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Wuchereria bancrofti and Brugia
malayi are filarial nematodes
Spread by several species of night feeding mosquitoes
Causes lymphatic filariasis, also
known as Elephantiasis
Commonly and incorrectly
referred to as Elephantitis
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Humans are the definitive host for the
worms that cause lymphatic filariasis
There are no known reservoirs for
W.bancrofti.
B.malayi has been found in macaques,
leaf monkeys, cats and civet cats
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Anopheles
Aedes
W.bancrofti is transmitted by
Culex, Aedes, and Anopheles
species
B.malayi is transmitted by
Anopheles and Mansonia species.
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Culex
Mansonia
Endemic in 83 countries
1.2 billion at risk
More than 120 million people infected
More than 25 million men suffer from
genital symptoms
More than 15 million people suffer from
lymphoedema or elephantiasis of the
leg
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Adult: White and thread-like. Two
rings of small papillae on the head.
Female:5~10cm in length
Male: 2.5~4cm and a curved tail
with two copulatory spicules.
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Microfilaria: 177~296 m in length,
a sheath with free endings. Bluntly
rounded anteriorly and tapers to a
point posteriorly. A nerve ring with no
nuclei at anterior 1/5 of the body.
Wuchereria bancrofti
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Brugia malayi
B.malayi microfilariae are slightly smaller than
those of W.bancrofti.
Microfilariae are sheathed, and about 200 to
275 m.
Not much is known about the adult worms, as
they are not often recovered
One distinctive feature of B.malayi is that the
microfilarial nuclei extends to the tip of the
tail
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W.bancrofti
Size
Cephalic space
Nuclei
Terminal nucleus
244~296 m
Shorter
Equal sized
B. malayi
177~230 m
Longer
Unequal sized
clearly
coalescing
countable
uncountable
No
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Host: Mosqutoes (intermediate host)
Human (final host)
Location: Lymphatics and lymph
nodes
Infective stage: Infective larvae
Transmission stage: Microfilariae
Diagnostic stage: Microfilariae
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Life cycle
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Wuchereria Life Cycle
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Phenomen which the number of
microfilariae in peripherial blood is very
low density during daytime, but
increase from evening to midnight and
reach the greatest density at 10p.m to
2 a.m.May be related to cerebral
activity and vasoactivity of pulmonary
vessels.
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Larva deposited by mosquito bite
Travel through dermis to lymphatic vessels
Growth (approx 9 months) to mature
worms(20-100mm long)
Worms live 5-7 years (occasionally up to15
years)
Mate->Microfilariae (1st stage larva)
Females->release up to 10,000
microfilariae/day into bloodstream
Microfilarie taken up by mosquito bite
Develop into 2nd and 3rd stage larva over
10-14 days inside mosquito vector
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Network of vessels
that collect fluid that
leaks out of the blood
into tissues (lymph)
Redirects lymph back
into the blood stream
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Initially asymptomatic
Symptoms develop with increasing numbers
of worms
Less than 1/3 of infected individuals have
acute symptoms
Clinical Course is 3 phases:
Asymptomatic Microfilaremia
Acute Adenolymphangitis (ADL)
Chronic/Irreversible lymphedema
Superimposed upon repeated episodes of
ADL
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Presents with sudden onset of fever
and painful lymphadenopathy
Retrograde Lymphangitis
Inflammation spreads distally away
from lymph node group
Immune mediated response to dying
worms
Most common areas: Inguinal nodes
and Lower extremities
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o
o
o
o
o
o
o
Inflammation spontaneously resolve
after 4-7 days but can recur frequently
Recurrences usually 1-4 times/year
with increasing severity of
lymphedema
Secondary bacterial infections in
edematous(elephantatic) areas
Filarial fever (fever w/o lymphangitis)
Tropical Pulmonary Eosinophilia
Hyperresponsiveness to microfilariae
trapped in lungs
Nocturnal Wheezing
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Lymphedema
Mostly LE and inguinal, but can
affect UE and breast
Initially pitting edema, with gradual
hardening of tissues
hyperpigmentation & hyperkeratosis
GenitaliaHydroceles
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Renal involvement
Chylurialymph discharge into
urine
o Loss of fat and protein
hypoproteinemia & anemia
o Hematuria, proteinuria from ?
immune complex nephritis
o
Secondary bacterial/fungal infections
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Elephantiasis: accumulation of lymph in
extremeties, fibrosis, and thickening of
skin.
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Debilitates millions of humans by
scarring eyes & causing
permanent blindness
Caused by Onchocerca volvulus
Affects people along rivers in
West & Central Africa (native) &
South America (introduced via
slavery)
Adult females are up to 500mm
long & males up to 40mm long
Adults live up to 14 years
Restricted to humans (no known
animal reservoirs)
Transmitted by black flies
(Simuliidae)
Larvae live in fast-flowing water
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Black flies ingest microfilariae from
blood
Move from gut to flight muscles &
mature into infective larvae (L3)
L3 larvae migrate to head & enter
humans via bite wound; mature
into adults (2-4 months)
Adults accumulate in subcutaneous
nodules (1cm diameter) which
dont cause much damage
Mating in nodules produces
microfilariae
Nodules
Live under skin causing rashes &
wrinkles
Cause blindness when invade
eyes tissues & die there
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Damaged eye tissues
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Early stages of eye damage can
be reversed by drug treatment
Transfer of worms affected by
feeding behaviour of flies
Parasiticide ivermectin is most
popular
Waggle mouth parts during biting
to increase wound size & create
pool of blood (pool feeders)
Main vector = Simulium
damnosum
Complex of >40 sibling species in
West & East Africa
Not all sibling species transmit
worms
Insecticide applications used to
control larvae in rivers
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Microfilariae in human blood
Caused by infection with Loa loa
Transmitted by horse flies (Tabanidae)
in genus Chrysops
Adult worms move under human skin
Observed beneath skin or passing
through conjunctiva of eyes (eye
worms)
Worms = 2 races (attack humans or
arboreal primates)
Day-feeding & forest-dwelling
Rare case of Tabanidae = biological
vectors
Adult in human eye
Disease endemic to rain forest regions
of West & Central Africa
Generally mild & painless (chronic)
with 10-15 year incubation period
May cause swellings of skin (Calabar
swelling)
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The standard method for diagnosing
active infection is the identification of
microfilariae by microscopic
examination
However, microfilariae circulate
nocturnally, making blood collection
an issue
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A card test for parasite antigens
requring only a small amount of blood
has been developed
Does not require laboratory equipment
Blood drawn by finger stick
Urinalysis, CBC and Comprehensive
Chemistries
Foot Biopsy: Normal Skin with areas of
chronic inflammation
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Microfilariae are seen in blood
smears and are DIAGNOSTIC
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Blood Smear - Microfilaria
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Note wavy
microfilarial
worm in the thick
part of blood film.
Dark blue
structures are
nuclei
Tail end tapering
(no nuclei)
Sheath covering
worm.
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Blood Smear - Microfilaria
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Note wavy
microfilarial
worm in the
thick part of
blood film.
Head end of the
worm rounded
(no nuclei)
(Sheath is not
clearly seen)
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Blood Smear - Microfilaria
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Note wavy
microfilarial worm
in the thick part of
blood film.
Dark blue
structures are
nuclei
Tail end - tapering
sheath (no nuclei)
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. Hydrocele fluid cell block
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Note wavy
microfilarial
worms.
Inflammatory
cells
lymphocytes.
Hemorrhagic
fluid sediment
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. Hydrocele fluid cell block
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Note wavy
microfilarial
worms.
Inflammatory
cells
lymphocytes.
RBC
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. Hydrocele fluid cell block
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Note wavy
microfilarial
worms.
Inflammatory
cells
lymphocytes.
RBC
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. Hydrocele fluid cell block
Inflammatory
cells
lymphocytes.
RBC
Microfilaria.
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As with malaria, the most effective method
of controlling the spread of W.bancrofti and
B.malayi is to avoid mosquito bites
The CDC recommends that anyone in atrisk areas:
Sleep under a bed net
Wear long sleeves and trousers
Wear insect repellent on exposed skin,
especially at night
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Covering water-storage containers and
improving waste-water and solid-waste
treatment systems can help by reducing
the amount of standing water in which
mosquitoes can lay eggs.
Killing eggs (oviciding) and killing or
disrupting larva (larviciding) in bodies of
stagnant water can further reduce
mosquito populations.
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Treatment of filariasis involves two
components:
Getting rid of the microfilariae in
people's blood
Maintaining careful hygiene in infected
persons to reduce the incidence and
severity of secondary (e.g., bacterial)
infections.
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Anti-filariasis medicines commonly used include:
Diethylcarbamazine (DEC)
reduces microfilariae concentrations
kills adult worms
Albendazole
kills adult worms
Ivermectin
kills the microfilariae produced by adult
worms
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The disease is usually treated with singledose regimens of a combination of two
drugs, one targeting microfilariae and
one targeting adult worms (i.e.,either
diethylcarbamazine and albenadazole, or
ivermectin and albendazole
In some areas, DEC laced table salt is
used as a prophylactic
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