1. Lymphatic Filariasis / Elephantiasis
Onchocerciasis (river blindness)
Loiasis
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What is it ?
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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Definitive Host
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
Intermediate Host
Aedes
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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6. Lymphatic Filariasis by the numbers
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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Morphology I
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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Morphology II
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.
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Wuchereria bancrofti
Brugia malayi

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Morphology - B.malayi
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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10. The morphological differences between two microfilaria
W.bancrofti B. malayi
Size ~296 µm ~230 µm
Cephalic space Shorter Longer
Nuclei Equal sized Unequal sized
clearly coalescing
countable uncountable
Terminal nucleus No Two
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11. 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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15. 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.
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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 days inside mosquito vector
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Lymphatic System
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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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
Acute Adenolymphangitis (ADL)
Chronic/Irreversible lymphedema
Superimposed upon repeated episodes of ADL
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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
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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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21. Chronic Manifestations
Lymphedema
Mostly LE and inguinal, but can affect UE and breast
Initially pitting edema, with gradual hardening of tissues  hyperpigmentation & hyperkeratosis
GenitaliaHydroceles
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22. Chronic Manifestations
Renal involvement
Chylurialymph discharge into urine
Loss of fat and protein hypoproteinemia & anemia
Hematuria, proteinuria from ?immune complex nephritis
Secondary bacterial/fungal infections
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Elephantiasis: accumulation of lymph in extremeties, fibrosis, and thickening of skin.
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24. 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)
Transmitted by black flies (Simuliidae)
Larvae live in fast-flowing water
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25. 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 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
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Damaged eye tissues

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27. 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
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
Generally mild & painless (chronic) with year incubation period
May cause swellings of skin (Calabar swelling)
Adult in human eye
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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
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Diagnosis
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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32. Microfilariae are seen in blood smears and are DIAGNOSTIC
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33. 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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34. 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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35. 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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36. Hydrocele fluid – cell block.
Note wavy microfilarial worms.
Inflammatory cells – lymphocytes.
Hemorrhagic fluid sediment
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37. Hydrocele fluid – cell block.
Note wavy microfilarial worms.
Inflammatory cells – lymphocytes.
RBC
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38. Hydrocele fluid – cell block.
Note wavy microfilarial worms.
Inflammatory cells – lymphocytes.
RBC
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39. Hydrocele fluid – cell block.
Inflammatory cells – lymphocytes.
RBC
Microfilaria.
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Control
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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Vector control
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
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
Ivermectin
kills the microfilariae produced by adult worms
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…And more drugs!
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
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45. thank you for your attention
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