Module: Livestock diseases

Credit hour 10
Tutor :Mr Magazini N.E

Code: AHT 05101

Credit hours: 11

Tutor: Mr. Magazini N.E

Date:oct -2019
 Module outlines
Diagnose disease/conditions
Explain causes of diseases
Describe clinical signs of diseases of livestock.
Describe methods of disease diagnosis
Describe the procedure of conducting disease
diagnosis
Conduct disease diagnosis
 Module outlines
Describe common livestock diseases and
conditions
Describe common bacterial diseases
Describe common viral diseases
Describe common protozoan diseases
Describe common mycotic diseases
Describe common metabolic and poisoning
conditions
Explain the importance of helminthes in livestock
production
 Diagnosis of diseases/conditions

 Aim: To teach students different ways of diagnosing

diseases so that they able to apply them in diseases
diagnosis.

 Objectives: at the end of this period students

should be able to:-
 Define important terms
 Outline causes of diseases
 Explain causes of diseases
 Describe clinical signs of diseases of livestock.
 Describe methods of disease diagnosis
 Describe the procedure of conducting disease
diagnosis
 Conduct disease diagnosis
 Introduction

• Diseases:- An alteration in the state of the

body which interferes with normal
performance of vital processes e.g.
Reproduction. OR
• Condition or state of animal showing
changes in the normal functioning of the
body system.
• i.e The changes may be anatomical
(broken leg) physical (rise in body
temperature) or change in behavior
(Demeanour).
 Intro cont..
• Diagnosis: Is the science of deducing from
clinical signs the nature of the prevailing
disease. OR
• Process of attempting to determine and
identify of possible disease or disorder and
the opinion reached by this process
 Cont..
• Clinical signs: is an observable evidence of
abnormalities of structure of function in animal
with the disease.
• This can be qualitative or quantitave clinical
signs or both changes in the structure of an
organ, tissue or its functions as well as behavior
of the whole individual.
• Qualitative: refers to status e.g. Discoloration of
mucous membrane, behavior, loss of appetite.
 Intro cont..
• Lession: Is a visible morphological signs of
disease in some parts of an animal e.g.
wound, ulcer, abscess or tumour.
• Prognosis: Expresing an opinion as to the
probable duration and outcome of the disease
i.e grave / fatal or Good / encouraging
 Intro cont..

• Demeanour: Response of an animal to normal

stimuli i.e. Bright or dull.
• It is said to be bright when an animal responds
to normal external stimul e.g. movements,
sounds etc. e.g. when the laying animal rise up
on approaching bright demeanour. .
 Intro cont..
• Gait: Refers to rate range, force and direction of
limbs. All legs must take equal weight during walking
• Posture: Is the carriage of the body in relation to the
earth (Ground surface) (Distribution of body weight
on legs).
• Epidemiology: Is the study of the disease in
population and factors that determine its
occurrence. Or The study of relationship between
various factors that determine the frequency and
distribution of the disease within animal
populations.
 Intro cont..
• Pathogenesis: Is the mechanism by which
disease develops. Or The origin of a disease
and the chain of events leading to that disease
which can be acute, sub acute or chronic.
• Sporadic disease: These are disease seen
occasionally e.g. Tetanus, BQ or Actinomycosis.
• Why occasionally: You can encounter tetanus
in horse when you have undergone castration
in horse or docking in sheep
 Intro cont…
• Health: is the state of being physically,
physiologically and mentally fit.
• Morbidity: Describe the rate of animals that suffer a
particular disease when exposed to the same
infection and it is expressed in percentage.
Morbidity rate
= No of animals manifesting the disease x 100%
No of animal at risk

• Mortality: Express the number of animals which die

as a result of disease. Expressed as a percentage of
death (measure of the number of death in a
population).
• Mortality rate:
= No of animal dying of the disease x 100%
No of animal at risk
• Fatality:
= No of animal dying of the disease x 100%
No of animal manifesting the disease
 Intro cont..
• INFECTIOUS DISEASE: The disease that is caused by
living organisms, often microorganism, that infects
animals and are transmissible from one infected
animal to another. The Microorganisms are bacteria,
Viruses, Protozoa, Mycoplasm etc.
• NON-INFECTIOUS DISEASE: Diseases that are not
transmissible from one animal to another, they are
caused by a number of factors, such as poisons,
abnormal growth of the body (cancer or tumor),
inadequate or excessive nutrition and secretion.
 Intro cont..
• QUARANTINE: Implies governmental regulations for the
prevention of the spread of infectious disease by which
an animal or animal products, which have come from
infected countries or areas, are detained at the frontiers
or ports of entrance, or at other official centers, for a
period of isolation, before being allowed to mix with
stock of the country/area.
• OR is the physical separation of sick animals from healthy
ones, or the placing of restraints on the movements of
exposed or infected animals or its items that may have
contaminated.
 Intro cont..
• NOTIFIABLE DISEASES: Are those which, when
they break out upon farm premises, must be
notified to the police or government
department concern. For example: Anthrax,
CBPP, Rabies, African Swine Fever etc.
 Causes of animal diseases

• Diseases in animals are caused by many factors including:-

(i) Living organisms causing diseases are subdivided into:
• (a) Microorganisms – These are small organisms which
cannot be seen with naked eyes. They are further
subdivided into:
• Viruses: These are living particles that do not survive
outside a living cell. They can not seen by ordinary
microscope but require special powerful microscope.
• Rickettsia: Are smaller than bacteria but larger than
viruses.
 Causes cont..
• Bacteria: One celled organisms.
• Protozoa: Most protozoa require an
intermediate host to complete their life cycle.
They cause important animal diseases in
tropics e.g. ECF. Trypanosomosis etc.
• Mycoplasma: The most important ones are
those cause CBPP and CCPP.
• Fungus
 Causes cont..
b) Parasites – These are larger organisms that
can be seen with naked eyes. They live on or
in the body of their hosts, deriving their
nutrient from the host tissue. The most
important parasites are:
• Helminthes (worms)
• Insects (tsetse flies, biting flies)
• Arachnids (Ticks, mites, fleas).
 Causes cont..
(ii) Chemicals that may interfere with the
normal functioning of the animal tissues and
organs e.g. poisons.
(iii) Physical damages to the body such as
bruises and fractures.
(iv) Mineral deficiency
 Predisposing factors (FACTORS THAT
FACILITATE THE DISEASE TO OCCUR )
• The development of diseases in individual animals is not dictated
only by the presence of causative agents. There are certain other
factors that predispose animals to develop clinical signs of the
disease:
 environment
 host
 causative agent
Epidemiologic triad
Agent

• Host Environment
 Agent factors;
 Pathogenicity (ability to cause diseases)
 Dose of pathogens

 Host factors;
 Behavior (mating practice, hygiene and feeding)
 Age: The age of an animal has influence on the susceptibility
of individuals to certain disease. e.g Adult indigenous cattle
show more resistance to ECF than calves. This is attributed to
the underdeveloped immune system in calves relative to adult
cattle. On the other hand very old animals tend to succumb
more easily to some disease than younger animals partly
because changes in the physiology of the animal body induced
by age weaken the defence system of aged animals.
 Poor nutrition: Animals in poor state of nutrition succumb
more easily to disease.
 Factor cont..
Sex
Genetic composition, Certain individual breeds or
groups of animal have different level of genetically
controlled capacity to resist to animal disease. These
characteristic are passed from one generation to
another. e.g Certain local breeds of cattle in central and
West Africa are highly resistance to Trypanosomosis
while other breeds else where are not.
 Presence of diseases or medications
Stress
 Factor cont..
Environment factors
Physical factors; Geology and Climate
Biological factors; crowding, Poor hygiene
Distribution and transmission of diseases

disease distribution: refers to the

extent/intensity of diseases
occurrence in a certain area at a
specified period of time.
According to disease distribution
diseases are classified as :- sporadic,
epizootic/epidemic,panzootic/pandem
ic and enzootic.
 Disease distribution:
 Epizootic/epidemic:- Diseases which are wide
spread among many animals in the same place ,
district, region or country for a short time e.g.
chorela, FMD (Foot and Mouth Disease), Lumpy
skin Disease
 Panzootic/ pandemic; Diseases which are
wide spread among many animals in the whole
country, continent, and other continents e.g. ASF
(African Swine Fever)
 Enzootic: The time enzootic describes the time
factor of epidemiological intensity in a given
place or zone. It can occur sporadically or
epizootically e.g. swine Enzootic
Encephalomyelitis ‘’Teshena disease’’ Enzootic
Muscular Destrophy (White Muscle Disease).
 Diseases transmission: refers to the
mechanism by which a disease causative
agent gains entry to the host.
Mode of disease transmission:
• Vertical transmission: occur from individual to
its offspring. E.g foetus in eteroneonates via
colustrum.
• Horizontal transmission: Occur from infected
individual to a susceptible contemporary.
• Direct transmission: require a close proximity
of infected to susceptible individual either by
physical interaction e.g bite in rabies.
 Mode cont…
• Indirect transmission: By vectors such as ticks
by vehicle i.e. in animate e.g. food, water,
milk, dust formities etc.
• By droplet nuclei: small pathogenic particles
suspended in air e.g. FMD, New castle disease
virus.
 Routes of infection

• Direct contact: infectious agent are picked by health

animals from infected animals with whom they have
close contact e.g. a calf picks up ringworm, fungus
from the skin of another calf. Or a cow leaks the
muzzle of another cow with FMD. Also mange
• Inhalation of contaminated material: These occur
where micro-organism survive in the air long enough
the infected air to be inhaled by clean animal. It is
facilitated by animals being in close, contact.
 Rout cont..
• Ingestion of contaminated feeds, water.
• Coitus: some disease of the reproductive organs are
transmitted during coitus e.g. Trichomonas in cattle.
• mechanical transmission: Created by a doctor. It
involves introduction of pathogens by dirty
instruments or through contaminated prophylactic
or therapeutic preparation.
• Transfer of an infected animal from infected herd
to a clean herd through livestock trade.
 Strategies of control and eradication of
Animal disease
• Do nothing: Enables natural change between host
and parasite relationship without intervention by
man.
• Quarantine: Infected or suspected area restriction.
Physical separation of sick from health. Permit
system: Gvt. Legislation on notifiable diseases.
• Selective slaughter: Chronically or infectious
disease cases should follow mass diagnosis by use
of simple testing techniques.
 Strategies cont..
• Control of mechanical vectors by destruction
and disinfection.
• Formite disinfection: Elimination of sources of
contamination e.g. surgical equipments.
• Education: The success of disease control
programme depend on overcoming and
modification of human cultural practices
 Strategies cont..
• Vaccination: Mass
immunization.
 Strategies cont..
• Therapeutic and
prophylactic
chemotherapy: Mass
treatment for sudden
disease incidence or
when disease prevailing
is high.
 Strategies cont..
• Improvement of
husbandry and feeding.
Host resistance is
improved.
• Genetic screening
through selective
breeding to reduce
defective gene pool.
 Cont..
• NOTE: If people are made to undertake the
importance and necessity of controlling
animal diseases a great social and economic
benefit will be obtained at an acceptable cost
level. Hence control programme like
vaccination campaigns, selective slaughter,
quarantine and culling will be smoothly
effected.
 Types of infections
• Monoinfection:- condition in which only one
etiological agent is involved-caused only by one
aetiological factor.

• Secondary infection: is when in the same

animal the second disease occur on the expense
of the first one while the first one is not yet
cured. All diseases are caused by different
etiological factors (two infections at one period)

• Mixed infections:- diseases caused by more

than one or two agents
 Types of infections
 Reinfections:- When an animal repeats
contacting a disease by the same aetiological
factors after the primary illness has been
cured. E.g.having a challenge after days from
a super strain

 Superinfections:- when an animal contacts a

disease of the same aetiological agent while
the ongoing illness is not cured. E.g. infection
in infective individuals
 Types of infections
 Contagiousness:- able to spread by contact

 Bacteremia/virusaemia:- when
bacteria/viruses circulated or transported in
blood or lymph to other body tissues while
multiplying first

 Septicaemia:- when microorganism

multiply in the blood and then get
transported to other parts of the body as in
anthrax, pasteurelosis and erysipelosis
 Types of infections
Pyaemia:- formation of second foci of
pus diffused in organs

Septicopyaemia :- combination of
pyaemia and sepsis
Sepsis:- contamination
 Clinical signs:-

• Clinical sign:- is a qualitative or quantitative or

both changes in the structure of an organ/tissue
or its functions as well as in the behavior of the
whole individual.

• Health: is the state of being physically,

physiologically and mentally fit.
 Signs of health:-

 General attitude:- a health animal should be

alert and enquisitive
 Appetite:-the animal should be interested in
food almost any time
 Cudding:-at a certain time of the day the
animal should chew curd
 Eyes and nose:- should be bright and no
discharges respectively and cool and dry
respectively.
 Coat:- clean and glossy
 Faeces:- should be firm and pelleted in small
ruminants
 Signs of health:-
 Urine:- should be straw colored and not blood
stained
 Breathing

 Purse rate:- should be regular and normal for a

particular spot

 Gait:-should be steady i.e.all limbs take equal

weight as it walks

 Milk:- sudden change should be noted

e.g.content, clots, blood, consistence and odour.
 Clinical signs

Physical signs
Emaciation: various parts of the skeleton are
prominent

Obese:- overweight

Abnormal body conformation:- changes in symmetry,

shape, relative size of different body parts due to
dropsy of the fetal membranes, ascites, chronic
exudative peritonitis, rickets.
 
General demeanor :-Abnormalities of behavior

Dullness/apathy:- the ‘’dummy’’ state : an

advanced degree of failure to respond to
external stimuli although the animal remains
standing and capable of movement. Occurs in
liver fibrosis and encephalomyelitis (horse),
Listeriosis, Lead poisoning and ketosis in cattle.

Comma:- an advanced stage of apathy where

the animal is unconscious and fails to respond
to painful stimuli.e.g. in parturient
hypocalcaemia in cattle.
 Cont..
Restlessness:-where an animal exhibits
constant movement consisting of lying
down,rolling, getting up again, looking at the
flanks, kicking at the belly, and groaning e.g.
colic syndrome in horse.
 Gait:- abnormal gait include

Lameness
Stiffness
Staggering
Forced movement
Abduction of one or more limbs
The above occurs due to :- diseases of muscles e.g.
BQ, Enzootic muscular dystrophy, diseases of
bones e.g rickets, Osteomalacia, diseases of joint
e.g. Athritis, Diseases of feet e.g .FMD and Foot rot
 Posture:-
 Posture:- is the carriage of the body in relation
to the earth (ground surface). When approached
in lying position most animals will get up.
 Changes in postures can be:-
• Curvature of the spine either upward (kyphosis)
or downward (lordosis)
• High or oblique carriage of the head and neck
torticolis or opistotornus
• Unusual position of limbs
 Examples of abnormal posture:-

Inability to extend the knees- streptococcal or E.coli

Athritis
Dog sitting- in acute gastric distention in horse due to
acute pressure on the diaphragm
Sterna recumbency with s-shaped neck-
hypocalcaemia
Standing on three limbs in fracture of one limb
Bow legged- as in rickets and osteomalacia
Walking on knees e.g.in sheep and goats when they
have foot rot
  Abnormal coat

Dry and rough coat due to nutritional

disturbances
Loss of hair (alopecia) due to skin diseases
Severe dehydration due to salmonellosis,
enteric colibacillosis, Gastroenteritis,
vomiting, paratuberculosis and white scours
  Skin surface:-

Color and structure:

Changes in color and structures may be due to

primary and secondary diseases of common
integument e.g. Vesicular and pustular exanthema
(skin eruptions). Also common in canine
distemper, swine erysipelas , subcutaneous
inflammatory edema in Anthrax and in horses the
condition might occur, in cattle it occurs in
pasteullosis.
 Read on the following signs as an assignment

• Cutaneous Lesions
• Skin pigmentation
 Odour:
Bacteria and chemical decomposition of the
secretion apocrine sweat gland and the
holocrine secretions of sebaceous gland lead to
animal ‘s species odor
Halitosis:- foul smell of the breath

Ketosis:-In ruminants and in advanced stage of

Diabetes Mellitus there is an odor of acetone
and in uraemia there is an odor of urine
 Methods of conducting disease diagnosis:

The methods are divided into:

a)General Observation/inspection
• This is carried out at some distance away from the
animal visually examining gait, behavior, demeanor
and inspection of the environment.

• Scan the patients appearance closely, watch the play

of motion, abnormalities, colour, smoothness and
texture of the skin, mucus membranes, presence of
swelling, haemorrhages, discharges and other signs.
• b) physical examination
• ii) Auscultation:-
• Means listening to the sounds produced by the
functional activity of an organ located within a part
of the body in order to assess its condition by using
a stethoscope indicated in the examination of lungs,
heart, and parts of the G.I.T
• Rhythm and character of respiratory sounds, groan
(sounds produced after obstruction near to die),
moan signs made by the patient.
• -It is traditional to associate certain sounds with
discomfort or pain in the head and others with pain
in the stomach or extremities.
• -Any of these sounds may have conclusive and
diagnostic values *sounds of pain differs from
sounds of plays.
Percussion:-
• Is achieved by striking a part of the body, its
surrounding tissues and deeper lying parts. The
value of this method comes from the vibrations
imparted at the point of impact producing audible
sounds, which vary when reflected back because of
the difference in density of the tissue.

• Indicated in examination of the thorax (lung heart)

paranasal sinuses in subcutaneous emphysema.

• Equipment for percussion—Hammer and pleximeter

-Sounds produced
a) Resonant:-is a characteristic sound emitted by air
containing organ e.g.lung

b) Tympanic:-sound gas under pressure of rumen

(Rumination), caecum

c) Dull:-sound emitted by a solid organ like liver or heart

(tumour)
iii) Palpation
• Consists of handling the tissue by means of fingers or
palm of the hand. The main objective is to detect the
presence of pain in tissue by noting increased sensitivity,
variation in size, shape, consistency and temperature.
• TERMS USED
• Resilient:-when the structure quickly resume its normal
shape
• Doughy:- when pressure causes pitting as in oedema
• Firm:- when the resistance to pressure is similar to that
of normal liver
• Hard:-when the structure possesses bone like
consistency.
• Fluctuating:-when a wave like movements is produced
in a structure by the application of alternate pressure
• Emphysematous:- when a structure is swollen and
yields on pressure with the production of crepitating or
crackling sound.
• note: structural changes in size, weight, volume
lobulation and texture of a given tissue
iv) INQUIRING
Ask conventional questions such as:
-What is wrong with animal x (mention the name of
an animal)
-At what time of the day the first sign appeared
-What was the patients mental state when the illness
was first noticed-refer to diseases of the CNS e.g
rabies and Tetanus.
-Have there occurred cases of epidemic diseases in
the viscinity surroundings.
-Have there been unusual draught, dump, heat or
cold
- What is the feeding regime (routine) refer to the
plan of nutrition required to the animal
v) FEELING THE PULSE RATE
• This may supply some missing information
determining whether the problems lies in the heart
itself, liver, kidneys, lungs, spleen etc.
Location site:
• Hose: The pulse rate is taken at the external
maxillary artery on the medial aspect of the ventral
border of the mandible where the vessel is
associated with the corresponding vein and the
parotid ducts as itself as the facial artery.
• Other position: The transverse facial artery at a
posterior between the base of the ear and the eye
at median artery beneath the posterior superficial.
• Bovine: Facial artery on the lateral aspect of
the mandible or the transverse facial artery.
• Small animals: The pulse rate in small animals
is taken at the femoral artery.
The table below shows the pulse rate of
different animals
 The physiological factors affecting pulse rate:-

• Species
• Size
• Age
• Physical condition
• Sex
• Pregnancy
• Parturition
• Posture
• Environment
vi)DETERMINING THE RESPIRATORY RATE
• Supply the information regarding to the
respiratory system of e.g.lungs, bronchi,
trachea.
• -dyspnoea, apnoea, hypnoea the larger the
animal the lower the respiratory rate and vice
versa.
Respiration rate of different species
 Abnormal respiratory noises

• Hiccough: Is a short jerky inspiration caused

by stimulation of the phreme nerve producing
sudden contraction of the diaphragm.
• Sneezing: Due to nasal irritation.
• Snoring: Caused by pharyngeal occlusion as in
TB lymphadenits of the retropharyngeal
lymphnode.
 CONT..
• Grunting: It’s a freed respiration against a
closed glottis associated with painful condition
of the respiratory track.
• Wheezing/Whistling: Due to paralysis of the
intrinsic muscle of the larynx.
• Yawning: Is a prolonged inspiration with the
mouth widely and the soft.
• Coughing: Is due to irritation of the pharynx,
larynx bronchi, trachea.
vii) RECORD BODY TEMPERATURE
• Normally taken per rectum or per vagina.
• Supply the information regarding the
thermal regulatory state of a patient. The
temperature can rise due to an infection,
poisoning or metabolic disorder.
 Steps of taking animal body temperature

• Shake the thermometer to allow the mercury to drop

down.
• Moisten (lubricate) the bulb thermometer by water/saliva
to facilitate easily entry per rectum.
• Insert the thermometer into rectum then place the bulb on
the rectal wall.
• Retain it for about 2 minutes.
• Withdraw the thermometer and read by holding it against
the light.
• Record the reading, clean the thermometer and return into
the case.
Table shows the body temperature of different animals:
viii) Sampling
• normally are taken in order to isolate the
causative agent.
• Samples should be taken in a sterilized
equipment
• All procedures of asepsis should be adhered.
 PROCEDURES OF CONDUCTING CLINICAL /DISEASE DIAGNOSIS

Diagnosis (Dx)-Greek word “Diagnositikas”

Procedure
1.Registration (Animal profile)
A general information is required regarding the
patient
• Address of client
• Breed / species
• The identification number/name
 Registration cont…
• Age
• Sex
• Colour of the coat
• Production class / type of animal
• Body condition – good/poor
• Posture – recumbent, collapse, normal / back
arched.
• Demeanour: dull, bright, poor and good.
2. Anamnesis-History taking
i) Anamnesis Vitae-life history
• Condition of the animal before illness
• Type of management and husbandry practices
• The plane of nutrition/animal nutrition
• Water supply (individual or communal)
• Animal use e.g.Draught, beef, dairy dual purpose
etc.
• Previous illness
ii) anamnesis morbi- disease history
Consider
• The date of the animal discovered to be sick
• Under which or what conditions e.g. after vaccination,
after a longer drought
• The possible causes of illness
• Clinical signs observed
• Was there any attempt to treat the animal and what was
the response of the drug used.
• Is the condition improving or worsening
• What are the common infectious diseases in the locality
• Any common food poisoning
• Is there any possible animal contact and contact with
game animals
3.Examination of the herd and environment
(i) Examination of the environment. The
environment to be investigated include :
• The grazing areas used by the relevant herd.
• The sheds where the animals are being housed.
• The type of feeds used etc.
• The veterinary technician should be observant
of all things that could hazardous to animal
health e.g weeds that may be poisonous Close
examination of an animal
 Cont..
(ii) General inspection of the herd.
Before the sick animals are examined
in detail the technician should inspect
the entire herd / flock. Inspection of
the herd as whole is important for it
may point the general health / status
of the herd / flock
 4. Examination from a distance:

• The animal should be examined from a

distance without disturbance. Some significant
clinical findings could be picked up from a
distance such as the way the animal is eating,
walking, posture, gait and the general body
condition, Skin coat, Abdomen, Demeanour
 5. Close examination:

• This is the actual examination of the body systems. In close

examination one is starching for signs and lesion which can
not be detected (ascertained) at a distance observation.
• -digestive system
• -circulatory system
• -urogenital system
• -intergumentary system
• -nervous system
• -lymphatic system
• Skeletal and muscular system
 Close exam cont..
• Examination of Cardinal parameters such as
body temperature, pulse rate, respiratory
rate, Heart beat and rumination should be
done before doing system by systems
examinations.
• Different methods which are used in close
examination during clinical diagnosis includes:
Palpation, Percussion and Auscultation.
6. Local status- status localis
• Location of clinical signs and the tentative diagnosis
7. prognosis
• Expressing of an opinion as to the probable duration
and the outcome of the disease. Fatal/grave or
Favourable 50/50.
8. Recommendations
• Destroyed or disposed
• Treatment course and drug of choice
• Disease control
• Prophylaxis/ disease control
• Hygienic measure
• Better husbandry practices
 EAST COAST FEVER
Synonyms:Ndigana kali

• Definition
Is a non contagious highly fatal, febrile disease
predominantly of cattle characterized by
coughing, high fever, dyspnoea, hyperemia of
mucus membranes, profuse lachrymation,
bilateral nasal discharge, focal hyperplasia and
damage to the lymphatic system and frothing
from mouth at the point of death
• Etiology: Caused by a protozoan parasite “Theileria
parva parva”
• In the bovine host it first appears in lymphocytes as
macroschizonts and later as microschizonts and as an
intraerythrocytic pirplasm in the blood.
• The macroschizonts are within the cytoplasm of the
lymphocyte and have chromatin granules and have 10 -
20 nuclei or more.
• They may break away from the host cell and are seen
free, in stained smears from infected tissues and are
known as "KOCHS’ BLUE BODIES"
• The microschizonts develop from macroschizonts
and appear as a mass of deeply staining cocci
almost filling the cytoplasm of a lymphocyte.
• These cocci, in one microschizont may be as
many as 100 or more and when the cell ruptures,
they become free MICROMEROZOITES which can
enter the RBC to form the characteristic
piroplasms, which are comma or rod-shaped or
small irregular anaplasma-like organisms.
 Epidemiology
• Prevalence: ECF is endemic to Southern Sudan, Uganda, Kenya,
Tanzania, Eastern Congo, Malawi and possibly Ethiopia and
Southern Somalia. At the moment the disease is considered to
be eradicated from S. Africa, Swaziland, Mozambique and
Zimbabwe

• Infection is limited to areas of suitable or high rainfall and

suitable temperatures for the survival of the tick Rhipicephalus
appendiculatus, a 3- host tick.

• ECF is essentially a disease of cattle although similar parasites

have been seen in African buffalo, Indian buffalo, the eland and
antelopes.
• These might have been Theileria lawrencei
• Adult animals are more susceptible than immature animals
• Morbidity and mortality high 80 -90%
• Transmission is transtadial (larval stages not infective)
• Needs at lest 2 -3 days to feed prior to transmission,
this delay transmission is referred to a "Trigger
Mechanisms". Trigger mechanism is vital for spacing
dipping routines to twice a week.
• Loss of infectivity following engorgement but without
feeding infectivity may remain for 9 months
• Pasture spelling 12 -15 months ticks will die
• Loss of infectivity following engorgement can be used -
by exposing susceptible stock
 IMMUNITY TO THEILERIOSIS (ECF)

• It is generally agreed that there is innate resistance to all animals

except cattle and buffaloes
• Adult cattle, especially those without previous exposure are the
most susceptible
• Calves especially those in endemic areas are most resistant, due
both to contact and colostral antibodies
• Animals recovered from ECF have a strong and sterile immunity
(parasite disappears) this can be life long, however the immunity
may wane if there is no re-exposure Immunity
• Spleenectomy of recovered animals does not provoke relapses
compared to Theileria annulata
• It seems that immunity in ECF is cellular rather than humoral but is
yet to be confirmed.
 Transmission

• Is effected by a 3- host tick Rhipicephalus appendiculatus and is a

transtadial transmission (stage to stage -i.e. If the larva picks the
disease, the nymph will transmit the disease and if the nymph picks
the infection, the adult will transmit the disease.
• The tick is a cyclic transmitter and not a mechanical one. Transmission
is effected after the tick has fed for 1 -3 days -thereby passing infective
particles from the tick to the host.Studies have shown that Hyalomma
spp. (H. anatolicum, H. dromedarii and H. impressum also transmit the
disease but they are possibly of little significance as opposed to the
Rhipicephalus spp. Because, their larval and nymphal stages do not
feed on cattle and thus do not transmit the disease -.
• Infection remains in the tick for roughly 9 months but once the tick
feeds, the tick loses its infection. There is no transovarial infection
whatsoever .
 Transmission
• In endemic areas most adult cattle may have an average of
ticks which normally attach around the ear (Brown Ear tick)
causing swelling of the parotid glands.
• Under bad managemental conditions, epidemics of East Coast
Fever may occur (resistance, fencing, under strength etc).
• Experimentally transmission may be achieved by inoculation
with infected bovine tissues e.g. spleen, lymphoid tissues and
blood. Intraperitoneal and intra-splenic routes also very
effective
• You can also transmit by using infected-engorged ticks or use
tick stabilates
 Clinical features:

• Incubation period is 8 -30 days (13 days)

• Under experimental conditions it is 10 -21 (15 days)
• The disease can be depicted in five syndromes such as Acute , subacute , Mild ,
inapparent, Cerebral

• Acute
• Is the commonest form of the disease seen
• Affected animals are usually dull and have a starry coat and inappetent
• The external Lymphnodes starting with the parotids (around the ear -predilection site)
become swollen then prescapular and precrural lymphnodes follow
• A rapid rise of temperature of 105 -106oF follows and tends to remain high until
terminally
• There is a marked drop in milk production
• There can be profuse lacrimation as well as a bilateral serous nasal discharge compare
from from rhinitis)
• There is usually tacchycardia and tacchypnoea
 Acute

• There is difficult breathing due to lung oedema and this

is responsible for death due to asphyxiation
• There is increased salivation
• Usually diarrhoea with blood stained faeces is a feature
• Generally many calves in endemic areas show no
symptoms beyond enlargement of superficial LNs and a
transient fever
• Anaemia is not a feature but petechiation can be evident
under the tongue, eyelids, vulva and even nostrils
• Coughing is a feature. There is no jaundice
• Subacute: Occurs in calves or indigenous zebus and although
symptoms .are similar to those of acute form but less severe.
• Mild Seen in calves and immune animals, characterized by a
mild temperature rise.
• Inapparent: There is no obvious clinical reaction. It is a type
of reaction you get in experimental animals -however
demonstration can be achieved histologically.
• Cerebral: (Turning Sickness/Olmilo?).
• Seen in enzootic areas and is characterized by nervous
symptoms
• Commonly seen in zebus
• In this form there is increased leucocytes (lymphocytes) in
circulation which becomes deposited in the brain capillaries
causing thrombosis and necrosis of the brain
• Koch's blue bodies may be seen if a brain biopsy is taken
• Generally mortality is 80 -100% in susceptible stock
 Postmortem features

• There is often frothing from the nostrils

• Subcutaneous tissues and connective tissue as well as fat are
gelatinous and watery or yellowish and pale
• There is accumulation of fluids in body cavities i.e. Hydrothorax,
hydropericardium and Ascites
• Lymph Nodes are enlarged, oedematous and haemorrhagic. The cut
surface is uniformly creamy and there is loss of differentiation in its
structure
• Spleen rarely enlarged, although trabeculae and nodule may be
prominent
• There is aggregations of lymphocytes in various organs in particular in
kidneys and liver (infarcts)
• 1nfarcts contains dead lymphocytes and streaking of haemorrhages
 Postmortem features
• Lungs -1nterstial emphysema, oedema, sometimes-lobar
pneumonia and hepatisation
• Heart -marked petechiation especially at the apex median and
coronary grooves. Coronary fat may be gelatinous
• Much of the serosa is petechiated including peritoneal and
intestinal etc.
• Most of the GIT is hemorrhagic starting from the abomasum
downwards and the rectum may have "Zebra-markings"
(compare from rinderpest, Babesiosis, Anaplasmosis)
• The abomasum is more haemorrhagic and may have ulcers (cigar
burn type) mainly in the pyloric region
• Liver is usually enlarged with mottled gray areas.
• Diagnosis:
• Based on epidemiology -areas, animal susceptibility,
movements, history, dipping and spraying routines
• On clinical grounds
• LN biopsy -earliest appearance of parasites will be on the
second day (temperature + I) following pyrexia, either
schizonts or microschizonts will be evident
• Piroplasms appear coincidentally with the pyrexic phase
• Serological tests such as Complement fixation test,
Fluorescent Antibody Technique and agglutination test have
been used with some degree of success.
• Differential Diagnosis
• Ephemeral Fever
• Other tickborne diseases (Anaplasmosis, Babesiosis, Trypanosomosis)
• CBPP
• Bovine Lymphosarcomas

• Chemotherapy:
• Is of f little value
• Tetracycline have been used with some success
• Halofuginone (antimalarial, anticoccidial) by HOESCHT now under field
trial and may prove useful
• Clexon (parvaquone) has proved effective as well
• Other preparations include (Buparvaquone, fruvexone, parvexon)
• Lasix against pulmonary oedema
• Prednisolone (anti-inflammatory agent)
•
• Control
• Factors to consider
• Managemental factors: e.g.
• Nomadism -Masais, Sukumas -literally no tick control
• Extensive grazing -where animals are literally in contact like it is in
the whole of Africa, semi-permanent settlement
• Ranching conditions with good degree of control (spraying)
• Intensive management -dairy farms (fencing, movement control,
dipping, spraying,
• pasture spelling etc but Acaricide resistence is common
• Movement control, imports, exports, use of stock routes with
dipping facilities
• Thus control
• The vector
• Cattle movement
• The parasite by chemotherapy, vaccine? (ground up stabilate
+ tetracycline),
• Pasture spelling,
• Graze non-susceptible stock e.g. donkeys, goats or sheep etc.
• Dipping -vector control
• Movement control (fencing, pasture etc.).
• Check acaricide strength ? Prophylaxis
 BABESIOSIS

• Definition
Etiology
• Is a febrile tick-borne protozoan disease of most domestic and wild
animals characterized by extensive heamolytic crisis resulting into
anaemia, jaundice, haemoglobinuria
• Protozoan parasite of the Genus Babesia" first recorded in USA in
1976 by a man known as "Babes" and hence the name
• There are several species some of which are large and others small,
and in general large forms have less susceptibility to chemotherapy
as opposed to smaller forms for example against Trypan blue.
• These parasites multiply in the red blood cells by either budding or
Binary fission
 Summary:

• Host Large Forms Small Forms

• Cattle B. bigemina B. bovis / B. Argentina

B. major B. divergens

• Horse B. cabali B. equi (Nuttalia)

• Sheep B. Motasi B. ovis

• Dogs B. Canis B. gibsoni

• Cats B. felis (Nuttalia)

• Pigs B. trautmani B. perroncitoi

• Fowls - Aegyptionella pullorum

• They are generally pear shaped with their narrow in apposition.
Irregular or amoeboid
• forms are also seen. Large forms are about 6 while small ones are
1.5.
•
• Revise shapes and positions in the red blood cell
•
• Prevalence:
• The disease is world wide in distribution coinciding with vector ticks
• B. divergens occurs in most part of Europe (temperate countries)
• B. bovis in South and Central America, Europe, USSR, Africa, Australia,
Southern USA
• B. major in Europe, USSR, N. Africa
• B. bigemina in America (North, Central and South), Europe, Africa
(East, North, Central and South).
• Babesia parasites affects cattle mainly but also water buffaloes, sheep,
goats and wild ruminants like Deers, gazelles as well as human beings
following splenectomy. Animals other than cattle act as carriers.
•
• Transmission
• Rhipicephalus (Boophilus) annulatus in Americas, B. decoloratus in
Africa, B. microplus in Australia and TRASMISSION IS BY
TRANSOVARIA( a 1 host tick)
• Haemophysalis spp, and Rhipicephalus spp can also transmit the
disease and TRANSMISSION IS BY TRANSTADIAL in 2 and 3 host ticks
• MECHANICAL TRASMISSION with inoculation of infected blood
• In one host tick all the stages are completed in over host.
• Thus an engorged female falls to the ground to lay eggs and after
hatching the larvae infest another host where they moult to nymph
and nymphs to adults without falling down.
• The larvae thus transmit the infection but some authors think its only
the nymph and adult that are responsible for transmission.
• It takes about 11 -17 days (14 average) from the time of infestation
with the larva to the time of appearance of the parasites in the host
i.e.
• Larva attachment to nymph 7 -12 days;
• Nymph to adult 5 -19 days;
• Adult to engorgement 15 days
• It therefore takes roughly 3 weeks for full cycle
• Clinical features:
• Incubation period is 11 -17 days (average 14 days)
• Calves often show no symptoms at all and adults are more susceptible
• Affected animals are dull, remain isolated, anorexic and have a
rumenal stasis
• There is pyrexia of a sudden onset up to 41°C
• There is a starry coat with an arched back
• Tachycardia, Tachypnoea and Dyspnoea.
• There is increased heart beat sound -so much so that you may hear
without a stethoscope “ANAEMIA“
• In the early stages mucus membranes are congested and later a high
degree of anaemia. There is weakness and unsteadness
• Constipation followed by colics and tenesmus

• Faeces are usually dry, brown with sometimes yellowish streaks followed by a watery
diarrhoea (note: A huge lump of hard faeces is also regarded as diarrhea not only the watery
or fluid faeces

• There is haemoglobinuria but not haematuria. This is a result of haemolytic crisis thus there is
hyperbilirubinuria
• Jaundice is often a feature
• Central nervous system signs characterized by aggressiveness, muscular tremors and
staggering gait (compare from rabies, Anaplasmosis, heart water, cerebral form of ECF etc)
• There is a drop in milk yield in lactating animals and pregnant ones will abort
• Death may be within 3 weeks or earlier
• In fully susceptible animals mortality may be as high as 90%.
• It could be lower in endemic areas due to premunity
• Recovery may be very protracted. With B. argentina the nervous signs more common.
•
 Pathology:

• In acute disease, lungs are oedematous and there is sanguinous fluid in the
pericardial sac
• Petecchae are obvious in the myocardium and endocardium as well as the
mucus membranes of the urinary bladder
• There is hepatomegally and may be yellowish in colour
• The gall bladder is distended with dark green thick granular bile
• The spleen is very enlarged, soft and fragile compare from Anthrax
• Kidneys may be congested with petechiations
• The bladder may contain pink to dark red urine
• The carcase is anemic and jaundiced
• There are catarrhal streaks of haemorrhages and erosions in abomasum,
intestines
• and especially rectum compare from rinderpest.
• There are haemorrhages in serious cavities.
• In chronic cases there is emaciation and jaundice
• There is general oedema
• The spleen is enlarged but not so soft
• In most cases the urine is normal in colour
 Diagnosis:

• Epizootiology
• On clinical gounds Aneamia, jaundice haemoglobinuria
• Blood smears NOT LN smears
• brain smears taken at postmortem
• PM lesions
• Serological tests (CFT, CAT)
• Biological inoculation of splectomised animals with infective blood

• Specimen for diagnosis

• Good blood smears from ear or tail (thin and thick)
• Use fresh or citrated blood (EDTA)
• Dead animal recently take spleen, kidney, heart, liver brain and for that
had died long time take spleen, brain, heart muscle
 Treatment:

• A number of drugs used

• Imidocarb also for Anaplasmosis
• Diminazene aceturate (berenil) 8.8 mg/kg Bw.
• Phenomidine
• Amicarbalide
• Quinuronium sulphate
• Trypan blue -toxic

• Control: similar to anaplasmosis and ECF.

• Including vaccination
 TRYPANOSOMIASES
Synonyms
Trypanosomosis
Nagana

Definition
• These are a group of protozoan, zoonotic diseases of both
domestic and wild animals alike and clinically manifested by a
wide spectrum of features depending on the species of
parasite and shot involved but most commonly by intermittent
fever (parasitaemia), anaemia, emaciation, reduced
productivity and high mortalities.

• Although our major emphasis is to talk about bovine

trypanosomiasis; it is worthy while to mention at this point
other allied diseases in other animal species and the names
used to describe them
Nagana
• Refers broadly to the tsetse transmitted disease of domestic animals in Africa
and it is infections caused by T. vivax, T. Congolense, T. simiae, T. suis, T. brucei
and T. uniforme.

Sleeping sickness
• Is the tsetse-transmitted infection of man by T. gambiense and T. rhodesience,
a zoonosis

Surra disease
• Is a vector borne (Tabanids, stomoxys etc) trypanosomal infection of equids
and camels with T. evansi and T. equinum which is an evansi like organism Also
known as T. venezuelae. This disease will thus occur in tsetse free areas.

Dourine
• Is a venereal trypanosomiasis of horses and donkeys and transmission being
effected at coitus with the parasite penetrating the m2 of vagina and urethra.
Caused by T. equipeidum.
Chagas’ disease
• Is a zoonotic disease and less important in
domestic animals with pigs and dogs being
infected with T. Cruzi. Transmission via kissing
bugs (reduvidae). Is a stercoraxian parasite
with development in bugs and transmission
via faecal contamination.
 BOVINE TRYPANOSOMIASIS:
• Bovine trypanosomiasis perhaps emerges at the top of the list as one of the most
important diseases of cattle in Africa where it covers more or less 67% of the continent
making livestock production a problem or limiting it only to certain tsetse free areas.
Its importance lies mainly on the direct losses. It causes in cattle, stunted growth,
inefficient breeding, retarding expansion of national herds, hindering of mixed farming,
all of which finally result into deficient protein requirement for human beings.
Inevitably human resources are drawn to fight the disease (research, control) in order
that animals can be raised in wider areas and thus increasing protein production.

• Trypanosomiasis also prevents the development of donkeys and horses, which would
otherwise be used as draft animals and the pig industry may be interfered with due to
T. Simiae infections.

• All species can be infected with T. brucei, T. congolense and also T. evansi while T.
vivax will affect all animals except the pig, dog and other experimental animals. Viz.
• Etiology
• Trypanosomes – which are protozoan parasites.
• Needless to go into classification, Morphology, Developmental stages as
these should have been covered adequately in protozoology.

• However it is important to not that there are two main groups of

trypanosomes:
• Salivanian group which get transmitted in the process of the vector biting
or feeding on a susceptible host e.g. T. vivax, T. rhodesiense, T.
congolense, T. gambiense, T. Brucei T. evansi, T. suis

• Note:
• T. brucei is also a connective tissue parasite: Lymph smears
• T. equinum T. congolense – capillary parasite (blood)
• T. equiperdum,T. vivax – capillary and large vessel parasite (smears)
• Stercorarian group – whose transmission is mainly via faecal
contamination e.g. of kissing bugs T. cruzi.

• These classifications are based on the mode of development and

method of transmission by the insect vector as well as
developmental stages and morphology in the vertebrate host.

• The stercorarian trypanosoms develop as epimastigotes in the

midgut of the insect vector and complete their development to the
metacyclic (infective) stage in the hind gut (or posterior station) New
hosts are infected by contaminative means through insects faeces
(bugs). With the exception of T. cruzi (chagas Disease), these
trypamosomes are not very pathogenic.
• The salivanian trypanosomes: These are important parasites
and may develop as trypanosomes (procyclics) in the midgut
of tsetse flies, migrate anteriorly to the fly mouthparts or
salivary glands where they develop as epimastigotes. They
complete development in the anterior station and the infective
metacyclic trypamosomes are introduced in the new host by
inoculation through the insect mouth parts. They multiply
continuously in the trypanosome form in the vertebrate.

• These organisms parasites blood and in some instances, the

tissues and tissue fluid of their vertebrate hosts where they
multiply extracellulary by longitudinal binary fision.
Prevalence
• African typamosomiasis is basically found within equatorial
Africa 10oS – 29oS of the equator coinciding with the distribution
of tsetse flies which are the main vectors.

• Basically more than two third of Africa (41/2 million square

miles) is tsetse infested making livestock production a problem.
Tsetse flies are all dependent on shade and humidity therefore
rainfall is important.

• Trypanosomosis which is non-tsetse transmitted is to be seen

outside this region e.g. T. evansi and T. equipeidum are to be
found in N. Africa and Asia as well as S. America. This is also true
with T. vivax which can be transmitted mechanically.

• The prevalence also depends on the presence of pathogenic

tryponosomes e.g. T. brucei, T. vivax, T. congolense.
Transmission:
• In Africa, the pathogenic salivanian trypanosomes are transmitted naturally
by tsetse flies of the genus Glossina, where they undergo a cycle of
development before being transmitted to a new host via bite i.e. cyclical
transmission:
• e.g. T. brucei  Develops in the gut, salivary glands and mouth parts of the
fly. (pp 5-12 days)

• T. congolense develops in the gut and mouth parts. (pp 12 – 16 days). T.

vivax develops in the mouthparts only. prepatent period 8 – 10 days (short)

• Forest group:
• G. tabaniformis, G. migrofusca G. hanington, G. medicorum G. brevipalis and
G. longipenis. These are of little importance economically because their
habitat is unsuitable for raising livestock.

• Riverine group
• G. palpalis, G. fuscipes, G. tachnoides G. caligenea, G. palliceta
• These are more important because they are to be found near essential water
supplies where both man and livestock come for their supplies.
 Savannah group.
• G. morsitans, G. austerni, G. longipalpis G. pallidipes, G. swynnertoni. These
have the greatest impact in livestock production and development as they
occupy vast areas of land otherwise suitable for grazing animals.

• Animals are infected with trypanosomes via a bite of an infected tsetse fly which
also acquire infection on feeding on and infected animal. The infested
trypanosomes undergo a cycle of development in the fly lasting between 8- 35
days before infected metacyclic trypanosomes are produced; and once infected,
flies are always capable of transmitting trypanosomes for the rest of their lives.

• It is important to note that mechanical transmission can occur both in tsetse flies
(T.vivax) and other biting flies (Tabanus spp, Stomoxys spp). Generally the
infection rate in tsetse flies is very low 1-20% and anything in excess of 20% is
considered to be pretty high.

• Most wild animals are known to harbour these parasites for considerable periods
with little or no clinical evidence. Their infectivity varies kudus, giraffes,
bushbucks etc. 30-45% while Buffaloes, wild pigs, antelopes have 10-16%
infective rate. The baboon is the only animal not affected with any infective
African Trypanosome.
Clinical signs
• These are evident following incubation period of variable lengths
depending on the strain and species of infecting trypanosomes and on
the number of trypanosome introduced by the tsetse fly during bite e.g.
T.vivax 10 days.
• There is usually intermittent fever which coincides with the fluctuating
parasitemia and this may result into sudden deaths in ACUTE cases of T.
vivax in cattle, T. brucei in Horse, T. Simiae in pigs
• Affected animals are anaemic – macrocytic, hypochronic – haemolytic?
Anaemia (trypanolytic!)
• Affected animals are usually weak, emaciated, have a stair coat and a
moderate enlargement of superficial lumpy modes.
• Oedema is usually a feature in the horse and dog (T. brucei) but also in
chronic cases of cattle.
• Infection with T. brucei which invades the CNS sometimes may result into
Nervous signs and paralysis.
• Lachrymation and photophobia may be a feature in cattle infected with T.
vivax where as dogs affected by T. brucei may manifest corneal opacity.
 Although animals may be dull they nevertheless continue to eat until their last minute.
• Chronic form of the disease is characterised by emaciation, weakness, anaemia, Oedema of
the ventral parts of the abdomen, prostration and death. LN enlargement is a feature.

• Trypamosomiasis is exacerbated by stress, work, vaccinations, malnutrition, other intercurrent

disease particulary Anaplasmosis, ECF etc. Some breeds are considered to be more tolerant to
Tryps are trypanotolerant breeds e.g. N’dama and Muturu breeds of west Africa.

• The real cause of death is unknown BUT at times considered to be due to some sort of
terminal shock!!!!! As mentioned earlier anaemia is a prominent feature with T. vivax and T.
congolense (haemoparates) and there is an obvious fall in both PCV and HB concentration.
There is extensive haemodilution which results from something similar to shock.

• The shock syndrome is due to a break down of FIBRINS releasing KININS which are
pharmacologically active causing vascular permeability resulting into the release of fluids into
tissue spaces. The half life of RBC is considerably reduced and adds to the degree of anaemia.
Erythrocytes are mopped up by a process of erythrophagocytosis and most lymphocytes will
have RBCs in them resulting into anaemia without jaundice. It is an immunological reaction
• Epidemilogical factor:
• There is always a variability in the course of the disease and that
not all trypamosomes a will kill all animals they infect. Death
results from repeated exposure. Tsetse challenge is an important
feature, because tsetse densities and hence exposure tend to vary
from one area to another, this influences the chemoprophylactic
approach which might be required.

• Stress factors e.g. malnutrition, other intercurrent diseases will

precipitate severe clinical disease.

• Age; calves are more resistant to tryps than adults due to maternal
antibodies and also due to high milk and fat diets (Good nutrition).

• Breed and race of cattle e.g. Zebu are less susceptible than Bos
Taurus cattle and N’dama and Muturu are even more resistant.
• PATHOLOGY:
• Usually emaciated carcases and Anaemic.
• There is enlarged lymphnodes and spleen
• A swollen and congested liver
• There may be mild gastritis and multiple haemorrhages involving most mucous
membranes and serous surfaces, common in acute trypanosomiasis.

• Diagnosis
• Based on epidemiological features e.g. Presence of tsetse flies.
• History of recent introduction of animals in an endemic area.
• Clinical manifestation – progressive loss of condition anaemia etc in chronic
cases but sudden deaths in acute cases anthrax.
• With wasting consider other conditions characterised by unthriftness e.g.
malnutrition, johns disease, Lymphosarcoma, Tuberculosis etc.
• Demonstration and identification of trypanosomes in blood:
• Wet blood films – of limited value useful in early stages of disease mainly for T.
vivax and T. simiae which both move very fast. T. Congolense moves very
slowly WHILE T. brucei is somewhere in between. However, it gives an instant
diagnosis.
• Dry Smears:
• THICK  best method as it gives a high chance of spotting the
parasite after staining with Giemsa and examining with x40 or x100
objective. However morphology is deformed. Dehaemoglobinise in
tape or distilled H20 prior to staining.
• THIN  Smears are good for the identification of species. It is
advisable to sample the animals more than once due to the
fluctuating intermillent parasitaemias. Mornings and evening better
chance sample 10% of any herd you are presented with.

• Haematocrit centrifugation method of blood:

• Use capillary tubes filled with suspect blood and centrifuge and
tryps will appear in top of buffy coat. It should be heparinised
blood.
• Commonly used for T. vivax and brucei BUT T. congolense tends to
sink down. Use a x10 objective to check.
• DEAE (DES2) Cellulose:
• A cellulose filter is used to filter tryps suspect blood and allows only trips to go
through. It is a very sensitive test and will show as low as 4 trips/ml BUT it takes
time and is expensive.

• Multiplication method:
• By inoculation of suspect blood into mice, rodents intrapecitoneally 0.5 – 1ml of
blood. Good for T. brucei and T. congolense but poor with T. vivax. Following
inoculation you need to observe and take smears constantly for 4-6 weeks to
develop.

• Lymphnode smears and Cerebral spinal fluid

• Used in special circumstances especially when T. brucei is suspected, T. vivax can
also be seen in LNs
• Tissue sections have been used as a diagnostic tool only if you know exactly what
you are looking for.
• Cultivation of trypanosomes on solid media:
• Possible with T. brusei and T. congolense which can be grown in blood again
media.
• However the non pathogenic T. theileri tend to grow ubiquitously and confuse
diagnosis. Tryps have also been grown on embryonated eggs.
• Serodiagnostic tests:
• A number of serological tests have been used to indicate infection
with tryps but the variability of antigens may be a problem (i.e. the
different species). These tests include:
• CFT
• Fluorescent antibody technique very widely used.
• Capillary Agglutinition test easy to use
• Checking for raised levels of immunoglobulin M. This test has also
been used for the diagnosis of sleeping sickness.
• ELISA test (Enzyme linked Immuno sorbent Acid test). Done in plastic
trays with multiple wells into which antigens re put and then washed
to remove excess antigens.
• Serum samples (antiserum) are added to the wells, followed by the
addition of Elisa conjugate, which should be absorbed, to the
Enzyme linked substrate. This gives a colour reaction whose
intensity is used as the basis for the estimation of the amount of
substrate released and the reading is done by a photo spectrometer.
• Treatment
• A number of drugs are available for the treatment of various
trypanosomes BUT. T. Simiae does not respond to any of the drugs
with any degree of satisfaction.
•
• Generally these are toxic drugs and may cause a local (Necrosis,
sloughing, lameness, abscesses) or systemic (Fever) reaction e.g.
Antrycide prosalt (Quinapyramine) causes toxicity manifested by
salivation, trembling, recumbency etc and CNS signs.
• There can be a drop of milk production following treatment.
• Chemotherapy can either be curative or proplhylactic.
•
• Common drugs used are:
• Diminazene aceturate (Berenil, Babesin) 3.5 mg/kg Bw 1m (for T.
vivax, congolence, brucei, evansi in cattle)
• Quinapyramine sulphate (Antrycide sulphate) 2.2 – 4.4 Sc as above
for cattle and for brucei, evansi equiperdum Horses evansi camels.
• Homidium chloride (Novidium, Ethidum bromide (vivax,
congolense, brucei cattle , vivax, congolense – Horses)
• Isometamedium chloride (samorin) 0.25 – 1 mg/kgBw
1m Typamidium (vivax, congolense, brucei cattle,
Horses), Congolense, brucei Dogs)
• Suramin (antrypol) 7-10 mg/KgBw 1v
• T. brucei, T. evansi (Horses)
• T evansi (camels)
• T. brucei, T. evansi (dogs).
• May be used prophy/actically.
• Drug resistance is the main problem mainly because most of the drugs are
chemically similar, so that resistance in one results into resistance to the other
(cross-resistence). This happens because all too often sub-curative does are used
or trypanosomes have developed alternative metabolic pathways. In such cases it
is advisable to change the drug rather than continue increasing the dosage (i.e.
creating resistance at a higher level.)
• e.g. Cross resistence “curative Doses”

• Trypanosomes
• primarily resistant to Berenil Antrycide Ethidium Samorin
Samorin 0 + + R
•
• Berenil R 0 0 0
•
• Antrycide + R + +
•
• Ethidium 0 + R +
•