FILARIASIS

Dr. Suhaemi, SpPD, Finasim

Filariasis
commonly known as elephantiasis
caused by a parasite transmitted by mosquito
Signs and Symptoms
Pain and swelling of the breast, vagina, scrotum, legs
and arms Fever Cough Chills Wheezing
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
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

Intermediate Host
W.bancrofti is transmitted by Culex, Aedes,
and Anopheles species
B.malayi is transmitted by Anopheles and
Mansonia species.
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
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.

Anopheles

Aedes

Culex

Mansonia

 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

Brugia malayi

B. 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
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nuclei extends to the tip of the tail

The morphological differences between two microfilaria

W.bancrofti

Size
Cephalic space
Nuclei

Terminal nucleus

244~296 m
Shorter
Equal sized
clearly
countable
No

B. malayi
177~230 m
Longer
Unequal sized
coalescing
uncountable
Two

Characteristic of life cycle

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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Nocturnal periodicity
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.
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
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Microfilarie taken up para-lab
by mosquito
bite

Lymphatic System
Network of vessels that collect
fluid that leaks out of the blood
into tissues (lymph)
Redirects lymph back into the
blood stream

Clinical Course

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
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Acute Adenolymphangitis (ADL)

Acute ADL
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
o Inflammation spontaneously resolve after 4-7 days but
can recur frequently
o Recurrences usually 1-4 times/year with increasing
severity of lymphedema
o Secondary bacterial infections in
edematous(elephantatic) areas
o Filarial fever (fever w/o lymphangitis)
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o Tropical Pulmonary Eosinophilia

Chronic Manifestations
o Lymphedema

o Mostly LE and inguinal, but can affect UE and breast

o Initially pitting edema, with gradual hardening of
tissues hyperpigmentation & hyperkeratosis
o GenitaliaHydroceles
o Renal involvement

o Chylurialymph discharge into urine

o Loss of fat and protein hypoproteinemia & anemia
o Hematuria, proteinuria from immune complex nephritis
o Secondary bacterial/fungal infections
o Elephantiasis: accumulation of lymph in extremeties, fibrosis,
and thickening of skin.

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Onchocerciasis (river blindness)

Debilitates millions of humans
by scarring eyes & causing
permanent blindness
Affects people along rivers
in West & Central Africa
(native) & South America
(introduced via slavery)
Caused by Onchocerca
volvulus
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)

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Onchocerciasis (river blindness)

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
Live under skin causing rashes & wrinkles
Cause blindness when invade eyes tissues &
die there
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Onchocerciasis (river blindness)

Early stages of eye damage can be reversed by
drug treatment
Parasiticide ivermectin is most popular
Transfer of worms affected by feeding behaviour
of flies
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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Loiasis
Caused by infection with Loa loa
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)
Transmitted by horse flies (Tabanidae) in genus
Chrysops
Day-feeding & forest-dwelling
Rare case of Tabanidae = biological vectors
Disease endemic to rain forest regions of West &
Central Africa
Generally mild & painless (chronic) with 10-15
year incubation period
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May cause swellings
ofmenawi
skin (Calabar
swelling)

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Diagnosis
The standard method for diagnosing active
infection is the identification of microfilariae by
microscopic examination
However, microfilariae circulate nocturnally,
making blood collection an issue
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

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

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

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.
Note wavy
microfilarial
worms.
Inflammatory
cells
lymphocytes.
Hemorrhagic
fluid sediment

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Hydrocele fluid cell

block.
Note wavy
microfilarial
worms.
Inflammatory
cells
lymphocytes.
RBC

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Hydrocele fluid cell

block.
Note wavy
microfilarial
worms.
Inflammatory
cells
lymphocytes.
RBC

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Hydrocele fluid cell

block.

Inflammatory
cells
Microfilaria.
lymphocytes.
RBC

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Control

Vector control

Covering water-storage
As with malaria, the most
containers and improving
effective method of
controlling the spread of
waste-water and solidW.bancrofti and B.malayi is
waste treatment systems
to avoid mosquito bites
can help by reducing the
The CDC recommends that
anyone in at-risk areas:
amount of standing water
Sleep under a bed net
in which mosquitoes can
Wear long sleeves and
lay eggs.
trousers
Wear insect repellent on Killing eggs (oviciding) and
exposed skin, especially
killing or disrupting larva
at night
(larviciding) in bodies of
stagnant water can further
reduce mosquito
populations.
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Treatment
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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Drugs, Drugs, Drugs!

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

The disease is usually treated with single-dose

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
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prophylactic