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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 ElephantiasisCommonly 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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W.bancrofti is transmitted by Culex, Aedes, and Anopheles species
B.malayi is transmitted by Anopheles and Mansonia species.
Anopheles
Aedes
Culex
Mansonia
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Endemic in 83 countries1.2 billion at riskMore than 120 million people infectedMore than 25 million men suffer from
genital symptomsMore 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 lengthMale: 2.5~4cm and a curved tail with
two copulatory spicules.
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Microfilaria: 177~296 µm 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
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B.malayi microfilariae are slightly smaller than those of W.bancrofti.
Microfilariae are sheathed, and about 200 to 275 µm.
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 B. malayi
Size 244~296 µm 177~230 µm
Cephalic space Shorter Longer
Nuclei Equal sized Unequal sized
clearly coalescing
countable uncountable
Terminal nucleus No Two
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Host: Mosqutoes (intermediate host) Human (final host)Location: Lymphatics and lymph
nodesInfective stage: Infective larvaeTransmission stage: MicrofilariaeDiagnostic 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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io 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)o Tropical Pulmonary Eosinophiliao Hyperresponsiveness to microfilariae
trapped in lungso Nocturnal Wheezing
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o Lymphedemao Mostly LE and inguinal, but can
affect UE and breasto Initially pitting edema, with gradual
hardening of tissues hyperpigmentation & hyperkeratosis
o GenitaliaHydroceles
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o Renal involvement o Chylurialymph discharge into
urineo Loss of fat and protein
hypoproteinemia & anemiao Hematuria, proteinuria from ?
immune complex nephritiso Secondary bacterial/fungal infections
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Elephantiasis: accumulation of lymph in extremeties, fibrosis, and thickening of skin.
para-lab by l. wafa menawi 23
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) Transmitted by black flies
(Simuliidae) Larvae live in fast-flowing water
para-lab by l. wafa menawi 24
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 don’t cause much damage
Mating in nodules produces microfilariae Live under skin causing rashes &
wrinkles Cause blindness when invade eyes
tissues & die there
Nodules
Damaged eye tissues
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para-lab by l. wafa menawi 26
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
para-lab by l. wafa menawi 27
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 May cause swellings of skin (Calabar
swelling)
Microfilariae in human blood
Adult in human eye
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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 developedDoes not require laboratory
equipmentBlood 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)
para-lab by l. wafa menawi 35
HYDROCELE FLUID – CELL BLOCK. Note wavy
microfilarial worms.
Inflammatory cells – lymphocytes.
Hemorrhagic fluid sediment
para-lab by l. wafa menawi 36
HYDROCELE FLUID – CELL BLOCK.
Note wavy microfilarial worms.
Inflammatory cells – lymphocytes.
RBC
para-lab by l. wafa menawi 37
HYDROCELE FLUID – CELL BLOCK.
Note wavy microfilarial worms.
Inflammatory cells – lymphocytes.
RBC
para-lab by l. wafa menawi 38
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 at-risk areas:
Sleep under a bed netWear long sleeves and trousersWear 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 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 prophylactic