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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 3 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
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W.bancrofti

is transmitted by Culex, Aedes, and Anopheles species B.malayi is transmitted by Anopheles and Mansonia species.

Culex

Mansonia
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 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.
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Wuchereria bancrofti

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

B. malayi
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Size Cephalic space

244~296 m Shorter

177~230 m Longer

Nuclei

Equal sized
clearly countable

Unequal sized
coalescing uncountable

Terminal nucleus

No

Two
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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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para-lab by l. wafa menawi

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 17 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 18 and Lower extremities

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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 Eosinophilia o Hyperresponsiveness to microfilariae trapped in lungs o Nocturnal Wheezing
o

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Lymphedema

o
o

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
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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

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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

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

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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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24 Damaged eye tissues

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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) Complex of >40 sibling species in West & East Africa Not all sibling species transmit worms Insecticide applications used to control larvae in rivers

Main vector = Simulium damnosum

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Microfilariae in human blood

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

Adult in human eye

Generally mild & painless (chronic) with 1015 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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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

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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 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 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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