely rejected because
“it takes too many years to show results” ’; A.-E. Birn, and A. Solórzano, ‘The
Hook of Hookworm: Public Health and Politics of Eradication in Mexico,’ in A.
Cunningham, and B. Andrews, eds., Western Medicine as Contested Knowledge
(Manchester: Manchester University Press, 1997), 147–171, at 163.
56 Annual Report, 1915 (New York: Rockefeller Foundation, 1915), 12; cited by S.
Franco-Agudelo, ‘The Rockefeller Foundation’s Antimalarial Program in Latin
America: Donating or Dominating?,’ International Journal of Health Services,
13, 1, 1983, 51–67, at 54. S.P. James, too, would ponder the irony of Rockefel-
ler Foundation anti-malarial projects in 39 areas of eastern and southern Europe
‘when so much has been left undone in the tropics’; in Presidential Address,
‘Advances in Knowledge of Malaria Since the War,’ Transactions of the Royal
Society of Tropical Medicine and Hygiene, 31, 3, Nov. 1937, 263–280, at 274.
57 See note 37.
58 Malaria pharmacotherapeutic research within the LNMC also was ignored by
the Rockefeller Foundation; James, ‘Advances in Knowledge of Malaria,’ 274.
59 Kavadi, Rockefeller Foundation and Public Health, 78; Kavadi, ‘Wolves Come
to Take Care,’ 104.
60 P.F. Russell, ‘Malaria in India: Impressions from a Tour,’ American Journal of
Tropical Medicine, 16, 6, 1936, 653–664, at 663. Twelve years earlier Balfour
had also acknowledged the costliness of anti-mosquito measures that in many
areas did ‘not justify the expense,’ recognizing that such measures were feasible
only in enclave settings; Health Problems of the Empire, 237, 249. See also
Kavadi, Rockefeller Foundation and Public Health, 81. In 1942 Russell would
qualify his ‘pessimism’ based on later work with pyrethrum . . . at per capita
costs around $0.08 per year; P. Russell, F.W. Knipe, and T.R. Rao, ‘Epidemiology
of Malaria with Special Reference to South India,’ IMG, 77, 1942, 477–479.
61 Russell, ‘Impressions from a Tour,’ 661.
62 Proceedings of the Water-logging Board, Punjab, Dec. 6, 1930, ‘Principles to be
observed in the preparation of canal projects and in their execution,’ RMSI, 3,
2, Dec. 1932, 269–270; P.F. Russell, ‘Malaria due to defective and untidy irriga-
tion,’ Journal of the Malaria Institute of India, 1, 4, 1938, 339–349; W.C. Sweet,
‘Irrigation and malaria,’ Procs. Nat. Inst. Sci. Ind., 4, 1938, 185–189.

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63 Russell, ‘Malaria due to Defective and Untidy Irrigation,’ 342.

64 It would later be acknowledged that the technique ‘may interfere with the
growth of rice crops and the question is one which requires further investiga-
tion’; Famine Inquiry Commission (1945) Report on Bengal, Pt. II (New Delhi:
GOI, 1945), ch. 6, ‘Malaria and Agriculture,’ 170–175, at 173.
65 Russell, ‘Impressions from a Tour,’ 662.
66 P.F. Russell, and M.K. Menon, ‘A Malario-economic Survey in Rural South
India,’ IMG, 77, Mar. 1942, 167–180, at 179.
67 Causes of unemployment in 1946–1947 for West Bengal agricultural labourers
were estimated at 3.1 per cent for sickness, 8.2 per cent for ‘want of work’ and
9.1 per cent for ‘miscellaneous’; 1951 Census of India, VI West Bengal, Pt. I-A,
98. At the same time, the Russell study was silent on the possibility that access to
irrigation substantially reduced seasonal hunger and may well have outweighed
the wages lost due to more frequent malaria infection. Unconsidered as well was
the likelihood of labour inefficiencies entailed with wage levels often below sub-
sistence levels, or that debt-servicing costs are likely to have been highly skewed
against the poorest households.
68 Kavadi, Rockefeller Foundation and Public Health, 92.
69 Ibid., 94, 109. Unlike in China where the limited presence of Western medical
institutions allowed a free hand to the Foundation in establishing Peking Union
Medical College, in India negotiations would drag on for years over how such
public health training would be integrated into existing medical training facilities
and who would be in control. Proposed initially in 1923 by the All-India Confer-
ence of Medical Research Workers, and recommended in 1927 by the IHD as
a teaching and research institute, the institute was inaugurated only in Decem-
ber 1932. Thereafter relations were fraught with administrative dissatisfaction
on both sides. On intra-professional tensions between European and Indian
membership on the AIIHPH Governing Body, see D. Arnold, ‘Colonial Medicine
in Transition: Medical Research in India, 1910–47,’ South Asia Research, 14, 1,
1994, 10–35, at 27–28.
70 S. Amrith, Decolonizing International Health: India and Southeast Asia, 1930–
65 (Basingstoke: Palgrave Macmillan, 2006), 104.
71 Kavadi, Rockefeller Foundation and Public Health, vi, 94, 109.
72 In the case of mosquito control programs, Amrith notes gently satirical reaction
to such projects in Phanishvarnath Renu’s 1954 novel, Maila Anchal. The Soiled
Border (Delhi: Chanakya Publ., 1991); Decolonizing International Health, 122.
73 Kavadi, Rockefeller Foundation and Public Health, 92, citing R.B. Watson of the
Rockefeller Foundation in his 1946 India tour. See also V.R. Muraleedharan, and
D. Veeraraghavan, ‘Anti-malaria Policy in the Madras Presidency: An Overview of
the Early Decades of the Twentieth Century,’ Medical History, 36, 1992, 290–305.
74 Kavadi, Rockefeller Foundation and Public Health, 92, 137.
75 GOI, Report of the Health Survey and Development Committee (New Delhi:
GOI Press, 1946), vols. 1 & 2.
76 See also ch. 3 at note 15 for the influence of the Rockefeller-funded AIIHPH
on ‘nutritional’ thought. Perhaps the most valuable IHD work in India was in
nurse training, a health field of otherwise markedly low status, although here
too public health nursing appears to have been directed primarily to disease-
transmission interventions and maternal (behavioural) education.
77 Kendrick to Sawyer, October 28, 1925, cited in Kavadi, Rockefeller Foundation
and Public Health, 49–50.
78 Kavadi, Rockefeller Foundation and Public Health, 50. In 1929, 489 Punjab
villages were treated with carbon tetrachloride; PPHA 1929, 2; PPHA 1934,

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19. This, though Forster had testified one year earlier that the ‘hookworm is
not a disease of any consequence in Punjab’ (RCAI, vol. 8, 524), a conclusion
supported by the Chandler study that had found a ‘fairly high incidence (60 to
70%) of very light infections . . . along the eastern and northern borders of the
Punjab . . . but infections severe enough to be of pathogenic significance are
practically unknown’; Chandler, ‘The prevalence and epidemiology of hook-
worm,’ 717.
79 Kavadi, Rockefeller Foundation and Public Health, 44.
80 P.F. Russell, ‘Some Social Obstacles to Malaria Control,’ IMG, Nov. 1941,
681–690.
81 GOI, Famine Inquiry Commission (1945) Report on Bengal (New Delhi: GOI,
1945), Pt. II. ‘Death and Disease in the Bengal Famine,’ ch. VI ‘Malaria and
Agriculture,’ 170–175, at 171.
82 P.F. Russell, ‘Some Aspects of Malaria in India,’ Jul. 5, 1941, as cited in Farley,
To Cast Out Disease, 123.
83 P.F. Russell, L.S. West, and R.D. Manwell, Practical Malariology (Philadelphia:
W.B. Saunders, 1946), 541.
84 R. Packard, and P.J. Brown, ‘Rethinking Health, Development, and Malaria:
Historicizing a Cultural Model in International Health,’ Medical Anthropology,
17, 1997, 181–194, at 184. Patrick Zylberman similarly describes the ‘widening
gulf’ that had emerged between what he has termed ‘American malariology’ and
the ‘social malariology of a European ilk’; ‘A Transatlantic Dispute: The Etiology
of Malaria and Redesign of the Mediterranean Landscape,’ in S.G., Solomon, L.
Murard, and P. Zylberman, eds., Shifting Boundaries of Public Health: Europe
in the Twentieth Century (Rochester: University of Rochester Press), 2008,
269. According to Lewis Hackett’s notes to the Rockefeller Foundation, the 33
attendants at a June 1928 ‘special meeting of critics and advocates’ of the second
Malaria Commission report quickly fell into two groups: ‘mitigators’ and ‘eradi-
cators’; as cited in H. Evans, ‘European Malaria Policy in the 1920s and 1930s:
The Epidemiology of Minutiae,’ ISIS, 80, 1989, 40–59, at 51. Hackett similarly
described the gulf as between ‘the Anglo-Saxons’ and the ‘Europeans’; ‘Address
by Dr. Lewis W. Hackett,’ Proceedings of the Fourth International Congress on
Tropical Medicine and Malaria (Washington, D.C., May 10–18, 1948), 10–15.
85 S.P. James, ‘The Disappearance of Malaria from England,’ Proceedings of the
Royal Society of Medicine, 23, 1929–30, 71–87, at 84–85.
86 M. Watson, ‘The Lesson of Mian Mir,’ Journal of Tropical Medicine and
Hygiene, Jul. 1, 1931, 183–89 at 189. On the Mian Mir ‘debate’ and its signifi-
cance for colonial malaria policy, see Zurbrigg, Epidemic Malaria and Hunger,
12–13, 210–212; W.F. Bynum, ‘An Experiment that Failed: Malaria Control at
Mian Mir,’ Parassitologia, 36, 1994, 107–120.
87 R. Ross, ‘Malaria and Feeding,’ Journal of Tropical Medicine and Hygiene,
May 1, 1929, 132.
88 Zurbrigg, Epidemic Malaria and Hunger, 242–245.
89 Litsios describes Fred L. Soper, a quintessential Rockefeller vector ‘eradication-
ist,’ as one who ‘prided himself on having made the word eradicate “respectable
once more” . . . . His world was a world of action . . . there was little room in
that world for “esoteric” issues such as the relationship between malaria control
and agriculture. He believed in getting a specific job done with the conviction
that job would contribute to the wider good, however “good” was defined’;
The Tomorrow of Malaria (Wellington, NZ: Pacific Press, 1996), 78. Worboys
also notes in early twentieth-century Britain the ‘relative decline in the influ-
ence of epidemiology signalling declining interest in social factors, as disease was

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constituted in relations between bacteria and individual bodies’; M. Worboys,

Spreading Germs: Disease Theories and Medical Practice in Britain, 1865–1900
(Cambridge: Cambridge University Press, 2000), 285.
90 P.F. Russell, Man’s Mastery of Malaria (London: Oxford University Press, 1955),
202, 204–205. In his generally appreciative summary of the work of the LNMC,
L. Bruce-Chwatt also interpreted its reports as ‘prejudice[d] . . . show[ing] a
regrettable neglect of anti-anopheline methods of control’; ‘History of Malaria
from Prehistory to Eradication,’ in W.H. Wernsdorfer, and I.A. McGregor, eds.,
Malaria: Principles and Practice of Malariology (Edinburgh: Churchill Living-
stone, 1988), vol. 1, 1–60, at 41.
91 LNMC, Report of the Malaria Commission on its Study Tour of India (Geneva:
League of Nations, 1930), 74 [hereafter, LNMC, India report].
92 For details on Rockefeller Foundation funding of the LNHO, see M.D. Dubin,
‘The League of Nations Health Organisation,’ in Weindling, International
Health Organisations, 56–80, at 72. Already in the case of the 1927 U.S. study
tour, where deep differences in perspective existed between the socio-economic
and vector control interpretation of malaria decline in the country, a compro-
mise of sorts had resulted in no official report being issued; James, ‘Advances in
Knowledge of malaria since the War,’ 266. Yet even within the Rockefeller Foun-
dation itself there were individual consultants who by the late 1920s had come
to address a broader economic understanding of the malaria burden. I.J. Kligler’s
study of malaria in Palestine, for example, pointed clearly to the primacy of
economic conditions in malarial epidemiology. ‘Malaria may be classified among
the social diseases of a country,’ he concluded, ‘most prevalent and of greater
severity in countries of low social and economic status’; The Epidemiology and
Control of Malaria in Palestine (Chicago: University of Chicago Press, 1928), 12.
93 W. Schüffner, ‘Notes on the Indian Tour of the Malaria Commission of the
League of Nations,’ RMSI, 11, 3, Sept. 1931, 337–347, at 339. Yet the cen-
tral importance of economic and agrarian conditions in relation to the malaria
health burden would continue to be documented; J.A. Sinton, ‘Rice cultivation
in Spain.’ For an overview of ‘social medicine’ thought of this period, and its sub-
sequent sidelining in the early years of the WHO, see J. Farley, Brock Chisholm,
the World Health Organization, and the Cold War (Vancouver: University of
British Columbia Press, 2008), 111–118.
94 Litsios, ‘Malaria Control, the Cold War,’ 267.
95 Malaria deaths declined from an estimated 16,000 per year in 1900 to 2,045 in
1914; F. Snowden, The Conquest of Malaria: Italy, 1900–1962 (New Haven:
Yale University Press, 2006), 89, 120. Malaria mortality appears to have declined
from the later nineteenth century, along with general death rates. Nájera shows
funding for ‘land reclamations’ to have begun as early as 1901 and that for
mass quinine distribution in 1904; ‘ “Malaria Control” Achievements, Problems
and Strategies,’ Parassitologia, 43, 2001, 1–89, at 12; A. Celli, ‘The restriction
of malaria in Italy,’ in Transactions of the Fifteenth International Congress on
Hygiene and Demography, Washington, September 23–28, 1912 (Washington,
D.C., 1913), 516–531, at 529–530.
96 M.F. Boyd, ed., Malariology: A Comprehensive Survey of All Aspects of This
Group of Diseases from a Global Standpoint (Philadelphia: W.B. Saunders,
1949), 22, 698, 1470. In his 1955 text, Russell devotes 10 pages to the LNMC’s
anti-larval work, expresses regret over the Commission’s emphasis on ‘epidemi-
ology and drugs,’ and in a single-sentence reference to the India study tour report
points to inadequate urban anti-mosquito measures; Man’s Mastery of Malaria,
198–208.

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97 S.R. Christophers, ‘Endemic and Epidemic Prevalence,’ in M.F. Boyd, ed.,

Malariology (Philadelphia: W.B. Saunders, 1949), ch. 27, 698–721.
98 Siddiqui notes the India study tour report but mirrors Russell’s 1955 assess-
ment of the LNMC; World Health and World Politics, 128. Litsios provides
perhaps the most specific account of the LNMC policy dispute; The Tomor-
row of Malaria, 56–69. Curiously, in a later overview of pre-eradication era
malaria control work, the LNMC is omitted; S. Litsios, ‘Malaria Control and
the Future of International Public Health,’ in E. Casman, and H. Dowlatabadi,
eds., The Contextual Determinants of Malaria (Washington, D.C.: Resources
for the Future, 2002).
99 Among the few references to the India study tour report, William Bynum notes
its ‘striking’ conclusions regarding the ‘economic and social dimensions’ to
the malaria problem in both Bengal and Punjab; ‘Malaria in inter-war British
India,’ Parassitologia, 42, Jun. 2000, 25–31, at 29–30. Gordon Harrison refers
to the European and U.S. study tours of the LNMC but not that to India, inter-
preting LNMC reluctance to embrace the anti-mosquito approach as ‘defeat-
ist,’ ‘pessimis[tic],’ and ‘close-minded,’ and overlooking the Italian success in
‘removing the terror’ of malarial infection; Mosquitoes, Malaria, and Man:
A History of the Hostilities since 1880 (London: John Murray, 1978), 185.
100 An important exception appears in the work of José A. Nájera, where the
decline in the ‘pernicious’ form of malaria well in advance of the DDT era is
discussed for a number of regions in Europe; J.A. Nájera, Malaria Control:
Achievements, Problems and Strategies (Geneva: World Health Organization,
1999), 10–31. See also, Farley, To Cast Out Disease, 114–118.

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 6
MALARIA AND THE W.H.O.
The ‘Human Factor’ set aside

The seminal role played by malaria activities in shaping the nascent World
Health Organization following the Second World War has been highlighted
in recent historiography of the agency. This important work has explored the
backgrounds of key medical figures selected in early 1947 as initial members
of an Expert Committee on Malaria (ECM), as well as the larger geopoliti-
cal context and interests underlying the choice of malaria as an initial focus
for the emergent organization.1 Several key questions within this work how-
ever remain largely unexplored: how decisions regarding expert input came
about in the formative deliberations taking place in late 1946; the empirical
evidence underlying inclusion of global malaria transmission control within
the initial mandate of the new organization; and above all for the purposes
of this study, what pre-existing epidemiological understanding of malaria
was set aside in the process. How was it that the wealth of earlier insights
arrived at by the League of Nations Malaria Commission into the socio-eco-
nomic determinants of malaria’s global ‘burden’ – a good portion derived
from South Asian epidemiological experience2 – came to be circumvented in
the two-year interval leading up to the convening of the first World Health
Assembly in June 1948? This chapter considers the events of this formative
period of the World Health Organization that, beginning in late 1946, consti-
tute the final stage of the abandonment of the ‘Human Factor’ in twentieth-
century Western malaria thought.

Beginnings: UNRRA and the

Interim Commission
In the wake of the dissolution of the Geneva-based League of Nations and its
Health Organisation over the course of WW2, public health advisors from
18 member countries of the fledgling United Nations Economic and Social
Council (ECOSOC) met in Paris in March 1946 to establish a successor
global health organization.3 A provisional body, the Interim Commission
(IC), was constituted in July of that year,4 tasked with setting out a struc-
ture and preliminary program of work for the new agency while awaiting

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final ratification by member countries and formal inauguration as the World

Health Organization in 1948. One of the first tasks of the Interim Commis-
sion was the establishment of an Epidemiology and Quarantine Committee,
mandated to assume the international epidemic surveillance work which
the United Nations Relief and Rehabilitation Administration (UNRRA) had
taken over from the League of Nations Health Organisation (LNHO) in
1944 at the invitation of the U.S. government.5 This was quickly followed
by deliberation on the global health issues to be taken up by the organiza-
tion on a priority basis.
Among the several issues selected by the Interim Commission was a DDT-
based anti-malaria program.6 Widespread media reporting of war-time
successes in typhus control employing the new ‘miracle’ insecticide (dichloro-
diphenyl-trichloro-ethane) had already fanned professional aspirations for
global extension of malaria control. DDT had become ‘one of the heroes
of the war, heralded and praised in as many as twenty-one thousand news-
paper articles by the end of the war . . . reportedly saving some five million
lives by 1950.’7 By early 1947, preliminary success with DDT-based malaria
control in U.S.- and UNRRA-funded demonstration projects in Venezuela,
Italy, and Greece had won over many Interim Commission delegates to the
possibility of eradicating the disease globally. Adding to the euphoria was a
general sense of optimism engendered by the new medical technology devel-
oped during and leading up to the war: among the ‘magic bullet’ discoveries
were synthetic anti-malarial medicines, antibiotics such as penicillin, and in
1943 the anti-tuberculosis antibiotic, streptomycin.
But acceptance of malaria control as an urgent priority for WHO derived
also, it is argued in this chapter, from a carefully constructed strategy on
the part of the handful of malaria workers already engaged in the above
anti-malarial projects. The initial proposal for an Expert Committee on
Malaria was submitted at the second meeting of the Interim Commission
on November 6, 1946 by Arnoldo Gabaldón, director of the DDT-based
malaria program initiated under U.S. direction in Venezuela. From the ear-
liest days Gabaldón had aspired to the goal of malaria eradication for his
country. But he also recognized that effective control required eradication
well beyond its borders, a realization that likely underlay his enthusiasm for
a global program.8
More crucial, still, in the Interim Commission’s acceptance of the malaria
control mandate was the role of UNRRA as initial funding source for the
provisional WHO. The agency had been proposed in June 1943 by U.S.
President Roosevelt, anxious to pre-empt a replay of the mass starvation,
epidemics, and revolution that had followed in the wake of WW1.9 Estab-
lished as a temporary body in late 1943 by the 44 non-occupied Allied
Nations, UNRRA provided $3.8 billion in food and medical supplies to
liberated populations in the final days of WW2 and immediate post-war
period to help alleviate widespread hunger and typhus, venereal disease, and

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tuberculosis epidemics among the war-torn regions of Europe and China.10

Its activities were funded by member countries at the rate of 1 per cent of
GDP. However, given the size of the U.S. war economy and the catastrophic
economic destruction in the war theatres of Europe, the agency’s activities
were highly dependent on U.S. contributions, funding that was itself condi-
tional on year-to-year Congressional approval. UNRRA staffing was headed
by the New York State Governor, Herbert H. Lehman, as Director General,
while the key post of Director of the Health Division was held by Wilbur A.
Sawyer, former Director of the International Health Division of the Rock-
efeller Foundation. Under Sawyer, health funding was directed to short-term
relief, sufficient to avert ‘disease and unrest,’11 rather than to longer-term
economic reconstruction.12
With the establishment of the Interim Commission in June 1946, the UNRRA
administration announced its intention to wind down its activities and to trans-
fer all the agency’s remaining funds to the new emerging UN institutions.13
The decision presented the Interim Commission with the urgent obligation of
assuming, in addition to UNRRA’s epidemiological surveillance functions, its
ongoing medical operations. Despite objections from some IC delegates that
‘only the epidemiological work of UNRRA should be assumed by the Commis-
sion,’ UNRRA officials made the transfer of its funds conditional on maintain-
ing all of the agency’s existing health activities ‘without interruption.’14
During the final years of the war, experimental DDT malaria control
activities had been conducted in military theatres in southern Italy and the
Pacific, undertaken by the Allied military command.15 At the close of the war,
UNRRA, under Sawyer, immediately extended DDT-based malaria control
programs to civil war–torn Greece,16 and to Sardinia in April 1946.17 Thus,
included in the UNRRA mandate handed to the fledgling Interim Commis-
sion in mid-1946, alongside tuberculosis and venereal disease control activi-
ties were civilian DDT spray programs in several countries.
Up to this point, malaria does not appear to have figured prominently in
initial Interim Commission discussions on global epidemic conditions. Nor
was malaria included among the diseases listed by the Interim Commission
in early November 1946 as requiring ‘expert missions to countries with
special needs.’18 Indeed, at a subsequent IC meeting on November 13, the
Norwegian delegate queried spending so much of the Commission’s very
limited resources on one disease, and the French and British delegates ques-
tioned the urgency, and the idea itself, of eradicating malaria in the world.19
But with much of Europe and the Soviet Union preoccupied with relief and
reconstruction, U.S. influence in the shaping of the new UN institutions in
these early post-WW2 days prevailed.20 U.S. delegate to the IC, A. Doull,
also a former senior UNRRA official, strongly urged formation of a special
expert malaria committee, to be financed through UNRRA funds, while
Sawyer opined that ‘the malaria programme [in Greece and Italy] had been
extremely popular and that eventually complete control might be possible.’21

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In the event, in addition to assuming ongoing responsibility for the existing

DDT-based malaria control programs, other conditions came attached to the
offer of a portion of the UNRRA funds being directed to the Interim Com-
mission. Activities ‘would be limited to countries already receiving UNRRA
assistance,’22 with additional but very limited funding going to finance small
groups of ‘consultative’ experts as envisaged in Gabaldón’s ‘nuclear’ malaria
committee. Sawyer also stipulated that ‘[n]either UNRRA nor the Interim
Commission should be responsible for financing the importation or purchase
of supplies.’23 Thus, all supplies required for malaria activities undertaken by
WHO would require external funding through bilateral arrangements, ulti-
mately occurring primarily through U.S. government agencies.24 A minimal-
ist size and framework to the Expert Committee on Malaria was ensured
by the total level of funding, $1.5 million, offered for continuation of all
UNRRA health activities, a sum representing barely 10 per cent of the annual
UNRRA health program expenditures for 1946. Of this, less than one-tenth
was allocated to malaria ‘consultations and assistance.’25 The bulk of residual
UNRRA funds was channelled instead to the newly created United Nations
International Children’s Emergency Fund (UNICEF).26
With the WHO charter still awaiting U.S. ratification, there appeared to be
little choice but to accept the UNRRA terms if the Interim Commission was
to continue to function. On November 6, 1946, Gabaldón presented a formal
proposal for the establishment of an expert committee on malaria, to ‘speed
up the diffusion of new methods of control’ for a disease that ‘remained a
scourge.’27 Although few details on the post-war priority of malaria were
included in the Gabaldón proposal,28 the Committee on Epidemiology and
Quarantine one week later ‘agreed unanimously that the problem of malaria
was sufficiently urgent and important to warrant immediate action’ and the
decision was taken to ‘appoint a Sub-committee of five experts to study and
advise on the important problem . . . and submit a report.’ On December 31,
1946, UNRRA officials formally handed over responsibility for its ‘field
health activities,’ and assigned US$1.5 million to the Interim Commission.29
The ‘nuclear’ committee on malaria30 so formed in the early days of 1947
would soon be named the Expert Committee on Malaria (ECM), and would
formally meet for the first time in April 1947. But well before its first official
meeting, the future WHO had already been placed on an institutional course
that would lead nine years later to the global Malaria Eradication Program
(MEP). In the process, the precedent of purely ‘technical assistance’ and a
narrowly constituted expert advisory framework for the new organization
had also been established.

The Expert Committee on Malaria

Scant details appear in the official records of the Interim Commission
regarding the selection process of initial members of the Expert Committee

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on Malaria. Even less clear is the basis upon which Emilio Pampana himself
came to be elected as convenor and secretary of the Expert Committee on
Malaria. Described as ‘an exceptional administrator,’ Pampana had served
as a staff member of the Health Organisation of the League of Nations,
and more recently as Health Bureau Director of the U.S. League of Red
Cross Societies. His epidemiological malaria experience however appears
to have been primarily industrial-enclave in nature, as medical officer to a
Colombian mining population in the mid-1920s.31 Nonetheless in the early
weeks of 1947, with his strong ‘pro-DDT sentiments’ and ‘staunch’ support
of eradication plans,32 Pampana was appointed to the permanent WHO.
IC Secretariat as secretary to what would soon formally become the Expert
Committee on Malaria, his first task that of ‘suggest[ing] names for a pre-
paratory [malaria] group.’33
The five members of the ECM appointed included Paul Russell of the
Rockefeller Foundation, Arnoldo Gabaldón, N. Hamilton Fairley (UK), a
senior military officer during the war in charge of testing new synthetic
anti-malarial drugs among Allied troops, and Mihai Ciuca, a Romanian
malaria researcher and former Secretary to the League of Nations Malaria
Commission. A fifth seat was reserved for a USSR representative who had
‘not yet been appointed.’ Officially, Expert Committee members were cho-
sen by the Executive Director of the Interim Commission, Brock Chisholm.
As a psychiatrist, however, Chisholm was hardly in a position to question
the candidacy of prominent figures such as Russell and Gabaldón who were
among the few malaria workers with substantial DDT experience. Before
transferring funds to the Interim Commission, UNRRA officials had stip-
ulated that ECM members be chosen ‘for their technical proficiency and
experience.’34 On leave from the Rockefeller Foundation during the final
years of WW2, Russell as Chief Malaria Officer for the Allied Forces had
coordinated the initial DDT-based malaria and typhus control programs in
southern Italy and the Pacific, experience that made him a leading candi-
date for appointment to the new committee. In recommending candidates
for ECM membership, Pampana consulted with Dr Melville Mackenzie of
the U.K. Ministry of Health, and with Dr Thomas Parran, U.S. Surgeon-
General and former General of the U.S. Army, the latter also likely to strongly
support candidates committed to global DDT-based eradication plans.35
Organizationally, the structure and functioning of the ECM – its small size
and requirement that members be ‘free to attend’ twice yearly meetings36 –
also favoured independently funded figures such as Russell. Funded by the
International Health Division of the Rockefeller Foundation, Russell was
not bound by demanding national official responsibilities – arguably a situ-
ation inherently favouring candidates working in corporate philanthropic
agencies. J. Jackson offers detailed insights into the backgrounds and per-
sonalities of each of the members of the Expert Committee on Malaria (the
‘epistemic community’), as well as the limits imposed from the beginning on

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ECM deliberations. He describes a ‘forsaking [of] research,’ a ‘ridiculing’

of alternative (earlier) approaches to malaria control, and notes how ‘the
epistemic community used their individual prestige to insert the DDT gospel
into the technical forums of the WHO.’37
At its first formal meeting in April 1947, four of the five members of the
new committee were in attendance, the absence of a USSR representative
possibly one of the early casualties of the rapidly emerging Cold War: one
month earlier, President Truman had announced the U.S. doctrine of Com-
munist ‘containment.’38 Gabaldón was elected as Chairman, with Pampana
as Secretary to the committee. Listed as ‘also present’ at the April 1947 ECM
sessions were J.M. Vine, UNRRA medical director in Greece and author of a
report on the recent DDT anti-malaria operations there,39 and N.M. Good-
man, former UNRRA Director of the European Health Division, and now
Director of Field Services, WHO.
The official report of the first meeting of the Expert Committee on
Malaria, held April 22–25, 1947, set out a spare description of the future
functions and organization of the Committee. Prefaced with a description
of malaria as ‘one of the world’s greatest afflictions,’40 malaria was pre-
sented as an urgent priority, threatening ‘doubtless . . . severe epidemics,’
and ‘the greatest obstacle in the way of the objective of the World Health
Organization.’ But with the new insecticides and anti-malarials, the report
stressed, ‘malaria epidemics can be stopped effectively and quickly when a
suitable organization and the supplies are available’: the advent of ‘new era’
technologies meant that ‘malariology has come of age.’41 Few data how-
ever accompanied the report’s assessment of malaria as ‘the world’s greatest
affliction,’ an omission only marginally made up a year later in a ‘Note by
the [IC] Secretariat.’ The latter cited, unreferenced, a global figure of 3 mil-
lion malaria deaths a year and an estimated 1 per cent case mortality rate
for malaria,42 alongside a 1936 statement by J.A. Sinton, former Director of
the Malaria survey of India, that malaria cost India ‘unbelievable millions
of pounds Sterling each year.’43
Missing also from the ECM proceedings was a definition of what ‘malaria
control’ constituted: whether it meant reduction or global elimination of
malaria transmission (infection), or illness (morbidity), or malaria mor-
tality.44 Though a question central to the work of the League of Nations
Malaria Commission only 15 years earlier, and to malaria policy in India
before that, by mid-1948 such distinctions appeared to many as no longer
relevant: the dramatic power of DDT to interrupt malaria transmission
was already evident in Greece and Italy, as well as U.S.-funded programs in
Venezuela. Thus in skirting discussion of the meaning of malaria ‘control’ in
these formative years, deliberations foreclosed the possibility of epidemio-
logical experience informing post-war malaria policy.45

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First meeting of the ECM, April 1947

A sense of how basic decisions were made within the Expert Committee on
Malaria can be gleaned from ‘summary minutes’ of the first meeting, the only
ECM session for which minutes of the proceedings appear to be available.46
A dominant theme to the proceedings quickly emerged. Earlier approaches to
malaria control were now outdated. ‘In the past,’ Fairley noted, ‘it was custom-
ary for malariologists to be satisfied with a state of premunity in malarious
countries; their aim was to prevent the devastating mortality of epidemics. Now
it is different.’47 Previous policy of the League of Nations Malaria Commis-
sion (LNMC) that had focused on preventing severe illness and mortality from
malaria was explicitly set aside. Limiting goals to mortality prevention was now
imbued with a tone of professional negligence. The new tools had opened up
possibilities for ‘malaria control and even of practical eradication . . . unthink-
able in pre-war days.’48 A subsequent ‘Note by the [IC] Secretariat,’ perhaps
penned by Pampana, suggested that the ‘new synthetic drugs and insecticides
have . . . revolutionized malaria control . . . [and] raised hopes of the complete
eradication of the disease – even of anopheles – from entire countries.’49
Moreover, with Gabaldón’s November 1946 proposal ‘taken as a basis for
the discussion,’50 the agenda for the first meeting of the Expert Committee
on Malaria had evidently been set in advance. From the outset, demonstra-
tion and dissemination of DDT-based control methods was assumed to be
the centrepiece of WHO malaria activities. Through the course of the three
days of meetings, Ciuca would attempt to incorporate perspectives from ear-
lier LNMC research activities in areas such as chemotherapeutics and local
entomological studies of insecticide efficacy. But in each case his suggestions
were dismissed or left unanswered in the recorded minutes, Russell at one
point opining that ‘the present Malaria Committee should not necessarily
take over the functions of the old League of Nations Malaria Commission
but should determine its own policy in relation to present conditions.’51
Dr N. Goodman, former UNRRA official and an observer to the meeting,
urged attention instead be directed to the ‘really urgent work . . . such as
getting out publications and reports in relation to DDT for the benefit of
those countries which had been out of touch with the latest developments.’52
Ciuca also advocated for a larger membership for the Expert Committee,
arguing that ‘the various problems [associated with malaria] are so different
that it was necessary to choose the members according to their competence
in the matters discussed,’ reminding his colleagues that the LNMC had been
made up of ‘some 50 members.’ Here too, however, Russell prevailed, rec-
ommending a six-member committee for the first two years, with subse-
quent expansion to nine members.53
Most perplexing perhaps for Ciuca, given earlier emphasis on the risk of
post-war malaria epidemics, was the response of the committee to his resolu-
tion requesting supplies of anti-malarial medication for an epidemic in the

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Tulcea district of Romania, the single example of post-war epidemic condi-

tions cited by committee members in earlier discussion of malaria urgency.54
His request, relegated to the final (‘Miscellaneous’) agenda item, elicited tepid
interest. When the Committee secretary suggested Ciuca present more details
at the subsequent meeting of the Interim Commission set for the follow-
ing September, Chisholm as IC Executive Secretary and an observer to the
April 1947 ECM meeting, interceded. ‘[I]t was not necessary to wait,’ he sug-
gested, and offered the services of his office to vouch for an application to the
League of Red Cross Societies for anti-malarial drugs.55 But by this point any
confidence Ciuca might still have had in the Expert Committee’s interest in
malaria control beyond DDT is likely to have been shattered. A narrow DDT
framework to the remainder of the deliberations was ensured by the Commit-
tee ‘proceeding point by point’ through Gabaldón’s DDT-framed proposal.56
In the event, the second meeting of the Expert Committee on Malaria
convened only in April 1948. Again, the USSR chair was vacant, but this
time so also was that of the Romanian delegate, Ciuca.57 Without specific
expertise in DDT there now seemed perhaps little purpose to participation.58
Even in relation to basic chemotherapeutics, ECM policy was constrained.
Ciuca would go on to conduct clinical trials of chloroquine and paludrine in
the epidemic area of his country with the drugs supplied by the Red Cross.
But despite the inclusion in the first ECM report of a thorough overview by
Fairley of the efficacy of recent synthetic anti-malarial drugs and a detailed
outline of further drug trials required, no action on drug testing was taken
by the ECM, ‘[o]wing to the absence of funds for the purpose.’59 By the fol-
lowing year’s meeting, Fairley had resigned from the Expert Committee, and
priority had unequivocally been accorded anti-mosquito work over thera-
peutics: ‘the primary consideration in the communal control of malaria,’
the Committee asserted, ‘is interruption of transmission at the mosquito
level.’60 At its third meeting, in 1949, the ECM formally advised leaving
anti-malarial drug research to ‘existing institutions,’ an area of malaria
research consistently eschewed also by the Rockefeller Foundation in its
inter-war malaria work in India.61 In the meantime, a new Expert Commit-
tee on Insecticides had been formed in response to the emerging problem of
vector resistance, a potential problem flagged as early as January 1948 in
Greece with observed DDT-resistance among houseflies.62
Thus in the earliest days of the formative WHO, the Expert Committee on
Malaria assumed an organizational and programmatic structure that lent lit-
tle space to broader views and approaches to the malaria problem.63 Earlier
epidemiological perspectives on underlying determinants of the malaria bur-
den explored earlier by the LNMC were expressly set aside, and along with
them, the colonial South Asian literature as well.64 Several Interim Commis-
sion delegates had attempted earlier on ‘to ensure representations of various
schools of thought and experience’ in the formation of expert committees,
but this recommendation subsequently was deleted at the suggestion of the

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Indian and Mexican delegates.65 Here, added irony attaches to the fact that
Ciuca, as Secretary to the former LNMC, had participated in the Commis-
sion’s study tour of India less than two decades earlier and had co-authored
its ensuing report.
Even with respect to DDT, the purpose of the program drawn up by the
ECM in these early years was intended solely as demonstration. Funding
was limited to expert consultancy costs. Like the Rockefeller Foundation
before it, the goal was one of paradigm building, not service or supplies
provision. The role of the WHO and its Expert Committee on Malaria was
one of disseminating technical advice, with most funding coming through
bilateral agreements. Such funds, coming almost entirely from the U.S. at
this point, were directed largely to regions of the world aligned with its
strategic interests.66 ‘In postwar history,’ James Gillespie observes, ‘UNRRA
has been relegated to a footnote, written off as a temporary experiment in
international enthusiasm, of interest mainly as the site of some of the open-
ing manoeuvres of the cold war.’ To the contrary, he suggests,

UNRRA’s Health Division was the theatre for a complex battle over
the future direction of international health work. . . . UNRRA’s field
operations, especially in health, drew on models developed by the
Rockefeller Foundation’s International Health Division during the
interwar years, and became the progenitor of fieldwork in the UN
system. . . . International health became one arm of the struggle by
the United States and its allies to build stable, politically sympa-
thetic regimes on the periphery.67

It was a legacy destined to continue.

The 1948 U.S. proposal

At the second meeting of the Expert Committee on Malaria in May 1948,
membership had expanded to include D.K. Viswanathan, then intensely
involved in DDT-spray operations in Kanara district, India, and M.A. Vaucel,
of France; with Gordon Covell, a former director of the Malaria Survey of
India, now a U.K. delegate, taking the place of N.H. Fairley. At this meet-
ing, too, the agenda had largely been set in advance. Four months earlier,
a ‘US Proposal’ had been presented to the Interim Commission by U.S. del-
egate H. Van Zile Hyde that added a new dimension to the argument for
urgent malaria control, one that framed the WHO malaria task in much more
explicit terms of malaria as a block to economic development.68 Aside from
being the ‘the prime world health problem’ in itself, the proposal asserted that

the direct suffering caused by malaria is multiplied by the hun-

ger and malnutrition resulting from lowered food production in

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malarious areas. Malaria is a direct and important contributing

cause of the current world food shortage. . . . This situation is being
allowed to continue in the face of new discoveries of major impor-
tance in the field of malaria control.69

The Van Zile Hyde submission concluded that ‘the WHO should direct a
major share of its energy and resources during its first years to the applica-
tion of [malaria control] measures to . . . the major food-producing areas
afflicted by malaria.’70
Dated January 23, 1948, the U.S. proposal contained other advisements.
The Interim Commission, it suggested, ‘should seek the opinion’ of the Food
and Agriculture Organization (FAO) in selecting agricultural regions for
demonstrating the impact on agricultural productivity of a ‘mass attack’
on malaria, and went on to recommend a collaborative joint FAO-WHO
Working Party on Food Production and Malaria Control.71 Three days
later, the IC Secretariat embraced the proposal’s arguments, submitting a
draft resolution in near identical language for consideration by the World
Health Assembly at its inaugural meeting the following June. Concurring
that malaria ‘impoverishes the world,’ the Secretariat urged that ‘[a]t a time
when the world is poor, it seems that control of malaria should be the first
aim to achieve in order to increase agricultural output, . . . [and] entrusts
to its Expert Committee the study of a general plan for world malaria con-
trol.’ It further recommended that ‘a major share in the WHO’s energy and
resources during its first years be directed [to malaria],’72 and endorsed the
U.S. proposal for ECM collaboration with the FAO. Included was a detailed
budget for joint ECM-FAO ‘malario-economic surveys’ in selected areas to
document the health and economic benefits of malaria control.73 ‘Everybody
knows,’ the draft resolution suggested, ramping up the professional onus,
‘what has been achieved in selected areas of such countries, once malaria
has been controlled.’74 Thus well before the second meeting of the ECM,
the U.S. proposal had pre-emptively framed malaria as a major contributing
cause of world hunger and ‘block’ to global development.
As the single malaria worker on the Secretariat of the Interim Commis-
sion, it seems likely Pampana played a major role in shaping the Interim
Commission’s response to the U.S. January proposal – though it is unclear
where the procedural precedents lay for this direct submission of a proposal
to the Interim Commission by a single member government rather than
through the Expert Committee on Malaria. Nonetheless, the ECM at its sec-
ond official session in May 1948 ‘heartily endorse[d]’ the view that malaria
‘directly contributes to the world shortage of food.’ To the U.S. propos-
al’s argument for urgent anti-malarial action, the expert committee added
‘wide-spread . . . mental and physical deterioration . . . [and] serious loss of
working efficiency.’ One week earlier, in his address to the Fourth Interna-
tional Congresses on Tropical Medicine and Malaria held in Washington,

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D.C., U.S. Secretary of State George Marshall had added a further argument
for urgent action on malaria control: the ‘profound’ impact of the disease in
undermining of ‘any hopes of social stability.’75
The relationship between the May 1948 Malaria Congress in Washing-
ton and the ECM is an interesting one. At the first ECM meeting one year
before, Russell had piloted a resolution ensuring an invitation for ECM
members to attend the 1948 Congress, with the Committee’s second malaria
meet scheduled to follow one week later.76 Indeed, the U.S. ‘proposal’ in
January 1948 specifically called on the ECM to seek advice ‘in consulta-
tion’ with the International Congress on Malaria, part of the larger confer-
ence where Marshall, soon to unroll what would come to be known as the
Marshall Plan, gave the opening address,77 and where DDT-based malaria
control practitioners, including Indian delegate D.K. Viswanathan, reported
their initial results.78 With Sawyer as Executive Secretary of the Malaria
Congress and still actively directing the anopheles eradication campaign in
Sardinia, the portion of the Congress agenda devoted to malaria not surpris-
ingly was heavily weighted toward recent experience with DDT.79
But the January 1948 U.S. proposal contained yet a further directive. It
requested a clear ‘statement of commitment’ from the ECM ‘in regard to
such an attack [on malaria].’80 It is difficult to read the request as stem-
ming from doubts on the part of the U.S. IC delegates about the technical
merits of the DDT ‘demonstration’ projects proposal. More likely, broader
‘commitment’ to an insecticide-based global malaria control program was
being sought by U.S. members in the face of lingering doubts amongst other
national delegations about the priority and feasibility of such a plan. At
the sixth meeting of the Fifth Session of the Interim Commission, on Janu-
ary 27, 1948, the Soviet representative, for example, had called for ‘speedy
case-finding’ and treatment of malaria cases alongside spray programs and
‘hydraulic sanitation.’ British and French delegates had in turn warned of
the ‘danger . . . of giving the impression that the Organization was attempt-
ing world control of malaria. That was quite impossible.’81 With the WHO
constitution still awaiting U.S. ratification, endorsement by the U.S., along
with its funding contribution, appears to have hinged upon unequivocal
commitment by Interim Commission member states to the vector eradica-
tion approach to malaria control in advance of the first official meeting of
the World Health Assembly set for the following June.82
Included also within the U.S. proposal, moreover, was a request for
endorsement of collaboration with the Food and Agriculture Organization.
By this point the FAO, inaugurated in 1945, was already involved in a major
global campaign to increase food production. As Litsios highlights, it was
‘politically expedient’ on the part of the ECM to garner support from the
increasingly UN-prominent FAO, collaboration that would enhance both
the scientific credibility of the MBD thesis underlying the WHO’s call for
urgent malaria control, and the humanitarian profile of the WHO. Short

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on analytic or methodological detail, the only empirical evidence the U.S.

proposal cited for its argument that malaria was a barrier to global food
production and development was Russell’s 1942 South Indian malario-
economic study.83 Evidence to the contrary was ignored. In the case of Pun-
jab, for example, the malaria transmission associated with canal irrigation
across the colonial period had not ‘blocked’ cultivation expansion where
basic care was taken to avoid waterlogging.
The FAO delegate on the joint FAO-WHO Working Party on Food Pro-
duction and Malaria Control would be W.R. Aykroyd, recently appointed
to head the FAO’s nutrition division. Familiar with at least some of the
larger dimensions of the hunger problem in India through his earlier work in
India at the Coonoor nutrition laboratory, Aykroyd expressed some doubts
about malaria eradication as a major route to increased food production,
suggesting ‘other hindrances to efficient production’ such as ‘lack of capital
or credit . . . [and] systems of land tenure and taxation.’84 Nevertheless, the
joint WHO-FAO study proposal was adopted on February 5, 1948, by the
Interim Commission at its Fifth Session.85 Some governments no doubt were
swayed by Marshall’s promise of ‘social stability’ through removal of the
malarial ‘brake’ on food production. Others, it appears, were reluctant to
jeopardize U.S. engagement in the new WHO. U.S. cooperation in purely
technological programs at least, would foster, it was hoped, the ‘habit’ of
participation in the wider UN process and advance prospects for world
peace.86 Thus in June 1948 at the first World Health Assembly of the newly
ratified WHO, a global ‘demonstration’ program of malaria control based
on residual insecticide spraying was formally endorsed.87
In the event, little visibility would accrue to the project’s subsequent fail-
ure to document any substantive evidence regarding the impact of malaria
control on agriculture.88 The FAO quietly withdrew from the joint study in
1953 and the project withered away – though not before the MBD thesis
arguably had helped derail the pre-WHO momentum within the new UN
institutions for addressing deeper structural causes of poverty, global hun-
ger, and food insecurity.89

Post-war hunger politics

That an urgent international food crisis existed in the final years of WW2
and immediate post-war days is beyond dispute. But it was not one induced
by malaria. Depression unemployment had already brought hunger con-
cerns to the fore in the committee halls of the League of Nations Health
Organisation and the ILO through the 1930s, as we have seen.90 With the
outbreak of war at the end of the decade, war-induced hyperinflation dra-
matically compounded difficulties in food access globally, triggered by mili-
tary foodgrain demand throughout the European and colonial theatres of
war, as witnessed so catastrophically in India in 1942 and 1943. Even before

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the 1943–1944 Bengal famine, Roosevelt was acutely attuned to a possible

repeat of the starvation, epidemics, and revolution triggered in the after-
math of WW1, as seen with the establishment of UNRRA. In a further effort
to pre-empt similar events, Roosevelt had invited Allied governments in
1943 to a conference at Hot Springs, Virginia, to deliberate on coordinated
efforts, beyond emergency relief measures, to ‘[p]revent . . . speculative and
violent fluctuations in the prices of food . . . [and] conditions of scarcity
that appear certain to prevail after the war.’ In addition to formation of
UNRRA, the Hot Springs initiative laid the groundwork for establishment
of the FAO in 1945.91
Earlier LNHO concern over global conditions of agriculture and hunger
with the Depression already had been directed primarily to issues of sup-
ply (foodgrain availability) and micronutrient quality of foodstuffs rather
than to structural determinants of low productivity, or inadequate and inse-
cure access to available staple foods. Crisis conditions during the war, how-
ever, had forced far more explicit acknowledgement of the consequences
of unregulated foodgrain markets in terms of price volatility and epidemic
mortality.92 Resolutions coming out of the Hot Springs conference in 1943
stressed ‘the dominant role played by adequate food in the reduction of
sickness and death rates,’ in turn warning that ‘the most fundamental neces-
sity . . . required to promote freedom from disease . . . [was] adequate food.’
Proposed solutions lay overwhelmingly in the sphere of increased purchas-
ing power, it was argued. This was to be achieved through expansion of ‘the
whole world economy.’93

It is useless to produce more food unless men and nations pro-

vide the markets to absorb it. There must be an expansion of the
whole world economy to provide the purchasing power sufficient
to maintain an adequate diet for all. With full employment in all
countries, enlarged industrial production, the absence of exploita-
tion, an increasing flow of trade within and between countries, an
orderly management of domestic and international investment and
currencies, and sustained internal and international economic equi-
librium, the food which is produced can be made available to all
people.94

Issues of ‘social security’ also were raised at the Hot Springs meet, as were
underlying structural issues such as control of global foodgrain specula-
tion, the need for buffer grain stocks, agricultural credit, and land reform.
Clearly, the Hot Springs deliberations were an ideological battle ground.
Ultimately, however, the measures adopted were set largely in neo-liberal
terms of free trade, ‘enlarged industrial production,’ and scientific advances
in agriculture and promotion of ‘protective foods,’ a technological frame-
work that would largely come to shape the subsequent work of the FAO.

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In its final recommendations the 1943 conference acknowledged that

‘[a]gricultural productivity and efficiency and the well-being of the tiller of
the soil depend largely upon the system of land tenure and conditions of
farm labour’; but these were qualified as voluntary or short-term measures,
the report advising ‘each nation . . . [to] make a careful survey of existing
systems of land tenure . . . to ascertain whether changes in these systems and
conditions are necessary or desirable.’95 Nevertheless, the Hot Springs con-
ference marked a moment of exceptional political (and professional) trans-
parency, one where the curtain was pulled back on the primacy of hunger in
determining epidemic mortality96 – akin in one sense to the publication of
Malaria in the Punjab three decades earlier in British India.
Recognition of the importance of public policy on foodgrain regula-
tion was of course a matter of acknowledging facts on the ground. Over
the course of the war the dire food crisis had forced governments to take
unprecedented measures to control foodgrain prices and ensure access by
public rationing. Food distribution policies had been embraced in Britain
and in many other countries at war, if tragically belatedly in India. Such
wartime conditions had also prompted calls for permanent measures to insu-
late populations from the vagaries of international grain markets through a
world system of buffer foodgrain stocks. On October 16, 1945, 42 countries
met in Quebec City to create the Food and Agriculture Organization on the
basis of the resolutions from the Hot Springs conference. John Boyd Orr, a
leading U.K. nutritionist responsible for Britain’s school-milk program, was
appointed founding director-general, Western delegates perhaps assuming
him to be a ‘moderate’ head for the agency. The dire late- and post-war food
situation97 however had turned Orr’s attention sharply from dietary qualita-
tive issues to the glaring question of staple food sufficiency (acute hunger).
Riding a tide of deep public anxiety, Orr recommended a policy of global
foodgrain reserves as a central goal for the FAO, one that would give the
emerging ‘united nations’ system the capacity to actively buffer international
foodgrain price fluctuations and then-rampant commodity speculation. The
call for an international buffer foodgrain system (World Food Bank) how-
ever would soon be overridden by U.S. and U.K. delegates who together suc-
ceeded in limiting Orr’s tenure to a two-year term as FAO director-general.98
It was in this mid-1940s period of extraordinary international engage-
ment in, and contestation over, questions of global food security that the
WHO (IC) was also taking shape. With the backdrop of unparalleled politi-
cal and economic failings – the ‘unprecedented carnage’99 of two European
imperial wars, a world-wide economic depression, and decolonization and
revolution ushering in sweeping shifts in global political relationships – it
was thus also a point where, for Western governments, ideological hegem-
ony and boundaries had appeared seriously vulnerable: a period of political
contestation within countries as much as between them.100 The wars and the

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Great Depression had left North Atlantic societies ripe for alternate symbols
of accomplishment and sources of belief.
But the same wars had also thrown up dramatically powerful new tech-
nologies. ‘Good news’ in the ashes of 1945 lay in the optimistic promise of
science. With DDT, here was a demonstration of science and technology
used for social good, to advance civilization, decrease suffering and deaths,
and to relieve the tedium and exhaustion of laborious work. Thus by enjoin-
ing the FAO to collaborate with the WHO in documenting the economic
benefits of DDT-based malaria control, the U.S. joint-study proposal in Jan-
uary 1948 in effect was attempting to harness the tide of Western scientific
humanism to the malaria eradicationist cause via MBD.101
Paul Russell may not have been closely conversant necessarily with the
fierce contest between Orr and the U.S.-British delegates within the FAO.
But positioned at the centre of the new UN institutional processes, it is
unlikely he could have been unaware. By engaging the FAO with the DDT
campaign, the Expert Committee on Malaria was able to finesse the global
food crisis issue at the close of the war. Appropriating the prevailing sense
of crisis to the cause of DDT-malaria control, it strategically harnessed the
FAO’s new profile of competency to buttress the malaria eradicationist argu-
ment as an alternate route to food production security,102 thereby redirecting
attention away from the underlying structural determinants of hunger and
related ill-health.

Global eradication questioned: the

Kampala Conference, 1950
A food security rationale to the Expert Committee on Malaria’s global erad-
ication project arguably was necessary for other reasons as well. For as
momentum for malaria control drew to its ‘logical’ conclusion103 of ultimate
global eradication, the ECM faced an even more awkward question. Such
a vision inevitably hung on eradication also in the exceptionally intense
(holoendemic) malaria transmission areas of west and central sub-Saharan
Africa. In this region, the prime mosquito vector, Anopheles gambiae, feeds
almost exclusively on humans rather than animals, resulting in almost daily
infective bites in many areas. Such extreme inoculation rates induce high lev-
els of protective acquired immunity among the adult population, but intense
infection rates in the as yet non-immune infants and young children, amongst
whom the malaria mortality impact is considerable. Attempts at control of
malaria transmission in this context thus raised serious questions: among
them, the possible consequences of undermining high levels of acquired
immunity in regions where permanent eradication could not be guaran-
teed for reasons of prohibitive long-term costs and likely re-introduction
of infection from surrounding rural tracts.104

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In November 1950, members of the Expert Committee on Malaria,

now nine in number, joined colonial malaria workers with extended Afri-
can malaria experience to debate in Kampala, Uganda, the wisdom and
feasibility of extending the WHO malaria control program to include hol-
oendemic Africa. Deliberations between the two groups, not surprisingly,
were marked by intense disagreement. As something of a compromise, an
experimental malaria transmission control project was agreed upon for the
Pare-Taveta region of Tanzania and bordering Kenya: the goal to assess
the impact on mortality levels of transmission control, and of subsequent
malaria ‘rebound’ with discontinuation of spray operations in a population
where acquired immunity levels likely had declined.105 Yet without waiting
for the results of the trial, the ECM continued to argue for a ‘global’ eradi-
cation program,106 and its proposal would subsequently be endorsed at the
Eighth World Health Assembly in 1955.107
The many complex ethical and technical questions raised by the early tri-
als of residual insecticide spray operations at Pare-Taveta and other hyper-
and holoendemic regions of Africa, at the time unresolved, involve a subject
well beyond the scope of this study. They have recently, however, begun to
be revisited in historiographic analysis.108 Here, one can simply note the
considerable irony at play in Russell’s strong advocacy at Kampala, along-
side Macdonald’s, for residual-insecticide malaria eradication efforts in
Africa – policy that could be predicted to reduce protective levels of acquired
immunity – while in contemporaneous academic writing both workers con-
tinued to interpret the ‘notorious’ malaria epidemics in India to be a func-
tion of declining acquired immunity.109

The ‘Human Factor’ set aside

The reductive triumph of the Expert Committee on Malaria within the nas-
cent World Health Organization between 1946 and 1948 lay in two spheres.
First, international malaria policy formation was divested of any linger-
ing association with the ‘social medicine’ leanings of the former League of
Nations Health Organisation, the latter based on understanding of the role
of hunger as a major determinant of malaria’s lethality burden. The global
Malaria Eradication Program thus came at the expense of any serious con-
sideration of alternate, or additional, approaches to malaria ‘control’ such
as ensuring access to effective anti-malarial medication and addressing sub-
sistence and livelihood precarity.110
Second, through the joint FAO-WHO project that framed malaria as a
block to agricultural development, the Expert Committee on Malaria had
succeeded in wresting institutional attention to hunger away from its struc-
tural determinants and the para-United Nations agencies attempting to
address issues of livelihood.111 It would thus leave health advocacy solidly
in the technological and behavioural domains rather than in the economic

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arena of working conditions, resource disparities, and international grain

markets, issues the ILO and a minority of FAO members were attempting
to address. The joining of WHO-FAO in a malaria-agriculture alliance in
the earliest days of the IC-WHO effectively sealed the technological frame-
work to post-war international cooperation in the field of health, and a U.S.
prominence within it.
Like the Rockefeller Foundation before it, the ECM agenda involved par-
adigm building, not service or supply provision. The opportunity to forge
a practical and encompassing approach to malaria globally thus would be
deferred a half-century. Also deferred was the possibility of turning human
subsistence, and the foodgrains upon which it depended, from a tool of
geopolitical influence112 and coercion to an expression of common human-
ity and tool of peace.113 Staples observes that with regard to removing
global foodgrain supply from economic power politics, ‘this road was not
taken. . . . Instead, the countries of the world slid into the Cold War, and
food remained just another trade commodity, just another weapon in the
superpowers’ arsenal.’114 By 1949, she notes, the issue of land tenure was
sidelined from the FAO’s agenda, as also rural agricultural credit for small
farmers, and supplanted by largely voluntary and often equally abstract
‘community development.’115 Amrith describes parallel efforts of the U.S.
to remove health as an enforceable ‘right’ within the UN’s Commission on
Human Rights, leaving ‘technical assistance . . . as a substitute for rights,’116
and the definition of human health in the covenants of the WHO shorn of
socio-economic context.
The reductive triumph in understanding of human health that took place
within the formative World Health Organization was not wholly attribut-
able to the Expert Committee on Malaria. Nor was Russell alone in view-
ing malaria, and health more generally, as simply a technological problem.
A parallel shift was taking place in many academic realms, as seen in the
emergence of nutritional science. Yet in his long-term influence on the
Expert Committee, Russell nonetheless played a distinctive role in shaping
its policies and exerted a dominant influence in the sidelining of a broader
perspective on the malaria burden and approaches to malaria ‘control.’117
Though membership was notionally on a rotating basis, Russell would sit
on the committee throughout the 1947–1956 period until commitment to a
program of global malaria eradication was assured, the only member to do
so; Gabaldón was a delegate to four of the six meetings.
Moreover, with respect to the central question of this study, Russell also
played a pivotal role in the obscuring of the rich epidemiological litera-
ture from colonial South Asia on determinants of malaria lethality.118 In his
1946 text, Practical Malariology, Christophers’s study of the 1908 Punjab
epidemic was accorded a cameo appearance, but without reference to pre-
ceding harvest failure and ‘scarcity.’ Russell recounted Christophers’s obser-
vations on the characteristic ‘sudden onset’ of the epidemic in Amritsar city,

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but interpreted its lethality in terms of the epidemic ‘upset[ting] . . . the

entire routine of the city. . . . Food was difficult to obtain and prices became
prohibitive,’ thus inferring scarcity prices were a consequence of malaria
transmission rather than of preceding harvest failure.119 While secondary
debility no doubt was a later aspect to the 1908 Punjab epidemic, such a
reading leaves out the key dimension Christophers identified as underly-
ing malaria fulminancy in the province: epidemic (semi-)starvation.120 Else-
where in his 1946 text Russell claimed that the commonplace association
of epidemic malaria with famine could be explained by ecological condi-
tions triggering enhanced transmission, repeating his earlier assertion that
‘[a]rmies of well-fed, robust individuals go down with malaria to all appear-
ances just as rapidly and as seriously as any other group.’121 Nine years later,
Russell would publish his influential Man’s Mastery of Malaria, a history
of malaria research and control efforts. Indian malaria research would fig-
ure prominently in the accompanying 24-page bibliography. Yet among the
more than 500 references listed, both Malaria in the Punjab and Malaria
in the Duars were missing, as also Bentley’s studies on malaria and agricul-
ture in Bengal – though the collection did include two 1866 Indian Medical
Gazette articles on the use of cobwebs to treat malaria fever.122
It stretches credulity that Russell had not come across the earlier work of
Bentley, or was not aware of the economic content of Malaria in the Punjab,
findings cited in much of the Indian malaria literature through to the late
1930s. One can only speculate about the reasons that impelled him to omit
Christophers’s economic conclusions, and in the case of Bentley his entire
body of epidemiological analysis of malaria and agriculture in Bengal.123
Russell may have genuinely believed that the omissions were justified in
the belief that ‘social’ science was not true science – though here one might
have expected that cobweb treatment of malaria might have merited similar
omission. Whatever the reasoning for Russell personally, within the span of
a single generation of malaria workers, recognition of an historical role for
hunger in shaping the mortality burden of malaria had essentially vanished
from the post-WW2 medical literature.124

‘Not a policy to be recommended’

Even in the earliest days of DDT-euphoria in the new World Health Organi-
zation, there were many who were uneasy with a purely microbiological
understanding of the malaria problem and who warned against reliance
on the singular approach to malaria ‘control’ emerging within the WHO.
One of the more prominent sceptics in India was V. Venkat Rao, a lead-
ing malaria researcher whose own career was devoted to devising local,
often naturalist, measures of transmission control. In December 1949,
Venkat Rao published ‘a critical review’ of chemical-spray control meas-
ures employed to date in the subcontinent, a paper that identified ‘a large

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number of problems’ with DDT requiring ‘further study,’ among them the
question of DDT-resistance.125 Warning against sole reliance on DDT, he
argued that ‘though eminently suitable for emergencies and during periods
in which permanent or biological measures are under way, [DDT] cannot
constitute by itself an economic long-term policy of malaria control, even if
meanwhile the vector insects do not develop chemico-resistance against its
action.’126 It was a view that presciently predicted present-day Indian policy
where chemical spraying increasingly is reserved for serious outbreaks and
specific areas of hyperendemic transmission.127
But it is in his attention to agricultural conditions that Venkat Rao’s
broadest insights lay, noting that entomological conditions favourable
to malaria transmission were generally associated also with agricultural
decline. Here he pointed to the moribund rivers tracts of lower Bengal,
and to the waterlogged soils of the Terai, reminding readers that malaria
was mainly a disease of poor and economically backward countries: ‘a dis-
ease of waste land, waste water and waste men.’ ‘Bonification measures,’
he stressed, ‘are the best and most effective in the long run as they do not
involve the use of chemical larvicides but, on the other hand, include works
which gradually raise the economic level of the people and increase their
resistance to disease.’128 Such works were costly, he acknowledged, yet their
potential longer-term impact relative to initial costs clearly warranted care-
ful consideration.
In the final paragraphs of his overview, Venkat Rao went further, ques-
tioning Russell’s dismissal of the importance of ‘nutrition’ as a factor in
the epidemiology of malaria. ‘A study of most epidemics,’ he pointed out,
‘indicates the presence of this economic factor.’

The great epidemic of 1917 in the U.S.S.R. followed widespread

famine caused by a total breakdown of agriculture after the revo-
lution. In Ceylon, failure of the south-west monsoon, which must
affect the delicately balanced economy of the people, was the prime
factor of the 1934 epidemic. The famines of Bengal and the North
Madras Coast in 1942–43 were quickly followed by large-scale epi-
demics in the affected areas. The chronic low economic conditions
of the inhabitants of most hyperendemic areas is too well known to
require emphasis. One cannot, therefore, entirely agree with Russell
et al., (loc. cit.) that susceptibility to infection is not dependent on
the state of nutrition.129

He concluded by urging ‘a fresh approach to the problem of malaria con-

trol,’ adding ‘[i]f this paper dispels even to some extent, the popular notion
that, after the advent of D.D.T., malaria research has become a luxury and
all that needs to be done is only periodical spraying of D.D.T. on the walls,
its purpose is served and . . . the author is amply rewarded.’130

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In his concern over the rush to chemical-based malaria eradication

Venkat Rao was not alone. Several delegates at the Interim Commission
deliberations, as we have seen, had also questioned, for perhaps varying
reasons, the urgent priority directed to eradication of malaria transmission.
Six years later, in August 1955, at the height of eradication enthusiasm, an
82-year-old Christophers submitted a characteristically thoughtful article to
the Indian Medical Gazette highlighting a number of insights gained from
malaria control work in the Indian subcontinent. Beginning with a brief sec-
tion on ‘Economic Status’ aspects, the paper quietly hinted at key questions
missing from the global malaria eradication program about to be embraced
formally by the World Health Assembly the following month, and warned
against ‘smash and grab’ approaches to malaria control.131

It is not usually that a country is uniformly malarious, or even that

there are not extensive areas where malaria is not a serious prob-
lem. . . . On these accounts the urgency or even the desirability of
taking action under such conditions has been considered by some
authorities to be doubtful. . . . Without some system of ascertain-
ing what areas and communities are in need of action to be taken,
wide-scale institution of some particular method of control is not a
policy to be recommended.132

Christophers had retired from the Indian Medical Service 24 years earlier,
and as professor of ‘Malaria Studies’ at the London School of Hygiene and
Tropical Medicine he had gone on to pursue research on malaria chemother-
apeutics, quinine, and the new synthetic anti-malarials, an area of malaria
research consistently eschewed by the Rockefeller Foundation. Reluctant as
ever to directly contradict his medical colleagues, his 1955 paper nonethe-
less conveyed a deep concern with malaria policy direction.
Here we return, then, to consider at broader levels why the thesis of
malaria as a ‘block to development’ remained so compelling, even in colo-
nial South Asia with its well-documented history of malaria in relation to
destitution.

Notes
1 S. Amrith. Decolonizing International Health: India and Southeast Asia, 1930–
65 (Basingstoke: Palgrave Macmillan, 2006); J. Siddiqui, World Health and
World Politics: The World Health Organization and the UN System (London:
Hurst, 1995); J. Farley, Brock Chisholm, the World Health Organization, and
the Cold War (Vancouver: University of British Columbia Press, 2008); J. Jack-
son, ‘Cognition and the Global Malaria Eradication Programme,’ Parassitolo-
gia, 40, 1998, 193–216; S. Litsios, ‘Malaria Control, the Cold War, and the
Postwar Reorganization of International Assistance,’ Medical Anthropology, 17,
1997, 255–278; R.M. Packard, ‘Malaria Dreams: Postwar Visions of Health and

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 M A L A R I A A N D T H E W. H . O .

Development in the Third World,’ Medical Anthropology, 17, 1997, 279–296;

R.M. Packard, ‘ “No Other Logical Choice”: Global Malaria Eradication and the
Politics of International Health in the Post-War Era,’ Parassitologia, 40, 1998,
217–229; J.A. Gillespie, ‘Social Medicine, Social Security and International
Health, 1940–60,’ in E. Rodríguez-Ocaña, ed., The Politics of the Healthy Life:
An International Perspective (Sheffield: European Association for the History of
Medicine and Health, 2002), 219–239; A.-E. Birn, ‘Backstage: The Relationship
between the Rockefeller Foundation and the World Health Organization, Part I:
1940s–1960s,’ Public Health, 128, 2014, 129–140. For an historical overview
of the establishment of the Rockefeller Foundation and early decades of its inter-
national health activities and influence, see A.-E. Birn, ‘Philanthrocapitalism,
Past and Present: The Rockefeller Foundation, the Gates Foundation, and the
Setting(s) of the International/Global Health Agenda,’ Hypothesis, 1, 12, 2014,
1–27, at 1–8.
2 In 1938, for example, the League’s Malaria Commission re-published, in full, the
Punjab Public Health Department’s 1937 policy report on epidemic forecasting,
as well as an accompanying memorandum on ‘naturalist’ anti-malaria measures
employed in Punjab. In the province’s forecast calculation based on ‘quantum of
infection’ and ‘immunity in the population,’ the latter was based on child spleen
rate and ‘state of nutrition as calculated from availability of staple articles of
diet in any year’; LNMC, ‘Report on The Method of Forecasting the Probably
Incidence of Malaria in the Punjab,’ Geneva, 28 May 1938, C.H./Malaria/258.
3 The term ‘United Nations’ was first used in the ‘Declaration by United Nations
of 1 January 1942’ when representatives of 26 nations pledged their govern-
ments to continue fighting together against the Axis Powers.
4 World Health Organization, Official Records of the World Health Organization,
No. 2, 110–12 [hereafter WHO OR]. For a concise history of the institutional
origins of the Interim Commission and WHO in relation to preceding organiza-
tions of the League of Nations Health Organisation and UNRRA, see ‘Historical
Introduction,’ WHO OR, No. 9, 20–27. See also Farley, Brock Chisholm, 7–26,
48–57.
5 Amrith, Decolonizing International Health, 64; N. Howard-Jones, International
Public Health between the Two World Wars – The Organizational Problems
(Geneva: World Health Organization, 1978), 75–79.
6 For discussion of other infective diseases addressed initially, see Farley, Brock
Chisholm, chs. 8–11.
7 K.S. Davis, ‘Deadly Dust: The Unhappy History of DDT,’ American Heritage,
22, Feb. 1971, 44–47; A.L.S. Staples, The Birth of Development: How the
World Bank, Food and Agriculture Organization, and World Health Organiza-
tion Changed the World, 1945–1965 (Kent, OH: Kent State University Press,
2006), 162.
8 WHO OR, No. 5, 52; P.F. Russell, Man’s Mastery of Malaria (London: Oxford
University Press, 1955), 161; WHO OR, No. 8, 9. See also J.A. Nájera, ‘Epidemi-
ology in Strategies for Malaria Control,’ Parassitologia, 42, 2000, 9–24, at 15.
9 ‘Historical Introduction,’ WHO OR, No. 9, 23. China under the Kuomintang
government was the largest beneficiary, Amrith observes, of UNRRA medi-
cal supplies ($117 million); Decolonizing International Health, 56. Weindling
details parallel interest in ‘prevent[ing] socialist uprisings’ underlying the Ameri-
can Relief Administration’s food aid to central Europe immediately post-WW1;
‘The Role of International Organizations in Setting Nutritional Standards in the
1920s and 1930s,’ in H. Kamminga, and A. Cunningham, eds., Science and Cul-
ture of Nutrition (Atlanta, GA: Rodopi, 1995), 319–32 at 320.

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10 For the official history of UNRRA, see G. Woodbridge, UNRRA: The History
of the United Nations Relief and Rehabilitation Administration (New York:
Columbia University Press, 1950), 3 vols.
11 UNRRA Papers, British Library of Political and Economic Science (LSE), Com-
mittee for Coordination in Far East (44), 11, Sept. 28, 1944, ‘Relief Require-
ments for Certain Areas in the Far East,’ quoting a report by the British War
Cabinet’s Official Committee on Supply Questions in Liberated and Conquered
Areas SLAO/ER (44) 16; cited in Amrith, Decolonizing International Health,
55–56.
12 J. Gillespie notes that ‘[a]t the first UNRRA Council, at Atlantic City in 1944,
ILO observers, supported by the British delegation, urged that social security
organizations, which have survived remarkably intact in all occupied territories
except Poland, would be the most efficient method of distributing medical sup-
plies and services. All references to this proposal were dropped however in the
final report “in deference to the views of the State Department members of the
United States delegation” ’; ‘Social Medicine, Social Security and International
Health, 1940–60,’ in E. Rodríguez-Ocaña, ed., The Politics of the Healthy Life,
221–222. See also, J. Gillespie, ‘International Organisations and the Problem
of Child Health, 1945–1960,’ Dynamis: Acta Hispanica Ad Medicinae Scien-
tiarumque Historiam Illustrandam, 23, 2003, 115–142, at 130. Also, Amrith,
Decolonizing International Health, 84.
13 T. Patterson, On Every Front: The Making and Unmaking of the Cold War
(New York: W.W. Norton, 1992), 85, as cited in Litsios in ‘Malaria Control and
the Cold War,’ 269. Farley traces the geopolitical manoeuverings underlying this
decision; Brock Chisholm, 67–68.
14 WHO OR, No. 4, 104–109, 154.
15 Snowden describes ‘[m]assive welfare spending’ of a billion dollars by the Allies
and UNRRA in Italy between 1943 and 1947, ‘hoping to prevent epidemics,
restore the shattered Italian economy, and forestall an outburst of revolutionary
activity’; F. Snowden, The Conquest of Malaria: Italy, 1900–1962 (New Haven:
Yale University Press, 2006), 204.
16 M.J. Vine, ‘The Malarial Campaign in Greece,’ Bulletin of the WHO, 1, 1947,
197–204.
17 J. Farley, ‘Mosquitoes or Malaria? Rockefeller Campaigns in the American South
and Sardinia,’ Parassitologia, 36, 1994, 165–173. Snowden relates that proceeds
from the sale of UNRRA goods provided free to the post-war Italian govern-
ment were used to fund the DDT spray program (ERLAAS) in Sardinia; F.M.
Snowden, and R. Bucala, eds., The Global Challenge of Malaria: Past Lessons
and Future Prospects (Hackensack, NJ: World Scientific Publishing, 2014), 80.
18 WHO OR, No. 4, Minutes of the Second Session of the IC, 4–13 Nov. 1946,
112. The three-volume official history of UNRRA makes only brief reference to
DDT use for malaria control in southern Italy and post-war Greece, although
extensively used for typhus control; Woodbridge, UNRRA: The History, vol. 2,
134–135, 281.
19 IC, Fifth Session, WHO OR, no. 7, 23–25. See also Farley, Brock Chisholm, 229.
20 Farley, Brock Chisholm, 23, 63.
21 WHO OR, No. 4, 65, 107.
22 WHO OR, No. 4, 108. In June 1946, UNRRA-directed health programs were
heavily weighted in a handful of countries: of 353 Class 1 professional health
personnel in the field, 54 were in Italy, 114 in Greece, and 174 in China; Wood-
bridge, UNRRA, the History, 22–23.
23 WHO OR, No. 4, 108.

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24 ‘Congress,’ Gillespie observes, ‘remained reluctant to meet its budgetary com-

mitments to WHO and other multilateral agencies, while providing generous
funds to aid programmes that were more closely controlled by the United States.
A senior U.S. Public Health Service member of the American delegation to WHO
complained bitterly that: “It is difficult for many people to understand the atti-
tude of a Government which, having worked for the establishment of interna-
tional machinery to deal with these problems . . . nevertheless restricts use of
this machinery to minimum activities while at the same time setting up its own
or different international machinery, to which it contributes liberally to carry
out activities which an international organization like the WHO was created to
perform” ’; ‘Social Medicine, Social Security,’ 233–234.
25 WHO OR, No. 4, 111, 157–158.
26 Farley, Brock Chisholm, 68.
27 WHO OR, No. 4, 60, 21, 164–166.
28 Ibid., 168; WHO OR, No. 5, 52. In referring to UNRRA’s work in controlling
epidemics ‘aggravated by the war,’ malaria is not specified, although elsewhere
the DDT campaigns in Greece and Italy are mentioned; ibid., 109, 112.
29 WHO OR, No. 4, 27, 108, 115, 168.
30 Nuclear Committee on Malaria, First Session: Geneva, April 21–24, 1947, Draft
Agenda; WHO OR, No. 4, 160.
31 Jackson, ‘Cognition,’ 206, 208.
32 Jackson, ‘Cognition,’ 206. Pampana’s support for eradication goals continued,
despite being already aware of the possible emergence of insect resistance to
DDT in 1947 from his tour of spray operations in Greece and Italy; ‘Jackson,
‘Cognition,’ 206, as detailed in his ECM report, Report on Dr Pampana’s Mis-
sion to Greece and Italy, WHO.IC/Mal/8.
33 Jackson, ‘Cognition,’ 209.
34 WHO OR, No. 4, 160. ‘A technical committee must be made up of a small
number of real experts,’ their competency based upon ‘knowledge of the health
techniques concerned’; Note by the Secretariat, ‘Appointment of Expert Mem-
bers of Technical Committees,’ Oct. 21, 1946, in WHO OR, No. 4, 158. An
UNRRA memorandum to the IC advised that ‘[m]any experienced members of
the staff of the UNRRA Health Division will soon be released, and among them
there should be a considerable number who would be useful in the programme
of the Interim Commission. Every assistance will be given . . . in helping the offic-
ers of the Commission to make contacts with such personnel and to learn of their
qualifications’; WHO OR, no. 4, 112. Birn describes UNRRA as ‘a pipeline for
WHO’s first generation of personnel’; ‘Backstage,’ 131.
35 Jackson, ‘Cognition,’ 209.
36 ECM, Summary Minutes of the First Session, April 22–25, 1947, WHO.IC/
Mal./6, 21, 27; Jackson, ‘Cognition,’ 209.
37 Jackson, ‘Cognition,’ 193.
38 Farley, Brock Chisholm, 60–63. The Soviet delegate to the Epidemiology and
Quarantine Committee, Dr Fedor Krotkov, repeatedly expressed ‘apprehen-
sion . . . about the creation of too many committees’ and urged more attention
to responding to specific post-war relief needs ‘as judged by individual govern-
ments’; WHO OR, No. 4, 18, 20.
39 Vine, ‘The malarial campaign in Greece.’ The DDT program in Greece was
directed by Colonel D.R. Wright, a Rockefeller consultant engineer, ‘lent’ to the
IC, who had begun his career with Gorgas in Panama; G. Harrison. Mosquitoes,
Malaria and Man: A History of the Hostilities Since 1880 (New York: E.P. Dut-
ton, 1978), 230–231; WHO OR, No. 9, 31.

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40 ECM, Report on the First Session, Geneva, April 22–25, 1947, WHO.IC/Mal./4, 3.
41 Ibid., 5.
42 WHO OR, No. 7, Minutes and Documents of the Fifth Session of the IC, 22
Jan – 7 Feb. 1948, Annex 44, 223.
43 Ibid., 223; J.A. Sinton, Health Bulletin, No. 26 (Simla: GOI, Malaria Bureau,
1939), 13; J.A. Sinton, ‘What Malaria Costs India,’ Records of the Malaria Sur-
vey of India, Dec. 1935, 418.
44 The third ECM Session in 1949 suggested ‘the ultimate aim of WHO should be
to eliminate this disease as a public-health problem from the world,’ though this
too skirted the definitional question of ‘problem’; WHO Technical Report Series,
No. 8, ECM, Report on the Third Session, Aug. 10–17, 1949, 7.
45 ‘Malariologists in the United States,’ however, Nájera observes, ‘continued to
equate malaria control with anopheline control’; J.A. Nájera, ‘Malaria Control:
Achievements, Problems and Strategies,’ Parassitologia, 43, 2001, 1–89, at 21.
46 ECM, ‘Summary Minutes,’ 22–25 April 1947. As of August 1947, it was noted
at the fifth meeting of the IC, ‘documents of Technical Committees are not
printed in the Official Records’; WHO OR, No. 5, 128.
47 ECM, ‘Summary Minutes,’ 14–15. ‘Premunity’ refers to a sufficient level of natu-
rally acquired immunity where clinical symptoms from continuing re-infection
are limited or nil.
48 WHO OR, No. 8, 9.
49 WHO OR, No. 7, 224; ECM, ‘Extract from the Report on the First Session,
Note by the Secretariat,’ Bulletin of the WHO, 1, 1, 1948, 21–28, at 23.
50 ECM, ‘Summary Minutes,’ 13.
51 Ibid., 6, 16, 24. On U.S.-UK ‘hostility’ to the LNHO, see Gillespie, ‘Social Medi-
cine, Social Security,’ 222. Nájera describes the functioning of the subsequent
WHO Malaria Eradication Program in similar terms, as involving ‘the estab-
lishment of a central power, which recruited and trained its own peripheral
cadres . . . [and] took over and displaced previous antimalarial services, and the
early dissociation of operational planning from research, including epidemio-
logical and field research’; in ‘Malaria Control: Achievements, Problems,’ 5.
52 ECM, ‘Summary Minutes,’ 11.
53 Ibid., 17, 19, 32.
54 WHO OR, No. 8, 9.
55 ECM, ‘Summary Minutes,’ 39–41. Ciuca’s request for a three-week fellowship
for two Romanian entomologists to acquire field experience with DDT residual
spraying to assist in malaria control in the country also was turned down for
lack of funds; WHO OR, no. 7, 84–85.
56 ECM, ‘Summary Minutes,’ 14.
57 In an April 27, 1948, memorandum submitted in advance of the second ECM
meet that he would not attend, Ciuca urged ‘WHO’s aid’ in covering costs of
‘anti-malarial products (medicaments and insecticides)’ for non-producing
countries through the UN and co-ordination of their distribution through the
Economic and Social Council (ECOSOC); WHO.IC/Mal.24. Siddiqui notes con-
cerns by Eastern European member states that distribution of WHO funding
did not ‘correspond to actual needs,’ and the larger ‘political’ manoeuvering
around such issues as Chinese membership; World Health and World Politics:
The World Health Organization and the UN System (London: Hurst, 1995),
104–116.
58 With the 20 states of Latin America now under a Soper-headed Pan American
Health Organization (PAHO) and voting as a bloc, Soviet views routinely were
outvoted. Farley details Soviet objections to the direction in which the Executive

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Board was taking WHO, prompting its withdrawal from the organization in
February 1949, returning only in 1956; Farley, Brock Chisholm, 80–93. For a
detailed account of U.S. influence in opposing integration of the Pan American
Sanitary Bureau and the WHO, see, ibid., 97–110.
59 WHO OR, No. 8, ECM, Report on the First Session, 8–16, at 11.
60 WHO OR, No. 11, 59 [emphasis added].
61 WHO OR, No. 8. ECM, Report on the Third Session, 39–40; S.P. James,
‘Advances in Knowledge of Malaria Since the War,’ Transactions of the Royal
Society of Tropical Medicine and Hygiene, 31, 3, Nov. 1937, 263–280, at 266.
62 WHO OR, No. 7, 224.
63 For general discussion of the restrictive character and functioning of UN agency
expert committees, see K.J. Carpenter, Protein and Energy: A Study of Changing
Ideas in Nutrition (Cambridge: Cambridge University Press, 1994), 227–228.
Reliance on the authority of the expert committee was exemplified at the Jan. 27,
1948 (5th) session of the IC with the Brazilian member and vice-president sug-
gesting with reference to the joint WHO-FAO study proposal ‘that the [Interim]
Commission was not the appropriate body to enter into technical discussions
about the recommendations submitted by experts’; WHO OR, No. 7, 24.
64 A photo of the 34 delegates to the 1928 LNMC conference offers an interesting
contrast to the size of the ECM; International Public Health between the Two
World Wars, 63.
65 WHO OR, No. 4, 22. Amrith points out how India ‘played a central role in
shaping consensus around “modern” technological methods of disease control,’
presenting a willing and ‘ideal ground for “pilots projects” [and] demonstra-
tion areas,’ an outlook which ‘after 1945 accorded closely with the assumptions
of India’s new technocratic elite’; Decolonizing International Health, 12–13.
Administratively, Bombay was considered to provide a model of malaria control
organization as the work of Viswanathan was expanded to cover the whole
state; WHO OR, No. 11, 45. Lee notes that it was only in the early 1970s with
China’s entry into the World Health Organization that complete reliance on the
Western medical model and on technical aid was challenged with a ‘call to a new
politicization, based not on global transfers of wealth but on the reordering of
domestic political priorities’; Sung Lee, ‘WHO and the Developing World: The
Contest for Ideology,’ in B. Andrews, and A. Cunningham, eds., Western Medi-
cine as Contested Knowledge (Manchester: Manchester University Press, 1997),
24–45, at 36.
66 Litsios observes, ‘The Cold War’ [political contest] . . . led to a distortion of the
priorities of global programs being carried out under the various UN agencies.
Preference was given to countries where the threat of communism was judged
to be greatest. Preference was also given to more quickly achieved results that
placed anti-communist governments in a “good light” ’; ‘Malaria Control and
the Cold War,’ 271.
67 J. Gillespie, ‘Europe, America, and the Space of International Health,’ in Shift-
ing Boundaries Boundaries in Public Health: Europe in the Twentieth Century
(Rochester: University of Rochester Press, 2008), 117–119. Gillespie suggests a
larger U.S. concern with disease control lay with enhancement of trade. ‘Accord-
ing to the new approach to international public health associated with the
American architects of WHO, the first tactic against disease was eradication
at its source. International quarantine, with its restrictions on movements of
people and commerce, must finally be supplanted by programs that drew on
UNRRA’s experience – namely, vertically driven disease-eradication programs’;
‘Social Medicine, Social Security,’ 127. Indeed, from its first meeting onward, the

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ECM agenda included anopheline quarantine measures for air traffic ‘to prevent
the inadvertent transportation of malaria vectors across national boundaries’;
WHO OR, No. 8, ECM, Report on the First Session, 10. See also E. Pampana,
‘Malaria as a Problem for the World Health Organization,’ in U.S. Department
of State, Proceedings of the Fourth International Congress on Tropical Medicine
and Malaria, Washington, D.C., May 10–18, 1948, vol. 2, 940–946, at 644.
68 For discussion of the wider application of the thesis, see P.J. Brown, ‘Malaria,
Miseria, and Underpopulation in Sardinia: The “Malaria Blocks Development”
Cultural Model,’ Medical Anthropology, 17, 3, May 1997, 239–254.
69 ‘Malaria Programme: Proposal from the Representative from the United States
of America,’ Jan. 23, 1948, in WHO OR, No. 7, 222–223 [emphasis added].
70 Ibid.
71 Ibid.
72 ‘Note by the Secretariat’ WHO OR, No. 7, 223–225.
73 Ibid., 224–226; subsequently adopted by the IC on Feb. 3, 1948; ibid., 254.
74 Ibid., 223.
75 Report on the Second [ECM] Session, May 19–25, 1948, WHO OR, No. 11,
44, 48.
76 ‘Summary Minutes,’ 26.
77 United States. Department of State. ‘Address of welcome by the honorable
George Marshall, Secretary of State,’ Proceedings of the Fourth International
Congresses on Tropical Medicine and Malaria, Washington, D.C., May 10–18,
1948, vol. 2, 1–4 [hereafter, Proc. 4th Int. Cong. Mal.].
78 Viswanathan would report the rapid decline in malaria incidence that followed
1946 initiation of the Kanara district DDT spray trial; D.K. Viswanathan,
‘Activities of the Bombay Province Malaria Organization, 1942–27,’ Proc.
4th Int. Cong. Mal., 873–880. But discussion of the study’s finding of limited
mortality impact awaited a final report published in 1949; D.K. Viswanathan,
‘A Study of the Effects of Malaria Control Measures on Population and Vital
Statistics in Kanara and Dharwar Districts as Compared with the Rest of the
Province of Bombay,’ Indian Journal of Malariology, 3, 1, Mar. 1949, 69–99
[hereafter, IJM].
79 Of the 37 malaria papers presented, 17 were authored by U.S. malaria work-
ers, 3 by U.K. delegates, and a further 7 by delegates of other countries already
actively engaged in DDT-based campaigns.
80 WHO OR, No. 7, 222.
81 Ibid., 23–24. Amrith recounts the serious questions raised by the Liberian del-
egate to the 1955 World Health Assembly, Dr Togba, regarding feasibility of
eradication in Africa; Decolonizing International Health, 118–119. Nájera sug-
gests serious misgivings were ‘voiced in private talks’ by many World Health
Assembly delegates, despite a large majority vote in favour’; ‘Malaria Control:
Achievements, Problems and Strategies,’ Parassitologia, 43, 2001, 1–89, at 35.
82 Gillespie, ‘Social Medicine, Social Security,’ 225. Litsios reports that ‘Soper
claimed that it was the lack of this money that gave him time, as the Director of
the Pan American Sanitary Bureau, to mobilize such an important regional pro-
gram, as to preclude the PASB [Pan American Sanitary Bureau] being absorbed
by WHO’; ‘Malaria Control, the Cold War,’ 273.
83 WHO OR, No. 7, 223; P.F. Russell, and M.K. Menon, ‘A Malario-economic
Survey in Rural South India,’ Indian Medical Gazette, 77, Mar. 1942, 167–
180. For details, see ch. 5 above. A comprehensive 1978 bibliography of eco-
nomic aspects of malaria includes few documented examples of rural economic

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benefits; J. Sotiroff-Junker, A Bibliography on the Behavioural, Social and Eco-

nomic Aspects of Malaria and its Control (Geneva: World Health Organization,
1978). A Rockefeller-assisted 1951 study in Mysore State estimated an ‘annual
per-family lost earnings attributed to malaria’ of Rs 656 was reduced to Rs 68
‘post-DDT’; S.R. Bhombore, C. Brooke Worth, and K.S. Nanjundiah, ‘A Survey
of the Economic Status of Villagers in a Malarious Irrigated Tract in Mysore
State, India, before and after D.D.T. Residual Insecticidal Spraying,’ IJM, 6, 4,
Dec. 1952, 355–366; C.S. Narahari Rao, and S.R. Bhombore, ‘A Survey of the
Economic Status of Villages in a Malarious Tract in Mysore State (India) after
residual insecticide spraying,’ Bull. Nat. Soc. Ind. Mal. Mosq. Dis., 4, 1956,
71–77. These figures are puzzling, however, given that annual income for 60 per
cent of surveyed households was less than Rs 500.
84 ‘Memorandum prepared by FAO at the request of the Expert Committee on
Malaria,’ WHO OR, No. 11, 60.
85 Report of the Fifth Session of the IC, 5 February 1948, WHO OR, No. 7, 254.
86 Amrith notes that the British government viewed U.S.-UNRRA engagement as
key to ensuring American participation in a future international health organi-
zation, co-operation that officials believed otherwise ‘might be very difficult to
obtain’ after the war; Decolonizing International Health, 68. Siddiqui also sug-
gests a functionalist purpose in the preamble to the WHO’s constitution that
begins, ‘the health of all peoples is fundamental to the attainment of peace and
security and is dependent upon the fullest cooperation of individuals and states’;
World Health and World Politics, 45, 51, 42. See also Staples, The Birth of
Development, 169.
87 WHO OR, No. 13, 300, 306; WHO OR, No. 10.
88 Litsios, ‘Malaria and the Cold War,’ 259–260. Packard recounts Russell’s sub-
sequent whitewashing of the absence of data on economic benefits of malaria
eradication in a 1959 presentation to the WHO Director-General; R.M. Pack-
ard, ‘Malaria Dreams: Postwar Visions of Health and Development in the
Third World,’ Medical Anthropology, 17, 1997, 279–296, at 285. For a more
recent critique, see R. Packard, ‘ “Roll Back Malaria, Role in Development”?
Reassessing the Economic Burden of Malaria,’ Population and Development
Review, 35, 1, 2009, 53–85. Amrith observes that ‘[w]hen it could not be
shown that malaria control was transforming agricultural productivity, par-
ticularly as the Indian economy moved towards agrarian crisis in the 1960s,
or when other inventions – viz., population control – seemed more “cost-
effective”, support for malaria control ebbed’; ‘Political Culture of Health
in India: A Historical Perspective,’ Economic and Political Weekly, Jan. 13,
2007, 114–21 at 118.
89 Litsios, citing E. Goldman, The Crucial Decade and After: America, 1945–60
(New York: Alfred A. Knopf, 1960), details the profound impact that politi-
cal (‘anti-communist’) concerns within the ‘ “troubled American mind” ’ had in
shaping malaria and broader health policies of the WHO and FAO through this
formative period; ‘Malaria and the Cold War,’ 267–271.
90 LN, Final Report of the Mixed Committee of the League of Nations on the Rela-
tion of Nutrition to Health, Agriculture and Economic Policy (Geneva: LNHO,
1937); ILO, ‘Workers’ Nutrition and Social Policy,’ Studies and Reports (Social
and Economic Conditions), No. 23 (Geneva: ILO Office, 1936); E. Burnet, and
W.R. Aykroyd, ‘Nutrition and Public Health,’ LN, Quarterly Bulletin of the
Health Organisation, 4, 2, June 1935, 323–474.

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91 ‘United Nations Conference on Food and Agriculture: Text of the Final Act,’
American Journal of International Law, 37, 4, Supplement: Official Docu-
ments, Oct. 1943, 159–192, Resolution XIII, 172–173. The FAO was the single
UN organization the USSR did not join, though Soviet delegates attended the
1943 Hot Springs conference. In 1946 an unofficial American Famine Mission
under T.W. Schultz visited India to assess foodgrain supply adequacy; Indian
Famine Emergency Committee, India’s Hunger: Report of the American Fam-
ine Mission to India (New York, 1946), as cited in H. Knight, Food Adminis-
tration in India 1939–47 (Stanford: Stanford University Press, 1954), 253.
92 Zurbrigg, Epidemic Malaria and Hunger, ch. 12.
93 ‘Conference on Food and Agriculture,’ 163, 166, 171, 173.
94 Ibid., 163.
95 Ibid., 163, 175, 177, 183, 184–185.
96 In January 1946 ‘Montgomery reported to the cabinet that the existing ration
in Germany was only 1500 kilocalories per person per day, which was a bare
minimum to prevent starvation and disease. . . . The army was making arrange-
ments for handling an epidemic; Montgomery believed that if it occurred it
would probably spread to Britain’; J. Perkins, Geopolitics and the Green Revo-
lution: Wheat, Genes, and the Cold War (New York: Oxford University Press,
1997), 128.
97 Zurbrigg, Epidemic Malaria and Hunger, 390.
98 On Jan. 24, 1947, the final report of the FAO’s preparatory committee ‘recom-
mended creation of the World Food Council and emphasized industrial devel-
opment, full employment, and self-help,’ signaling defeat of the World Food
Bank proposals; Staples, Birth of Development, 78–81, 94.
99 S.G. Solomon, L. Murard, and P. Zylberman, Shifting Boundaries of Public
Health: Europe in the Twentieth Century (Rochester: University of Rochester
Press, 2008), 1.
100 See also, Packard ‘ “No Other Logical Choice”,’ 227. As the Eighth World
Health Assembly delegates gathered in Mexico City in 1955, they realized,
Packard observes, ‘that they had only two choices, they could jump on the
eradication train or get out of the way. Eradication was rapidly being adopted
by national malaria programs whether or not WHO adopted it’; ibid., 228.
101 D. Porter, ‘Social Medicine and the New Society: Medicine and Scientific
Humanism in mid-Twentieth Century Britain,’ Journal of Historical Sociology,
9, 2, June 1996, 168–187.
102 Present as ‘Counsellor’ at the Second ECM session on ‘Agriculture and
Malaria’ was Frank McDougall, co-architect of the 1930s ‘marriage of health
and agriculture’ efforts within the LNHO’s ‘Mixed’ Nutrition Committee that
interpreted global hunger as principally a problem of inadequate extension of
modern agro-technology. See above, ch. 3, at note 67.
103 Packard, ‘ “No Other Logical Choice”.’
104 The extreme efficiency of the main vectors (An. gambiae) in many regions of
central and west Africa (several hundred infective bites per person per year) led
to acquired immunity levels so high as to leave most of the population clini-
cally asymptomatic, a state referred to as ‘premunition,’ except among young
children.
105 For detailed accounts of the Kampala conference and larger issues raised,
see M.J. Dobson, M. Malowany, and R.W. Snow, ‘Malaria Control in East
Africa: The Kampala Conference and the Pare-Taveta Scheme: A Meeting
of Common and High Ground,’ Parassitologia, 42, 2000, 149–166; Far-
ley, Brock Chisholm, 159–169. The study would proceed through the years

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1954–1966, ultimately with inconclusive results regarding mortality impact

of initial transmission control and subsequent rebound, in part due to con-
founding effects of drug treatment; Dobson, et al., ‘Malaria Control in East
Africa,’ 160–164.
106 Ibid., 150.
107 WHO, ‘Minutes of Discussion of Committee on Programme and Budget, Eighth
World Assembly, 105, as cited in Packard, ‘ “No Other Logical Choice”,’ 228.
‘As a group,’ Packard observes, World Health Assembly ‘members were not in
a position to seriously question the proposal’s scientific merit. They could and
did raise questions concerning the feasibility of the proposal in terms mostly
of finances and the underdeveloped state of much of the world within which
malaria was a problem. But that was all. Few had first hand experience combat-
ing malaria. Those who did, as noted above, were among the most vocal critics
of the proposal’; ibid., 224.
108 J.L.A. Webb, ‘The First Large-Scale Use of Synthetic Insecticide for Malaria
Control in Tropical Africa: Lessons from Liberia, 1945–1962,’ Journal of the
History of Medicine and Allied Sciences, 66, 3, July 2011, 347–376; J.L.A.
Webb, The Long Struggle Against Malaria in Tropical Africa (New York: Cam-
bridge University Press, 2014), 88–95; M. Graboyes, The Experiment Must
Continue: Medical Research and Ethics in East Africa, 1940–2014 (Athens,
OH: Ohio University Press, 2015), 155–186.
109 Webb suggests that the severe 1958 malaria epidemic in the Ethiopian high-
lands, among a famished population with limited acquired immunity levels,
dampened advocacy for malaria eradication in tropical Africa; J.L.A. Webb,
Humanity’s Burden, 166; R.E. Fontaine, A.E. Najjar, and J.S. Prince, ‘The 1958
Malaria Epidemic in Ethiopia,’ The American Journal of Tropical Medicine
and Hygiene, 10, 795–803.
110 The influence of the malaria eradication program on the early WHO is reflected
in the fact that ‘five of the six WHO regional directors were ex-malariologists,
alongside the Director-General Candau himself’; M.A. Farid, ‘The Malaria
Programme – from Euphoria to Anarchy,’ World Health Forum, 1, 1–2, 1980,
8–33, 12.
111 For discussion of inter-agency competition through this period, see also,
Gillespie, ‘Social Medicine, Social Security.’ Gillespie notes that the Interna-
tional Labour Office (ILO) was ‘the only significant survivor from the wreck-
age of the LN to become the main international force in social and health
policy. . . . With a strong prewar record of support for reform of labor condi-
tions in dependent territories the ILO argued that the new standards of “social
security” developed for postwar Europe and America must apply equally in
their colonial possessions’; ‘Europe, America,’ 127–129. See also P. Weindling,
‘Social Medicine at the League of Nations Health Organisation and the Inter-
national Labour Office compared,’ in P. Weindling, ed. International Health
Organisations and Movements, 1918–1939 (New York: Cambridge University
Press, 1995), 134–153, at 138–141; P. Weindling, ed., The Social History of
Occupational Health (London: Croom Helm, 1985).
112 For discussion of the impact of surplus food ‘dumping’ on rural African agri-
culture and livelihood, see e.g., E. Boserup, ‘The Primary Sector in African
Development,’ in M. Lundahl, ed., The Primary Sector in African Development
(London: Croom Helm, 1985), 43–55; E. Holt-Giménez, and R. Patel, Food
Rebellions: Crisis and the Hunger for Justice (Cape Town: Pambazuka Press,
2009), 37–49; M. Ishii-Eiteman, ‘Perspectives on the IAASTD Report,’ Devel-
opment, 5, 14, 2008, 570–573.

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113 Susan George recounts how in 1965–1966 when India was in the throes of
the Bihar famine U.S. Food for Peace shipments ‘were suddenly placed on a
month-to-month basis and threatened with curtailment . . . India had no choice
but to accept America’s terms for resuming the Food for Peace programme.
These conditions consisted largely of greater freedom for US private invest-
ment . . . and for the American management of India’s fertilizer industry’; How
the Other Half Dies (Harmondsworth, England: Penguin Books, 1977), 118;
D. Morgan, Merchants of Grain (New York: Viking Press, 1979), chs. 10–12.
114 Staples, Birth of Development, 96; Litsios, Malaria Control, Cold War, 269.
On the eve of yet another ‘great’ war, Nagendranath Gangulee in 1939 decried
the use of hunger as among the most coercive weapons of war, describing post-
WW1 policies of ‘embargoes, war debts, [and] financial restrictions’ by the
victorious Powers as ‘victory with vengeance’ and rued ‘the supreme illusion of
the post-war world . . . that armed conflict alone is war’; Health and Nutrition
in India (London: Faber and Faber, 1939), 20.
115 Staples observes that ‘the preamble to the [FAO] constitution was not as forth-
right as the Hot Springs declarations had been. Instead of calling for freedom
from hunger, it merely called on all signatories to better standards of living and
nutrition’; Birth of Development, 78.
116 Amrith, Decolonizing International Health, 88–89 [emphasis in original].
117 Jackson highlights Russell’s particular role in controlling the ECM agenda;
‘Cognition,’ 207.
118 In a 1980 WHO article, for e.g., the subject of epidemic forecasting dealt exclu-
sively with entomological variables, with no reference to the human host; E.
Onori, and B. Grab, ‘Indicators for the Forecasting of Malaria Epidemics,’ Bul-
letin of the WHO, 58, 1, 1980, 91–98.
119 P. Russell, L.S. West, and R.D. Manwell, Practical Malariology (Philadelphia:
W.B. Saunders, 1946), 375. This reading by Russell may well be the source
for recent accounts of the 1908 epidemic where high prices are interpreted
as secondary to malarial debility; I.A. McGregor, ‘Malaria and Nutrition,’ in
W.H. Wernsdorfer, and I.A. McGregor, eds., Malaria: Principles and Practice
of Malariology (London: Churchill Livingstone, 1988), 754–777, at 754. See
Introduction, at note 9.
120 Russell, et al., Practical Malariology, 374–375.
121 Ibid., 541. See above, ch. 2 at note 116. Russell conceded that famine possibly
influences relapse rate of malaria infection, yet qualified even this admission
with a behaviouralist hue: famine victims ‘attempt[ing]to work before they are
fit’; ibid. Missing was any reference to the massive malaria mortality in famine-
stricken 1943–1944 Bengal in the absence of any change in entomological con-
ditions; Zurbrigg, Epidemic Malaria and Hunger in Colonial Punjab, ch. 12.
122 Man’s Mastery of Malaria. Only one of Christophers’s 215 published articles
and reports is included in Russell’s 1955 bibliography: a paper co-authored
with J.A. Sinton; ‘The Correct Name of the Malignant Tertian Malaria Para-
site,’ British Medical Journal, 3, Dec. 2, 1938, 1130. Three decades earlier,
Andrew Balfour’s single reference to Christophers’s malaria research would
appear in a passing general phrase as ‘pioneer work on mosquitoes’; A. Balfour,
and H.H. Scott, Health Problems of the Empire: Past, Present and Future (New
York: Henry Holt, 1924), 78.
123 Nor, in Pampana’s 1933 overview of LNMC epidemiological research, is men-
tion made of the 1930 India Study Tour report, though earlier European ‘tours
of investigation’ reports are discussed: E.J. Pampana, ‘Malaria Research and
the Malaria Commission of the League of Nations,’ Annals of Tropical Medi-
cine and Parasitology, 28, 1, 1934, 63–65.

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124 ‘[U]nder the all powerful gaze of the western eradicator,’ Packard observes,
‘local knowledge of malariologists built up over decades of experience became
irrelevant’; ‘Malaria dreams,’ 290. For on-going influence of the Rockefeller
Foundation and World Bank in shaping of the WHO, see T. Brown, M. Cueto,
and E. Fee, ‘The WHO and the Transition from International to Global Public
Health,’ American Journal of Public Health, 96, 1, Jan. 2006, 62–72. Interest-
ingly, in the 1963 second edition of Russell’s Practical Malariology, the section
on ‘regional epidemics’ is rewritten, much of the content replicating an article
previously published by G. Macdonald, now a fourth co-author to Russell’s
collaborative text. Here, brief reference to Malaria in the Punjab did include
acknowledgement of pre-existing economic hardship in relation to fulminant
epidemic malaria conditions; P. Russell, L.S. West, R.D. Manwell, and G. Mac-
donald, Practical Malariology (London: Oxford University Press, 1963), 473.
125 Already, he pointed out, there were reports of vector resistance ‘from Italy
and other countries including India,’ and that mud surfaces of village houses
absorbed 70 to 90 per cent of the DDT applied; also the problem of exophily:
the mosquito habit of resting outdoors after a human blood meal rather than
inside, in the case of some important vector species; V. Venkat Rao, ‘A Critical
Review of Malaria Control Measures in India,’ IJM, 3, 4, Dec. 1949, 313–326,
at 317–318. Venkat Rao was not among the 15 Indian delegates to attend the
May 1948 Malaria Congress in Washington.
126 Venkat Rao, ‘A Critical Review of Malaria Control,’ 319 [emphasis added].
127 In 1999, V.P. Sharma reported that DDT coverage in India in 1996 extended
to a population of 56 million, with another 7 to 10 million protected with syn-
thetic pyrethroids, the aim ‘to substantially reduce morbidity and mortality and
control malaria without contaminating the environment, and therefore wher-
ever feasible insecticides are being phased out’; ‘Current Scenario of Malaria in
India,’ Parassitologia, 41, 1999, 349–353. For an overview of recent malaria
control policy based on early diagnosis, prompt treatment, and alternate vector
control methods including larvivorous fish, wherever feasible, see L.M. Barat,
‘Four Malaria Success Stories: How Malaria Burden was Successfully Reduced
in Brazil, Eritrea, India, and Vietnam,’ American Journal of Tropical Medicine
and Hygiene, 74, 1, 2006, 12–16, at 13.
128 Venkat Rao, ‘A Critical Review of Malaria Control,’ 314, 322–323.
129 Ibid., 324.
130 Ibid.
131 S.R. Christophers, ‘Policy in Relation to Malaria Control,’ IJM, 9, 4, Dec.
1955, 297–303, at 299.
132 Ibid., 300. In 1969, several U.S. malaria workers would rue ‘the diminish-
ing number of “malariologists” and proliferation of “eradicationists” ’; R.
Scholtens, R. Kaiser, and A. Langmuir, ‘An Epidemiological Examination of
the Strategy of Malaria Eradication,’ International Journal of Epidemiology, 1,
1, 1972, 15–24, at 23.

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ALLURE AND LEGACIES OF THE
GERM PARADIGM

Tropical Hygiene . . . [can] give us a complete knowledge of the

dynamics of infections of all types and thus enormously con-
centrate our powers of prevention . . . [a] strategy of disease
prevention which would give us complete power over virtually
all communicable diseases.
—– G. Macdonald, ‘On the Scientific Basis of
Tropical Hygiene,’ Presidential address,
Transactions of the Royal Society of Tropical
Medicine and Hygiene (1965), 59, 618–619

We do a disservice to the weight of evidence, past and present,

on social inequalities in health if we suggest that what chiefly
hampers efforts to promote social equity in health is a lack of
knowledge.
—– N. Kreiger, ‘Historical Roots of Social
Epidemiology,’ International Journal of
Epidemiology, 30, 4, Aug. 2001, 899–900.

The allure of eradication

For medical scientists and practitioners in the post-1897 era, attraction to a
narrowed biomedical model of malaria – and the promise of the parasite’s
eradication – lay in myriad realms. Most basic was the common-sense maxim
that prevention is better than cure. Eradication’s appeal in turn lay also in its
inherent democratic aura. Interrupting malaria transmission meant eradica-
tion for everyone, including for the poor who suffered most. Conversely, to
question the eradication approach could open oneself to the professional
opprobrium of depriving those same poor of such benefits: ‘unwarrantably
attacking proven prophylactic measures,’ Ronald Ross would urge in 1909,
constituted ‘a very grave scientific crime.’1
Through the 1920s the eradicationist promise was fuelled by triumphalist
accounts of malaria control in the Panama Canal zone. No other sanitary

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campaign exemplified the heroic motif so powerfully, the challenge defined

overtly as a ‘battle’ against nature, an enthusiasm that would culminate with
U.S. Surgeon General William Gorgas’s knighthood in Britain. This, despite
evident questions about the broader applicability of the Panama example
in relation to cost and the confounding contributions to malaria mortality
decline in the canal zone of unlimited quinine and ‘a well-fed labour force’ –
despite, in other words, its enclave and imperially funded character.2 The
Panama campaign, nevertheless, would continue to serve as reference point
for vector eradication advocacy, no more so than within the Rockefeller
Foundation’s International Health Board as it turned away from hookworm
and embraced malaria in the 1920s as the new microbiological enemy of
global development.3
Across this same period, momentum for a war on malaria was building
also at the institutional level as tropical medicine schools proliferated. ‘[I]n
the scramble for imperial power and wealth,’ Bynum observes, ‘schools
of tropical medicine . . . represented tangible monuments to the power of
medicine and medical research,’4 a common central plank within the intra-
Western imperial contest. ‘Before the outbreak of World War I,’ he notes,
‘there were schools of tropical medicine in Germany, France, Belgium, the
Netherlands, and the United States, in addition to research stations in India,
Indochina (now Viet Nam), the Sudan, and Malaysia.’ Increasing cohorts of
graduates through the 1920s and 1930s were trained in ever more sophisti-
cated entomological and anti-larval techniques, imbued with the challenge
of the Gorgas example and Ross’s exhortation that ‘malaria has done more
than anything else to prevent the settlement and civilization of the vast trop-
ical areas which would otherwise be most suitable for the human race.’5 In
time, medical historians contributed to nourishing the heady heroic appeal,
with dramatic accounts of the discovery of new vectors and extirpation
campaigns incidentally offering a ‘darn good story.’6
The allure of malaria eradication was fuelled at a quite different level, by
the complexity of the microbe’s transmission cycle as a vector-borne disease.
Recognition of the fragility of that cycle, and of the numerous points at
which it potentially could be broken, endowed each new entomological dis-
covery with the promise of a technological breakthrough around the corner.
The tropical (colonial) world with its ‘wealth . . . of pathogenic organisms,’
in Manson’s terms,7 offered unlimited research possibilities, Worboys notes,
for ‘stak[ing] out new professional territory.’8 One of the more promising
entomological developments in the 1920s was identification of the different
feeding habits of Anopheles vectors: the observation that some anopheline
species such as An. culicifacies fed mainly on animals (zoophilic) rather than
humans. This helped to explain the perplexing phenomenon of ‘anophelism
without malaria,’ but also suggested that interruption of transmission
might be more feasible in regions where the main vector was zoophilic.
This entomological advance ultimately failed to bring about the hoped-for

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breakthrough in vector control in most endemic regions, but it did rekindle

and reinvigorate confidence in an entomological solution.9
Arguably, however, it was the rise of private ‘public health’ philanthropy
that ultimately gave financial legs to the reductive trajectory in the case of
malaria work, greatly expanding enthusiasm for the idea of vector-control
and development of related technical skills. Corporate funding, most promi-
nent in relation to the Rockefeller Foundation, made possible the conveni-
ent format of the short-term expert consultant, allowing heroic aspirations
to flourish. Very quickly the new medical subdiscipline of ‘malariology’ was
being shaped by professionals whose expertise lay primarily in laboratory
training or circumscribed anti-larval field trials, technical experts who had
little in-depth epidemiological experience of malaria in human populations,
or indeed none at all.10 More and more, Packard observes, the ‘problem
of malaria’ was coming to be defined in terms of the tools the professional
‘malariologist’ had for dealing with the disease, ‘as a case with a positive
blood smear, of plasmodia seen on a microscope slide . . . an infection by a
microorganism transmitted by anopheline mosquitoes.’11
For many of the new malaria professionals, agricultural development
(‘bonification’) was a less attractive malaria control strategy than sharply
defined, if painstaking, anti-larval campaigns. The former was not their
mandate, an arena where there was little interest or comfort, and even less
skill. To younger cohorts, the experience in Italy under Celli – where land
reclamation had left vectors and infection levels still abundant – appeared
to leave malaria workers without a role, except for perhaps the seem-
ingly undignified task of confirming that malaria transmission levels were
unchanged, though the ‘terror’ of that transmission had largely vanished.12
Such a job description hardly conjured up the heroic victories epitomized
by the Panama Canal campaign: a role antithetical to the ‘action man.’ Nor,
Amrith notes, did ‘the patient, unglamorous task of building up local health
services.’13 For some like Lewis Hackett, a prominent Rockefeller consultant
pursuing anti-larval trials in Italy through the 1920s, the Malaria Commis-
sion’s gravitation to a ‘social disease’ definition of malaria was viewed as
a professional threat, ‘doom[ing] . . . the medical field malariologist . . . to
extinction in Europe.”14 Hackett for his part would acknowledge a role for
poverty in malaria’s toll, conceding at one point that ‘[i]gnorance, poverty,
and disease constitute the vicious triangle of human social inadequacy. An
attack on any one of them helps to dissipate the other two.’ Yet ultimately,
he urged, the most practical point of intervention in that vicious cycle was
an attack on the infective agent, arguing that

the causes of malaria, at least, are in the main independent of the

ignorance and poverty of its victims and can be separately handled.
It is easier to believe that release from the burden of malaria will

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help to bring prosperity and knowledge than that a higher standard

of living and education must precede the eradication of malaria.15

There is a disarming candour to Hackett’s expression of belief. Still, it

begged the question: ‘easier’ for whom? As public health physicians one
might expect some acknowledgement – if not satisfaction – from Hackett
and Rockefeller colleague, Paul Russell, that by the 1920s the malarial ‘ter-
ror’ of the Pontine marshes had largely been lifted, though transmission of
the Plasmodium parasite remained. Instead, it was as if the two perspec-
tives, microbial and social, were in competition. And here, for experts such
as Hackett and Russell, there was no contest.
But the socio-economic route for malaria control was unattractive for
other reasons as well. Addressing economic determinants was frankly
impossible within the time-frame imperatives set for overseas consultancy.
‘Probably time has been wasted by assumptions that malaria is a socio-
logical rather than sanitary problem,’ Russell would argue, adding ‘it would
probably be a good deal quicker and cheaper to induce prosperity through
malaria control.’16 In very concrete ways, in other words, public health
approaches to malaria control were being moulded to conform to the time
constraints of that new institutional entity, the short-term international
expert. In the process, understanding of the malaria problem – indeed its
very definition – was being reshaped as well.

Myriad conveniences
A malaria model shorn of conditions of the human host was convenient
at other levels. For local elites, the prospect of malaria eradication offered
relief from fear of contamination from the poor, that unlimited reservoir
of disease. For the British Raj in the context of 1920s fiscal retrenchment,
formal embracing of the doctrine of malaria as a block to development also
held out the prospect of Rockefeller funding for programs that could be
pointed to as ‘doing something,’ ‘managing a problem or crisis.’ Many writ-
ers have also highlighted broader corporate interests in the promotion of a
unidirectional view of malaria as a principal cause of world poverty.17 ‘The
International Health Division,’ Farley observes,

played a crucial role in saving the Rockefeller name from almost

universal condemnation. In 1913 the American public associated
his name with the very worst features of brutal, unbridled, unprin-
cipled capitalism; today that is no longer the case. . . . Through the
Health Division in particular, the Rockefeller Foundation gained a
worldwide reputation for medical benevolence and enhanced the
reputation of the Rockefeller name.18

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Indeed, the public relations value of the anti-hookworm campaign was

articulated unabashedly in private proceedings in the formative years of the
Foundation.19
Such broader interests did not exclude genuine belief in the doctrines of
germ sanitation, as Ettling has pointed out.20 Indeed, a good deal of the force
of the reductive sanitary model lay in the ardent conviction of its field-level
advocates. But that conviction in the case of Rockefeller philanthropy was
inseparable from the ideological: a notion of the Western civilizing mission,
cultural supremacy expressed quintessentially in ‘Western’ science, above all
medical science.
Moreover, ideological beliefs were inseparable from the geopolitical:
expanding markets for goods, ensuring raw materials access and oppor-
tunities for investing capital; thus fashioning compliant relations with
governments in regions of the world of strategic and corporate interest.21
Such broader conveniences were openly acknowledged, Randall Packard
points out, by prominent U.S. public health figures22 such as James S. Sim-
mons, Dean of the Harvard School of Public Health who urged in a 1950
address to the conference of Industry and Tropical Health that the ‘health
and manpower of the free nations of the world are now the most vital
resources in our fight against Communism.’23 In the context of the post-
WW2 accelerating Cold War and nationalist movements in many regions
of the developing world vowing to ensure food and land for the poor and
malaria-afflicted, an urgent need existed on the part of Western powers
to be offering alternative ‘solutions’ to disease and underdevelopment in
place of the structural and political reforms sought by revolutionary move-
ments.24 In this political contest, international health and development
agencies became a central champs de bataille.25 Russell himself in 1955
described malaria as ‘a factor that, among others, helps to predispose a
community to infection with political germs that can delay and destroy
freedom.’26 In the task of winning hearts and minds the promise of an
immediate fix was an essential tool.
In the case of DDT, the value of eradication was two-fold: powerfully
reinforcing the technological paradigm; but also planting the donor’s flag of
goodwill and beneficence in regions of particular economic interest or politi-
cal concern. From its earliest days, WHO funding, as we have seen, was
both extremely limited and highly insecure, with most of the actual funding
of DDT ‘demonstration’ programs coming instead through U.S. bilateral aid
in the case of southern Europe, Iran, Venezuela, and of course India, regions
of strategic U.S. interest.27 As D.K. Viswanathan described:

If you take a DDT drum with the stars and stripes on one side and
the tricolour on the other side to each of the forty million homes
in the country . . . the psychological impact would be so great that
public opinion would swing back again in favour of democracy.28

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Ideological aspirations did not preclude the possibility of local benefits

along the way for some among recipient populations. But it did mean that
the needs of the poor could never be the central informing purpose of Rock-
efeller work, nor inform understanding of the broader roots to the disease
problem.
The political convenience of malaria eradication could of course apply
as well to recipient governments. ‘Alongside the redemptive narrative of
malaria eradication,’ Amrith observes, ‘stood a militarised, disciplinary nar-
rative that presented malaria eradication as an assertion of the state’s power,
its technology and its sovereignty.’ In post-Independence India, he observes,

The [DDT] programme found ritual expression in a way that

underscored the state’s presence in the lives of its citizens. To com-
memorate ‘World Health Week’ in 1955, for example, ‘two planes
of the India Air Force dropped leaflets’ on malaria eradication on
Hyderabad and Secunderabad . . . just seven years after Hyderabad
was subject to forcible incorporation into independent India by
‘police action.’29

The larger sanitationist dilemma

Yet as politically and professionally convenient as the reductive view of
malaria as a block to development proved to be, interpreting the exclusion
of the ‘Human Factor’ in malaria analysis in such terms alone is unsatisfying
on a further level. The inherent power of the sanitationist paradigm merits
analytic consideration on its own terms: the practical dilemma faced by
the individual public health worker charged with applying preventive germ
policies where understanding of disease etiology was narrowed conceptually
by the turn of the twentieth century to external, and invisible, pathogens –
or vectors. This is demonstrated in the case of South Asian malaria history
in the ardent defence, by a local British Indian civil surgeon, A. Hooton, of
Ronald Ross’s advocacy of vector sanitation at the Bombay Medical Con-
gress in 1909. ‘Is there a Civil Surgeon in the country,’ he would ask, ‘who
does not – if only in his own compound – undertake anti-mosquito opera-
tions?’30 Once vector information was available, the onus upon individual
sanitary officers was real. In sight of potential breeding sites, individual
local officials post-1897 were obliged to act, in situations where it was gen-
erally not possible to tell if the ‘dangerous’ specific vector was present, or
could be, with every fresh rainfall – and if so, if any might be infective. In
the absence of a broader predispositionist context of malaria lethality, the
quandary the new knowledge of malaria presented to those working ‘on the
ground’ was inescapable – unless another voice was also present, reminding
of other approaches: ensuring treatment access, and addressing a key lethal-
ity risk factor, human destitution. It was precisely this quandary that made

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the eradicationist argument so appealing: interruption of malaria transmis-

sion, once and for all.
Moreover, the dilemma is seen at government levels as well, the narrow
germ paradigm posing an equally inescapable, if different, bind. Unable to
acknowledge the larger, predisposing determinants of the malaria burden in
India, the British Raj soon came to see that it had little choice but to publicly
embrace vector extirpation, despite having little intention of, or practical
capacity to, follow through as general policy.31

Parallels and legacies

In the demise of the ‘Human Factor’ in malaria epidemiology, many paral-
lels exist with the ‘uncoupling’ of disease and destitution one century earlier
in industrializing Britain. Where nineteenth-century sanitarians sought to
fix public gaze exclusively on environmental (neighbourhood) filth, the gaze
one century later was directed to the plasmodium parasite and its anophe-
line vector. As in the nineteenth century where the sanitary promise was
fuelled by the possibility of real benefits, so too a goal of malaria eradica-
tion offered the practical possibility of reducing periodic malarial fever and
incapacity, at least for some. As in 1840s Britain, advocates of species sani-
tation a century later would portray malaria control policy in oppositionist
terms: optimists ‘versus’ pessimists – the latter term referring to those who
appealed to include socio-economic measures, thereby misguidedly depriv-
ing the poor of immediately available technical benefits, ‘the Luddhites of
public health.’32 And as a century earlier, rejection of this false dichotomiza-
tion came from within the medical community and from its most experi-
enced and insightful medical members.
In both eras, too, there were much larger propelling concerns in the back-
ground. The 1842 Sanitary Report, Hamlin suggests, was to a major extent
a political document. What was originally presented as a managerial strat-
egy for summoning financial commitment to necessary public infrastructure
was also a strategy of covering up unpleasant, inconvenient economic reali-
ties, ‘divert[ing] attention from the charges . . . that the new Poor Law itself
bore responsibility for fever. . . . At risk were the survival of the state in the
face of revolution, and the grand question of whether the class relations of
liberal industrial society could work.’ The Sanitary Inquiry, he concludes,
not only advanced Chadwick’s personal career ‘by inventing a field in which
he could be the authority,’ but also ‘helped the hated Poor Law Commission
to survive,’ an agency which under his stewardship was markedly reducing
relief to the destitute.33
In this much larger political drama, Chadwick, in his parallel role as Poor
Law Commission secretary, was but a single actor. Nonetheless, his contri-
bution included a studied excising of hunger from medical debate, literally
removing ‘starvation’ as a cause of death category from the vital registration

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system.34 In doing so, he helped remove not just incriminating statistics, but
a concept, and indeed vocabulary, central to the predispositionist argument,
making it that much more difficult to engage in broader health debate. As
for Ross or Russell, this hardly means the sanitary doctrine, or Chadwick’s
belief in it, was a fraud.35 But nor need it deter historians, Hamlin urges,
from considering the consequences of its limitations. For in both cases there
were costs.
In both eras, the role of carefully selected technical experts made ques-
tioning of broader economic roots of the epidemic disease problem diffi-
cult, as seen above with the WHO’s early Expert Committee on Malaria.36
As Hamlin observes with respect to the miasma thesis of urban typhus,
‘[t]he mode of investigation’ by Chadwick’s selected medical commission-
ers through summary tours of England’s fetid industrial slums ‘put a pre-
mium on what could be seen or smelled and counted on a brief stay. . . .
The epidemiologists’s searching inquiries or the casual conversations that
lead the ethnographer or journalist to sense the tapestry of social relations
were impossible.’37 One century later the phenomenon of the ‘international’
health consultant would be institutionalized under private corporate phil-
anthropic agencies where short-term assignments similarly lent themselves
to narrowly constructed expertise.38 The resulting constraints led predict-
ably to limited ‘demonstration’ projects, or to enclave activities, such as the
anti-malarial field work of the Ross Institute in India that remained ‘chiefly
occupied with industrial malaria in tea gardens.’39 As Gordon Harrison has
observed, such a ‘crusade for human life, organized selectively, could easily
become a defence of the privileged.’ He adds that ‘it is hard to see how the
first [malaria] fighters could otherwise have retained the optimism to act
at all and so to keep alive the possibility of extending the fight later on.’40
Indeed, but this was surely the point. The external expert was inherently
caught within a short-term framework where ‘success’ if it were to happen
at all depended on a limited technological approach.
Yet South Asian colonial malaria history suggests – as does the Italian –
that a very different framework for action was possible, as was a different
basis for ‘optimism.’ The choice was not to extirpate or do nothing. Chris-
tophers, Rama Rao, Gangulee, Bentley, and Venkat Rao were all ‘acting.’
Another choice existed: to assess, articulate, and address determinants of
lethality by advocating action on broader levels, alongside factors of trans-
mission where appropriate.
Reliance on external public health philanthropy was problematic not just
in terms of content of the programs promoted, however. It was problematic
also for the absence of accountability: of the consultant institution, of the
models offered, and of the central paradigm itself. Unlike government-based
public health services where an obligation for accountability existed at least
notionally, the question of whether a philanthropic scheme or pilot project
worked or not was hardly an issue. It was enough that the project bore the

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mantle of modern medical science, though in practice the scientific content

applied in the case of much Rockefeller Foundation work in India was often
limited simply to confirming the presence of a specific microbe in a popu-
lation. For the funding agencies themselves, it concretely did not matter
if a project was flawed, or failed entirely. In the wake of the failure of its
anti-hookworm campaign in Sri Lanka and southern India, the Rockefeller
Foundation could quietly move on to another disease, another experimental
‘field’ study or ‘demonstration’ project, in another area. And did. In the case
of India, the Foundation ultimately turned to malaria in the 1930s. Once
malaria eradication was in place within the World Health Organization
however, in 1951 it would again move on to seek technological solutions to
what Rockefeller directors viewed as the new and more pressing threat to
geopolitical stability and global business: population growth and foodgrain
production.41 The Foundation thus stepped away from malaria just when
serious research attention was required to face the emerging problems of
insecticide, and soon chloroquine, resistance.
In both Chadwick’s England and post-1920 British India, endemic under-
nourishment continued, if in South Asia accompanied by acute hunger in
endemic form as well. Increasingly however the new science of dietetics
would interpret such hunger in behavioural terms as bad personal dietary
habits, or in Britain, ‘inefficient mothers,’ and sideline underlying causes
of deep poverty: insecure, irregular, ill-paid, and exhausting conditions of
work and living. In the narrow application of nutritional science, the poor
in India would lose any authority to speak of their hunger.42 Officials sitting
on the Royal Commission on Agriculture in India would rail against the
vexatious ignorance of the poor who understood little of the new theory of
nutrition and insisted on eating too much bulky rice. Lectures and tonics
would be offered in the place of structural reforms, and common experi-
ence was lost or ignored. With disease and hunger now in the domain of the
microbiologic, there was no longer common authority to speak.
But there was another equally problematic ‘cost’ side to short-term expert
consultancy and related unaccountability: a general absence of scientific
testing.43 Moreover, the operative paradigm made it seemingly unneces-
sary. Where microbes were equated with disease burden, and their absence
defined as health and economic productivity, quantitative measurement of
the impact of eradication of particular microbes or their vectors on mor-
tality rates could be seen as superfluous. In the case of malaria, the eradi-
cation of the protozoa responsible was an incontrovertible good: proof
enough. Indeed, the frequent absence of scientific testing with the embrace
of modern sanitary science was perhaps the most deeply ironic of all the
parallels with the nineteenth-century British experience. In his 1842 Sani-
tary Report, Chadwick simply assumed, incorrectly, a miasmic explanation
of the fever (typhus) epidemics he had been commissioned to investigate.44
Subsequent decline in typhus outbreaks likewise was assumed attributable,

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also inaccurately, to sanitation measures (clean streets, eliminating environ-

mental human waste, i.e., sewage disposal and water supply).45 One century
later, in the case of South Asia, elimination of vector transmission of malaria
has been assumed responsible for post-WW2 decline in mortality from the
disease. In this latter case, however, the absence of empirical assessment is
even more puzzling because the opportunity for tracking such relationships
through vital registration records was that much greater. Yet in the rush to
act, elementary scientific practice was set aside.46 Did it matter, after all,
when eradication of the malaria plasmodium was by any standards a cat-
egorical good?
Here we turn to this largely neglected question of the mortality impact
of malaria transmission control in mid-twentieth-century South Asia, an
issue that casts light on both the continuing power of the germ paradigm
and the enduring invisibility of hunger in contemporary health history
analysis.

South Asian post-WW2 mortality

decline revisited
Within global malaria historiography, assessment of the impact of DDT-
based malaria control programs on mortality levels in post-WW2 South Asia
has been remarkably limited. Analysis undertaken by Western commenta-
tors has often focused on the experience in Sri Lanka, with DDT assumed
early on to be responsible for the notable decline in mortality levels in the
immediate post-war years. Particularly influential in this literature was the
reading offered by Kingsley Davis, a prominent U.S. historical demographer
of South Asia. ‘The main cause of the spectacular decline of mortality in
Ceylon is well known. It was the use of D.D.T.,’ he argued in 1956.47 That
death rates for all disease categories over this period had declined as sharply
as that for fever was acknowledged by Davis, but was attributed to malar-
ia’s debilitating effect, ‘mak[ing] people susceptible to other diseases.’48 Very
likely the Davis assessment reflected recent remarks from members of the
World Health Organization’s Expert Committee on Malaria. One year ear-
lier, Paul Russell had described the results of the DDT program in Ceylon
as ‘astonishingly good,’ pointing to plummeting malaria prevalence indices
and infant mortality rates that by 1951 ‘had fallen to about half what they
were in 1938,’ inferring a causal relationship.49 At a regional World Health
Organization conference in Bangkok in 1953, summary proceedings con-
tained a similar causal inference.50
In the case of India, highly influential commentary on DDT’s impact in
the country appeared in 1958 within a larger study of India’s economic and
demographic ‘prospects’ by U.S. demographer, Ansley Coale, and economist,
Edgar M. Hoover.51 Here, the two authors arrived at an estimate of 2 mil-
lion lives saved annually by the National Malaria Eradication Programme

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(NMEP) through the 1950s. Their estimate, however, was not based on
vital registration data, under the assumption that ‘[n]o adequate . . . Indian
data exist.’ The figure was reached indirectly, instead, by extrapolating
from the experience of Sri Lanka where marked post-WW2 crude death
rate decline had already been assumed largely due to DDT. Major post-war
decline in mortality in India was simply assumed to have begun after 1951,
corresponding to initiation of the residual insecticide spray program in the
country.52
This latter assumption has since been recognized as inaccurate. Much of
the post-WW2 mortality decline in India in fact preceded initiation of the
DDT spray program in the early 1950s. In Punjab, for example, an abrupt
fall in crude death rates took place in the mid-1940s (Figure 7.1),53 as Dyson
and Murphy also show for Maharashtra, Gujarat, and Tamil Nadu, associ-
ated more generally, they suggest, with an economic and employment boom
in developing countries in the immediate post-war period related to sudden
very favourable terms of trade.54 Admittedly, the Coale-Hoover estimates
were not presented as epidemiological in purpose, the goal of their 1958

60

50

40
CDR
30
CBR

20

10

0
1920 1930 1940 1950 1960

Figure 7.1 Mean annual crude death rate,* crude birth rate (per 1,000), 11 plains
districts,** (East) Punjab, 1920–60.
Sources: 1920–1947: PSCR, PPHA; 1948–1950: Directorate General of Health Services, Report
for the Quadrennium, 1949–1952, 28; 1951–1960: Census of India, 1961. Punjab. District
Handbooks. See S. Zurbrigg, Epidemic Malaria and Hunger in Colonial Punjab (London/New
Delhi: Routledge, 2019), p. 385.
* Plague deaths omitted. For discussion of the 1948–9 dip in vital rates associated with Parti-
tion, see ibid., pp. 386–7.
** Hissar, Rohtak, Gurgaon, Karnal, Amballa, Hoshiarpur, Jullundur, Ludhiana, Ferozepur,
Amritsar, Gurdaspur.

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report lay instead in conveying the authors’ apprehension regarding the eco-
nomic effects of post-war demographic growth in India. Yet their academic
prominence, as in the case of Davis, ensured that their conclusions would
be influential.55 Likewise, the earlier view of Sri Lankan crude death decline
as substantially related to malaria control – upon which the estimates of
lives saved by DDT-based malaria control in India were based – continues to
inform South Asian post-WW2 experience and much contemporary global
health analysis as well.56 In addressing current understanding of modern
South Asian malaria mortality history, then, familiarity with malaria control
in Sri Lanka is a necessary starting point – if risking some tedium in revisiting
earlier debate.

Post-WW2 mortality decline in Sri Lanka (Ceylon)

In the case of Sri Lanka, the thesis that DDT was responsible for much
of the decline in mortality in the immediate post-WW2 period would be
questioned by a number of Sri Lankan analysts. In his 1958 Demography
of Ceylon K.N. Sarkar pointed out that mortality levels on the island
were already in decline before initiation of the DDT spray program in
mid-1946. Economic development programs along with school feeding
and primary health care initiatives were undertaken in the late 1930s
and early 1940s, programs that were greatly expanded in the immediate
post-WW2 period.57 S.A. Meegama notes that neonatal tetanus deaths in
Colombo had declined by 75 per cent in the early years of the twentieth
century and puerperal sepsis deaths by 67 per cent between 1930 and
1939.58 In 1960, Harald Frederiksen, a program officer with the U.S. Pub-
lic Health Service and USAID advisor to the National Malaria Eradica-
tion Programme in India, concurred with Sarkar, pointing out additional
gaps in the Coale-Hoover assessment of DDT’s role. In a series of arti-
cles59 Frederiksen showed that the malaria control explanation failed to
take into account the timing of DDT spraying in different regions of the
country. The major drop in crude death rate in Sri Lanka, he pointed out,
occurred very rapidly between 1946 and 1947 across the island. Both the
malarious and non-malarious regions experienced similar proportionate
declines in mortality between 1945 and 1947 (Table 7.1), although only
28 per cent of the population at that point was covered by the DDT spray
program. Moreover, most of the decline in crude death rate occurred in
the second half of 1946, the July–December death rate for the country
as a whole declining from 21.3 in 1945 to 15.4 in 1946 (Table 7.2), at a
time when only 18 per cent of the population was included in the DDT
program.60
Frederiksen also stressed, as had Sarkar, that death rates were already
in decline pre-DDT, and that some of the major stepwise decline post-war
likely represented resumption of this earlier trend interrupted by the wartime

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Table 7.1 Death rates (all causes) in the malarious and non-malarious areas of
Ceylon [Sri Lanka] during the second semesters, 1944–1948 and 1953

Second semester Malarious area Non-malarious area Ceylon

(spleen rate > 10%) (spleen rate < 10%)
1944 21.0 19.2 19.9
1945 23.8 19.1 20.8
1946 17.6 14.5 15.7
1947 14.6 13.7 14.0
1948 13.6 14.1 13.9
1953 10.9 11.3 11.2
Source: H. Frederiksen, ‘Malaria control and population pressure in Ceylon,’ Public Health
Reports, 75, 10, Oct. 1960, p. 867, Table 4.

Table 7.2 Percentage of population protected against malaria by residual spraying

of insecticides and semestral death rates (all causes), Ceylon, 1944–1953

Semiannual death rates* Percent of population

protected

First semester Second semester

1944 21.6 21.1 0

1945 22.6 21.3 3
1946 25.1 15.4 18
1947 15.2 13.2 28
1948 13.5 13.2 40
1949 13.0 12.1 36
1950 12.3 12.9 35
1951 13.1 12.7 36
1952 12.3 11.7 38
1953 10.8 11.1 36
Source: H. Frederiksen, ‘Malaria control and population pressure in Ceylon,’ Public Health
Reports, 75, 10, Oct. 1960, p. 866, Table 2.

exigencies of plummeting rice imports.61 He went on to identify improve-

ment in a range of economic indicators, among them a substantial rise in
personal consumption between 1938 and 1947.62 Beginning in the final
years of WW2, irrigation development and colonization was undertaken in
the highly malarious dry zone, prompted by the cut-off of rice imports in
late 1942 with the Japanese occupation of Burma.63 Moreover, in the imme-
diate post-war period food security programs were greatly expanded such
that coverage of the wartime program of subsidized rice rations (2 kgs per
person per week) was universal by 1948.64 By that year, 3,500 milk feeding
centres were distributing free milk to pregnant women, infants, and pre-
school children, its beneficial effect reaching ‘colonist’ families in the highly

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malarial dry zone in particular.65 As well, government spending on school

meals increased four-fold between 1943 and 1947 from Rs 1.6 to 7.1 mil-
lion,66 and rural school enrolment rose to over 870,000 children with the
1945 abolition of school tuition fees.67
In other words, far-reaching shifts in food security – and in agricultural
employment in the dry malarious zone – took place in the immediate post-
war period. Though exact timing, month to month, of coverage of such
programs over the 1946–1947 period is unclear, it seems probable that
much of their expansion began in 1946 itself. Additionally, as mentioned
above, the immediate post-war years saw an economic boom in developing
countries, including in Sri Lanka.68 ‘Improvements in the whole range of
economic indices,’ Frederiksen observed, ‘were more or less concurrent with
the decline in the death rate.’69 Nutritional anthropometric data also sup-
ports the view of major improvement in post-war food security, the mean
weight of school children 6 to 18 years of age increasing by 10 per cent
between 1945 and 1950.70 Government health care spending also increased
post-war.71 However, taking inflation into account, Frederiksen estimated
that total health care expenditure in 1947 was still roughly at 1938 levels,
suggesting such services were unlikely to have played a major role in the
abrupt decline in mortality between 1946 and 1947.72

The Newman assessment

Despite much evidence to suggest alternate explanations for Sri Lankan
post-war malaria mortality decline, the DDT thesis has remained prominent
in Western academic literature. In the 1963 edition of Practical Malariol-
ogy, for example, Russell would repeat his earlier assertion as to the role of
DDT, with no mention of the questions raised in 1960 by Frederiksen in the
[U.S.] Public Health Reports.73 In 1965, Peter Newman acknowledged Fred-
eriksen’s critique, but argued that there were too many factors at play in the
key period of 1946–1947 to allow for a ‘disentangling’ of determinants of
death rate decline. He offered instead an indirect method of analysis, one
based on pre-DDT spleen rate levels (1938–1941) in relation to ‘post-1945’
mortality decline in the malarious ‘dry zone’ and non-malarious ‘wet zone’
divisions of the island. Regression analysis, he concluded, showed DDT to
have contributed 42 per cent of post-war mortality decline nationally.74
The Newman analysis was problematic methodologically in a number of
ways, in addition to eschewing the opportunity for direct analysis of timing
of mortality decline in relation to DDT coverage. The validity of the regres-
sion model employed itself was seriously at question where confounding
variables clearly were at play, among them major shifts in food security
pre- and post-1945 associated with government programs and the post-war
economic boom.75 Moreover, use of spleen rate data as a measure of malaria
transmission rates was also questionable, malarial splenic enlargement

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having long been recognized as influenced by socio-economic factors

beyond local malaria transmission levels.76 Langford rightly observes that
‘in some degree improvements in nutrition and general state of health would
be expected to reduce spleen rates, and malaria morbidity, and malaria mor-
tality, even if exposure to the risk of malaria remained unchanged.’77
It would not be until the early 1990s that the questions raised by Fred-
eriksen with respect to post-war mortality decline in Sri Lanka would be
revisited however, this time from the pen of an historical demographer. As
Frederiksen had done, C.M. Langford tracked timing of DDT initiation in
relation to regional patterns of general and infant mortality decline. Like
Sarkar, Langford placed post-war crude death rate decline in the context of
longer-term post-1920 patterns of mortality decline in the country. He also
attempted to take into account expansion in health, anti-malarial, and school
feeding programs over the period from 1930 through to 1954, remarking
that ‘there was clearly a great deal going on’ across the 1936–1949 period in
addition to DDT spraying.78 Even without factoring in post-war economic
expansion or most food security and agricultural support measures (for
which less specific data was available), Langford concluded that DDT inter-
ruption of malaria transmission could explain little of the largest stepwise
drop in mortality, that which occurred between 1946 and 1947. At most,
DDT interruption of malaria transmission on the island might explain some
of the more modest subsequent decline in crude death rate that occurred
between 1948 and 1951 (Langford estimates less than 16 per cent), itself an
assessment based upon counterfactual estimates about potential increase in
malaria mortality in the two subsequent low-rainfall years of 1948–1949
had there been no DDT-spraying, and assuming drought-enhanced transmis-
sion on the island.79 As Langford points out, however, even this post-1947
estimate of DDT impact is open to question for not taking into account very
different conditions of food security and quinine access in the later period.80
Despite the compelling questions raised by analysts such as Frederiksen,
Sarkar, and Langford, the influence of the early literature positing a primary
role for DDT in post-WW2 global mortality decline remains strong, with
1950s malaria transmission control continuing to be cited as a major con-
tributor to post-war mortality decline in South Asia and among low-income
countries in general.81

Privileging the microbiologic

The indirect and highly tenuous statistical modelling approach employed by
Newman to arrive at a microbiological (parasite transmission) explanation
of post-war mortality decline in Sri Lanka contrasts starkly with the casual,
indeed negligible, treatment accorded by the same author to shifts in food
security in post-war Sri Lanka. In this, Newman was not alone. The analytic
invisibility of food security can be seen as well in analysis by R.H. Gray who

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in 1974 reworked the Newman analysis ostensibly to take into account the
methodologically confounding variable of ‘nutrition’ and the question of
longer-term mortality trend.82 Gray acknowledged that possible differences
in nutritional status between the malarious and non-malarious regions of
the country undermined the validity of the regression model employed by
Newman. To rectify the problem, he turned to a 1940–1941 dietary survey
which showed, he suggested, that ‘[i]f anything . . . the endemic areas had
marginally better diets’ than did the ‘wet’ non-malarial zone of the island,83
a conclusion he considered to allow the Newman regression analysis to
stand methodologically.
Given the well-recognized limitations of dietary surveys, the choice of
the 1941 survey as a means of assessing nutritional status is curious84 –
all the more so given that it was conducted over a single 10-day interval in
the post-monsoon agricultural harvest months from late February through
March, a period unlikely to capture the seasonal hunger typical of the dry
endemic zone where only single harvests per year were then feasible.85 The
choice was that much more puzzling in light of the availability of direct
data on nutritional status. A nutritional anthropometry study published in
the same journal in 1949, for example, indicated greater nutritional stunt-
ing prevalence in 1948 among students from the dry malarial zone relative
to the wet zone,86 a finding consistent with abundant accounts of extreme
food insecurity and poverty in much of the dry northern zone of the coun-
try.87 There also was evidence of major post-war improvement in nutritional
status apparently in all regions of the country as Frederiksen had earlier
pointed out, the Director of Health Services reporting a 10 per cent increase
in weight and heights of children between 1945 and 1950.88
What is remarkable here is that despite empirical evidence of substantial
improvement in post-war food security and nutritional status, neither New-
man nor Gray attempted to incorporate these data in their assessment of
post-war mortality decline in Sri Lanka.89 It is difficult to avoid the conclu-
sion that the 1941 dietary survey was employed in the latter’s analysis not so
much to investigate shifts in hunger, but rather to set aside methodological
concerns relating to a confounding influence of food security in the origi-
nal Newman analysis. Notwithstanding serious limitations to the Newman-
Gray analyses, Samuel Preston, a leading U.S. demographer and economist,
concluded in 1975 that Frederiksen’s ‘arguments have been convincingly
refuted by Newman.’90 From there, the Newman analysis has continued to
appear in contemporary literature, interpreted as confirming a substantial
role for DDT in post-war Sri Lankan mortality decline.91
The first half of the twentieth century was a seminal period in the health
history of the Sri Lankan people. In the years immediately preceding initia-
tion of the DDT spray program, there were dramatic shifts in food security
brought about by social welfare policies, resumption of pre-war levels of
foodgrain imports, and the post-war boom in economic growth. These years

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brought employment growth, food rationing programs, and undoubtedly

also subtle but key shifts in conditions of women’s work affecting child
care and feeding, above all in the dry zone of the country. A major impact
of these policies is suggested in improved nutritional anthropometric indi-
ces, as noted above. Improvement is seen as well in decline in those causes
of infant mortality associated with severe hunger.92 With the exception of
the work of Frederiksen, however, there has been a near-complete absence
of investigation of food security trends across the period of post-war Sri
Lankan mortality decline in Western demographic and health literature, a
neglect that stands in contrast to analysis by Sri Lankan historians.93
We have seen the invisibility of human subsistence in malaria control
analysis before, in relation to the construction of the Panama Canal. Frank
Snowden suggests a similar omission of economic factors in accounts of the
WW2 malaria control campaign in Italy.94 Once the global residual insecti-
cide program had begun, assumptions with respect to mortality impact came
to be more or less ‘locked in’ – slipping into certitude within the broader
historiographical domain.95 Yet even before the era of residual insecticides,
an academic privileging of the ‘germ’ side of the epidemic equation was evi-
dent in relation to the 1934–1935 Sri Lankan epidemic, as seen in chapter
two. In his analysis of the epidemic presented to the Royal Society of Medi-
cine meeting in November 1935, Briercliffe, chief medical officer of colonial
Ceylon, omitted any reference to destitution, though his administration had
been fully occupied throughout the epidemic with famine relief efforts in
addition to malaria treatment. Interestingly, included in Briercliffe’s Royal
Society presentation was a photograph of a young child in a state of extreme
emaciation (marasmus) with typical signs of skeletal upper arm circumfer-
ence and hair depigmentation. The photo revealed the classic lower-body
swelling (‘kwashiorkor’) of end-stage starvation, yet was entitled ‘Child
with post-malarial oedema.’96 One year later, Lewis Hackett, a leading pro-
ponent of vector control with the Rockefeller Foundation, suggested in his
prominent text, Malaria in Europe, that

[e]pidemics of any disease seem to develop a sinister character which

tempts observers to assume either an unusual susceptibility on the
part of the population produced by famine, economic stress etc. . . .
We no longer resort to any influence more mysterious than summer
heat, an abundance of anopheles, and a few good infectors . . . [that
allow] new infection [to] increase by geometrical progression.97

Unintentionally perhaps, Hackett here epitomizes the wider epistemic shift

where consideration of ‘social’ factors in epidemic disease causation is now
seen as unscientific (‘mysterious’) and unprofessional.
Clearly, this is not to suggest that malaria transmission in Sri Lanka was
innocuous among the well-fed. Malaria’s inherent case fatality rate is not

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 ALLURE, LEGACIES OF THE GERM PARADIGM

negligible, particularly falciparum malaria among the non-immune, above

all in regions of intense holoendemic transmission. It is a toll that includes
substantial stillbirth risk among pregnant women as well – if here too the
historical mortality toll in South Asia appears to have risen markedly under
conditions of food crisis. Yet in assessing historical determinants of malaria
mortality decline, the question, Frederiksen reminds us, ‘is not whether
malaria is a potential killer but whether malaria control actually had a
major role in the dramatic post-war island-wide reduction in mortality in
Ceylon.’98 Empirical evidence from South Asia suggests it did not. Indeed,
post-WW2 experience in Sri Lanka has direct parallels with that in Punjab
one decade later where little evidence exists of substantial mortality decline
with the 1950s DDT-based interruption of malaria transmission in the
state.99 Nor is the view of malaria as the ‘great debilitator’ (in the absence
of acute hunger-debility) supported by subsequent mortality patterns with
the resurgence of malaria transmission from the late 1960s in Sri Lanka or
India.100 It is Frederiksen’s larger question that frames the conclusions of
this study.

Notes
1 R. Ross, ‘Malaria Prevention at Mian Mir,’ Lancet, Jul. 3, 1909, 43–45. See
S. Zurbrigg, Epidemic Malaria and Hunger in Colonial Punjab: ‘Weakened by
Want’ (London and New Delhi: Routledge, 2019), 245. For similar pressures
evident in the 1950 debate regarding extension of residual insecticide-based
malaria transmission control programs to holoendemic regions in Africa, see
WHO Registry files. WHO.2.DC.Mal.2. Africa Reports, 3, as cited in M.J. Dob-
son, M. Malowany, and R.W. Snow, ‘Malaria Control in East Africa: The Kam-
pala Conference and Pare-Taveta Scheme: A Meeting of Common and High
Ground,’ Parassitologia, 42, 149–166, 2000, 157–158.
2 On the food and labour policy changes initiated by Gorgas, see Zurbrigg, Epi-
demic Malaria and Hunger, 230; S.R. Christophers, and C.A. Bentley, Malaria
in the Duars: Being the Second Report to the Advisory Committee Appointed
by the Government of India to Conduct an Enquiry regarding Black-water and
Other Fevers Prevalent in the Duars (Simla: Government Monotype Press, 1911),
56–57; P. Hehir, Malaria in India (Oxford: Oxford University Press, 1927), 9.
3 ‘Perhaps after the great demonstrations are over and money begins to fail a lit-
tle,’ Lewis Hackett would surmise regarding potential waning public interest in
continued DDT spraying in rural Kanara district, India, ‘the control of malaria
could be continued with the collateral effect on flies, cockroaches, fleas, lice
and all the insects which we have including also some mammals like bats and
mice which seem to disappear at the same time’; L. Hackett, Proceedings of the
Fourth International Congresses on Tropical Medicine and Malaria, Washing-
ton, D.C., May 10–18, 1948, vol. 2, 879.
4 W. Bynum, and C. Landry, The Western Medical Tradition: 1800 to 2000 (Cam-
bridge: Cambridge University Press, 2006), 239.
5 R. Ross, Memoirs: With a Full Account of the Great Malaria Problem and Its
Solution (London: Murray, 1923), 115. In McLeod’s colourful phrasing, the his-
tory of tropical medicine is written in ‘the language of military and political

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conquest; the history of conflict in biblical dimensions, between the heroic

endeavours of human beings and the vast microscopic armies and resources of
the animal kingdom. Memoirs of tropical doctors are the journals of medical
Caesars confronting microbial Gauls’; R. Macleod, and M. Lewis, eds., Disease,
Medicine and Empire: Perspectives on Western medicine and the experience of
European expansion (London: Routledge, 1988), 6.
6 R. Packard, and P. Gadehla, ‘A Land Filled with Mosquitoes: Fred L. Soper, the
Rockefeller Foundation, and the Anopheles Gambiae Invasion of Brazil,’ Medi-
cal Anthropology, 17, 1994, 215–238, at 233.
7 P. Manson, Tropical Diseases: A Manual of the Diseases of Warm Climates
(London: Cassell, 1898), xvi.
8 M. Worboys, ‘Germs, Malaria and the Invention of Mansonian Tropical Med-
icine: From “Diseases in the Tropics” to “Tropical Diseases”,’ in D. Arnold,
ed., Warm Climates in Western Medicine: The Emergence of Tropical Medicine,
1500–1900 (Amsterdam: Redopi, 1996), 181–207 at 195. Arnold notes similar
professional opportunities in nutritional science; ‘The “Discovery” of Malnutri-
tion and Diet in colonial India,’ Indian Economic and Social History Review, 31,
1, 1994, 1–26, at 17.
9 G. Harrison, Mosquitoes, Malaria and Man: A History of the Hostilities since
1880 (New York: E.P. Dutton, 1978), 198, 208; S. Litsios, The Tomorrow of
Malaria (Wellington, NZ: Pacific Press, 1996), 61. S.P. James and E. Brumpt
would both question shifts in vector species and human exposure associated with
agriculture modernization as the explanation for the disappearance of malaria in
Europe; S.P. James, ‘The Disappearance of Malaria from England,’ Proceedings
of the Royal Society of Medicine, 23, 1, Nov. 1929, 71–87; E. Brumpt, ‘Ano-
phélisme sans paludisme et régression spontanée du paludisme,’ Ann. Parasit.
hum. comp., 20, 1944, 67–91.
10 Worboys notes the late nineteenth-century ‘relative decline in the influence of
epidemiology [that] signaled declining interest in social factors, as disease was
constituted in relations between bacteria and individual bodies where personal
behaviour, not social structures and social relations, determined the balance of
disease and health’; M. Worboys, Spreading Germs: Disease Theories and Medi-
cal Practice in Britain (Cambridge: Cambridge University Press, 2000), 285.
11 R. Packard, and P.J. Brown, ‘Rethinking Health, Development, and Malaria:
Historicizing a Cultural Model in International Health,’ Medical Anthropology,
17, 1997, 181–194, at 191–192.
12 N.H. Swellengrebel, ‘Some Aspects of the Malaria Problem in Italy,’ in League
of Nations Malaria Commission, Report on its Tour of Investigation in Certain
European Countries in 1924 (Geneva: League of Nations, 1925), Annex 11,
168–171, at 171. See ch. 1 at note 44.
13 S. Amrith, ‘Political Culture of Health in India: A Historical Perspective,’ Eco-
nomic and Political Weekly, Jan. 13, 2007, 114–121.
14 Hackett to Russell, October 18 and November 3, 1924; cited in J. Farley,
To Cast Out Disease: A History of the International Health Division of the
Rockefeller Foundation (1913–1951) (New York: Oxford University Press,
2004), 118.
15 L. Hackett, Malaria in Europe: An Ecological Study (London: Oxford University
Press, 1937), 320. Prefacing his 1937 text as an effort for ‘reconciliation of these
two points of view,’ Hackett acknowledged the distinction between malaria
infection and debilitating disease, yet returned to a singular concern with trans-
mission, concluding, ‘[t]here has never been any indication that malaria will
spontaneously die out under such conditions’: returning, in other words, to the

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view that infection per se was the principal problem and its interruption needed
to be the goal; ibid., xiv–xvi. Hackett’s argument parallels that expressed by
Chadwick’s sanitarian colleagues, that ‘filth was the [factor] most easily rem-
edied’; C. Hamlin, ‘Predisposing Causes and Public Health in Early Nineteenth-
Century Medical Thought,’ Society for the Social History of Medicine, 5, 1, Apr.
1992, 43–70, at 66.
16 P. Russell, L.S. West, and R.D. Manwell, Practical Malariology (Philadelphia:
W.B. Saunders, 1946), 555. Yet, arguably, even here, the socio-economic and
basic chemotherapy route for removing or abating the mortality-morbidity bur-
den of malaria was hardly long, as seen in the case of Italy or indeed even Pun-
jab, though such measures were not within the direct power of the consultant
vector eradicationist.
17 Litsios notes that ‘the Cold War undermined the possibility of addressing
politically sensitive issues, such as rural indebtedness and iniquitous land ten-
ure systems’; ‘Malaria Control, the Cold War, and the Postwar Reorganization
of International Assistance,’ Medical Anthropology, 17, 1997, 255–278, at
267–271. See also R. Packard, ‘Malaria Dreams: Postwar Visions of Health and
Development in the Third World,’ Medical Anthropology, 17, 1997, 279–296;
S. Amrith, Decolonizing International Health: India and Southeast Asia, 1930–
65 (Basingstoke: Palgrave Macmillan, 2006), 83–85; J. Siddiqui. World Health
and World Politics: The World Health Organization and the UN System (Lon-
don: Hurst, 1995); H. Cleaver, ‘Malaria and the Political Economy of Public
Health,’ International Journal of Health Services, 7, 4, 1977, 557–79 at 568–73
[hereafter, IJHS]; J. Farley, Brock Chisholm, the World Health Organization,
and the Cold War (Vancouver: University of British Columbia Press, 2008); J.A.
Gillespie, ‘Social Medicine, Social Security and International Health, 1940–60,’
in The Politics of the Healthy Life: An International Perspective (Sheffield: Euro-
pean Association for the History of Medicine and Health, 2002), 219–239.
18 Farley, To Cast Out Disease, 296.
19 J. Ettling, The Germ of Laziness: Rockefeller Philanthropy and Public Health
in the New South (Cambridge, MA: Harvard University Press, 1981), 185. See
also, E. Richard Brown, ‘Public Health in Imperialism: Early Rockefeller Pro-
grams at Home and Abroad,’ American Journal of Public Health, 66, 9, 1976,
897–903 [hereafter, AJPH]; J.C. Goulden, The Money Givers (New York: Ran-
dom House, 1971), ch. 2.
20 Ettling, Germ of Laziness, 206–208. Likewise, it is impossible to doubt Paul
Russell’s belief in the technological approach, if deeply shaped by ideological
geopolitical views. His personality was complex: for example, he criticized neo-
Malthusian arguments of colleagues who argued against malaria eradication
over population ‘explosion’ concerns. As an ardent eradication proponent, Rus-
sell’s rejection of that argument was of course logically required. But he went
further, to include a relatively sophisticated (in the prevailing Western academic
climate) articulation of demographic transition, an exposition on the economic
need for children under conditions of poverty and precarious survival; in Man’s
Mastery of Malaria, 254. Russell would also warn against exclusive reliance
on insecticides, and even acknowledged in 1936, if obliquely, the importance
of drainage as an economic measure. Yet it is difficult to square this with the
concerted exclusion of socio-economic perspective in policy formation within
the ECM.
21 Over half of all Foundation funding between 1925 and the late 1930s was chan-
nelled to yellow fever research and programs; Farley, To Cast Out Disease,
88. Arguably Rockefeller Foundation funding of the LNHO reflected a similar

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interest in protecting global trade, where a large portion of its work was directed
to epidemiological surveillance, and standardization of microbiologic measure-
ments, all congruent with the Rockefeller Foundation germ philosophy but also
with rampant U.S. fears of imported microbes. At the first meeting of the trustees
of the newly formed Rockefeller Foundation in 1913, concern over immigrant
hookworm carriers loomed large: ‘Every Indian coolie already in California was
a center from which the infection continued to spread throughout the state’;
Farley, To Cast Out Disease, 4.
22 In 1906, William H. Welch, the first dean of the Johns Hopkins Medical School
and its School of Hygiene and Public Health, would praise the facilitating role of
medical science in European and American ‘efforts to colonize and to reclaim for
civilization vast tropical regions’; H.H. Welch, ‘The Benefits of the Endowment
of Medical Research,’ in Addresses Delivered at the Opening of the Laboratories
in New York City, May 11, 1906 (New York: Rockefeller Institute for Medical
Research, 1906); as cited in Brown, ‘Public Health in Imperialism,’ 902.
23 J.S. Simmons, ‘Welcoming Address at the Conference on Industry and Tropi-
cal Health. Conference Proceedings, Industry and Tropical Health,’ Industry
and Tropical Health 1, 12; as cited in Packard, ‘Malaria Dreams,’ 282. See also
Marcos Cueto, Cold War, Deadly Fevers: Malaria Eradication in Mexico, 1955–
1975 (Washington, D.C.: Woodrow Wilson Centre Press, 2007), 49–69. Rieff
notes Andrew S. Natsios, head of USAID and former vice president of World
Vision, describing USAID as ‘ “a key foreign policy instrument . . . an important
tool for the President to further America’s interests . . . help[ing] nations prepare
for participation in the global trading system and become better markets for U.S.
exports” ’; A Bed for the Night: Humanitarianism in Crisis (New York: Simon
and Schuster, 2002), 236–237, 120.
24 R. Packard, ‘Visions of Postwar Health and Development and Their Impact on Pub-
lic Health Interventions in the Developing World,’ in F. Cooper, and R. Packard,
eds., International Development and the Social Sciences: Essays on the History and
Politics of Knowledge (Berkeley: University of California Press, 1997), 93–115.
25 S. Franco-Agudelo, ‘The Rockefeller Foundations’ Antimalarial Program in
Latin America: Donating or Dominating?,’ IJHS, 13, 1, 1983, 51–67 at 59–60,
at 64. Packard observes ‘tropical disease control quickly became viewed as a
critical weapon in the war against international Communism. . . . Malaria con-
trol programs were defined by the US Special Technical and Economic Missions
to Vietnam and Thailand as “impact programs” . . . designed to have a rapid
positive effect on local populations in order to build support for local govern-
ments and their US supporters’; ‘Malaria Dreams,’ 282–283.
26 P.F. Russell, Man’s Mastery of Malaria (London: Oxford University Press, 1955),
221. Russell recounts the strategic origins of U.S. malaria control programs in
1940 in 18 Latin American countries, prompted by concerns for ensuring ‘stra-
tegic materials’; ibid., 222–227. A summary account of the economic and mili-
tary benefits accruing to the United States with global malaria control, including
elimination of a $175 million annual ‘malaria tax’ on resource imports (malaria-
related increased production costs) from developing countries, is given in P.F
Russell, ‘A Lively Corpse,’ Tropical Medicine News, Jun. 5, 1948, 25.
27 Cleaver, ‘Malaria and the Political Economy of Public Health.’ Roger Jeffrey has
estimated that, in the period 1950–1959, foreign aid to India accounted for 14 per
cent of the total expenditure on health. ‘Of this the UN (WHO and UNICEF) . . .
accounted for only 15 per cent, most of the remainder coming from U.S. bilateral
aid to India, channeled through the Public Law 480 programme’; The Politics of
Health in India, (Berkeley: University of California Press, 1988), 102.

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28 D.K. Viswanathan, The Conquest of Malaria in India: An Indo-American

Co-operative Effort (Madras: Law Institute Press, 1958), 3–4, 58. See also K.
Mankodi, ‘Political and Economic Roots of Disease: Malaria in Rajasthan,’
Economic and Political Weekly, Jan. 27, 1996, PE42–48; D. Kinkela, DDT
and the American Century: Global Health, Environmental Politics, and the
Pesticide That Changed the World (Chapel Hill: University of North Carolina
Press, 2011). Packard cites early 1950s Iran as ‘caught in a serious political
upheaval’ involving the 1953 U.S.-assisted overthrow of the Mossadegh govern-
ment, with a 1956 International Development Advisory Board report suggest-
ing that ‘ “the malaria component of the U.S. technical assistance program . . .
play[ed] an important role in supporting our diplomatic representations with a
concrete manifestation of our sincerity and mutual interest” ’; ‘Visions of Post-
war Health,’ 98–99.
29 Amrith, ‘Political Culture of Health in India,’ 118. For a similar pattern in Latin
America, see M. Cueto, ‘The Cycles of Eradication: The Rockefeller Foundation
and Latin American Public Health, 1918–1940,’ in P. Weindling, International
Health Organisations and Movements, 1918–1939 (Cambridge: Cambridge
University Press, 1995), 222–243, at 228.
30 A. Hooton, Major IMS, Agency Surgeon, Kathiawar, letter to the Indian Medical
Gazette, April 24, 1909, in Transactions of the Bombay Medical Congress, 93.
See Zurbrigg, Epidemic Malaria and Hunger, 264–265.
31 Ibid., 225–226, 265.
32 Hamlin, Public Health and Social Justice in the Age of Chadwick (Cambridge:
Cambridge University Press, 1998), 338.
33 Ibid., 157.
34 C. Hamlin, ‘Could You Starve to Death in England in 1839? The Chadwick-Farr
Controversy and the Loss of the “Social” in Public Health,’ AJPH, 85, 6, Jun.
1995, 856–866.
35 ‘Dominated solely by the actuarial problems of pecuniary profit and loss, Chad-
wick laid no claims to universal humanitarianism but frankly admitted his nar-
row interests in keeping the poor rates down’; S.E. Finer, The Life and Times of
Sir Edwin Chadwick (New York: Barnes and Noble, 1952), 157.
36 Margaret Jones recounts how reluctance on the part of the new indigenous gov-
ernment in Sri Lanka in the early 1930s to pursue aggressive weekly oiling of
municipal cesspools and stocking wells with larvivorous fish had ‘enabled hostile
commentators at the metropolitan centre to place responsibility for the loss of
life in 1934–35 at the feet of the new government . . . elected three years before’;
Health Policy in Britain’s Model Colony: Ceylon, 1900–1948 (New Delhi: Ori-
ent Longman, 2004), 187. Rieff observes a modern parallel, the ‘humanitarian’
content of development assistance ‘serv[ing] to immunize the public against any
political questioning’; A Bed for the Night, 170.
37 Hamlin, ‘Public Health and Social Justice,’ 289 [emphasis added].
38 Rieff observes in relation to recent USAID military-aid in Afghanistan that ‘[t]
he mainline relief agencies depend largely on young people who work on short
contracts . . . and quickly get back to start real careers’; A Bed for the Night,
236–237, 120.
39 S.P. James, Presidential Address, ‘Advances in Knowledge of Malaria Since the
War,’ Transactions of the Royal Society of Tropical Medicine and Hygiene, 31,
3, Nov. 1937, 263–280, at 276.
40 Harrison, Mosquitoes, Malaria and Man, 140. There were of course instances
where technical assistance was appropriate. Amrith for example describes a
technical assistance agreement between the GOI, WHO and UNICEF signed in

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July 1951 for construction of a penicillin factory near Pune, production begin-
ning in 1955; Decolonizing International Health, 105.
41 ‘The Rockefeller Foundation phased out its International Health Division in
1951, merging it with the medical sciences program’; P. Weindling, ‘American
Foundations and the Internationalizing of Public Health,’ in S. Gross Solo-
mon, L. Murand, and P. Zylberman, eds., Shifting Boundaries in Public Health:
Europe in the Twentieth Century (Rochester: University of Rochester Press,
2008), 63–85, at 79. A June 1951 Rockefeller Foundation report concluded:
‘The problem of food has become one of the world’s most acute and press-
ing problems; and . . . is the cause of much of the world’s present tension and
unrest. . . . Agitators from Communist countries are making the most of the
situation. The time is now ripe, in places possibly over-ripe, for sharing some of
our technical knowledge with these people. Appropriate action now may help
them to attain by evolution the improvements, including those in agriculture,
which otherwise may have to come by revolution’; ‘The World Food Problem,
Agriculture, and the Rockefeller Foundation,’ by Advisory Committee for Agri-
cultural Activities, June 21, 1951, RG 3, series 915, box 3, folder 23, Rockefeller
Foundation Archives; as cited in J.H. Perkins, Geopolitics and the Green Revo-
lution: Wheat, Genes, and the Cold War (New York: Oxford University Press,
1997), 138–139. Perkins concludes ‘[t]his specific report was instrumental in
leading the Rockefeller Foundation to start its Indian Agricultural Program. . . .
American plant-breeding science thus became part of the cold war’s defense of
capitalist political economies,’ although the Rockefeller Foundation was already
engaged in funding Borlaug’s hybrid grain research by the early 1940s; ibid.,107.
For a detailed account of the Foundation’s influence in population analysis in
India, see M. Rao, From Population Control to Reproductive Health: Malthu-
sian Arithmetic (New Delhi: Sage, 2004), 27, 106–111.
42 A century earlier the vice-chairman of the Cockermouth [Poor Law] Union
lamented, Hamlin recounts, that ‘[t]he people themselves are inert. . . . Their
thoughts are engrossed by the great business of finding daily food; and they will
not listen to any lectures upon the theory of infection, or the connexion [sic]
between dirt and disease’; Public Health and Social Justice, 204.
43 Farley observes that it was only in 1926, following failure to eradicate hook-
worm infection in the U.S. South and after international malaria control activi-
ties were well underway, that a statistician was appointed to the IHB to begin
analysis of projects’ effectiveness, to dubious account; To Cast Out Disease,
112–113, 120, 176.
44 See above, ch. 4, note 4.
45 With the claims of the sanitationist portrayed as simple common sense, Hamlin
observes, ‘their confirmation by independent inquirers has not seemed particu-
larly problematic to historians’; Public Health and Social Justice, 220, 160–161.
46 ‘Virtually nowhere,’ Packard observes, ‘was research conducted to investigate
local conditions, or to study in a scientific manner the relative effectiveness of
various approaches. The “R” word was not to be spoken and research activities
were certainly not funded’; ‘Malaria dreams,’ 290.
47 K. Davis, ‘The Population Specter: Rapidly Declining Death Rate in Densely
Population Countries: The Amazing Decline of Mortality in Underdeveloped
Areas,’ American Economic Review, 46, 2, 1956, 305–318, at 311. Davis’s
source for his DDT conclusion was H. Cullumbine, ‘An Analysis of the Vital
Statistics of Ceylon,’ Ceylon Journal of Medical Science, Dec. 1950, 134–135;
possibly also, E.J. Pampana, who by 1951 had concluded: ‘Il semble donc évi-
dent que cette baisse doit être en grande partie mise au crédit du DDT,’ in ‘Lutte

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antipaludique par les insecticides à action rémanents: résultats des campagnes

antipaludiques,’ Bull. Org. Mond. Santé, 3, 557–619, at 592. In neither arti-
cle was analysis of timing and location of mortality decline in relation to DDT
spraying offered.
48 Davis, ‘The Population Specter,’ 312; also, Pampana, ‘Lutte antipaludique,’ 600.
49 P.F. Russell, Man’s Mastery of Malaria (London: Oxford University Press, 1955),
167, 244. Early on, G. Macdonald offered a similar interpretation: ‘A similar
reduction [with malaria control], from 31.8 to 15.4 per 1000, has been seen in
the notorious North Central Province of Ceylon, which has for long been one
of the most malarious parts of that country’; ‘Community Aspects of Immunity
to Malaria,’ British Medical Bulletin, 8, 1951, 33–36, reprinted in L. Bruce-
Chwatt, and V.J. Glanville, eds., Dynamics of Tropical Diseases: The Late
George Macdonald (London: Oxford University Press, 1973), 77–84, at 84.
50 F.J. Dy, ‘Present Status of Malaria Control in Asia,’ Bulletin of the WHO, 11,
1954, 725–763, at 726, 736. This interpretation is puzzling given that the full
complement of Sri Lankan mortality data had been sent, Frederiksen relates, to
WHO officials in Bangkok for the 1953 conference and 1954 Taipei conference;
H. Frederiksen, ‘Malaria Control and Population Pressure in Ceylon,’ Public
Health Reports, 75, 10, Oct. 1960, 865–868. See also ‘First Asian Malaria Con-
ference in September 1953,’ Chronicle of the WHO, 8, 4, Apr. 1954, 117–123,
at 120.
51 A.J. Coale, and E.M. Hoover, Population Growth and Economic Development
in Low Income Countries: A Case Study of India’s Prospects (Princeton: Prince-
ton University Press, 1958), 62–67. A subsequent analysis of the 1950s Indian
malaria eradication program (MEP) was limited to assessing the ‘costs and ben-
efits’ of eradication versus simply ongoing control; E.J. Cohn, ‘Assessing the
Costs and Benefits of Anti-Malarial Programs: The Indian Experience,’ AJPH,
63, 12, Dec. 1973, 1086–1096, at 1095.
52 Coale, and Hoover, Population Growth and Economic Development, 14–15,
62, 65. The 2 million figure is also J.A. Sinton’s estimate in the mid-1930s; in
‘What malaria costs India, nationally, socially and economically,’ Records of the
Malaria Survey of India, 5, 3, Sept. 1935, 223–264, at 256, and that cited by
Paul Russell in 1941; ‘Some Social Obstacles to Malaria Control,’ Indian Medi-
cal Gazette, Nov. 1941, 681–690. One-quarter of all fever deaths, it appears,
was assumed due to malaria, an estimate first offered in the pre-1909 period. On
this, see Zurbrigg, Epidemic Malaria and Hunger, 102.
53 For discussion of possible factors contributing to this marked step-wise decline,
see Zurbrigg, Epidemic Malaria and Hunger, ch. 12.
54 T. Dyson and M. Murphy, ‘Macro-level Study of Socioeconomic Development
and Mortality: Adequacy of Indicators and Methods of Statistical Analysis,’ in
J. Cleland, and A. Hill, eds., The Health Transition: Methods and Measures.
Health Transition Series No. 3 (Canberra: Australian National University,
1991), 147–164, at 153. For analysis of economic and food security conditions
in post-WW2 Punjab, see Zurbrigg, Epidemic Malaria and Hunger, 389–394.
55 See, e.g., R.P Sinha, Food in India: An Analysis of the Prospects for Self-
Sufficiency by 1975–76 (Delhi: Oxford University Press, 1961), 39.
56 Harrison, Mosquitoes, Malaria and Man, 229; S. Anand, and R. Kanbur, ‘Public
Policy and Basic Needs Provision: Intervention and Achievement in Sri Lanka,’
in J. Drèze, and A. Sen, eds., The Political Economy of Hunger (Oxford: Claren-
don, 1991), vol. 3, 59–92 at 63–64; L.T. Ruzicka, and H. Hansluwka, ‘Mortality
in Selected Countries of South and East Asia,’ in WHO, ed., Mortality in South
and East Asia: A Review of Changing Trends and Patterns, 1950–1975 (Manila:

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 ALLURE, LEGACIES OF THE GERM PARADIGM

World Health Organization), 1982, 83–155, at 123, in WHO, Mortality in

South and East Asia: A Review of Changing Trends and Patterns, 1950–1975
(Manila: World Health Organization, 1982); D.F.S. Fernando, ‘Health Statistics
in Sri Lanka, 1921–80,’ in S.B. Halstead, et al., eds., Good Health at Low Cost
(New York: Rockefeller Foundation, 1985), 85; P. Jha, and A. Mills, Improving
Health Outcomes of the Poor: The Report of the Working Group 5 of the Com-
mission on Macroeconomics and Health (Geneva: World Health Organization,
2002), 38; M. Worboys, ‘Colonial Medicine,’ in R. Cooter, and J. Pickstone,
eds. Medicine in the Twentieth Century (Amsterdam: Harwood Academic Publ.,
2000), 79; R. Packard, The Making of a Tropical Disease (Baltimore: Johns
Hopkins University Press, 2007), 146.
57 K.N. Sarkar, The Demography of Ceylon (Colombo: Govt Press, 1958), at 123.
58 S.A. Meegama, ‘The Decline in Maternal and Infant Mortality and its relation
to Malaria Eradication,’ Population Studies, 23, 2, 1969, 289–302. Together,
if such efforts were extended widely beyond the urban population through the
1940s they potentially could have reduced infant mortality rate by as much as
40 per 1,000 live births, assuming near-universal mortality among those infants
without access to breastfeeding in cases of maternal deaths.
59 H. Frederiksen, ‘Malaria Control and Population Pressure in Ceylon,’ Public
Health Reports, 75, 10, Oct. 1960, 865–868; H. Frederiksen, ‘Determinants and
Consequences of Mortality Trends in Ceylon, Public Health Reports, 76, 8, Aug.
1961, 659–663; H. Frederiksen, ‘Economic and Demographic Consequences of
Malaria Control in Ceylon,’ Indian Journal of Malariology, 16, 4, Dec. 1962,
370–391; H. Frederiksen, ‘Dynamic Equilibrium of Economic and Demographic
Transition,’ Economic Development and Cultural Change, 14, 1, Oct. 1965,
316–322; H. Frederiksen, Book Review of P. Newman, ‘Malaria Eradication and
Population Growth 1965,’ American Journal of Tropical Medicine and Hygiene,
15, 2, 1966, 262–264; H. Frederiksen, ‘Determinants and Consequences of Mor-
tality and Fertility Trends,’ Public Health Reports, 81, 8, Aug. 1966, 715–727;
H. Frederiksen, ‘Malaria Eradication and the Fall of Mortality: A Note,’ Popula-
tion Studies, 24, 1, Mar. 1970, 111–113.
60 Frederiksen, ‘Malaria Control and Population Pressure,’ at 866, Table 2. Wer-
nsdorfer also supported Frederiksen’s analysis, noting that ‘[i]n the non-malar-
ious areas the average [death rate] decrease was 30.6%, in the malarious areas
33.5%. This difference is statistically significant (p < 0.001) but in absolute terms
it would account for only 784 lives saved from malaria during the second semes-
ter of 1953, representing some 1.7% of deaths from all causes and certainly
not enough to explain the major drop in mortality rates’; ‘Social and Economic
Aspects,’ 1434, in W.H. Wernsdorfer, and I.A. McGregor, eds., Malaria: Princi-
ples and Practice of Malariology (Edinburgh: Churchill Livingstone, 1988), vol.
2, 913–998.
61 Frederiksen, ‘Determinants and Consequences of Mortality Trends in Cey-
lon,’ 659. Per capita food imports, primarily rice, declined by 25 per cent in
1942–1943 relative to pre-war levels following the 1942 Japanese occupation
of Burma, triggering hyperinflation similar to that in Bengal; Frederiksen, ‘Eco-
nomic and Demographic Consequences,’ 380, 383. Meyer suggests the 1934–
1935 malaria epidemic marked a turning point in accountable governance in Sri
Lanka; E. Meyer, ‘L’Épidémie de malaria de 1934–1935 à Sri-Lanka: Fluctua-
tions économiques et fluctuations climatiques,’ Cultures et Développement, 14,
2–3, 1982, 183–226, at 186; 14, 4, 589–638, at 629–633.
62 Frederiksen, ‘Determinants and Consequences of Mortality Trends,’ 661–662,
Table 5.

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 ALLURE, LEGACIES OF THE GERM PARADIGM

63 With marked decline in rice imports in 1942, government ‘[i]nvestment on peas-

ant colonisation schemes in the dry zone was increased, and the range of free
services given by government to the colonists expanded well beyond what had
been envisaged in 1939’; K.M. De Silva, A History of Sri Lanka (Delhi: Oxford
University Press, 1981), 472. As in Punjab a war-economy boom was felt in Sri
Lanka ‘with Sri Lanka the main source of natural rubber for the Allied powers
after the Japanese overran Malaya and the Dutch East Indies,’ and Sri Lanka
established as the South East Asia Command with its network of bases on the
island; ibid., 470–471. Severe drought and harvest failure in 1945–1946, how-
ever, triggered a ‘sharp rise in the death rate from starvation, malnutrition and
malaria’; S.A. Meegama, ‘Malaria Eradication and its Effect on Mortality Lev-
els,’ Population Studies 21, 3, Nov. 1967, 207–237, at 217.
64 De Silva, A History of Sri Lanka, 470–472; W.A.A.S. Peiris, Socio-Economic
Development and Fertility Decline in Sri Lanka (New York: United Nations,
Dept. International Economic and Social Affairs, 1986), 57–58. On food ration-
ing in Sri Lanka, see P. Isenman, ‘Basic Needs: The Case of Sri Lanka,’ World
Development, 8, 1980, 237–258.
65 Imports of milk and milk foods into Ceylon rose exponentially from 2,184,000
lbs in 1942 to 8,112,000 in 1945, then to 28,880,000 lbs by 1947; Meegama,
‘Malaria Eradication and its Effect on Mortality Levels,’ 213, 222.
66 C. Langford, ‘Reasons for the Decline in Mortality in Sri Lanka Immediately
after the Second World War: A Re-Examination of the Evidence,’ Health Transi-
tion Review, 6, 1993, 3–23, at 15.
67 De Silva, A History of Sri Lanka, 198, 475.
68 Dyson and Murray, ‘Macro-level study of socioeconomic development and
mortality.’
69 Frederiksen, ‘Economic and demographic consequences,’ 386. Frederiksen was
not criticizing the program itself. As USAID consultant, by the mid-1960s he was
actively involved with the National Malaria Eradication Programme in India and
applauded both the reduced morbidity from the disease and increase in dry zone
acreage under cultivation; ‘Economic and demographic consequences,’ 391. Indeed,
a major concern for him, Litsios points out, was to refute the pessimism emerging
from Western analysts who, under a neomalthusian perspective, questioned DDT
programs as precipitating a population explosion that would ‘overwhelm result-
ing economic gains’; S. Litsios, ‘Malaria Control and Future of International Pub-
lic Health,’ in E. Casman, H. Dowlatabadi, eds., The Contextual Determinants of
Malaria (Washington, D.C.: Resources for the Future, 2002), 292–328 at 316.
70 Frederiksen, ‘Determinants and Consequences of Mortality Trends,’ 661.
71 Health expenditures increased from Rs 12.9 million in 1939 to 37.2 million in
1947, by 1952 reaching 82.5 million; Langford, ‘Reasons for the decline in mor-
tality in Sri Lanka,’ 15.
72 Frederiksen, ‘Mortality Rates and Economic Development,’ 17; Frederiksen,
‘Determinants and Consequences of Mortality Trends,’ 661–662.
73 P. Russell, L.S. West, R.D. Manwell, and G. Macdonald, Practical Malariol-
ogy (London: Oxford University Press, 1963), 501. One decade later, this view
would appear in an official Sri Lankan government report; The Population of Sri
Lanka (Colombo: Dept of Census and Statistics, 1974), 5.
74 P. Newman, Malaria Eradication and Population Growth with Special Ref-
erence to Ceylon and British Guiana, Bureau of Public Health Economics,
Research Series No. 10, School of Public Health (Ann Arbor: University of
Michigan, 1965), 157; P. Newman, ‘Malaria Control and Population Growth,’
Journal of Development Studies, 6, 2, Jan. 1970, 133–158; P. Newman, ‘Malaria

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 ALLURE, LEGACIES OF THE GERM PARADIGM

Eradication and Its Effects on Mortality Levels: A Comment,’ Population Stud-

ies, 23, 2, 1969, 285–288; P. Newman, ‘Malaria and Mortality,’ Journal of the
American Statistical Association 72, 358, 1977, 257–263. Newman, Frederiksen
observed, ‘prefers a more elaborate and circumstantial method . . . [one that] fails
to quantify the extension of insecticides in time and place . . . [and] overlooks or
ignores this opportunity to directly compare the reductions in mortality in areas
with malaria and with spraying of insecticides, and in areas without malaria and
without spraying of insecticides . . . substitut[ing] hypothetical extrapolation
of the regression technique for empirical observation of the [mortality] results
of the natural experiment’; Frederiksen, ‘Book Review of P. Newman’ [Malaria
Eradication and Population Growth, 1965], 262–264; Frederiksen, ‘Malaria
Eradication and the Fall of Mortality,’ 111–13).
75 Dyson and Murray, ‘Macro-Level Study of Socioeconomic Development,’
147–164.
76 See Zurbrigg, Epidemic Malaria and Hunger, 101, 191–192; Report on the Sani-
tary Administration of the Punjab, 1908, 14.
77 Langford, ‘Reasons for the Decline,’ 18.
78 Ibid., 14.
79 As suggested by Newman, ‘Malaria Control and Population Growth,’ 157.
80 Langford, ‘Reasons for the Decline,’ 21–22. Moreover, a significant ‘pre-
emptive’ role for DDT post-1947 is questionable, resting as it does on the
assumption that epidemic mortality was driven primarily by malaria transmis-
sion levels. Major drought in 1938 as severe as that in 1948 (79.0 inches rainfall
cf a mean of 99 inches) triggered increased malaria transmission, a high vector
infection (sporozoite) rate (4.97 per cent), and a four-fold rise in 1939 dispen-
sary fever cases; S. Rajendram, and S.H. Jayewickreme, ‘Malaria in Ceylon,’
Indian Journal of Malariology, 5, 1, Pt. 1, Mar. 1951, 1–73, at 57, 29, 67, 59.
Yet 1939 mortality increased only marginally to 21.8 per 1,000 compared to
21.0 the year before; Frederiksen, ‘Malaria Control and Population Pressure,’
866. Margaret Jones also notes the limited mortality outcome in 1939; Health
Policy in Britain’s Model Colony, 203–204.
81 See above, note 57.
82 R.H. Gray, ‘The Decline of Mortality in Ceylon and the Demographic Effects of
Malaria Control,’ Population Studies, 28, 2, Jul. 1974, 205–229.
83 Gray, ‘Decline of Mortality in Ceylon,’ Table 11, 219; citing L. Nicholls, and A.
Nimalasuriya, ‘Rural Dietary Surveys in Ceylon,’ Ceylon Journal of Science (D),
V, Pt. D, Nov. 12, 1941, 59–110.
84 League of Nations, ‘The Most Suitable Methods of Detecting Malnutrition due
to the Economic Depression, Conference Held at Berlin from December 5th to
7th, 1932,’ Quarterly Bulletin of the Health Organisation, 2, 1, Mar. 1933,
116–129.
85 Gray’s interpretation of the Nicholls study itself is questionable. The eight highly
malarious ‘dry zone’ study villages show caloric consumption to be slightly
lower, not ‘marginally better,’ than that in the wet-zone villages. Average daily
calorie consumption of the eight dry zone villages, listed as nos. 2–5 and 10–13,
is recorded as 2,390 compared to a mean of 2,461 calories per day in the remain-
ing five southwest wet-zone survey villages; in Nicholls and Nimalasuriya, ‘Rural
Dietary Surveys in Ceylon,’ 63. Bibile and colleagues observed that ‘in south-east
Uva province . . . peasants consume three meals a day during the harvest, ie. from
March onwards . . . [and in] August onwards, the number of meals become two
and sometimes one for a day. The traders and landed proprietors have a regular
supply of food throughout the years’; S.W. Bibile, H. Cullumbine, R.S. Watson,

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 ALLURE, LEGACIES OF THE GERM PARADIGM

and T. Wickremananake, ‘A Nutritional Survey of Various Ceylon Communi-

ties,’ Ceylon Journal of Medical Science (D), VI, Pt. 1, Mar. 21, 1949, 54.
86 H. Cullumbine, ‘The Influence of Environment on Certain Anthropomorphic
Characters,’ Ceylon Journal of Medical Science (D), 6, 3, (1949), 164–170, at
171, Table 3. Gray was aware of this later study and cited its anthropometric
findings, yet concluded that ‘on balance . . . disparities in diet could not account
for the mortality differences between zone of malaria prevalence before 1945’;
Gray, ‘Decline of Mortality in Ceylon,’ 220.
87 The climatically precarious agricultural economy in the dry malarial zone was
marked by ‘hungry seasons . . . [m]alnutrition, and even starvation’; conditions
Meegama described as ‘inherent in the type of cultivation forced by circumstances
on those people.’ He pointed to ‘innumerable references’ in the annual colonial
administrative reports to ‘famine conditions and distress in this region’ compared to
the ‘agriculturally prosperous’ wet zone with its more secure agriculture and diversi-
fied economy, hence ‘stable supply of food’; Meegama, ‘Malaria Eradication and its
Effect on Mortality Levels,’ 211. See also above, ch. 2, at notes 13 and 46.
88 Administrative Reports of the Director of Health Services, Ceylon, no date; cited in
Frederiksen, ‘Determinants and Consequences of Mortality Trends in Ceylon,’ 661.
89 Nor was there any attempt, as Brown points out, to incorporate any of the avail-
able literature on changing economic conditions in the dry zone, such as a 1952
International Bank for Reconstruction and Development report [The Economic
Development of Ceylon (Baltimore: Johns Hopkins Press, 1952)]; P.J. Brown, ‘Soci-
oeconomic and Demographic Effects of Malaria Eradication,’ Social Science Medi-
cine, 1986, 852–853. Curiously, Brown also comes to accept the Gray analysis.
90 S. Preston, ‘The Changing Relationship between Mortality and Level of Eco-
nomic Development,’ Population Studies, 29, 2, July 1975, 231–248, at 239;
S. Preston, ‘Causes and Consequences of Mortality Declines in Less Developed
Countries during the Twentieth Century,’ in R.A. Easterlin, ed., Population and
Economic Change in Developing Countries (Chicago: University of Chicago
Press, 1980), 296, 313. This, though in his own analysis Preston was unable to
establish a statistical relationship between life expectancy increase and pre-DDT
malaria endemicity; ‘Causes and Consequences,’ 311–312.
91 See, e.g., L. Molineaux, ‘The Epidemiology of Human Malaria as an Explanation
of its Distribution, Including Implications for Its Control,’ in Wernsdorfer and
McGregor, eds., Malaria: Principles and Practice, 974–976; R. Cassen, India:
Population, Economy, Society (London: Macmillan, 1978), 86; R. Carter, and
K.N. Mendis, ‘Evolutionary and Historical Aspects of the Burden Of Malaria,’
Clinical Microbiology Reviews, Oct. 2002, 564–594, at 584.
92 Among the four leading causes of infant mortality in Sri Lanka between 1935
and 1948, three were associated with undernourishment: ‘debility’; ‘rata’ (a
local term for a skin disease condition associated with malnutrition); and ‘pre-
maturity’ (a term applied to low birth weight newborns, often associated with
intrauterine undernourishment). Both ‘debility’ and ‘rata’ are recorded show-
ing marked decline between the periods 1935–1939, 1944–1946 and 1948; in
Sarkar, The Demography of Ceylon, 161. The fourth major cause of infant mor-
tality listed, ‘convulsions,’ also shows major decline, a diagnosis that Nicholls
suggested applies to ‘[m]any of the children who die within a week of birth
appear[ing] to be of low vitality’; in ‘A Nutritional Survey of the Poorer Classes
in Ceylon,’ Ceylon Journal of Science. (D), IV, Pt. 1, Apr. 30, 1936, 1–70, at
51–52. It is unlikely that many convulsion deaths were malarial, the large major-
ity (71 per cent) occurring under one month of age, half within one week of
birth; ‘A Nutritional Survey,’ 52.

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 ALLURE, LEGACIES OF THE GERM PARADIGM

93 ‘These [wartime] food subsidies . . . were continued thereafter to become one of

the island's social welfare services’; De Silva, A History of Sri Lanka, 476. Both
Frederiksen and Langford are acknowledged in Packard’s important critique
of the MBD thesis as questioning the DDT explanation of post-WW2 Ceylon
mortality decline, but the actual content of the latter’s analyses unfortunately
is left unarticulated; R. Packard, ‘ “Roll Back Malaria”? Reassessing the Eco-
nomic Burden of Malaria,’ Population and Development Review, 35, 1, Mar.
2009, 53–87, at 66.
94 F. Snowden, The Conquest of Malaria: Italy, 1900–1962 (New Haven: Yale
University Press, 2006), 219–220.
95 William McNeill’s reading is perhaps the most emphatic: ‘The sudden lifting
of the malarial burden brought by liberal use of DDT in the years immediately
after World War II was one of the most dramatic and abrupt health changes
ever experienced by humankind’; Plagues and People (Garden City, NY: Anchor
Press, 1976), 249. See also, P. Kennedy, Preparing for the Twenty-first Century
(New York: Random House, 1993), 25; A. Hardy, and E.M. Tansey, ‘Medical
Enterprise and Global Response, 1945–2000,’ in W. Bynum, et al., The West-
ern Medical Tradition (Cambridge: Cambridge University Press, 2006), 472;
R. Fogel, The Fourth Great Awakening (Chicago: University of Chicago Press,
1999), 46; A.K. Bagchi, The Political Economy of Underdevelopment (Cam-
bridge: Cambridge University Press, 1982), 204.
96 R. Briercliffe, and W. Dalrymple-Champneys, ‘Discussion on the Malaria Epi-
demic in Ceylon 1934–1935,’ Proceedings of the Royal Society of Medicine,
29, 1936, 537–562, at 554, Fig. 16. The severe edema in the child’s lower
extremities may have been exacerbated by malaria-induced anemia, but the
state of extreme undernourishment evident in the severe muscle mass loss and
sparse, depigmented hair indicates underlying severe undernourishment.
97 Hackett, Malaria in Europe, 227.
98 Frederiksen, ‘Malaria Eradication and the Fall of Mortality,’ 113. In 1970 Fred-
eriksen noted that despite ‘the dramatic and massive resurgence of malaria in
Ceylon,’ by early 1968 reaching a million cases, ‘[r]esident and visiting observ-
ers from the host government, the World Health Organization, the U.S. Public
Health Service and the Population Council have so far not noted any significant
increase in mortality since the start of the malaria epidemic’; ibid.
99 On this, see Zurbrigg, Epidemic Malaria and Hunger, ch. 12, analysis that
encompasses the eastern half of the colonial province of Punjab making up the
post-1947 Indian state of Punjab.
100 Ibid. See also, Wernsdorfer, ‘Social and Economic Aspects of Malaria,’ in Wer-
nsdorfer and McGregor, eds., Malaria: Principles and Practice, 1421–1472, at
1435. Limited impact of malaria transmission resumption on general death rate
levels has often been attributed to improved access to treatment; D. Bradley,
‘Malarial Old Infections, Changing Epidemiology,’ Health Transition Review,
2, Suppl. 1992, 137–153. But for much of rural 1950s India, assured access to
anti-malarials appears unlikely; Zurbrigg, Epidemic Malaria and Hunger, 387.

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 8
WHAT WAS LOST

When I teach the social impact of technology, I do not find

it difficult to make it clear to engineers that technology has a
social impact; however, it is almost impossible for me to make
it clear to them that they are being impacted.
—– Ursula Franklin, ‘Educating Engineers for the
Modern World,’ in Ursula Franklin Speaks:
Thoughts and Afterthoughts, 1986–2012 (Montreal:
McGill-Queen’s University Press, 2014), p. 155

A new scientific truth does not triumph by convincing its

opponents and making them see the light, but rather because
its opponents eventually die, and a new generation grows up
that is familiar with it.
—– Max Planck, Scientific Autobiography and
Other Papers, trans. F. Gaynor (New York
Philosophical Society, 1949), pp. 33–34

What was lost in understanding of human health with the nineteenth-

century ascendance of sanitationist epidemic theory and a laboratory-based
medicine was not just a single factor in infective disease causation. Set aside
amidst the enthusiasm for applying the new microbiological insights of
germ transmission were the broader discerning powers of observation of an
earlier era. In the annals of modern medical and public health history, early
twentieth-century figures in colonial India such as S.R. Christophers and
C.A. Bentley had their nineteenth-century European counterparts in W.P.
Alison, Rudolf Virchow, and Louis-René Villermé. The most prominent
amongst them have not been forgotten. But posterity has often remembered
their work selectively for their microbiologic or statistical contributions; less
for their broader epidemiologic insights to which that expertise led them.
In his 1840 descriptions of typhus fever amongst the Scottish poor, Alison’s
carefully detailed observations predicted with near-clairvoyant accuracy
the characteristics of spontaneous recrudescent typhus under conditions of

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 W H AT WA S L O S T

human destitution, a phenomenon that would be unravelled scientifically

only a century later as Brill-Zinsser disease.1 These were powers of observa-
tion that extended beyond infection transmission alone, encompassing that
‘tapestry of social relations’2 within which the specific disease epidemiology
was set, and discerning key relationships from this broader context. ‘It is
not asserted,’ Alison wrote in his treatise on typhus (‘fever’) and poverty in
Scotland

that destitution is a cause adequate to the production of fever

(although in some circumstances I believe it may become such); nor
that it is the sole cause of its extension. What we are sure of is, that
it is a cause of the rapid diffusion of contagious fever, and one of
such peculiar power and efficacy, that its existence may always be
presumed, when we see fever prevailing in a large community to an
unusual extent. The manner in which deficient nourishment, want
of employment, and privations of all kinds, and the consequent
mental depression favour the diffusion of fever, may be matters of
dispute; but that they have that effect in a much greater degree than
any cause external to the human body itself, is a fact confirmed by
the experience of all physicians who have seen much of the disease.3

It was the ‘peculiar power and efficacy’ of destitution (hunger-induced

immune-suppression and ‘mental depression’) that a handful of the early
malaria researchers in the Indian Medical Service also were recognizing
and attempting to assess in teasing apart the interaction of biological and
socio-economic factors underlying highly lethal malaria in India. Though
more constrained perhaps by imperial allegiances than was Alison, their
intellectual facility allowed them to consider and comprehend relationships
transcending the specific confines of the sanitary paradigm of germ trans-
mission. That they employed their scientific talents enthusiastically in the
service of the British imperial state cannot be doubted. It could well be
argued they could have done more, and that in their politically privileged
positions, the obligation to do so was there. But that is a different historical
question. Here what is considered is simply the significance of that broader
understanding, and its common fate: how such epidemiological insights and
experience were overshadowed and effectively set aside. ‘The role of predis-
position was not something that could be disproved,’ Hamlin observes in
the post-1842 context of industrializing England, ‘but it could be ignored.’4
These larger insights stand in stark contrast to the vision of public health
conjured in the nineteenth-century daily tasks of sanitary engineering, a
vision increasingly narrowed to the elimination of environmental ‘dirt’ or
‘moisture.’ In his re-examination of the Chadwickian legend, Hamlin antici-
pates something of the interpretative power of the sanitationist model evi-
dent in the accounts of W.J. Gilbert, an Assistant Poor Law Commissioner

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selected by Chadwick to co-compile testimony on urban filth and ‘bad air’

(mal-aria). ‘The diseases arising from malaria,’ Gilbert would lament on the
first page of the Local Reports (England and Wales) from which Chadwick
selectively synthesized the Sanitary Report of 1842, are ascribed to various
causes, ‘heredity or personal infection, to low or unsuitable diet, hard work,
exposure to cold, and other causes; but whenever such a regularly recurring
complaint is found, almost invariably there is some open drain, some stag-
nant pool.’5 Here, miasma-engendering filth functions as the default causal
explanation of disease: ubiquitous, and in its invisible mechanism of ‘nox-
ious vapours,’ impossible to disprove. The frailty of the logic is transparent.
‘Dirt’ not only trumps diet (hunger), but it does so even where its presence
is simply a theoretic possibility. Indeed, it was precisely the invisibility of the
miasmic threat that endowed sanitarianism with its power and correspond-
ing sense of professional obligation.
A parallel shift to the privileging of microbiologic factors external to the
human host in explanations of epidemic behaviour can be traced equally
clearly in the late colonial South Asian malaria literature, in Major A.
Hooton’s absorption with anopheline vectors in the Kathiar Agency of
Gujarat, as seen above in chapter seven.6 The invisible, but ever-present
potential threat of infected mosquitoes would soon be accompanied by
its counterpart, the twentieth-century risk of ‘hidden (micronutrient) hun-
ger.’ It is seen as well in Passmore and Sommerville’s 1940 paper where
Christophers’s 1911 ‘scarcity’ conclusions regarding malaria lethality are
set aside on the basis of their laboratory work on simian malaria, work that
addressed micronutrient-deficient dietaries rather than caloric insufficiency
(hunger).7 ‘Mere association,’ they argued in relation to the 1911 report,
‘cannot be taken as proof’ of a causal relationship.8 Despite the manifest
analytic limitations of the 1940 study, Paul Russell would make similar
arguments in his 1946 text, Practical Malariology, citing the Passmore-
Sommerville article. ‘A good deal has been said about famine as a causative
factor in regional epidemics, . . . [but] no proof of a causal relationship
has been found,’ he argued. ‘[F]requently the same climatic factor which
brought about famine also made conditions favorable for the breeding of
vector mosquitoes.’9 Here, the ‘exciting’ or ‘precipitating’ cause – ento-
mological conditions – of malaria epidemicity was accorded preferential
explanatory power over ‘predisposing’ factors and selectively relieved of
the burden of proof in the process, what Hamlin describes in nineteenth-
century sanitationist argument as ‘the arbitrary elevation of one set of
correlations to the status of the cause.’10 To qualify as scientific, the epide-
miological observations as contained in earlier studies such as Malaria in
the Punjab now required experimental (microbiologic) validation, where
the sufficiency of vector and related immunological aspects in explaining
epidemic mortality patterns, however uncorroborated by epidemiological
evidence, did not.

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 W H AT WA S L O S T

Had Russell been asked directly for his assessment of malaria mortality
in the absence of destitution, he might well have replied that the amount
of mortality was immaterial. It was enough that there was any mortal-
ity (which there was) and any economic debility associated with infection
(which again there unquestionably was), whether or not either became dra-
matically magnified under conditions of acute hunger (which they did). And
as a vector sanitationist or medical clinician, he was right. Yet in the context
of health policy decision-making, the amount of mortality did matter. As it
matters also to health historiography.
This ‘gravitational’ pull to factors external to the human host in epidemic
causation was not new. But it was becoming that much more exclusivist
within the confines of industrializing Europe. In his efforts to document
the class differentials in mortality he saw in early nineteenth-century Paris,
the French hygienist, Villermé, would lament that ‘[w]e far too often attrib-
ute . . . the very different life expectancies of the masses of individuals who
make up each nation, to difference in climate.’11 One century later, Ackerk-
necht would point to ‘the extraordinary brilliancy of the bacteriological era’
that has come to ‘obscur[e] . . . everything lying behind it in the field.’12 In
relation to the World Health Organization’s Malaria Eradication Program,
Packard similarly describes ‘a compelling logic’ to the idea of eradication of
the plasmodial parasite that

continually draws one into the narrow medical, technical and

organizational factors that shaped the program. . . . [O]ne needs to
continually work against the logic and resist its pull. For it is a logic
that isolated the history of malaria eradication from the world in
which it occurred, a logic that excluded from vision a wide range
of social, economic, and political forces that were operating during
this period.13

What drives this ‘extraordinary brilliancy’ and privileged status?

Beyond the undisputed effectiveness of microbiologic techniques in spe-
cific instances, explanations of epidemic behaviour narrowed to germ-
transmission are deemed more credible because microbes are identifiable
and in theory at least amenable to controlled experiment, hence grounded
by scientific proof. Hunger, in contrast, is viewed as not admitting of scien-
tific analysis, under the assumption perhaps that it is not possible to control
for myriad confounding social dimensions (‘complexities’). This privileging,
one can suggest, turns in part on the conflation of scientific and microbio-
logic. Microbial (also, micronutrient) explanations of ill-health are prefer-
entially ‘scientific’ because they are reproducible in laboratory conditions,
the bedrock of scientific investigation. Human destitution triggered by crop
failure, work injury, or death of a primary wage-earner, for self-evident
ethical reasons, generally is not. The microbiologic is academically ‘safe,’

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by comparison.14 Interestingly, in their 1909 paper on the ‘Human Factor,’

Christophers and Bentley themselves hint at this dichotomy, referring to
observations on economic conditions as ‘study whose object is not in one
sense scientific research but simply the getting of information absolutely nec-
essary to action.’15 Here, wage levels, grain prices, destitution, physiological
poverty (macrobiological conditions) comprise ‘information,’ while parasite
rates and entomological observations constitute scientific research.16
The consequences of the selective microbiologic focus for historical epi-
demic enquiry have been many. One example in relation to malaria is seen
in Macdonald’s mathematical modelling of malaria transmission, work in
which host recovery rate was assigned a constant value, presumed unmeas-
urable and unsuitable for statistical analysis and prediction. In the process,
however, the immense range in lethality (case fatality rate) of malarial infec-
tion was effectively removed from the epidemic equation, as we have seen:
and along with it, a dimension central to understanding much endemic dis-
ease mortality in history, and the larger question of secular trends in human
life expectancy, in turn.17 Quantifiability in this sense thus tends to shape
what data qualify as scientifically useful, but also what questions are asked,
and by whom investigated. Weindling points to the dilemma, observing in
the context of the International Labour Organisation’s early work on health
and economics, that ‘in seeking to justify its reformist demands in the uni-
versalist terms of science, [the organisation] had to devolve initiatives to sci-
entific experts whose empirically based approaches were necessarily limited
to what could be proven in the laboratory.’18
In relation to mid-twentieth-century South Asian epidemiological
thought, a particularly transparent window on the impact of the biomedi-
cal model’s ‘brilliancy’ can be seen in the official report on the 1943 Ben-
gal famine. In the deliberations of Famine Commission members regarding
the causes of epidemic mortality, a range of entomological and parasitic
factors were considered in seeking to explain the enormous malaria mor-
tality witnessed. Various vector explanations outlined in the earlier 1940
Passmore-Sommerville paper were discussed at some length.19 Unable to
identify ecological changes capable of affecting malaria transmission rates
across Bengal, the Commission turned to the recent ‘influx of refugees from
Burma [Myanmar]’ as creating conditions ‘propitious for the dissemination
of unfamiliar strains’ of malaria parasites, ‘exotic strains’ to which the pop-
ulation would have had little previously acquired specific immunity. This,
too, was an unlikely explanation, it ultimately was acknowledged, leading
members to ‘tentatively express . . . that the high mortality from malaria can
be largely accounted for without pre-supposing any change in the virulence
of the infecting organism.’20
Remarkably, this statement effectively brought the committee’s report
to a close. It was followed by a simple paraphrasing of a Croonian Lec-
ture recently given before the Royal Society, a quote inserted, it seems, as a

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concluding statement to the medical portion of the famine Inquiry report.

The Topley paper, the 1945 Commission members urged, ‘brings out the
complexity of the problem’ of epidemic causation in relation to famine.
Clarity was often elusive due to

[o]ur present lack of knowledge of all the factors concerned in the

rise and fall of epidemics and their interaction. . . . It may be dif-
ficult to account satisfactorily for the cause and course of epidemics
even in a well-fed static human population, even indeed, in a closed
colony of experimental animals. To do so in the case of a socially
disorganized famine-stricken population is an impossible task.21

A definitive explanation of the 1943–1944 Bengal famine’s soaring malaria

mortality, the medical enquiry report appears to suggest, was as yet out of
reach where an expanding list of potential microbiological factors could not
expressly be ruled out.
What is striking in the 1945 Famine Commission’s closing statement
on Bengal famine mortality is the degree of circumspection, a hesitancy
in marked contrast to the conclusions of earlier observers such as W.R.
Cornish and A.P. MacDonnell who linked malaria lethality in the late
nineteenth-century famines in British India indisputably to human starva-
tion.22 On the one hand, the 1945 enquiry commissioners clearly under-
stood at a common-sense level that starvation was the overriding driver of
lethality in Bengal in 1943–1944, indeed at one point acknowledging Chris-
tophers’s 1911 Punjab conclusions. On the other hand, such a relationship
could now only be viewed as, at best, ‘tentative,’ with both the micronu-
trient nutritional research and 1940 Passmore-Sommerville paper before
them – the latter quoted at length – and a growing range of entomological
theses also as explanatory possibilities.23 It is as if Commission members
were throwing up their hands in the face of such microbiologic ‘complexity.’
But for some perhaps also finding comfort in its academic safety.
One can suggest this was scientism at its most paralyzing, a forfeiting of
the basic capacity to weigh relative roles. But it was more than this, too,
because in the malaria literature such a tentativeness was often unequally
applied. As in the case of Ceylon, the microbial-immunological argument
often was privileged, less subject to interpretative caution, indeed, requiring
at times no empirical evidence at all. A similar example of microbiologic
privileging can be seen three decades later at an international famine and
nutrition symposium. In a paper addressing ‘different degrees of starvation,’
W.R. Aykroyd, leading medical contributor to the 1945 Bengal Famine
Commission report, would suggest that the common association between
famine and disease ‘is in the main social rather than physiological, i.e., it is
due to the disruption of society, facilitating the spread of epidemic disease,
rather than lowered bodily resistance to invading organisms.’24

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Consequences of the germ paradigm’s ‘brilliancy’

A similar tendency to gravitate to microbiologic explanations of epidemic
behaviour can be traced running through recent South Asian epidemic and
demographic historiography. Researchers of epidemic and mortality decline
history generally acknowledge the findings of prominent nutritionists such
as Nevin Scrimshaw that undernourishment compromises immune capac-
ity, and thus recovery, for many common (endemic) infections.25 But if rec-
ognized in theory, understanding of the large range in lethality of many
infective diseases often fails to be incorporated in assessing relative roles for
microbe transmission, public health interventions, and staple-food security
in historical mortality decline. It is often assumed, for example, that inter-
rupting transmission of one particular pathogen will effect a decline in mor-
tality levels equivalent to those deaths triggered by such infection preceding
the transmission ‘intervention.’ This may be the case for inherently virulent
infections such as smallpox; but not necessarily for the leading historical trig-
gers of death such as malaria, tuberculosis, typhus, the diarrhea-pneumonia
complex, and others where undernourishment and acute hunger have played
a prominent predisposing role in their lethality, and continue to do so among
impoverished populations. This of course raises the issue of ‘competing risk.’
As explored in relation to the 1950s DDT-based malaria control program,
the overall impact of the abrupt interruption in malaria transmission on gen-
eral mortality levels in (East) Punjab state appears to have been very limited.26
The most likely explanation is that many of the deaths averted by the DDT
program were simply postponed to subsequent seasons: those children most
vulnerable to dying of malaria by virtue of undernourishment remaining vul-
nerable to other common endemic infections at other times of the year.27
Conceptual consequences of the germ theory’s brilliancy for epidemic
historiography lie at other levels as well. In employing the tools and
microbiologic insights of the expanding medical subdisciplines for under-
standing human health history (secular trends in life expectancy), only
infrequently have historians addressed the interpretive constraints so posed.
The dilemma for them is considerable because the range of possible micro-
biological factors – and hence the number of potentially relevant medical
subdisciplines – involved in any particular epidemic event or time-trend
is essentially unlimited. The onus is there to take them sufficiently into
account, to ‘cover all biomedical bases,’ or at least to attempt to do so. This
has meant that in the face of complex technical questions, the historian
often defers to the medical literature, hesitating to ask for scientific ‘proof,’
or to pose self-evident questions. Here, Hamlin, in citing Gilbert’s example
of ‘some open drain,’ remarks that ‘we do not read other areas of social sci-
ence so naively.’28
The interpretive difficulty lies in the ease with which microbiological
findings come to be accorded explanatory power for epidemiological

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phenomena in advance of being tested adequately, or at times at all. In

the case of malaria, entomological hypotheses such as ‘vector devia-
tion’ continue to be cited as likely contributing explanations of epidemic
outbreaks – in this case, famine-induced livestock mortality posited as
resulting in a shift in mosquito feeding from cattle to humans – though
unaccompanied by substantive empirical examination.29 The difficulty lies
not in the citing of potentially relevant biological phenomena; but rather
in doing so in the absence of accompanying effort to weigh their con-
tribution in relation to other factors. Any possibility of a microbiologic
explanation – or simply its possibility – suffices often to sideline adequate
assessment of hunger.
In recent accounts, for example, of the emergence of an ‘exalted’ form of
malaria (‘Burdwan fever’) in the ‘dying river’ tracts of nineteenth-century
western Bengal, potential entomological effects of interrupted inundation
irrigation are generally cited alongside the economic effects of embankments
in lowering soil productivity.30 ‘[A]nother consequence of the declining
[inundation] flows through the western arms of the Ganges delta,’ Marshall
observes, was that ‘as the rivers became more stagnant, malaria-bearing
mosquitoes bred more freely.’31 In this, the author is taking into account
1940s studies that suggested a link between lower water-table levels in the
embankment-affected tracts and a more conducive habitat for the main
malaria vector in the region, An. philippinensis, ecological changes that may
well have enhanced malaria transmission levels.32 Here, again, the interpre-
tative difficulty arises where the citing of a microbiological aspect distracts
from, or arrests, deliberation regarding relative roles: viz., consideration of
broader context that could shed light on the likely contribution of each.33
In the case of Burdwan fever, a broader epidemiological perspective could
include post-1920 decline in mortality levels in the region;34 and as well,
the experience of epidemic malaria during the 1943–44 Bengal famine. In
the latter case, as explored in chapter three,35 malaria lethality soared as the
leading cause of mortality across the course of the famine although ecologi-
cal conditions (including subsoil water-table levels) remained unchanged – a
heightened malaria mortality that was sharply circumscribed to the period
of epidemic starvation. In other words, the famine was a dramatic demon-
stration of the power of human famishment to alter the lethality of malarial
infection.36 Of course, access to such broader context is not always so read-
ily at hand. Nonetheless, acknowledgement of the need for a weighing of
relative import remains.
Similar interpretive difficulties can be seen in relation to analysis of the
massive canal irrigation projects in colonial Punjab. Interpretation of their
‘malariogenic’ consequences has often focused on vector-transmission
parameters, overshadowing the economic impacts of blocked surface drain-
age and waterlogging.37 This has meant it has been difficult to place the
specific, and very real, deleterious effects in the context of mortality trends

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over time: an impasse that in turn has impeded integration of the region’s
‘public health’ history into the rest of South Asian history.
Faced with the seeming incongruity of continuing malaria transmis-
sion but declining epidemic and general mortality after 1920, historians of
South Asian epidemic history have turned at times to alternate microbio-
logical hypotheses, positing a general rise in acquired immunity levels in the
population38 – a thesis unsupported empirically, and itself a function of vec-
tor transmission.39 Macdonald earlier, as we have seen, also turned to an
immunologic hypothesis of malaria epidemicity, if in a somewhat differ-
ent framework: in this case, suggesting year-to-year fluctuation in numbers
of non-immunes in the Punjab population to explain the region’s epidemic
malaria history. Default reliance on acquired immunity hypotheses is of
course a much broader phenomenon within epidemic historiography:40 a
reflection of the continuing epistemic power of the germ-transmission par-
adigm, but arguably also an expression of the underlying absence of an
adequate epidemiological approach to hunger in historical analysis.

From too obvious to invisible

This study has sought to trace the decline in Western medical understanding
of hunger in human health and epidemic history. What was once obvious,
even ‘truistic,’41 by the mid-twentieth century now verged on the invis-
ible: the history of mortality decline, aside from famine control, was now
understood primarily in terms of the control of pathogen transmission and
chemotherapeutics. In one sense, the historical relationship between hunger
and infective disease lethality was too obvious, often failing to merit dis-
cussion within medical texts. In the 1894 edition of the Indian Manual of
Hygiene, for example, a single reference acknowledged that ‘[i]n a country
like India, the influence of rainfall upon General Health and well being of
the community is very marked.’ But the consequences of ‘failure of the crop’
were deemed ‘too well known to need any further explanation.’42 Hamlin
also reminds us that the ancient Hippocratic treatises addressed the medical
diseases of individuals, whereas those of society associated with crop failure
were not the domain, or within the capacity, of the physician.

Knowing that . . . a harvest had failed might allow one to anticipate

disaster but rarely allowed one to prevent it. Indeed, such events
marked the limits of a medicine based on individualized dietet-
ics. Powerless to . . . guarantee the crops, Hippocratic writers . . .
focused instead on what they could do.43

In the case of South Asia, hunger runs through the colonial records, but
largely obliquely. During the famine-related malaria epidemic of 1878, the
Sanitary Inspector for Jullunder city noted, for example, that ‘food tickets’

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distributed by the municipal committee ‘as recommended by the Native

Doctors . . . [had] done great good,’ while the insufficiency of such funds also
was acknowledged.44 Three decades later, hunger would weave inferentially
through the deliberations of the 1909 Imperial Malaria Conference held
at Simla, well beyond the ‘scarcity’ conclusions of Christophers’s Punjab
presentation. When a malaria ‘cess’ was proposed for funding anti-malaria
work, it was opposed by one of the few ‘Native’ delegates. Taxing the poor
for whom resistance to malaria was already low could not be justified, Mr.
Kishori Lal Goswami, Member of the Bengal Provincial Legislative Council,
argued: ‘poverty was accountable for malaria, poverty reduced the people’s
power of resistance, and if further taxation was to be imposed that resist-
ance would be further reduced.’45 He was not challenged, and the proposed
tax, it appears, was quietly abandoned.
This broader, seemingly self-evident, understanding of disease lethality as
shaped by the subsistence conditions of the human host was not limited to
South Asian experience. The relationship continued to be reappear episodi-
cally in Britain into the early twentieth century. In the 1902 annual oration
to the Medical Society of London, S. Mackenzie described the role of pov-
erty in tuberculosis as ‘a powerful predisponent,’ adding,

I remember many years ago, before the discovery of the bacillus,

someone pressing the late Dr. H.G. Sutton to define what tubercle
really was. He replied, ‘Tubercle is making shirts at 5s. a week.’46

But if the disease and destitution relationship was a commonplace, hun-

ger was also deeply incriminating, as seen in Edwin Chadwick’s efforts
to remove starvation as a cause of death category from vital registration
reports.47 Where obvious, hunger was often veiled linguistically. The vari-
ous epidemic ‘fevers’ (often typhus) seen typically among the livelihood-
desperate were grouped, for example, under the nineteenth-century English
category of ‘crowd diseases,’ the term connoting contagion as the central
dynamic underlying their epidemic manifestation, less so starvation.
In nineteenth-century colonial India as well, starvation deaths were rarely
registered as such, but rather slotted under categories of ‘old age’ or ‘fever’
by low-level functionaries, often for ‘fear of getting into trouble with the
authorities.’48 The commonly documented ‘exalted’ form of malaria evident
on colonial construction sites would be interpreted in miasmic terms of
‘turning up the soil,’ the indentured and often times semi-starving migrant
labourers who did the ‘turning,’ left out of sight.49 At the same time, the
heinous methods resorted to by the state to control the desperate actions
of the famished went largely unrecorded. Only a single reference to whip-
ping – a measure employed to discourage deliberate courting of imprison-
ment to access food – appears in the voluminous nineteenth-century British

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India famine commissioner reports, an inadvertent remark by a district offi-

cial that found its way into the Punjab provincial report on the 1899–1900
famine.50
Where specific measures to alleviate hunger appear in the colonial sani-
tary and malaria records, they too were phrased in oblique terms. In Chris-
tophers’s case, policies to prevent famine and the notorious associated
malaria epidemics were referred to as ‘general sanitary reforms’;51 flood-
related food relief in Punjab, simply as ‘other ameliorative measures.’52 At
the 1909 malaria conference, ‘great privation and hardship’ was openly
acknowledged to underlie the ‘very fatal’ form of epidemic malaria. But
such transparency was the exception,53 prompted, as I have suggested else-
where, by even greater ‘obloquy’ directed to the British Raj by prominent
figures publicly excoriating the government for its reluctance to embrace
vector eradication as a central malaria control policy.54
In historical records generally, reticence to record the human agony of
famishment prevails, as ‘that of which one cannot speak.’ One small glimpse
of the extremes of starvation misery appears in Aykroyd’s 1974 Conquest
of Famine. ‘Cannibalism occurred’ during the 1846–1847 Irish famine, ‘as
it does in many major famines,’ he acknowledged, ‘but it was apparently
confined to a few people driven mad by suffering. The [Quaker] Friends had
to give up buying cheap sausages when some were found to contain human
flesh.’55 Such stark accounts however are rare. As Millman and Kates have
pithily observed, ‘[t]he history of hunger is for the most part unwritten. The
hungry rarely write history, and historians are rarely hungry.’56
From being once ‘too obvious,’ hunger within professional circles by the
early twentieth century had swung to its socially ‘hidden’ form, increas-
ingly viewed in the micronutrient domain as largely a qualitative problem.
‘One of the most difficult problems facing the investigator,’ scientists with
the All-India Institute of Hygiene and Public Health lamented in 1949, ‘is
to determine the nutritional status of an individual without carrying out a
series of elaborate biochemical tests which are beyond the realm of practi-
cability in a survey . . . unless unmistakable signs of vitamin deficiency are
present.’57 Increasingly interpreted now as an educational problem, hunger
in turn came to be shorn of its ethical and emotive implications.
At the methodological level, reliance on aggregate economic measures
to assess ‘nutritional status’ within mortality decline analysis has further
contributed to hunger’s invisibility by obscuring differential access to food
within populations. When it became evident in the mid-twentieth century
that national Gross Domestic Product data poorly predicted life expectancy
across the world,58 ‘nutrition’ itself, along with the index, was sidelined as
a substantial factor in post-WW2 mortality decline, and the inherent inad-
equacies of aggregate indices such as GDP as a measure of hunger within
societies were overlooked. Within Western medical fora, the questions raised

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by Frederiksen in the 1960s in relation to post-WW2 Sri Lankan post-war

mortality decline were simply set aside as ‘not . . . realistic.’59

[T]he falls in mortality in the developing countries have been so

sharp, and the rise in living standards so gradual – indeed in some
there has been no rise at all – that on this score alone it is difficult
to accept his hypothesis. . . . We may therefore conclude that medi-
cal measures of one kind or another are responsible for the fall in
mortality.60

Here, a role for food security in rising life expectancy was not just invisible,
but verging on the inconceivable, with mortality decline credited instead to
medical measures ‘of one kind or another.’
Within Western academic thought, macroeconomic indices have con-
tinued to be employed as indicators of nutritional status in health analy-
sis, despite conveying little about distribution of food within societies,
shifts in security of staple food access, or the myriad constraints to access
presented by prevailing conditions of work.61 Moreover, the language
employed in recent epidemic historiography has added a further veil,
with aspects of food insecurity commonly grouped under the rubric of
‘social’ factors, leading to attributions of dysfunctional cultural or behav-
ioural practices.62 Equally problematic has been the increasing use of the
term ‘environmental’ to encompass both subsistence insecurity (economic
conditions) and exposure to infection,63 terminology generally directing
attention to the latter – conditions external to the human host related to
infection transmission.
Quantitative hunger – not enough to eat – would begin to be reclaimed in
clinical medicine in the 1960s and early 1970s through nutritional anthro-
pometry, where childhood undernourishment was rendered obvious as
cumulative faltering growth on paediatric weight (‘road-to-health’) charts,64
most prominently in low-income populations. Hunger’s impact on immune
capacity and the lethality of many infective diseases was also confirmed in
this period,65 if analysis of broader socio-economic determinants was often
limited.66 Ensuing historical nutritional anthropometry research also began
to reclaim visibility of ‘chronic’ hunger at this time by tracing secular trends
in human stature as a marker of cumulative endemic undernourishment.67
It was in this period as well that recognition of the immense variation in
lethality (case fatality rate) of infective diseases re-emerged in analysis of
mortality decline in nineteenth-century Britain in the work of Thomas
McKeown.68 Perceived in some instances however as a dismissal of public
health efforts to control infection transmission,69 the key issue of shifts in
the lethality of endemic infections tended to recede once again in epidemic
and public health historiographic analysis.70

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‘Good Health at Low Cost’

One example of waning visibility of subsistence (in)security in contempo-
rary health history analysis can be seen in the 1985 document Good Health
at Low Cost [GHLC].71 Addressing the dramatic post-WW2 rise in child
survival rates and life expectancy recorded in the low-income (GDP) ‘devel-
oping’ countries of Sri Lanka, China, and Kerala state in India,72 the GHLC
report identified four main contributing factors: ‘education for all’; public
health measures (immunization, protected water supplies and sanitation,
vector control); accessible primary health care; and ‘adequate caloric intake
by all.’73 Of the four, much of the conference report however came to focus
on the first three factors: primary health care, public health programs, and
female literacy. Aggregate per capita foodgrain figures and trends for each
population were reported,74 along with a brief review of the ‘linkages’
between nutritional status and mortality risk.75 But shifts in food access
within the case-study populations and specific economic reforms – such
as rural land reforms, public distribution programs, and minimum wage
legislation – and their consequences for access made up relatively little of
the 248-page report.76 Surprisingly as well, little attempt was made to assess
timing of the various programs in relation to observed mortality trends.
In light of the document’s considerable subsequent influence,77 several
questions unaddressed in the 1985 report are considered here.

China as case study

In regard to China, mortality decline appears to have been most rapid at
the beginning of the 1950–1980 case study period, that is, between the
years 1950 and 1957.78 In the absence of country-wide vital registration
before 1955, estimates of mortality levels in the immediate pre-1950 period
have generally relied upon local surveys conducted in the pre-revolution
period. Those data considered approximately representative of national
(viz., largely rural) conditions come from a 1929–1931 study conducted
in 16 provinces in rural areas not directly affected by then-prevailing war-
fare.79 Adjusted for under-registration, the 1929–1931 data have suggested
a rural crude death rate of 41.5 per 1,000 population, with life expectancy
estimated at 24.2 years.80 Such conditions, Judith Banister has suggested,
likely continued through the 1930s and 1940s: ‘In 1950, warfare had just
ceased and recovery from the ravages was just beginning.’81 The crude death
rate in 1949 for China as a whole she estimated as 38 per 1,000 population,
indicating life expectancy likely below 30 years.82
By 1957, national life expectancy had almost doubled to 50 years.83
By the early 1970s, a further 13 years in average life span had been
gained.84 Together, these figures translate into hundreds of millions of

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deaths averted, the population increasing from 542 million at the end of
1949 to 830 million in 1970.
What explains this rapid rise in survival rates? Certainly, the return of
peace, of rudimentary administrative capacity, and of a civilian economy,
played a major role, conditions directly affecting livelihood and food secu-
rity. A number of national disease control campaigns also were initiated in
the early 1950s. Among them, smallpox was effectively eradicated by 1957
through universal vaccination.85 As well, an anti-syphilis campaign saw the
entire adult population of Shanghai, for example, tested and treatment pro-
vided for positive cases, a government-funded program that extended sub-
stantially also to village level.86 These two diseases together however appear
to have accounted for only a small portion, possibly 8 per cent, of total
preventable mortality in the pre-1950 period.87 Other programs, such as the
Patriotic Health Campaigns were considerably less effective in controlling
transmission of major parasitic infections such as malaria and schistoso-
miasis in these early years.88 Major improvements in water and sanitation
infrastructure in the initial two decades also appear to have been limited, the
prevalence of intestinal parasitic infections remaining high through to the
early 1980s.89 Primary education was massively expanded post-1950, but it
is unlikely increased child literacy could explain a significant portion of the
initial rapid decline in mortality. Basic rural health care services, moreover,
largely awaited initiation of the barefoot doctor program in 1968–1969 and
its expansion in the 1970s,90 at a point in other words when a good deal of
the 1950–1980 gains in life expectancy nationally had already taken place.91
Measles immunization began in 1965, and expanded childhood immu-
nization campaigns in the later 1960s and early 1970s.92 Yet well before,
a major drop in the lethality of common endemic infections in the country
appears already to have taken place. Tuberculosis was a leading cause of
mortality in pre-1950 China, estimates suggesting 200–300 deaths annually
per 100,000 population.93 By 1957 the tuberculosis death rate in major cit-
ies was reported as 54.6 per 100,000 population, declining further to 36.2
six years later.94 Improved access to treatment through concerted efforts to
identify cases undoubtedly contributed.95 Yet levels of access to effective
treatment beyond the urban centres is unclear, with specialist tuberculosis
personnel numbering only 4 per million population in 1960.96 Moreover,
even in the major urban centres tuberculosis transmission rates, based on
Mantoux testing, appear to have remained high across the 1950s.97 A simi-
lar decline also appears to have occurred in the lethality of measles, a major
contributor to pre-1950 childhood mortality. The national case fatality rate
was estimated to be 8.6 per cent in 1950; six years later a figure of 1.6 per
cent was reported. A similar proportionate decline was recorded in Beijing.98
The sources and representativeness of the above few mortality data are
unclear, making definitive conclusions on lethality trends for many endemic
diseases yet out of reach. Improved access to preventive or curative care may

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well explain some decline in tuberculosis mortality, particularly in urban areas.

Health care services, however, are unlikely explanations for mortality decline
in the case of measles: a near-universal childhood viral infection for which
immunization or effective treatment, at the time, had yet to be developed.
The decline in death rates in post-1950 China clearly merits far more
detailed study, certainly more than is offered here. One development,
however, that suggests a major role for improved food security in declin-
ing infective disease lethality is the dramatic improvement documented in
child nutritional status. Between 1951–1958 and 1979, the mean height of
boys 12 years of age had increased by 8.4 centimetres; mean weight, by 4.2
kilograms, with comparable increases for girls.99 These figures reflect to a
large extent conditions of child feeding and care in early childhood and in
utero, and thus conditions preceding each of these two nutritional survey
periods, viz., the 1940s decade, and the mid- and later 1960s. This degree of
improved child nourishment after 1949 would have been accompanied by a
major increase in general immune-competence in the population.100
The magnitude and rapidity of nutritional improvement and rise in life
expectancy in China is historically unprecedented, an increase in human
survival that took over a century to achieve in far smaller populations in
nineteenth- and early twentieth-century Europe. In addition to the cessa-
tion of military invasion and civil warfare by 1949, the rise corresponds
temporally to initiation of major food security programs. Between 1950 and
1952, an estimated 30 to 45 per cent of China’s arable land was redistrib-
uted, bringing about an immediate narrowing of rural wealth and livelihood
disparity, and was accompanied by a 25 per cent increase in crop output by
1958.101 In urban areas, by 1955 a food ration system guaranteed access
to subsidized staple foodgrains, the ‘iron rice-bowl,’ that provided 1,800–
2,600 kcal daily per adult.102 No formal rationing system was established
for the almost 90 per cent of the population in rural China, but a system of
grain transfers from surplus to deficit areas was established to maintain ‘a
floor level of grain consumption.’103
Mortality decline would be reversed, tragically, with frank famine con-
ditions in 1960 that saw life expectancy fall that year to 1930s levels:104
an inverse example – quite possibly largely preventable – of the mortality-
hunger link. The earlier trend soon resumed, however, with life expectancy
reaching an estimated 61 years by 1969.105
The composition of the diet in China between 1950 and 1970 remained
essentially unchanged from its traditional content: based almost entirely on
traditional staple foodgrains and tubers.106 But it was much more secure,
and sufficient, it appears, to satisfy hunger for many. Few aspects, however,
of the food security programs established in these initial years are traced in
the GHLC report.107
Considerable undernourishment still remained in China in 1975, affect-
ing 23 per cent of young suburban children; and one-third of the population

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still lived in absolute poverty, levels that were far higher in the poorest west-
ern and southwestern provinces of the country.108 Thus further improvement
in child and adult nourishment nationally likely continued to contribute to
ongoing decline in mortality levels in the post-1975 period, life expectancy
reaching 71 years in 1999–2000.109

Kerala state
Infant mortality in the southwestern Indian state of Kerala fell rapidly from
120 deaths per 1,000 live births in the 1950s to 39.1 by 1981, and further
to 15 by 1990.110 The 1960s and 1970s was a period of major economic
reforms, policies that included modest land reforms, security of tenancy
legislation, a rural Public Distribution System (PDS or ‘fair price shops’)
program, minimum wage legislation, and in the 1970s agricultural labourer
pensions.111 These reforms were accompanied by important expansion of
rural health care services112 and primary education, overlap that makes
assessment of relative roles in mortality decline in the state more challenging.
Once again, however, trends in childhood nutritional status shed impor-
tant light. Despite below-average mean per capita calorie intake for Kerala
state as a whole compared to all-India figures, prevalence of severe malnu-
trition among young children (weight less than 60 per cent normal) in Ker-
ala by the 1970s was recorded already below levels in other states, at 10.2
per cent. By the 1980s, reported severe malnutrition prevalence was down
to 2.0 per cent.113 The significance of this decline lies in the five- to 10-fold
greater mortality risk for severely underweight children relative to normal
growth, or even to lesser degrees of undernourishment.114 By 1976 as well,
the height of rural school boys 6 years of age in the state had increased by
4.9 cm relative to 1963.115 In contrast to this improvement in child stature,
there is little evidence that sanitation and protected water supply improved
substantially. As in China, intestinal parasitic infection rates remained
extremely high as late as the early 1980s.116
Curiously, data on trends in prevalence of severe undernourishment in
young children are not included in the Kerala case study analysis, nor those
on increased child stature. Moreover, little exploration of the potential
impact of the economic reforms for food security was offered.117 Instead,
based upon aggregate (state-level) per capita caloric consumption figures
and Gini coefficients, the case study at one point concluded that ‘nutritional
differences cannot explain the lower mortality rate in Kerala’ relative to
other Indian states.118

Tamil Nadu
Twenty-five years later, a further series of case studies was undertaken as
a follow-up to the original 1985 Good Health at Low Cost report. In this

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case, the focus was directed even more specifically to ‘health systems’: pre-
ventive and curative care health services.119 Among the cases included in the
2011 report was that of the south Indian state of Tamil Nadu, neighbouring
to Kerala. Between 1983 and 2005, infant mortality had declined from 100
deaths per 1,000 live births to 35 across the state, a period that saw expan-
sion of rural primary health care services through ‘village health nurses’ and
a thorough overhaul of the rural supply of essential drugs and laboratory
services – both extremely welcome initiatives.120 Once again, however, little
information was provided on the timing of these programs in relation to the
trajectory of child mortality decline. But unmentioned also were major rural
food security programs launched in the state in the 1980s and early 1990s.
Initiated in the wake of the 1985 state election, a Public Distribution
System (‘fair price shops’) guaranteed rural access to 20 kgs of rice per vil-
lage household each month at controlled and subsidized prices. Its timing
appears to have corresponded to the initial major drop in infant mortality
to 65 per 1,000 live born by 1991, following a 1970s decade of stagnating
rates.121 And as in Kerala, this drop was associated with a major decline in
the prevalence of severe undernourishment in young children: from 13.9 per
cent in 1983–1984 to 4.2 per cent by 1988–1990122 – data that also do not
appear in the case study analysis.123 Subsequently, 25,000 village creches
were established for children 0 to 3 years of age, as well as maternity ben-
efits of Rs 300 for ‘nutritional support.124

View from a southern Tamil Nadu village

In light of the limited attention directed to basic subsistence issues in the
two GHLC documents, one glimpse of how the new food security pro-
grams in Tamil Nadu state were perceived at village level is offered here.
When asked by the author in early 1997 how child health conditions in the
southeastern district of Ramanathapuram had changed from 17 years ear-
lier, Rakku, traditional midwife of Puliyur village, turned to a small box on
the shelf of her thatched one-room home. Taking out her household ration
card, she pointed to the family’s rice allotments, marked in monthly instal-
ments. Then she gestured to the local ‘fair price’ shop at the village’s edge
and explained how she would ‘sell’ her sugar and kerosene ration to ‘big’
(landowning) households during periods of scarce daily wage employment,
the modest earnings helping her to purchase ragi, a local staple millet, to
bridge seasonal livelihood gaps. She went on to describe the more recent
establishment of a child care centre where women could leave their infants
and toddlers for care during field labour through the day.125
Beyond the impact, momentous enough, of stable foodgrain prices across
the agricultural year, and their modest subsidy through the ration shop,
what the midwife described might be considered a type of ‘micro-credit’
benefit of the PDS program – if unintended perhaps by administrators. Its

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impact went beyond the direct nourishing of young children. In a small but
concrete way, the PDS program appears to have effected a shift in relations
of dependency within the village: the ration card replacing to some extent
the traditional role of the village landlord-moneylender, a function now in
her own possession (if in her husband’s name) and that of other landless,
illiterate dalit women.126
The realities of hand-to-mouth subsistence, understood intimately by the
women of Puliyur village, are captured poorly, one can suggest, in aggregate
econometric analyses. Even less so are the constraints of time that subsist-
ence realities ordain for the feeding of their young children, including those
in utero – above all, the necessary frequency of ‘meals-per-day’ required
by infants and toddlers. Such constraints, and gaps, remain largely unre-
corded, and invisible. Likewise, too, it seems, their beginning alleviation,
and the shift in female empowerment that even modest food security poli-
cies instantiate.
Discussion of women’s ‘empowerment’ can at times be left at a some-
what abstract level, interpreted primarily in terms of access to health care
services. Such services are of course fundamentally important also for these
women and their children. But there can often be limited acknowledgement
of the importance of minimum food and employment security in allowing
women to access that care without jeopardizing the survival of other chil-
dren and the larger household. Similarly, minimally sufficient time and work
flexibility for women to attend to child feeding and care during episodes
of diarrhea and other common childhood infections is crucial for ensuring
recovery and lessening nutrient drain.127
The further removed by class, caste, and personal experience analysis is
from the subsistence lives of such women, the less comprehensible, it seems,
insufficient and insecure daily subsistence can become. There is some irony
in this. For in disciplines outside medical and health historiography, the con-
sequences of food insecurity on mortality are more evident. A central meth-
odological tool in historical demographic research, for example, involves
examining mortality patterns in response to foodgrain price levels (‘price
shocks’) as an indicator, if crude, of shifts in access to staple food.128 In a
different domain, the importance of food security was a founding premise
of the International Labour Organisation in 1919: an understanding that
‘[p]ay and social security benefits were the keys to good health.’129 Two
decades later, the hunger-epidemic relationship remained strategically self-
evident within the halls of post-WW2 Western geopolitical power, as we
have seen, giving rise to the 1942 Hot Springs food conference and subse-
quent establishment of UNRRA and the FAO.130
Yet in modern epidemic historiography such understanding has waned.
Disease epidemics are more comprehensible, and visible, than are epidem-
ics of hunger, or for that matter, is endemic hunger. ‘It is striking,’ Michel
Garenne and colleagues have observed of the 1987–1989 malaria epidemic in

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Antananarivo, Madagascar, ‘that malaria came back at about the same time’
as food shortage and soaring prices. ‘Perhaps more striking still,’ they add,

the malaria epidemic, which killed about 700 people in the city in
three years, has been well documented and studied. Indeed, several
scientific publications and many articles in local and international
newspapers have appeared on the subject. However, the more silent
food shortage which killed perhaps 11 times more people has been
ignored.131

‘News coverage and scientific publications,’ they suggest, ‘do not always
follow a demographic logic. . . . Diseases or causes of death which for some
reasons are considered to be shameful tend to be ignored.’132 The GHLC
and Antananarivo analyses are but two among many examples of a reced-
ing visibility of subsistence (in)security in contemporary health, and health
history, analysis, and of the limitations this poses for interpreting historical,
and recent modern, experience of mortality decline.133
It bears restating perhaps that the attempt in this study to reclaim human
subsistence in health historiography is not a dismissal of the value of mod-
ern medical and public health techniques or safe water supply. Each of the
health care programs detailed in the GHLC case studies is indisputably
important for saving lives. Anti-natal tetanus toxoid and anti-diphtherial/
pertussis immunization, two examples among many, are true ‘wonder’ tech-
niques in the ease of their administration and the numbers of newborns and
young children saved – deaths for which ‘daily bread’ in such cases could
offer limited or negligible protection. So also is emergency obstetrical care,
and assured access to a range of basic drugs. A right to all is fundamental.
Indeed, the importance of assured access to such preventive and curative
services is far greater for those who can least afford livelihood losses associ-
ated with even brief periods of physical incapacity.
Nor is attention to human subsistence a denial of public health ‘agency’
such as the efforts of those who struggled for reforms in housing and water
supply in early twentieth-century Beijing or in the slums of nineteenth-
century industrializing Britain. The importance of a strong public health
system in addressing continuing disease outbreaks and the emergence of
new ones is of eminent importance, as evidenced with recent HIV, Ebola,
SARS, and most recently, Zika epidemics. But public ‘agency’ clearly was
not limited to germ-transmission control interventions in the case study
countries above, nor indeed in Britain a century earlier where historic shifts
in conditions of work and livelihood security ultimately took place through
the efforts of the emerging trade unions and labour-oriented political move-
ments in achieving economic and social welfare legislation.134
Ultimately, measures of disease control cannot substitute for subsist-
ence security because hunger undermines survival chances not for a single

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infective disease, but for a host of common endemic infections. Those chil-
dren most at risk of succumbing to a specific infection such as measles or
pneumonia by virtue of undernourishment-compromised immune capacity
are more vulnerable to a range of other endemic infections at other times of
the year – including those microbes represented in the catch-all ‘pulmonary-
diarrhea complex’ category, still responsible for up to one-third of all pre-
ventable childhood deaths in the modern non-industrial world:135 in the
words of the 1878 Punjab Sanitary Commissioner, ‘distress for food . . .
render[ing] them incapable of resisting the assaults of any disease going.’136
At another level, when analysis is directed principally to technical interven-
tions to specific diseases one can suggest there is often limited comprehen-
sion of the magnitude of prevented deaths that underlie secular trends in life
expectancy for entire populations – indeed, of even a few years’ increase.
It is not a matter, then, of choosing between health care systems and food
security, but of addressing both. Yet the relative sidelining of food security
policies in recent analysis of the modern mortality decline suggests instead
a fundamental loss in understanding of the central role of staple-food secu-
rity in ‘good health,’ and of the importance of conditions of women’s work
upon which child nourishment depends.137 These are issues that take on
even wider contemporary significance with the challenges already unfold-
ing with global climate destabilization. In this context, perhaps one of the
more important insights from the 1985 GHLC report is the finding that the
composition of the diet for all three Asian populations studied had remained
essentially unchanged from its traditional content across the period of dra-
matically rising life expectancy: which is to say, staple food made up almost
entirely of traditional foodgrains and tubers.138 Nothing fancy, in other
words: sufficient daily ‘bread.’

A larger significance to South Asian malaria history

One example of the importance of staple-food security can be seen,
inversely, in the 1950s experience in Punjab139 where abrupt interruption in
malaria transmission appears to have had only a marginal effect, at most,
on general mortality levels – suggesting, in other words, that post-1920
decline in acute hunger accounted for most of the reduction in the region’s
historical malaria mortality burden, though much ‘chronic’ undernourish-
ment remained.140 Across the final years of the nineteenth-century, there
was increasing awareness in British India of malaria as the leading ‘vehi-
cle’ by which acute hunger markedly magnified death rates from autumnal
malaria infection. During this period and into the early twentieth century,
epidemiological analysis transcended the conceptual constraints of sanita-
tionist epidemic theory of the British metropole, where epidemic causality
had increasingly been reduced to ‘exciting’ or ‘precipitating’ factors. First
queried by W.R. Cornish in his painstaking account of famine mortality

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in the 1876–1877 Madras famine, those reductive conceptual constraints

were formally challenged two decades later in the pages of the 1901 Fam-
ine Commission Report.141 Moreover, for reasons that included looming
imperial exigencies, this understanding of the hunger-epidemic malaria
relationship was soon extended beyond episodic famine (epidemic acute
starvation), to include the general ‘difficulties under which the people
. . . get their food supply . . . throughout the year.’ In the wake of the 1918
influenza epidemic, the Madras Corporation in its 1919 annual report
stressed the ‘potent influence’ of economic conditions upon the death rates
of the population.

Supplies may exist and still be beyond the purchasing power of

many members of the population . . . the excessive mortality accom-
panying the diminution of the means of support though not caused
by actual starvation is brought about by disease. The working of
this factor so easily perceived when people are dying of starvation
is often overlooked when a population is decimated by disease.142

Such non-famine conditions of economic stress S.R. Christophers would

refer to as ‘private hardship’: acute hunger triggered by injury, debility, or
individual loss of employment or of a household wage-earner; but also man-
ifested in ‘hunger seasons,’ regular intervals where little agricultural employ-
ment was available and increasingly unremunerative work was resorted to
in an effort to stave off frank starvation.143
Already, at the third annual meeting of the General Malaria Commit-
tee in 1912, Bentley stressed the distinction between infection and disease,
and pointedly challenged the view ‘that our knowledge of malaria . . . [based
upon] blood examination, spleen counting, . . . dissection of anopheles, and
the mapping out of [vector] breeding places . . . is now so complete that it
can be reduced to mathematical formulae.’

[A]lthough the brilliant discoveries of Laveran and Ross have

extended our knowledge of the parasitology of malaria . . . we are
still ignorant of many of the factors responsible for the occurrence
of malaria disease, more especially when it appears in epidemic form
among populations like those to be met with in India; and there are
reasons for believing that until our conception of infectious diseases
in general and malaria in particular undergoes a radical change,
these gaps in our knowledge may not only remain unfilled but actu-
ally pass unrecognized.144

The ‘radical’ change envisioned by Bentley entailed recognition of the

immense variation in clinical morbidity and mortality historically observed
for common endemic infections under conditions of hunger-induced

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suppression of immune capacity. In a very concrete sense, a small hand-

ful of malaria researchers in early twentieth-century South Asia had found
themselves undertaking an epidemiology of what W.P. Alison in Scotland
articulated almost a century earlier as the ‘grand level of Poverty itself.’145
Bentley’s fears, and Forster’s a decade later, that comprehension of the
role of hunger in epidemic and endemic mortality patterns in British India
was being lost would prove well founded. In the case of malaria, the three
decades 1920–1950 were a key period of contestation in Western infec-
tious disease thought in which acknowledgement of the distinction between
infection and morbid disease was in marked retreat in international fora –
which is to say, at a point in time when subsistence precarity yet remained
a central dimension of public health in much of the then malaria-endemic
world.
In December 1949, with growing Western optimism for residual insecticide-
based malaria eradication, V. Venkat Rao would survey malaria control
efforts in India and conclude with a prophetic warning that ‘[t]he human
factor involved in epidemic malaria has not perhaps received the emphasis
that it deserves.’146 His reference was possibly the last to a concept which
had centrally informed malaria research and analysis three decades before,
in that ‘golden age’ of malaria research.147 That it could fade so thoroughly,
and so rapidly, from medical and intellectual discourse – though the practi-
cal reality of hunger remained pervasive in the society in which he worked –
speaks to how many fundamental concepts relating to disease and social
conditions had already been set aside. Ironically, across this period of con-
ceptual demise, a demonstrable ‘success’ in one area of malaria control was
unfolding quietly in the background: the near elimination after 1920 of the
once ‘fulminant’ malaria epidemics of northwest India, unfolding without
external philanthropic expertise, without vector sanitation, or indeed with-
out any perceptible decline in malaria transmission rates among the rural
population. But rather with the politically imperative control of epidemic
acute hunger. Yet this quiet pre-DDT success would fail to be reflected in
the new, post-WW2 World Health Organization, as the region’s exactingly
documented historical experience was set aside.
The demise in understanding of the role of destitution in South Asian
malaria history – and its inverse, the triumph of the ‘malaria as block to
development’ thesis – stemmed from a confluence of forces: academic, pro-
fessional, technological, and geopolitical, with antecedents that predated
the 1908 Punjab epidemic. In one sense, ‘malariology’ as a discipline could
no longer ‘see’ or know what was missing because, for new entrants to the
profession, elemental concepts and the very language of human hunger were
gone. Relatively few medical figures were left in modern tropical medicine
institutes who had extensive field experience of malaria in relation to acute
hunger, or the broader professional stature, to be in a position to argue suc-
cessfully those insights.

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Now in his mid-70s, Christophers did not attend the 1948 Washington
Malaria Congress. Though he would be formally lauded in absentia for his
life-time malaria research by congress attendees,148 economic dimensions to
malaria formed no part of the proceedings. At the very end of the twentieth
century, An Illustrated History of Malaria would commemorate the great
medical figures who contributed historically to the elucidation of malaria
science. Among the 129 photographic portraits and 346 names included in
the text’s index, S. Rickard Christophers was missing.149
What happened a century earlier in the lead-up to and formulation of the
1842 Sanitary Report, Hamlin suggests, was ‘not a beginning, but the kind
of revolutionary change that obliterates an earlier landscape,’ one where a
broader predispositionist understanding of disease came to be ‘intention-
ally effaced from professional memory.’150 With scarcely less efficiency, and
possibly no less intentionality on the part of key figures, a similar effacing
was re-enacted a century later with the relinquishing of earlier research and
understanding of the ‘Human Factor’ in malaria. In the process, historical
common experience, and arguably common sense itself, was set aside. Bind-
ing together the two (public) health histories was the Chadwickian sanita-
tionist legacy in which the very language of hunger had been erased.

Notes
1 See ch. 4, note 4.
2 C. Hamlin, Public Health and Social Justice in the Age of Chadwick (Cam-
bridge: Cambridge University Press, 1998), 289.
3 W.P. Alison, Observations on the Management of the Poor in Scotland, and Its
Effects on the Health of Great Towns, 2d ed. (Edinburgh: Blackwood, 1840),
10–11. For a comprehensive overview of Alison’s work as professor of medicine
at Edinburgh University and Edwin Chadwick’s ‘nemesis,’ see C. Hamlin, ‘Wil-
liam Pulteney Alison, the Scottish Philosophy, and the Making of a Political
Medicine,’ Journal of the History of Medicine and Allied Sciences, 61, 2, 2006,
144–186.
4 C. Hamlin ‘Predisposing Causes and Public Health in Early Nineteenth-Century
Medical Thought,’ Society for the Social History of Medicine, 5, 1, Apr. 1992,
43–70.
5 Hamlin, Public Health and Social Justice, 195–196.
6 See ch. 7, at notes 30 to 36; also, S. Zurbrigg, Epidemic Malaria and Hunger in
Colonial Punjab (London and New Delhi: Routledge, 2019), 264–265.
7 R. Passmore and T. Sommerville, ‘An investigation of the effect of diet on the
course of experimental malaria in monkeys,’ Journal of the Malaria Institute of
India, 3, 4, Dec. 1940, 447–455, 448 [hereafter, JMII].
8 In the specific case of epidemics among labour camps ‘[i]t seems more prob-
able,’ they concluded, that ‘labour forces are exposed to infection with strains of
malaria parasites to which they have previously had no opportunity of acquiring
immunity’; ibid.
9 P. Russell, L.S. West, R.D. Manwell, Practical Malariology (Philadelphia: W.B.
Saunders, 1946), 374. As had Ross in his criticism of the work at Mian Mir,
Russell would fault Christophers for ‘largely ignor[ing]’ the anopheline factor in

251
 W H AT WA S L O S T

the 1911 Punjab study, arguing that ‘methods for measuring anopheline density
have never been satisfactory’; ibid., 376.
10 Hamlin, Public Health and Social Justice, 196 [emphasis in original].
11 E. Ackerknecht, ‘Hygiene in France, 1815–1848,’ Bulletin of the History of
Medicine, 22, 1948, 117–155, at 141. For an overview of the work of Louis
René Villermé, see N. Krieger, Epidemiology and the People’s Health (Oxford:
Oxford University Press, 2014), 78–80.
12 Ackerknecht, ‘Hygiene in France,’ 144.
13 R.M. Packard, ‘Malaria Dreams: Postwar Visions of Health and Development in
the Third World,’ Medical Anthropology, 17, 1997, 279–296, at 280.
14 Noting Gill’s reference to famine as a contributing factor in the 1934–1935 Cey-
lon epidemic, Lewis Hackett responded: ‘What is lacking to this case is any
sound evidence, other than influential opinion, that it is true.’ In acknowledging
host factors, he argued, ‘we are no longer on solid ground. We have cut loose
from our experimental data and become engaged at once in a battle of opinion.’;
L. Hackett, Malaria in Europe (Oxford: Oxford University Press, 1937), 263,
261.
15 S.P. James, S.R. Christophers, ‘Malaria in India: What the State can do to pre-
vent it?’ Lancet, 26 Jun. 1909, 1860–1862, at 1862.
16 Of course hunger too could also be observed and investigated ‘scientifically’
under controlled conditions, as S.P. Ramakrishnan would pursue; S. Zurbrigg,
‘Did starvation protect from malaria?: Distinguishing between severity and
lethality of infectious disease in colonial India,’ Social Science History, 21, 1,
1997, 27–58.
17 It would be this question that framed Thomas McKeown’s 1970s analysis of
mortality decline from infective disease in Britain: ‘The virulence of an organ-
ism is not . . . a distinct character like its size or shape; it is an expression of an
interaction between a particular organism and a particular host’; T. McKeown,
The Modern Rise of Population (London: Edward Arnold, 1976), 73. For fur-
ther discussion in relation to colonial Punjab epi-/endemic mortality history, see
Zurbrigg, Epidemic Malaria and Hunger, 406–409.
18 P. Weindling, ‘Social medicine at the League of Nations Health Organisation and
the International Labour Office compared,’ in P. Weindling, ed. International
Health Organisations and Movements, 1918–1939 (New York: Cambridge Uni-
versity Press, 1995), 134–153. [emphasis added]).
19 Famine Inquiry Commission, Report on Bengal (New Delhi: Government of
India Press, 1945), 116–123.
20 Ibid.
21 W.W.C. Topley, ‘The biology of epidemics,’ Croonian Lecture, Proceedings of
the Royal Society of London. Series B, Biological Sciences, 130, 861, May 8,
1942, 337–359.
22 W.R. Cornish, Report of the Sanitary Commissioner for Madras for 1877
(Madras: Government Central Branch Press, 1877), 11, 142, xxviii [hereafter,
MSCR]; A.P. MacDonnell, Report of the Indian Famine Commission 1901 (Cal-
cutta: Government Printing Office, 1901), 2, 61–62. For details, see Zurbrigg,
Epidemic Malaria and Hunger, 187, 329.
23 Report on Bengal, 121.
24 W.R. Aykroyd, ‘Definition of Different Degrees of Starvation,’ in G. Blix, Y.
Hofvander, B. Vahlquist, eds. Famine: A Symposium dealing with Nutrition and
Relief Operations in Times of Disaster (Uppsala: Swedish Nutrition Founda-
tion, 1971), 17–24. Dissension among 1945 Famine Commission members as
to the role of starvation in epidemic mortality may explain the vacillation in

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emphasis, with Indian members perhaps stressing testimony from earlier famine
commission reports, and Aykroyd, judging from later statements, veering to the
microbial: some form of ‘consensus’ ultimately reached by deferring to Topley’s
‘complexity.’ In a subsequent overview of the Bengal famine, Aykroyd would
also refer to the ‘[r]efugees from Burma [who] poured into Bengal through
Assam and Chittagong, bringing with them a virulent form of malaria’; The
Conquest of Famine (London: Chatto & Windus, 1974), 72.
25 N.S. Scrimshaw, C.E. Taylor, J.E. Gordon, Interactions of Nutrition and Infec-
tion (Geneva: World Health Organization, 1968); N.S. Scrimshaw, ‘The Phe-
nomenon of Famine,’ American Review of Nutrition, 7, 1987, 1–21.
26 Zurbrigg, Epidemic Malaria and Hunger, ch. 12.
27 Ibid., 384, 281. Moreover, hunger itself likely has played a substantial role sec-
ondarily in maintaining transmission of major infective diseases such as tuber-
culosis; and certainly in the severity of others, as suggested by Punjab malaria
history in relation to dose of infection; ibid., ch. 5.
28 Hamlin, ‘Social Justice and Public Health,’ 11.
29 See, e.g., E. Whitcombe, ‘Famine Mortality,’ Economic and Political Weekly, 28,
1993, 1169–1179; B. Mohanty, ‘Case Study of the Indian Famines of 1896–97
and 1899–1900,’ in S.N. Singh, et al., eds., Population Transition in India, v. 2
(Delhi: B.R. Publishing, 1989), 371–379.
30 P.J. Marshall, Bengal: The British Bridgehead: Eastern India 1740–1838 (Cam-
bridge: Cambridge University Press, 1987); I. Klein, ‘Population Growth and
Mortality in British India Part I: The Climacteric of Death,’ Indian Economic
and Social History Review, 26, 4, 1989, 387–403 [hereafter, IESHR].
31 Marshall, Bengal: British Bridgehead, 4–5, 20.
32 M.O.T. Iyengar, ‘Studies on Malaria in the Deltaic Regions of Bengal,’ JMII,
Dec. 1942, 435–446.
33 Klein considers both, but ultimately argues the impact of increased vectors ‘far
outpaced any agricultural decline from soil decay’; ‘Development and death:
Reinterpreting malaria, economics and ecology in British India,’ IESHR, 38,
2, 2001, 147–179. Yet the effect of interrupted inundation flows on cropping
frequency would have been immediate, as Bentley conveyed; C.A. Bentley,
‘Some economic aspects of Bengal malaria,’ IMG, Sept. 1922, 321–326; Bentley,
Malaria and Agriculture in Bengal. How to reduce malaria in Bengal by irriga-
tion (Calcutta: Bengal Govt Press, 1925). For recent Burdwan fever analysis, see
ch. 1, note 56.
34 Zurbrigg, Epidemic Malaria and Hunger, 273–276.
35 See also, Zurbrigg, ‘Did Starvation Protect from Malaria?’
36 A. Sen, Poverty and Famines: An Essay on Entitlement and Deprivation (Oxford:
Oxford University Press, 1981); A. Maharatna, The Demography of Famines:
An Indian Historical Perspective (Delhi: Oxford University Press, 1996).
37 E. Whitcombe, ‘The Environmental Costs of Irrigation in British India: Water-
logging, Salinity, Malaria,’ in D. Arnold, R. Guha, eds., Nature, Culture, Impe-
rialism: Essays on the Environmental History of South Asia (Delhi: Oxford
University Press, 1995), 237–259; K. Wakimura, ‘Epidemic malaria and “Colo-
nial Development”: Reconsidering the Cases of Northern and Western India,’
Economic History Congress XIII, Buenos Aires, Argentina, July 2002, mimeo.
38 The apparent paradox has redirected interpretation of South Asian mortality
decline away from ‘nutritional’ explanations to instead immunological hypoth-
eses; Klein, ‘Population Growth and Mortality in British India,’ 392, 403; I.
Klein, ‘Population Growth and Mortality in British India Part II: The Demo-
graphic Revolution,’ IESHR, 27, 1, 1990, 33–63, at 60; Klein, ‘Development

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and Death,’ at 177–179. In contrast, others have pointed to initial shifts in food
security to explain beginning decline in mortality post-1920; S. Guha, ‘Mortality
Decline in Early Twentieth Century India: A Preliminary Enquiry,’ IESHR, 28,
4, 1991, 371–387; C. Guilmoto, ‘Towards a New Demographic Equilibrium:
The Inception of Demographic Transition South India,’ IESHR, 28, 3, 1992,
247–289.
39 Zurbrigg, Epidemic Malaria and Hunger, chs. 2, 4.
40 See, e.g., W.H. McNeill, Plagues and Peoples (New York: Anchor Books,
1976), 116.
41 ‘Malthus saw no need to appeal to learned medicine to support these claims,’
Hamlin points out, ‘for nothing he said about disease was controversial. It
seemed obvious, even truistic, that disease was deadlier to the weak than to the
strong’; Hamlin, Public Health and Social Justice, 26.
42 Surgeon-Captain H.E. Grant, The Indian Manual of Hygiene being King’s
Madras Manual, rev. ed., (Madras: Higginbotham & Co., 1894), 326.
43 C. Hamlin, More Than Hot: A Short History of Fever (Baltimore: Johns Hop-
kins University Press, 2014), 61–62.
44 Report on the Sanitary Administration of the Punjab (Lahore: Medical Depart-
ment, Punjab), 1878, 67.
45 GOI, Proceedings of the Imperial Malaria Conference held at Simla in Octo-
ber 1909 (Simla: Government Central Branch Press, 1910), 103 [hereafter Simla
Conf.].
46 S. Mackenzie, ‘The Powers of Natural Resistance, or the Personal Factor in Dis-
ease of Microbic Origin,’ The Annual Oration, May 26, 1902, Transactions of
the Medical Society of London, 25, 302–318, at 312.
47 C. Hamlin, ‘Could you starve to death in England in 1839? The Chadwick-Farr
controversy and the loss of the “social” in public health,’ American Journal of
Public Health, 85, 6, Jun. 1995, 856–866.
48 W.R. Cornish, MSCR 1877, 147.
49 P. Manson, Tropical Diseases: A Manual of the Diseases of Warm Climates
(London: Cassell and Co., 1898), 98. On this and the larger issue of malaria and
‘tropical aggregation of labour,’ see Zurbrigg, Epidemic Malaria and Hunger,
228–231.
50 Famine Commission Report (Punjab), 1900, Vol. I, 35. See Zurbrigg, Epidemic
Malaria and Hunger, 347; D. Arnold, ‘Looting, grain riots and government pol-
icy in South India 1918,’ Past and Present, no. 84, 1979, 111–145; D. Arnold,
‘Social Crisis and Epidemic Disease in the Famines of Nineteenth-century India,’
Social History of Medicine, 6, 3, Dec. 1993, 385–404, at 396.
51 See also, ch. 4, at note 52. Cornish, who attempted to tally 1876–1877 Madras
famine starvation-induced deaths, was very much the exception, sufficiently sen-
ior, experienced, and administratively and intellectually above reproach; MSCR,
1876–1877.
52 Simla Conf., 43; P. Hehir, Malaria in India (London: Humphrey Milford,
1927), 442.
53 Simla Conf., 5.
54 See, Zurbrigg, Epidemic Malaria and Hunger, chs. 7, 8.
55 Aykroyd, Conquest of Famine, 93.
56 S. Millman, R.W. Kates, ‘Toward Understanding Hunger,’ in L.F. Newman, et al.,
eds., Hunger in History: Food Shortage, Poverty, and Deprivation (Oxford: Basil
Blackwell, 1990), 3–24, at 22.
57 R.B. Lal, S.C. Seal, General Rural Health Survey, Singur Health Centre, 1944,
(Calcutta: GOI Press, 1949), 118.

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58 A.J. Coale, E.M. Hoover, Population Growth and Economic Development in

Low Income Countries: A Case Study of India’s Prospects (Princeton: Princeton
University Press, 1958), 62–67; S. Preston, ‘Causes and Consequences of Mor-
tality Declines in Less Developed Countries during the Twentieth-century,’ in
R.A. Easterlin, ed., Population and Economic Change in Developing Countries
(Chicago: University of Chicago Press, 1980), 296, 313.
59 T.W. Meade, ‘Medicine and population,’ Public Health, 82, 3, 1968, 100–110.
For a similar assessment, see, Editorial, ‘Malaria and the Population Explosion,’
Lancet, Apr. 27, 1968, 899–900.
60 Meade, ‘Medicine and population.’ In addition to GDP figures, Frederik-
sen referred to the public distribution system and agricultural development
programs.
61 Important exceptions are studies that investigate caloric consumption by income-
deciles, a rare example of which is seen in the 1937 rural Madras study discussed
in ch. 3 at note 78; W.R. Aykroyd, B.G. Krishnan, ‘Diets surveys in south Indian
villages,’ Indian Journal of Medical Research, 24, 3, Jan. 1937, 667–688.
62 That the poor continued to work despite illness is cited for its effect on infection
dissemination; less for the looming hunger that drove the sick to work, often to
death; A. Hardy, The Epidemic Streets: Infectious Disease and the Rise of Pre-
ventive Medicine, 1856–1900 (Oxford: Clarendon Press, 1993), 270–271.
63 S. Szreter, Health and Wealth: Studies in History and Polity (Rochester: Univer-
sity of Rochester Press, 2005), 313–328. McKeown, Modern Rise of Population,
156, 159. Curiously, McKeown also grouped ‘improvement in diet’ under the
umbrella term of ‘environmental’ factors, along with ‘conditions of exposure
to disease’; ‘Medicine and world population,’ Journal of Chronic Diseases, 18,
1965, 1067–1077.
64 D. Morley, Paediatric Priorities in the Developing World (London: Butterworth-
Heinemann, 1973).
65 R. Martorell, T.J. Ho, ‘Malnutrition, morbidity and mortality.’ In H. Mosley,
L. Chen, eds., Child Survival: Strategies for Research, Supplement to vol. 10,
Population and Development Review, 1984, 49–68; Scrimshaw and Gordon,
Interactions of Nutrition and Infection.
66 An important exception is seen in the work of R. Chambers, R. Longhurst, A.
Pacey, eds., Seasonal Dimensions to Rural Poverty (London: Frances Pinter,
Institute of Development Studies, 1981), 164, 167, 174.
67 For a comprehensive overview of this work, see R. Floud, R. Fogel, B. Har-
ris, Sok Chul Hong, eds., The Changing Body: Health, Nutrition, and Human
Development in the Western World since 1700 (Cambridge: Cambridge Univer-
sity Press, 2011). It is unclear however to what extent adult stature also captures
prevalence of acute hunger (semi- or frank starvation), given the much greater
associated mortality. For discussion of this distinction and likely implications for
interpreting trends in nutritional stunting in South Asia, see Zurbrigg, Epidemic
Malaria and Hunger, 25–32, 354, 410.
68 McKeown, Modern Rise of Population; McKeown, The Role of Medicine. In
part, lack of clarity regarding the meaning of ‘nutritional improvement’ left his
argument readily open to rebuttal on the basis of little demonstrable qualitative
(micronutrient) improvement in the late nineteenth- and early twentieth-century
period of initial rising life expectancy.
69 S. Szreter, ‘The importance of social intervention in Britain’s mortality decline,’
Social History of Medicine, 1, 1, 1988, 1–37.
70 Moreover, geographic and institutional distance from the dominant epis-
temic community often was too great to counter dominant germ-transmission

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paradigms in mortality decline analysis. Egyptian demographers ‘profoundly

disagreed’ with U.S. economists, for example, regarding timing of post-WW2
crude death rate decline in Egypt, finding most decline occurred in the immedi-
ate post-war years, thus pre-dating the country’s DDT malaria control program,
rather than in the 1950s as the latter argued. Their views, however, were appar-
ently disregarded; T. Dyson and M. Murphy, ‘Macro-Level Study of Socioec-
onomic Development and Mortality: Adequacy of Indicators and Methods of
Statistical Analysis,’ in J. Cleland, A. Hill, eds., The Health Transition: Methods
and Measures (Canberra: Australian National University, 1991), Health Transi-
tion Series No. 3, 147–164, at 149. On the marked mid-1940s drop in mortality
levels in Punjab associated with food rationing and a post-war economic boom,
see, Zurbrigg, Epidemic Malaria and Hunger, 392–393.
71 S.B. Halstead, J.A. Walsh, K.S. Warren, Good Health at Low Cost (New York:
Rockefeller Foundation, 1985) [hereafter, GHLC].
72 A fourth case study was Costa Rica, if somewhat less representative as a very
low-income country.
73 GHLC, 246.
74 GHLC, 200–213.
75 Ibid., 200; R. Martorell, R. Sharma, ‘Trends in Nutrition, Food Supply and
Infant Mortality Rates,’ GHLC, 200–213.
76 Food subsidies were listed in tabular form (203, 177), with a passing reference to
land reform (204, 62, 64). But brevity allowed little discussion of their potential
impact, or timing in relation to mortality decline. One contributor emphasized
that ‘the rapid growth of the national economy . . . [in China was] certainly the
material basis of the continuously progressing health status of the people,’ but
again without specific policy or timing details; ibid., 35.
77 ‘What matters most [in achieving high life expectancy] is that people come to
understand disease risks, and how to manage them. . . . Low-income countries
found low-cost ways to control these diseases, relying more heavily on educating
people to do things for themselves and less on public financing, expert interven-
tion, medical technology, or hospitals’; J.C. Riley, Low Income, Social Growth,
and Good Health: A History of Twelve Countries (Berkeley: University of Cali-
fornia Press, 2008), 5–7, 159.
78 J. Banister, China’s Changing Population (Stanford: Stanford University Press,
1987), 83; J. Banister, K. Hill, ‘Mortality in China 1964–2000,’ Population Stud-
ies, 58, 1, 2004, 55–75 at 55, reported 20 per 1,000 to 10.2 per 1,000 by 1958.
79 F.W. Notestein and Chi-ming Chiao, ‘Population,’ in J.L Buck, ed., Land Utiliza-
tion in China (Chicago: University of Chicago Press, 1937), vol. 1, 358–399. For
a summary, see Banister; China’s Changing Population, 79, Table 4.2.
80 G. Barclay, A. Coale, M. Stoto, J. Trussell, ‘A reassessment of the Demography
of Traditional Rural China,’ Population Studies, 42, 4, 1976, 605–635, at
608, 621.
81 Death rates (per 100,000) in Beijing for the 1937–1945 period also show no
decline relative to earlier decades; Campbell, ‘Mortality Change,’ 236, Table 11.3.
82 J. Banister, ‘Population Policy and Trends in China, 1978–83,’ The China Quar-
terly, 100, Dec. 1984, 717–741, at 740.; Banister, China’s Changing Population,
80. It is possible that rates of survival had improved somewhat prior to 1949
in Communist-held areas through land distribution measures; Liping Bu, Pub-
lic Health and the Modernization of China, 1865–2015 (London: Routledge,
2017), 192, 197–198.
83 Banister, China’s Changing Population, 116. See also, J. Banister, S.H. Preston,
‘Mortality in China,’ Population and Development Review, 7, 1, 1981, 98–110
at 107–108.

256
 W H AT WA S L O S T

84 Banister and Preston, ‘Mortality in China,’ 104.

85 Banister China’s Changing Population, 55; J. Salaff, ‘Mortality decline in the
People’s Republic of China and the United States,’ Population Studies, 27, 1973,
551–576 at 566.
86 Banister, China’s Changing Population, 53–54; Salaff, ‘Mortality decline,’ 563.
87 Smallpox in 1929–1931 reportedly contributed 7.7 per cent of total deaths;
Notestein and Chiao (1937) mortality survey, 393; cited in J. Banister, China’s
Changing Population, 51. Syphilis mortality is generally a later consequence
of the infection, thus lives saved due to treatment likely contributed only a
small proportion to the overall decline. Neonatal tetanus was also targeted in
the 1950s, mortality in Beijing declining from 7.2 deaths per 1,000 live births
in 1941 to 0.7 in 1957 with the shift to hospital deliveries (Salaff, ‘Mortality
decline,’ 566), though rural decline through rudimentary village midwife train-
ing is unclear. Priority was given to development of 2,379 Maternal and Child
Health (MCH) stations by 1952 (World Bank, China: The Health Sector, Wash-
ington, D.C., 1984, 14), yet each was responsible for a population of 250,000.
Moreover even had rural neonatal tetanus rates declined as fast as urban, the
contribution to infant and overall mortality decline would have been small.
88 Much has been written about the national ‘patriotic’ vector control campaigns
also initiated in the early 1950s. Their impact on transmission of endemic
infections such as malaria and schistosomiasis however has been questioned;
C. Campbell, ‘Mortality Change and the Epidemiological Transition in Beijing,
1644–1990,’ in Ts’ui-jung Liu, et al., eds., Asian Population History (Oxford:
Oxford University Press, 2001), 221–269, at 237–238; Salaff, ‘Mortality
Decline,’ 567; Banister, China’s Changing Population, 57–58. Farley points out
the extreme difficulties of controlling the snail vector of schistosomiasis; Bilhar-
zia: A History of Imperial Tropical Medicine (Cambridge: Cambridge University
Press, 1991), 284–285.
89 As of 1982, only half the urban population had access to piped water; in rural
areas, 6 per cent, with another 34 per cent benefitting from ‘improved wells.’ As
late as 1981, dysentery remained ‘the most commonly reported communicable
disease in China,’ with ‘great deficiencies’ remaining; GHLC, 192, 193; Banister,
China’s Changing Population, 64–66.
90 D. Zhang, P. Unschuld, ‘China's barefoot doctor: Past, present, and future,’ Lan-
cet. 372 (9653), 2008, 1865–1867; J. McConnell, ‘Barefoot No More,’ Lan-
cet, 341 (8855), 1993, 1275.
91 Estimated life expectancy in 1980 was 65 years; Banister, ‘Population Policy and
Trends,’ 740–741.
92 Campbell, ‘Mortality Change,’ 239.
93 GHLC, 15. Notestein and Chiao, ‘Population,’ cited in Banister, China’s Chang-
ing Population, 51; E.L. Opie, ‘Tuberculosis of first infection in adults from rural
districts of China,’ Chinese Medical Journal, 56, 3, 1939, 216–224; Bu, Public
Health and the Modernization of China, 257.
94 GHLC, 16.
95 Tuberculosis hospitals increased from 13 to 48 between 1949 and 1957; Camp-
bell, ‘Mortality Change,’ 233.
96 Ibid., 233. Much TB-control effort in the 1950s was directed to BCG produc-
tion and vaccination, the effectiveness of which has since been shown, however,
to be very limited in preventing pulmonary TB; the single exception being the
uncommon meningeal form in children; Centers for Disease Control, Morbidity
and Mortality Weekly Report, Apr. 26, 1996.
97 Salaff, ‘Mortality decline,’ 569.
98 Ibid., 566; Banister, China’s Changing Population, 56.

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99 By comparison, the ‘lack of any significant change in nutritional status during

1915–25 to 1951–58 is quite striking’; D.T. Jamison, A. Piazza, ‘China’s Food
and Nutrition Planning,’ in J.P. Gittinger, J. Leslie, C. Hoisington, Food Policy:
Integrating Supply, Distribution, and Consumption (Baltimore: Johns Hopkins
Press, 1987), 467–484, at 479; A. Piazza, Food Consumption and Nutritional
Status in the PRC (Boulder: Westview Press, 1986), 140–141, 154–155. This
improvement is all the more significant because the children represented in the
earlier 1915–1925 survey figures were school children likely from the least poor
subgroups, those attending school. No major differences in stunting prevalence
were observed between males and females in 1979; but significant regional and
urban (2.6%): rural (12.7%) differences remained; ibid., 481.
100 The leading causes of death in pre-1949 Beijing (respiratory and gastrointesti-
nal diseases, and tuberculosis) (Campbell, ‘Mortality Change,’ 235–236) are all
strongly linked to undernourishment. Reported incidence of low birth weight
(birth weight < 2.5 kg) in Shanghai also apparently declined from 6.3 per cent
in 1936–1940 to 3.2 per cent in 1950–1955; Salaff, ‘Mortality decline,’ 574.
101 Jamison and Piazza, ‘China’s Food and Nutrition,’ 477, 470, 472, Table 36.2.
102 Elizabeth Croll, The Family Rice Bowl: Food and the Domestic Economy (Lon-
don: UNRISD/Zed Press, 1983), 113.
103 Jamison and Piazza, ‘China’s Food and Nutrition,’ 470.
104 Banister, ‘Population Policy, 740.
105 Ibid., 741.
106 GHLC, 209.
107 Passing reference to ‘improvement in nutrition’ in China appears in a very
detailed account of the country’s health care system (GHLC, 24), but the reader
is directed elsewhere for data. The one case study where food security programs
were considered in somewhat more detail was Sri Lanka; GHLC, 114.
108 World Bank, China: The Health Sector, 174; Banister, ‘Mortality in China,’ 65.
109 Banister and Hill, ‘Mortality in China 1964–2000, 69.
110 GHLC, 41, 40–45; P.G.K. Panikar, and C.R. Soman, Health Status of Kerala:
Paradox of Economic Backwardness and Health Development (Trivandrum:
Center for Development Studies, 1984), 24. By 1990, infant mortality had
fallen to 15 deaths per 1,000 live births; S. Irudaya Rajan and P. Mohanachan-
dran, ‘Estimating Infant Mortality in Kerala,’ Economic and Political Weekly,
vol. 34, no. 12 (Mar. 20–26, 1999), 713–716.
111 GHLC, 64.
112 The number of primary health centres in Kerala doubled in the 1960s, as did
rural dispensaries a decade later.
113 National Nutrition Monitoring Bureau (NNMB), Report of Repeat Surveys:
1988–90 (Hyderabad: National Institute of Nutrition, Hyderabad, 1991),
55, Table 9.1. There are limitations to the earlier NNMB survey data; but the
trendline of decline in severe malnutrition prevalence in Kerala is consistent
from the late 1970s, and corresponds to trends in child stature over the same
period.
114 R. Martorell, and T.J. Ho, ‘Malnutrition, morbidity, and mortality,’ Popula-
tion and Development Review Suppl., 10, 1984, 49–68; J.C. Waterlow, et al.,
Protein-energy Malnutrition (London: Edward Arnold, 1992), 336, Fig. 18.4.
115 Panikar and Soman, Health Status of Kerala, 28. Between 1961–1962 and
1983, calorie intake in Kerala increased by 40 per cent; B.G. Kumar, ‘Quality
of Life and Nutritional Status: A reconsideration of some puzzles from Kerala,’
in P. Bardhan, M. Datta-Chaudhuri, and T.N. Krishnan, eds., Development
and Change: Essays in Honour of K.N. Raj (Bombay: Oxford University Press,

258
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1993), 318–340, at 321. For assessment of the impact of the PDS program
on low-income household food consumption, see e.g., S.K. Kumar, ‘Impact of
Subsidized Rice on Food Consumption and Nutrition in Kerala,’ International
Food Policy Research Institute, Research Report, no. 5, Jan. 1979.
116 Panikar and Soman, Health Status of Kerala 74–75. Over 90 per cent of school
girls in 1980 were found with intestinal nematode infections, and over 70 per
cent with ascariasis. Moreover, infant and child mortality rates were similar in
households with pipe water source compared to wells; also with flush toilet,
latrine, or neither; GHLC, 193, 194.
117 For example, in a single stroke the PDS program substantially mitigated sea-
sonal foodgrain price swings (‘hunger seasons’), and security of dwelling (own-
ership of housing plots) arguably would have helped empower the landless 30
per cent of households to insist on newly legislated minimum wage levels.
118 GHLC, 63, 73. To be fair, reliable data from initial 1970s NNMB survey work
may not have been available to analysts in the early 1980s, although it appears
data on child stature was. Based solely upon aggregate calorie availability,
Kerala continues to be seen as one with malnutrition levels ‘among the highest
in India’; D. Lal, The Hindu Equilibrium (Oxford: Clarendon Press, Oxford,
2005), 323.
119 D. Balabanova, M. McKee, A. Mills, eds., ‘Good Health at Low Cost’: Twenty
Years On (London: London School of Hygiene and Tropical Medicine, 2011)
[hereafter, GHLC-25]. The 2011 report’s overview of ‘lessons gained’ from the
earlier 1985 GHLC analysis pointed again, in the case of China, to the control
of communicable disease transmission and to barefoot doctors; with food secu-
rity policies unmentioned; ibid., 2–3, 236.
120 GHLC-25, 172, 176–177. Most recently 24-hour emergency medical ser-
vices has been extended through a growing network of rural health centres;
ibid., 188.
121 GHLC-25, 166, Fig. 6.2.
122 Report of the NNMB-NNSO Linked Survey, 1983–84, National Institute of
Nutrition: Hyderabad, Table 20; Report of the First Repeat Rural Surveys
[1988–90], National Institute of Nutrition: Hyderabad, 55. Though the 1988–
1990 NNMB survey reports ‘very little change in average income status’ in
the state, average calorie intake among children 1–3 years was found to have
increased by 9 per cent and among 4–6 year-olds by almost 13 per cent; NNMB
1988–90, 12, 18, 47.
123 The Tamil Nadu report mentions increased industrial and transportation
development across the state, as well as passing reference to the Noon Meal
Scheme for school children, but with little exploration of the impact on food
security or timing in relation to infant mortality decline; GHLC-25, 184–185.
Most recently, the PDS has expanded to include wheat flour and lentils; www.
tncsc.tn.gov.in/PDS.html; and Tamil Nadu has successfully implemented the
National Rural Employment Guarantee program; J. Drèze, A. Sen, An Uncer-
tain Glory: India and its Contradictions (Princeton: Princeton University Press,
2013), 168–176.
124 R. Chhabra, ‘Reaping rewards of social development,’ People and the Planet,
3, 3, 1994, 16–20.
125 Personal interview, February 1997.
126 ‘We have seen the close links between seasonality, poverty and dependence. If
counter-seasonal programmes can enable the poorer rural people to gain more
adequate flows of food and income and to become less vulnerable and less
dependent, they may then be more able and ready to assert themselves. More

259
 W H AT WA S L O S T

food and better health may provide the physical and psychological precondi-
tions for political organization and pressure to achieve reforms’; R. Chambers,
S. Maxwell, ‘Practical Solutions,’ in Chambers, Longhurst and Pacey, eds., Sea-
sonal Dimensions to Rural Poverty, 226–240, at 238.
127 Studies in contemporary West African agricultural populations vividly docu-
ment pronounced rainy-season weight loss and infant/toddler failure to grow;
M.G.M Rowlands, et al., ‘Seasonality and the Growth of Infants in a Gam-
bian Village,’ in Chambers, Longhurst and Pacey, eds., Seasonal Dimensions
to Rural Poverty, 164–174. See also, A.M.K. Chowdhury, S.L. Huffman, and
L.C. Chen, ‘Agriculture and Nutrition in Matlab Thana, Bangladesh,’ ibid.,
52–66.
128 See, e.g., Allen, R.C., T. Bengtsson, and M. Dribe, eds., Living Standards in the
Past: New Perspectives on Well-Being in Asia and Europe (Oxford: Oxford
University Press, 2005).
129 P. Weindling, ‘Social medicine at the League of Nations Health Organisation
and the International Labour Office compared,’ in Weindling, International
Health Organisations, 139.
130 See above, ch. 6 at notes 91–95. See also, J.H. Perkins, Geopolitics and the
Green Revolution: Wheat, Genes, and the Cold War (New York: Oxford Uni-
versity Press, 1997), 128.
131 M. Garenne, D. Waltisperger, P. Cantrelle, O. Ralijona, ‘The Demographic
Impact of a Mild Famine in an African City: The Case of Antananarivo, 1985–
87,’ in T. Dyson, C. Ó Gráda, eds., Famine Demography: Perspectives from the
Past and Present (Oxford: Oxford University Press, 2002), 204–217.
132 Ibid.
133 In a 2015 analysis of post-1949 mortality decline in China, food security poli-
cies were hardly mentioned. Nor were child nutrition indices reported. ‘Nutri-
tion’ was addressed solely in terms of per capita provincial grain production,
price trends, and an undefined ‘campaign against malnutrition’ in four west-
ern provinces, possibly a local selenium micronutrient deficiency program
(Table 2); the authors concluding that ‘increases in educational attainment and
public health campaigns jointly explain 50–70 per cent of the dramatic reduc-
tions in infant and under-five mortality between 1950 and 1980’; K.S. Babiarz,
et al., ‘An Exploration of China’s mortality decline under Mao: A provincial
analysis, 1950–80,’ Population Studies (Camb), 69, 1, 2015, 39–56. Interest-
ingly, almost four decades ago, Chambers and colleagues observed, ‘[t]he very
high life expectancies and low fertility of Sri Lanka and Kerala are usually
attributed to education, health services, and late marriage. It is at least possible
that a major factor is the exceptional food security of poor families in those two
regions’; Chambers, et al., eds., Seasonal Dimensions to Rural Poverty, 231.
134 For a glimpse of the political impact of such efforts on hours and conditions of
work both in Britain and British India, see ch. 1, at notes 30–36.
135 C.L. Fischer-Walker, et al., ‘Global burden of childhood pneumonia and diar-
rhea,’ Lancet, 381 (9875), 2013, 1405–1416.
136 Punjab Sanitary Commission Report, 1878, 28–29.
137 The question of the ‘nutrition drain’ associated with recurrent infections, and
related impact of clean water and sewerage infrastructure interventions, can be
seen also within a wider additional context that encompasses subsistence (in)
security: the constraints of time available for nourishing young children through
the frequent infections of childhood. In this sense, the time- and energy-sparing
impact of ready access to safe water is likely also to encompass a ‘nutritional’
element.

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138 GHLC, 209. Moreover, decline in mortality levels was at least as great in the
Asian case study countries where staple foods were primarily grains and tubers,
as in Cuba and Costa Rica where the traditional diet included considerable
amounts of food of animal origin.
139 Zurbrigg, Epidemic Malaria and Hunger, ch. 12.
140 Ibid., 384.
141 See above, note 22.
142 Annual Report of the Madras Corporation, Health Dept, 1919, 2.
143 S.R. Christophers, ‘Endemic and Epidemic Prevalence,’ in M.F. Boyd, ed.,
Malariology (Philadelphia: W.B. Saunders, 1949), 698–721, at 715. For a con-
temporary portrait of seasonal hunger by women landless labourers in Mid-
napore district, West Bengal, see N. Mukherjee, A. Mukherjee, ‘Rural Women
and Food Insecurity: What a Food Calendar Reveals,’ Economic and Political
Weekly, Mar. 12, 1994, 597–599. See also note 127.
144 C.A. Bentley, ‘A New Conception Regarding Malaria,’ Proceedings, 3rd Meet-
ing of the General Malaria Committee, Nov. 18–20, 1912, held at Madras
(Simla: Govt. Monotype Press, 1913), 61–84 [emphasis added].
145 W.P Alison, Observations on the Management of the Poor in Scotland, x. I am
indebted to Christopher Hamlin for insights into the significance of Alison’s
work.
146 V. Venkat Rao, ‘A critical review of malaria control measures in India,’ IJM, 3,
4, Dec. 1949, 313–326, at 324.
147 Three years later, the Director of the Malaria Institute would highlight Christo-
phers’s ‘famous memoir,’ Malaria in the Punjab, that ‘has remained an authori-
tative report on the subject’ of malaria, yet refer to its economic conclusions
only obliquely: ‘In places like the Punjab . . . there is no well marked innate
immunity and there are periodic severe or fulminating epidemics . . . the result,
under certain circumstances, of exceptionally heavy rainfall accompanied by
river flooding, usually following one or more years of comparative drought’;
Jaswant Singh, ‘Malaria and its Control in India,’ Perspectives in Public Health,
72, 1952, 515–525, 515–516 [emphasis added].
148 In presenting the Laveran Prize to H.E. Shortt at the 1948 International Malaria
Congress in Washington, N.H. Swellengrebel referred to Shortt’s work (iden-
tifying the long-missing exoerythrocytic stage of development of the malaria
parasite in humans) as ‘a builder of bridges spanning chasms of ignorance . . .
like that other constructor of foundations, the man we admire so much, Sir
Rickard Christophers. . . . I want your name coupled with his.’ He added,
‘[s]ome of our friends from India and Pakistan called Sir Rickard their father.
In time to come they may call you by that name’; ‘Presentation of the Laveran
Prize to Prof. Henry E. Shortt by Prof N.H. Swellengrebel,’ Proceedings of the
Fourth International Congress on Tropical Medicine and Malaria, 19–20.
149 C.M. Poser, Geo. W. Bruyn, An Illustrated History of Malaria (New York:
Parthenon Publ., 1999). In a remarkable parallel, Hamlin notes how ‘Alison
is oddly absent from big-picture histories of public health’; ‘William Pulteney
Alison, the Scottish Philosophy,’ at note 1.
150 ‘Public Health and Social Justice,’ 18.

261
 Appendix I
MALARIA TRANSMISSION
IN PUNJAB

Malaria is caused by a single-cell protozoan parasite (Plasmodium), its

transmission involving a complex life cycle with two stages of development.
The first stage takes place in humans who form the ‘reservoir’ of infection;
and the second occurs in particular species of Anopheles mosquitoes. Trans-
mission of malaria to the human host occurs through the bite of an infected
female mosquito, its blood meal being required for egg production. Para-
sites (‘sporozoites’) are transmitted along with the insect’s saliva that acts
as an anticoagulant, and are rapidly sequestered in the liver of the human
host. After one to two weeks, large numbers of ‘merozoites’ are released
into the blood stream and infect red blood cells. Characteristic symptoms of
episodic fever and chills begin to appear as successive batches of the para-
site break down red blood cells, are released into the circulation, and infect
further blood cells. Subsequently some merozoites differentiate into male
and female gametocytes, at which point the human host becomes infective
to further feeding mosquitoes, initiating the second (‘extrinsic’) phase of
the parasite’s life cycle. With fertilization of the male and female gametes
inside the insect gut, sporozoites develop in the stomach wall, multiply, and
migrate to the mosquito’s salivary glands where the cycle begins again.
Successful completion of the Plasmodium life cycle thus requires two
blood meals by the vector mosquito a minimum of 10 days apart, an inter-
val allowing sufficient time for development of the parasite inside the insect.
Thus, transmission hinges upon anopheline lifespan, determined by both
temperature and atmospheric humidity. Under ideal conditions (28°C. and
60–80 per cent humidity), a single reproductive cycle for the P. falciparum
parasite requires 30 to 35 days.
Subtropical in latitude but nestled within the Asian continental land-
mass, the Punjab plains are subject to enormous extremes in temperature
and atmospheric humidity. With the exception of the Himalayan hill tracts,
annual rainfall is low. Thus for most of the year, low humidity reduces
anopheline lifespan well below that required for development of the para-
site. With the summer monsoon rains, however, the fine clay soil is quickly
saturated, causing further rainfall to collect in countless pools suitable for

262
 MALARIA TRANSMISSION IN PUNJAB

larval development. Atmospheric humidity levels rise dramatically, and in

turn mosquito longevity, such that malaria infection rates can increase expo-
nentially from extremely low pre-monsoon levels to near universal preva-
lence in the space of three reproductive cycles. With cessation of the rains in
mid- or late September, malaria transmission falls off quickly.
The two main malaria species transmitted in Punjab were P. vivax (‘benign
tertian’) and P. falciparum (‘malignant’ or ‘sub-tertian’ malaria), the latter
associated with greater morbidity and mortality related to proportionately
greater parasitization of red blood cells. In the Punjab plains, the autumn
rise in malarial fever typically appeared in late August, initially consisting of
vivax infection. In non-drought years, falciparum cases followed within 2 to
4 weeks, largely replacing vivax transmission by early October, its later tim-
ing related to the longer period (10 to 14 days) required for the appearance
of gametocytes in the human host.

263
 Appendix II
AN EPIDEMIOLOGICAL
APPROACH TO HUNGER
IN HISTORY 1

To trace the uncoupling of disease and destitution in modern epidemic

theory requires the reclaiming of fundamental concepts of human subsist-
ence. Here a tentative epidemiological framework is offered. Three dimen-
sions to hunger considered in this study involve: degree or severity of food
(calorie) insufficiency; duration; and prevalence (proportion of a popula-
tion affected at a given time). If self-evident, these differing aspects can be
obscured in modern usage of the terms ‘malnutrition,’ ‘undernutrition,’ or
‘undernourishment.’
Hunger involves a range of caloric levels of food consumption on a con-
tinuum of insufficiency: from slight and moderate inadequacy, at one end of
the spectrum, to nothing at all to eat, on the other. In very basic terms, this
encompasses two states: ‘not enough’ to eat (undernourishment), and ‘not
nearly enough’ (semi- or frank starvation). The two can be distinguished,
again in very general terms, in relation to basal metabolic rate, that level of
energy required for all internal metabolic and physiological functions in a
state of complete rest. In this study, ‘acute’ hunger refers to caloric intake
below basal metabolic rate, a level where weight loss is continuous and life
cannot be supported beyond the short term. In contrast, undernourishment
(often termed ‘chronic’ hunger) refers to food intake above basal meta-
bolic requirement but below that required to fully meet all external energy
demands (‘normal’ activity, and physical labour) as well as growth demands
(in children and in pregnant or breastfeeding women).
In both cases, duration largely determines general mortality risk, related to
direct effects on immunological capacity (immunosuppression).2 The mor-
tality risk with undernourishment (chronic hunger), though also elevated,
is less than absolute and less immediate compared to that for acute hunger
(the term ‘chronic’ reflects this lower lethality, allowing for a longer dura-
tion unremedied). Some physiological ‘adaptation’ to undernourishment is
often possible through reduced physical activity (energy expenditure), or
additionally in children, a reduction in physical growth rate (stunting). Both
such states of ‘adaptation,’ however, entail immunological and cognitive

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costs depending on extent of calorie deficit, as well as likely impairment of

(future) work capacity.
While the link between immune-suppression and both undernourish-
ment and semi-/frank starvation is clear, this relationship very likely encom-
passes immune-suppression effects beyond those directly due to calorie
insufficiency. A related component, if largely unmeasurable, derives from
the immune-suppression effects of extreme psychological stress associated
with food insecurity and acute hunger: the despair and human degradation
accompanying inability to protect oneself and family members, above all,
one’s children. Such despair was routinely expressed in the desperate resort
to offering children into servitude for the price of their being fed, or the
agony of watching them die in the streets and roadways absent of succour.3
Separating the two sources of immune-suppression associated with acute
hunger is an impossible – one might suggest, unnecessary – task. In this
study, both are assumed to be at play.
In young children, cumulative undernourishment is identified clinically by
‘stunting’ (low height-for-age), and acute hunger, by ‘wasting’ (low weight-
for-height) or emaciation. Both can be evident in the same child as levels of
food inadequacy fluctuate over time. In all states of caloric inadequacy, the
added energy drain of concurrent infections further reduces the net calories
physiologically available.
Prevalence of acute and chronic hunger cannot be traced in historical
research with the precision expected in modern clinical research. Never-
theless, with a clearer conceptualization of hunger, historical markers can
be identified from a range of archival sources. The two general categories
of hunger, acute and chronic, can be identified in South Asian historical
records, for example, in references to numbers of meals per day consumed:
two meals a day generally considered ‘enough to satisfy hunger.’ The catego-
ries of zero, one, and two meals per day encompass, albeit in very general
form, the two central aspects of hunger in human history: on the one hand,
reflecting (in)sufficiency of levels of food (caloric) intake, and on the other,
(ir)regularity of access to food, that is, the frequency with which subgroups
of a population slip below one square meal into semi- or frank starvation
(acute hunger). If one could graphically sketch acute and chronic hunger
through history, one would be tracing, in effect, the relative prevalence in a
population of persons with access to two square meals per day, one, or none
over time – the term ‘prevalence’ here being used in its epidemiological sense
of frequency, duration, and social extent.
Such a schematic framework requires qualification to take into account
the exceptional needs, for example, of infants and young children who
require far more than two meals a day because of their extremely high rela-
tive food requirements for growth, and their small stomach size. It is here,
of course, where conditions of work for women, productive and reproduc-
tive, play such a large historical role. Attention has been directed recently

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to the nutritional drain of repeated infections, again of special relevance

to young children. The concept of ‘net’ nutrition takes into account the
potential additional impact on food sufficiency of transient illness-induced
anorexia and added nutrient losses associated, in particular, with diarrheal
episodes. In addition to questions of water supply, ‘net nutrition’ thus also
reflects conditions of work: time and energy available to feed and care for
young children to compensate for such recurring nutrient losses.
Further, such a schema allows consideration of acute hunger well beyond
episodic ‘famine’ (epidemic acute hunger). Indeed, endemic acute hunger
plays possibly a greater role in health history than its epidemic form, encom-
passing regular ‘hunger seasons,’ intervals in the agricultural year where
little employment is available and increasingly unremunerative work is
resorted to in an effort to stave off frank starvation. Studies in contem-
porary agricultural populations document pronounced rainy-season weight
loss and infant/toddler failure to grow, related to women’s extreme time
constraints and depleted food stores.4 Undernourishment is ‘visible’ as well,
if indirectly, in conditions of work. Most obvious, historically, are wage lev-
els insufficient to meet even minimal calorie requirement; but also intensity
and hours of work, constraints that often bore disastrous consequences for
nourishing young children and constitute a large, if generally unwritten,
chapter of endemic hunger history.
The conceptual distinction between acute and chronic hunger is impor-
tant for historical analysis for several reasons. The most obvious relates to
mortality risk, as indicated above. Another is methodological: the means by
which the two states of hunger can be identified from historical records, and
potentially measured, often differ. Historical changes in mean physical stat-
ure in a population, for example, are likely to reflect change in general levels
of (under)nourishment over time more reliably than acute hunger,5 whereas
short-term fluctuations in foodgrain prices probably signal greater relative
increases in acute hunger compared to chronic.
The significance of this distinction is evident in the case of South Asia.
Recent nutritional anthropometric research for the colonial period suggests
little increase in mean stature,6 and indeed, possibly slight decline in height
amongst the poorer and most food-insecure subgroups across the colonial
period.7 This lack of improvement in adult stature appears paradoxical in
light of the beginning increase in life expectancy across the final three dec-
ades of British rule from very low levels pre-1920. Yet seen from the context
of both gaps in food access as well as levels of food intake, this pattern is
perhaps less surprising. More effective famine (acute hunger) control after
1901 likely meant proportionately greater improvement in survival chances
among the most poor and chronically undernourished, resulting possibly
in a net increase in nutritionally stunted individuals after 1920 within the
post-famine population. Seemingly opposite trends – decreasing or stag-
nant mean stature levels and rising life expectancy – may not necessarily

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be inconsistent, then, with improving food security, when the distinction

between acute and chronic hunger is taken into account.
Finally, the conceptual distinction between acute and chronic hunger is
particularly important in health and epidemic history because of poten-
tial differences in interaction between specific infectious diseases and type
of hunger. In South Asia, the case fatality rate for malaria, for example,
appears to have been heightened in particular by acute hunger and less so
by lesser degrees of hunger (undernourishment).8

Notes
1 For further discussion, see S. Zurbrigg, Epidemic Malaria and Hunger: In Colo-
nial Punjab: ‘Weakened by Want’ (London and New Delhi: Routledge, 2019),
28–32.
2 ‘Many of the body’s generalized defenses against infectious disease,’ Nevin Scrim-
shaw details, ‘are reduced by relatively mild degrees of nutritional deficiency.
These include, among others, cell-mediated immunity, phagocyte function, com-
plement function, and delayed cutaneous hypersensitivity. . . . With the more
severe deficiencies of famine [acute hunger], specific humoral antibody defenses
[macromolecules such as antibodies circulating in the bloodstream and tissues]
and capacity to produce phagocytes are also weakened’; ‘The Phenomenon of
Famine,’ American Review of Nutrition, 7, 1987, 1–121.
3 P.B. Mukharji addresses such mental misery, in ‘Verncularizing Political Medi-
cine: Locating the Medical betwixt the Literal and the Literary in Two Texts on
the Burdwan Fever, Bengal c. 1870s,’ in R. Deb Roy, and G.N.A. Attewell, eds.,
Locating the Medical: Explorations in South Asian History (New Delhi: Oxford
University Press, 2018), 235–263.
4 For further discussion, see Zurbrigg, Epidemic Malaria and Hunger, 410–412.
5 See for example, R. Floud, ‘The Heights of Europeans since 1750: A New Source
for European Economic History,’ in J. Komlos, ed., Stature, Living Standards, and
Economic Development: Essays in Anthropometric History (Chicago: University
of Chicago Press, 1994), 12.
6 A.V. Guntupalli, and J. Baten, ‘The Development and Inequality of Heights in
North, West, and East India 1915–1944,’ Explorations in Economic History, 43,
2006, 578–608.
7 L. Brennan, J. McDonald, and R. Shlomowitz, ‘Long-Term Change in Indian
Health,’ South Asia: Journal of South Asian Studies, 26, 1, 2003, 51–69; Guntu-
palli and Baten, ‘Inequality of Heights,’ 592.
8 Zurbrigg, Epidemic Malaria and Hunger.

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293
 INDEX

Abdul Majid, J. 32 – 33 93, 98; milk protein focus 88 – 90,

Ackerknecht, E. 144, 232 98; Nutritive Value of Indian Foods
Acton, H. W. 21 90; see also Bhore Report (Report of
Africa, holoendemic malaria in 15n34, the Health Survey and Development
29, 67, 145, 161n13, 183 – 184, 217 Committee); Report on Bengal
aggregation of labour (tropical, (1945)
migrant) 68, 39n46, 73n61, 238
Alison, W. P. 115, 229 – 230, 250, Balfour, Andrew 67, 143, 163n40,
261n149 164n60, 198n122
All-India Conference of Medical Bamber, C. J. 129 – 130
Research Workers 81, 144, 154, Bellew, H. W. 126 – 128, 130
165n69 Bengal 1943 – 44: Burdwan fever 27,
All-India Institute of Hygiene and 39n56, 140n57, 152, 236, 267n3;
Public Health 80, 149, 154, 239 famine 84 – 86; Permanent Settlement
All-India Labour Enquiry 122 (1793) 27, 39n55, 104n36; see also
All-India Sanitary Conference (1911) Malaria in the Duars (1909)
122, 129n49 Bentley, C. A. 16n42, 19, 21–23, 43,
Amrith, Sunil 154, 165n72, 185, 145, 186, 229, 249, 253n33; Burdwan
193n65, 195n86, 88, 202, 205, fever analysis inverted 147; nutrient
221n40 ‘imbalance’ queried 81–83, 86
Amritsar, analysis of epidemic malaria Bhore Report (Report of the Health
in 30, 71n22, 124, 185 Survey and Development Committee)
An. culicifacies 9, 34, 201; Ceylon (Sri 97 – 99
Lanka) 43, 45, 48, 61, 62 biomedical model of infective disease,
An. gambiae 15n34, 74n87, 183, epistemic significance of 1 – 6, 44,
196n104 57, 87, 148, 156, 216; contest, truce
anophelism without malaria 201 – 202 122 – 125; epistemic community
An. philippinensis 236 173 – 174; see also Human Factor
An. stephensi 28, 159 Birn, Anne-Emanuelle 164n55, 191n34
Antananarivo, Madagascar 247 Biswas, A. 39n56
Arnold, David 6, 22, 84, 101, 138n30, blackwater fever 19
165n69, 218n8 Bombay (municipality), malaria vector
Assam Labour Enquiry Committee control in 16n42, 28, 159
(1922) 24 Bombay Medical Congress (1909)
Aykroyd, W. R. 85 – 99 passim; 18 – 19, 134; see also Human Factor;
influence on policy 98, 234; LNHO Mian Mir vector control trial
88; malnutrition as technical problem Bombay Textile Labour Union 90

294
 INDEX

bonification 22, 143, 157, 187, 202; cholera 119; climatist theory of
Bengal 68, 152; Italy 25 – 26; Punjab 120 – 121; etiology debate 125 – 126;
124; see also Celli, Angelo; Hehir, malaria priority over 127; mapping
Patrick 131; and starvation 82; vaccine
Boyd, M. F. 68, 159 limitations 141n101; as zymone 124,
Boyd Orr, John 182 139n54; see also Snow, John
Briercliffe, R. 44, 48 – 59 passim, 60, Christophers, S. R. 1 – 2, 51;
73n61, 69, 216 antimalarial chemotherapeutic
British Medical Association conference research 188; blackwater fever 19;
(1904) 30, 140n59 Ceylon epidemic 65, 79 – 80, 85 – 86;
Burdwan fever see Bengal 1943 – 44 collegial personality 67 – 68, 76n107;
Burnet, Etienne 88 – 89 dose of infection research 8, 15n36,
Bynum, William 13n14, 168n99, 201 34; Duars report (1909) 18 – 20,
145; endemiology 11, 68; general
calorie consumption 88 – 91, 96, 99, vector-eradication questioned 188;
108n79, 109n108, 196, 226n85, Human Factor, academic-official
258n115; calorie availability 97, 244, recognition of 18 – 28, 42n100, 68,
259n118 123 – 124, 150; hyperendemicity
canal irrigation: abolition as malaria research 31 – 32; infection and disease
control measure 130; adverse effects distinguished 145; regional epidemics
on soil 127, 152; Ceylon, vector 1, 123 – 124; research misread 69,
breeding 45; ‘malariogenic’ critique 99 – 100, 185 – 186, 231; see also
(Punjab) 9, 152, 236; Bengal, Human Factor, as euphemism; Mian
interrupted inundation flows 236; Mir vector control trial
see also embankments; waterlogging Ciuca, Mihai 39n52, 173, 175 – 177,
Carpenter, K. J. 104n27, 110n110, 192n57
113n63 Coale, Ansley 209 – 210
Carter, H. F. 71n20, 36 ‘communal immunity’ 35 – 36, 43, 65
case fatality rate 15n35, 67, 216, 233, competing risk 235
240, 242, 267; see also malaria Coonoor Nutrition Research
lethality Laboratories 79 – 80, 85, 90, 99
Celli, Angelo 25, 157, 202 Cornish, W. R. 119 – 120, 234, 248,
Ceylon (Sri Lanka): malaria 254n51
transmission 44 – 45; regional Cotton, Arthur 140n57
economies 45 – 47 Covell, Gordon 177
Ceylon 1934 – 35 malaria epidemic: crowd diseases 238; see also typhus
class differentials 55 – 58; drought 44, Cueto, Marcos 164n55, 220n23,
62, famine conditions, Depression 221n29
52 – 54, 57 – 58; ‘epidemic area/zone’ Cuningham, J. M. 126
48 – 49; ‘Epidemic Figure mapping’
55 – 56; malaria species 48, 58; Davis, Kingsley 209, 211, 222n47
mortality by age 48; post-epidemic Dalrymple-Champneys, W. 60
commentary 60 – 67 DDT-based malaria control 2, 8, 15n38,
Chadwick, Edwin 113 – 116, 206 – 207, 161n25, 169n100, 170 – 179, 183,
208, 230 – 231; as Poor Law 209, 235; Ceylon 211 – 217 passim;
Commission secretary 116, 221n35 Egypt 256n70; Greece 170 – 171,
Chandler, Asa 151, 166n78; see also 174, 176; India 199n127; Italy 25,
hookworm (ankylostomiasis) 257, 167n95, 170 – 173, 190n15, 22,
Chisholm, Brock 173, 176 199n125, 202, 232, 235; Kanara
chloroquine 176, 208; see also Ciuca, district (Bombay province) 174, 177;
Mihai mortality decline assumed 209 – 211,

295
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228n95; Punjab 20, 64, 161n25, Expert Committee on Malaria see

193n65, 210, 217, 236; Sardinia World Health Organization (WHO)
179; UNRRA 170 – 177, 190n17,
22; vector resistance 176, 187, Fairley, N. H. 173 – 177
190n18, 191n32, 39, 199n125, 208; ‘fair price shops’ see Public Distribution
Venezuela 170, 174, 204; see also System (PDS)
mortality decline famine: Bengal (1943–44) 94 – 96;
Deb Roy, Rohan 39n56 Ceylon (1934–35) 54, 58; Ireland
Depression (1930s) 5, 44, 52 – 57, (1846–47) 116, 239; South India
88 – 90, 159 (1876–1877) 119 – 120, 249; Punjab
DeRenzy, A. C. C. 125 – 126 ((1879) 126; (1897) 129; (1900)
De Silva, K. M. 225n63 129 – 130, 239; (1942) 29, 75n93)
dose of infection 8, 15n36, 34, 62, 66, Famine Codes 86, 95 – 96, 100
74n79, 253n27 Famine Commission Reports: Bengal
drainage 9, 114, 118, 120, 127 – 128, (1945) 94, 96, 156, 233 – 234; India
132; see also Dufferin Inquiry (1888); (1901) 130, 249
rail construction famine control 28, 86, 96, 237
drought 126, 129; see also Ceylon famine foods 84, 96, 105n35
1934 – 35 malaria epidemic; non- famine mortality and malaria 94 – 96,
immunes, epidemic malaria theory of 130; see also malaria mortality
drought relief, policy change 124 FAO-WHO Working Party on Food
Duars tea plantations see Malaria in the Production and Malaria Control
Duars (1909) 178 – 180
Dufferin Inquiry (1888) 86 – 87, 127 Farley, John 151, 167n93, 190n13,
Dunn, C. L. 43, 66, 71n15, 72n54, 193n58, 203, 220n21, 222n43
73n63 Farr, William 115
Dyson, Tim 210, 256n70 Fayrer, Joseph 126
fiscal retrenchment 64, 132 – 150
Ehrlich, Paul 121, 139n42 passim, 203
embankments: deleterious impact of flood control measures 132
27, 127; disruption of inundation flooding: economic impact 27, 127,
irrigation (Bengal) 123, 234; see also 130; entomological influence 34;
bonification; Burdwan fever; flooding relief measures 124, 127, 134
Empire of India and Ceylon Tea Food and Agricultural Organization
Company 19, 86 (FAO) 89, 178 – 185, 193n63,
endemiology see Christophers, S. R. 195n89, 196n91, 98, 198n115, 246
epidemic causation: in British India foodgrain availability per capita 96,
117 – 120; mid-/late 19th century 241, 244, 260n133; see also calorie
reductive trajectory in Britain consumption
115 – 117; pre-modern theories of foodgrain exports 128, 130
114 – 115 foodgrain price control 140
epidemic disease, conceptual shifts: foodgrain prices see scarcity
accommodation between climatist foodgrain rationing: Ceylon 216,
and contagionist views 122 – 124; 227n93; China 243; Kerala 244;
conflated 117; infection and disease, post-WW2 India 99; Tamil Nadu 245
distinguished 22, 145; narrowed to forecasting, predicting malaria
germ-transmission 29, 36, 153 – 154 epidemics 1, 21, 30, 35, 60, 65,
epidemic figure 34 – 35, 42n96, 55, 62, 189n2, 198n118
71n35 Forster, W. H. C. 132 – 135, 143 – 144,
epistemic influence see biomedical 150, 154, 166n78, 250
model of infective disease, epistemic Frank, Johann 115
significance of Franklin, Ursula 229

296
 INDEX

Frederiksen, Harold 211 – 217, 223n50, significance of its eclipse 1 – 9; as

225n69, 226n74, 228n98, 240 euphemism 22, 124; fading visibility
fulminant malaria 1 – 3, 9, 16n40; see and eclipse of 44, 99 – 100, 147,
also malaria lethality 231 – 234; professional recognition
of 18 – 28, 42n100, 68, 123, 150; see
Gabaldón, Arnoldo 170, 172 – 176, 185 also sanitary reforms, ‘general’
Galdston, I. 117, 144 Hume, J. C. 121
Gandhi, M. K. 94 hunger: acute 2, 5, 264; acute hunger
Gangulee, Nagendranath 89, 91 – 93, and malaria lethality 12n8, 248;
98, 101, 108n86, 198n114, 207 ‘chronic’ hunger (undernourishment)
Garenne, Michel 246 – 247 as nutritional stunting 23, 215,
George, Susan 198n113 255n67, 264 – 265; declining visibility
Gill, C. A. 20, 27, 30–31, 35, 40n67, 43, 216, 228n96, 239 – 248 passim;
55, 60, 71n20, 72n46, 124, 132, 150 endemic vs. epidemic acute hunger
Gillespie, James A. 177, 190n12, 86, 249; hunger epidemiology
191n24, 193n67, 197n111 264 – 267; immune suppression
Good Health at Low Cost 224n56, 15n35, 135n4, 230, 235, 265,
241 – 245, 256n71 267n2; meals per day 5, 86, 106n49,
Goodman, N. N. 174 – 175 246; seasonal 86, 154, 165n67, 215,
Gorgas, W. C. 143, 150, 201, 217n2 245, 259, 261n143; time constraints
Goswami, Kishori Lal 238 for child feeding 23, 93, 105n33,
Grant, John Black 155 246; see also household income
Gray, R. H. 214 – 215, 226n85, 227n86, surveys; nutritional anthropometric
89 history; scarcity
Guha, Sunil 254n38 hyperendemicity 26, 28, 31 – 33, 52,
Guilmoto, Christophe 254n38 75n97, 104, 145 – 146

Hackett, Lewis 41n77, 166n84, immunity, acquired (specific) vs.

202 – 203, 216, 217n3, 218n15, immune capacity 2, 10, 15n34,
252n14 35 – 36, 240, 248; acquired and
Hamlin, Christopher 112n149, general capacity conflated 65,
113 – 117, 136n5, 14, 137n16, 116 – 117; see also communal
206 – 207, 222n42, 45, 230 – 231, immunity; hyperendemicity; non-
235, 237, 251 immunes, epidemic malaria theory of
Harrison, Gordon 44, 61, 74n79, immunology 29, 30, 67, 116
168n99, 207 Imperial Malaria Conference 1909 see
Harrison, Mark 120, 121 Simla Malaria Conference (1909)
Hay, C. Douglas 113, 136n14 Inchcape Commission (1923) see fiscal
Hehir, Patrick 22 retrenchment
Hicks, E. P. 33 – 34 Indentured Labour Act 19 – 20,
hookworm (ankylostomiasis) 22, 58, 24, 238
146, 148, 150 – 151, 155, 163n40, Indian (Madras) Manual of Hygiene
164n55, 204, 208, 220n21; see also (1880, 1894) 119 – 120, 237
Rama Rao Indian Rebellion (1857) 118, 125
Hooton, A. 205, 231 Indian Sanitary Policy Resolution
Hoover, Edgar 209 – 210 (1914) 134
Hot Springs, Virginia conference (1943) Infant mortality 56, 131, 209, 216,
181 – 182 244 – 245, 227n92, 258n110
household income surveys 6, 90, international consultancy, limitations of
105n33, 246 158, 171, 202 – 203, 207 – 208
Human Factor, in malaria analysis 1 – 2, International Health Board (IHB),
19; contested 185 – 186; epistemic Rockefeller Foundation 5, 148 – 152

297
 INDEX

International Health Division (IHD), Learmonth, A. T. A. 42n102, 76n114,

Rockefeller Foundation 6, 11, 64, 91n90
69, 152 – 155, 165n69, 76, 173 – 174, Lee, Sung 193n65
177, 191n34, 203, 222 lethality of infection see case fatality
International Labour Organization rate; malaria lethality
(ILO) 24, 90, 93, 180, 185, 190n12, life expectancy 233, 235, 239 – 241,
197n111 248; China 241 – 244; India 266;
International Tropical Medicine and McKeown 255n68
Malaria Congress (1948) 178 – 179, Litsios, Socrates 159, 166n89. 179,
194n78, 79 193n66, 194n82, 195n89, 219n17,
irrigation see canal irrigation 115n69
Italy see Celli, Angelo London School of Hygiene and Tropical
Medicine 67, 143, 149 – 150, 188
Jackson, J. 173, 191n32, 198n117
James, Sydney Price 24, 86, 164n56, McCay, R. 79, 83
167n92, 218n9; malaria as a ‘social McCarrison, Robert 79 – 83, 89, 94,
disease’ 157 – 158 101, 105n38
Jones, Margaret 221n36, 73n72, Macdonald, George 1, 61, 64 – 66,
226n80 75n95, 199n124; Karnal malaria
Jones, W. H. S. 134, 146 research 32 – 33
Jumna Canal realignment 118, 123 MacDonnell, A. P. 234
McGregor, I. A. 112n148, 198n119
Kampala Conference (1950) 183 – 184, McKeown, Thomas 15n35, 240,
196n105 252n17, 255n63, 68
Karnal Malaria Research Station McNeill, William 228n95, 254n40
32 – 36 MacLeod, Roy 12, 138n37, 218 – 19n5
Kavadi, S. N. 154, 162n37, 163n49 Madras famine (1876–77) 120, 247
Kazi, Ihtesham 39n56 Madras Manual of Hygiene (1880) see
Kerala 244 Indian (Madras) Manual of Hygiene
kesari dal see wage levels (1880, 1894)
King, William G. 144 – 145 Maharatna, Arup 60n61
Klein, Ira 253n33, 38 malaria as a block to development
Knight H. F. 110n115, 196n92 (MBD) 5, 134, 143 – 150 passim,
Krishnan, B. G. 90 154, 160, 179 – 180, 183; challenged
14n30, 145, 180, 195n88
labour conditions 23 – 24, 201; see also Malaria as a social disease 7, 22 – 28,
hunger, time constraints for child 63, 74n87, 158, 167n92, 202; as
feeding; Indentured Labour Act; ‘great debilitator’ 138n36, 217
wage levels Malaria Committee (General)
land revenue policy, shifts in 28 Conference (Madras 1912) 22 – 23,
Langford, C. M. 214 249
lathyrism 21 Malaria Committee (Royal Society)
League of Nations Health Organisation 41n80
(LNHO) 5, 10, 25, 38n37, 88, 159, malaria control policy, India117, 134,
169 – 170, 180 206, 239; see also League of Nations
League of Nations Malaria Commission Malaria Commission (LNMC)
(LNMC) 4 – 5, 7, 25, 67; policy malaria epidemic forecasting see
disputes 60, 73n72, 157 – 160; study forecasting, predicting malaria
tours (Europe 25–26; India 26–28, epidemics
42n100) malaria epidemics: Bengal (1943)
League of Nations Nutrition Committee 94 – 96, 234; Madagascar (1986–88)
88 – 89 246 – 247; Madras (1877) 119 – 120,

298
 INDEX

249; Punjab ((1908) 18, 34, 44, 130, non-immunes, epidemic malaria theory
185; (1942) 98n93); Russia (1922) of 30 – 35; see also Karnal Malaria
24; Sri Lanka (see Ceylon 1934–35 Research Station
malaria epidemic); Swaziland 40n69 nutritional anthropometric history
malaria eradication program (WHO 15n35, 266
1955) 184; bilateral aid funding 172, nutritional science: economic rationality
177, 204; ‘functionalist’ purpose of the poor 89; epistemic impact
195n86; questioning of 187, 188, Bhore and 1945 Famine Commission
194n81; political, geopolitical reports 96–99; ‘hidden hunger’
interests 169, 190n13, 204 – 205, 208; 84–85; IMG (1936) 87; institutional
post-DDT malaria rebound 228n98 80–81; League of Nations Nutrition
Malaria in the Duars (1909) 18, 20, 24, Committee 88–89; non-Western
68, 69, 100, 145, 186 dietaries as ‘backward’ 94; excess-
Malaria in the Punjab (1911) 3, 62, 68, rice, protein-deficiency thesis
99, 100, 123, 130, 182, 186 questioned 81–83, 86, 91–92; hunger
malaria lethality 12n8, 15n34, 35, 130, overshadowed in malaria-nutrition
157, 184, 207, 233 – 235; Bengal research 99–100; ‘malnutrition’
95 – 96 as ill-balanced diet 79; maternal
malaria species: Ceylon (1934–35) 48, inefficiency 85, 89; micronutrient
58; Ceylon 48, 55, 62, 65; falciparum deficiencies (beriberi 78–79, 84; iodine
8, 15n34, 34, 217, 262 – 263; vivax 83; North Circars 84; rice parboiled
15n34, 263 84, 87; scurvy 84; vitamin A 83–84);
Malaria Survey of India 43, 146, 152 responsibility redirected 92–93; see
malaria transmission: atmospheric also Aykroyd, W. R.; Bentley, C. A.;
humidity 33 – 35, 47, 262 – 263; Gangulee, Nagendranath
unstable malaria 13n16, 32
Manson, Patrick 138n36, 201 Osler, William 134
Marshall Plan 179
Meegama, S. 57, 211, 227n87 Packard, Randall: epistemic power
Mettur-Cauvery Canal 152 – 153 of vector transmission 202, 232;
Meyer, Eric 57 – 59, 72n53, 73n64 geopolitical interests 204, 220n25,
Mian Mir vector control trial 18 – 19, 221n28; LNMC divisions 157;
64, 73n70, 130, 140n59, 158, MBD 14n30, 195n88; research
251n9 and experience sidelined 199n124,
migrant labour see aggregation of 222n46; WHO 196n100, 197n107
labour (tropical, migrant) Palestine 39n47, 167n92
Mohapatra, Pranab 38n35 Pampana, Emilio 13n16, 173 – 175,
mortality decline: Ceylon (post-WW2) 178, 198, 222n47
209 – 214; Punjab ((post-1920) 2, 9; Panama Canal zone malaria control
(1940s) 210, 248); see also DDT- 150, 191n39, 200 – 202, 176,
based malaria control; life expectancy 230 – 232, 245, 129n36
Mukharji, P. B. 39n56, 267n3 Pare-Taveta scheme 184
Muraleedharan, V. R. 6, 84, 107n75 Passmore-Sommerville thesis 99 – 102,
Murphy, M. see Dyson, Tim 231 – 234
Pasteur Institutes 29, 79, 153
Nájera, J. A. 14n27, 74n76, 75n97, Pelling, Margaret 101, 102, 115
76n114, 167n95, 168n100, 192n45, Perkins, J. H. 222n41
51, 194n81 Perry, E. L. 30 – 31
Newman, Peter 213 – 215, 226n74 plague 18, 29, 120, 130, 132 – 133, 148
Newnham, H. E. 52 – 54, 60, 73n72 pneumonia 13n20, 235, 248
Nicholls, L. 226n85, 227n92 predisposition 115; in 19th British India
Niven, James 23 sanitation theory 118, 125, 128;

299
 INDEX

ignored 230, 231; reclaimed (post- Ross, Ronald 16, 200, 205; dismissal of
1908) 22, 60, 41n94, 150; see also Human Factor 158, 251n9; malaria as
epidemic causation; epidemic disease, block to development 145–146, 201;
conceptual shifts mathematical modelling 60; Mian Mir
premunity 175 trial criticism 73n70, 140n59
Preston, Samuel 215, 227n90 Ross Institute 207
protein (in)sufficiency see nutritional Royal Commission on Agriculture in
science India (RCAI) 34n43, 91, 104 – 110,
Public Distribution System (PDS) 241, 115, 173, 238
243 – 246 Royal Society of Tropical Medicine and
public health: narrowed to germ- Hygiene 44, 60 – 62, 65, 83 – 85
transmission control 117, 120 Royal Society of Medicine 245
Russell, Paul F. 1934–35 Ceylon
Qadeer, Imrana 17n46 epidemic 61, 186; 1911 Punjab
quinine, access to 28, 16n42, 153, inquiry questioned and omitted
201; limitations 132; safety; see also 186, 188, 203, 198n123; epistemic
blackwater fever influence 156–157, 198n121; malario-
economic study 153–154; political
rail construction: impact on surface views 204, 220n26; role of hunger
drainage 16n42, 120, 127 – 128; contested 69, 76n116, 99–100,
foodgrain exports and prices 128; see 157–158, 251n9; South India vector
also aggregation of labour (tropical, control 152–153; WHO-ECM 6, 11,
migrant) 173–176, 179–180, 183, 185–186
Ramakrishnan, S. P. 112n143, 252n16 Russia 24, 92
Ramanathapuram district 245
Rama Rao, Dr 151 Samanta, Arabinda 39n56
Ramasubban, Radhika 119, 137n26, Sanitary Boards 127; see also Stephen, A.
163n47 Sanitary conference, Bombay (1911)
Rao, Mohan 160n5, 222n41 123, 134
Ravindran, T. K. S. 17n46 sanitary reforms, ‘general’ 122–124, 239
recovery rate (malaria) 66 – 67, 233 Sanitary Report (1842) see Chadwick,
regional epidemic 1, 36, 64, 150, 231; Edwin
see also Christophers, S. R. sanitationist paradigm 117, 205
Report of the Royal Commission of Sarkar, K. N. 211, 214
Inquiry into the Sanitary State of the Sathyamala, C. 7, 84, 93, 104n27,
Army in India 118 109n99, 111n128
residual infection 22, 63, 66; see also Sawyer, Wilbur A. 171 – 172, 179
recovery rate (malaria) scarcity 1, 20, 128, 181, 186; definition
rice: parboiled 84, 87; polished 79, 28; wartime hyperinflation 75n93,
84, 94 94, 180
Rieff, David 162n34, 220n23, scarcity relief 28; see also foodgrain
221n36, 38 price control
Rockefeller Foundation, programmatic Schüffner, W. A. C. 26 – 27
and epistemic influence: hybrid grain Scrimshaw, Nevin 235, 267n2
research and Indian Agriculture Sen, Amartya 94 – 95
Program 208, 222n41; India Sharma, V. P. 199n127
149 – 156; LNMC funding 38n37; Siddiqui, J. 192n57, 195n86
UK 149 Sierra Leone, malaria in 31
Roe, W. A. 128 – 129 Silva, K. T. 61, 138n35
Rohilkand Terai 28; see also Simla Malaria Conference (1909)
hyperendemicity 20 – 22, 145, 238

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Singhbhum see hyperendemicity (IHD); League of Nations Malaria

Sinton, J. A. 15n38, 39n46, 146 – 148, Commission (LNMC); An. stephensi;
162n29, 167n93, 174 Watson, Malcolm
smallpox 116, 119, 127, 156, 235; in vector deviation (cattle mortality)
China 242, 257n87 thesis 99
Snow, John 121, 139n41; see also Venkat Rao, V. 186 – 188, 250, 199n125
cholera Virchow, Rudolf 115, 136n7, 157, 229
Snowdon, Frank M. 190n15, 17, 216 Viswanathan, D. K. 177, 179, 193n65,
spleen rate 40n66, 75n98, 189n2; 194n78, 204
Ceylon (1934–34) 45 – 48, 52, 54, vital registration 4, 103, 115, 117,
64 – 67, 71n35, 75n98; Ceylon 119 – 120, 129, 206, 209 – 210;
(1940s) 213 – 214; Punjab 30 – 35, England and Wales 115
85, 90
spleen surveys 30, 41n78 wage levels 21, 67 – 68, 90 – 91, 117,
Sri Lanka see Ceylon (Sri Lanka) 131, 150, 153, 157, 165n67,
Staples, Amy 185, 198n115 238, 244
starvation see hunger Wakimura, Kohei 16n39, 283n37
stature see nutritional anthropometric wartime hyperinflation see scarcity
history waterlogging 9, 118, 124, 127 – 128,
Stephen, A. 126 – 128, 130 – 131 134, 180, 236
stunting see hunger Watson, Malcolm 157 – 158
Swaroop, S. 31, 41n78, 64 Watts, Sheldon 16n39, 137n22
Swellengrebel, N. H. 25 – 26, 261n148 Webb, J. L. A. 197n109
Wernsdorfer, W. H. 224n61
Tamil Nadu 244 – 245 whipping 238 – 239
Topley, W. W. C. 234 Whitcombe, Elizabeth 16n39, 41,
tuberculosis 6, 23, 80, 126, 151, 157, 253n29, 37
164n55, 170, 235, 238, 253n27; Wigglesworth, V. B. 61, 66
China 242 Wilkinson, E. 130
typhus 24, 114 – 116, 161n16, 208; Worboys, Michael 41n87, 84, 93,
recrudescent (Brill-Zinsser disease) 106n55, 109n96, 97, 110n118, 116,
135n4, 229 – 230; see also Alison, W. 139n45, 166n89, 201, 218n10
P.; Chadwick, Edwin World Health Organization (WHO)
Tyssul Jones, T. W. 70n10, 13 Interim Commission: origins of the
malaria eradication program (MEP)
UNRRA 11, 169 – 174, 177, 181, 189, 6, 169 – 188 passim; see also UNRRA
190n12, 15, 17, 22, 191n24, 28, 34,
195n86, 246; and China 190n22 Yacob, M. 31, 41n78, 64

Van Zile Hyde, H. 177 – 178 Zinsser, H. 135n4

vector control see Celli, Angelo; Zylberman, Patrick 166n84
Ceylon 1934 – 35 malaria epidemic; zymonic see Christophers, S. R.
International Health Division zymotic disease 123 – 124

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