Lymphatic filariasis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Kalsang Dolma, M.B.B.S.[2]

Lymphatic filariasis, considered globally as a Neglected Tropical Disease, is a parasitic disease caused by microscopic, thread-like worms. The adult worms only live in the human lymph system. The lymph system maintains the body’s fluid balance and fights infections. Lymphatic filariasis is spread from person to person by mosquitoes. People with the disease can suffer from lymphedema and elephantiasis and in men, swelling of the scrotum, called hydrocele. Lymphatic filariasis is a leading cause of permanent disability worldwide. Communities frequently shun and reject women and men disfigured by the disease. Affected people frequently are unable to work because of their disability, and this harms their families and their communities.

Lymphatic Filariasis is thought to have affected humans since approximately 1500-4000 years ago and the first documentation of symptoms occurred in the 16th century, when Jan Huygen Linschoten wrote about the disease during the exploration of Goa.

Infective larvae are transmitted by infected biting mosquitoes during a blood meal. The larvae migrate to lymphatic vessels and lymph nodes, where they develop into microfilariae-producing adults. The adults dwell in lymphatic vessels and lymph nodes where they can live for several years. The female worms produce microfilariae which circulate in the blood. The microfilariae infect biting mosquitoes. Inside the mosquito, the microfilariae develop in 1 to 2 weeks into infective filariform (third-stage) larvae. During a subsequent blood meal by the mosquito, the larvae infect the vertebrate host. They migrate to the lymphatic vessels and lymph nodes of the human host, where they develop into adults.

Lymphatic Filariasis is caused by nematodes (roundworms) that inhabit the lymphatic vessels and lymph nodes of a human host. Wuchereria bancrofti, Brugia malayi and Brugia timori cause lymphatic filariasis.

Repeated mosquito bites over several months to years are needed to get lymphatic filariasis. People living for a long time in tropical or sub-tropical areas where the disease is common are at the greatest risk for infection. Short-term tourists have a very low risk.

Most infected people are asymptomatic and will never develop clinical symptoms, despite the fact that the parasite damages the lymph system. A small percentage of persons will develop lymphedema. Filarial infection can also cause pulmonary tropical eosinophilia syndrome. Most people develop these clinical manifestations years after being infected.

Serologic techniques provide an alternative to microscopic detection of microfilariae for the diagnosis of lymphatic filariasis. Patients with active filarial infection typically have elevated levels of antifilarial IgG4 in the blood and these can be detected using routine assays. The development of an immunochromatographic card test (ICT) with high sensitivity and specificity for detecting W. bancrofti infection has simplified diagnosis, and test kits are commercially available. The test requires 100 μl of fingerprick blood drawn at any time, day or night.

People infected with adult worms can take a yearly dose of medicine, called diethylcarbamazine (DEC), that kills the microscopic worms circulating in the blood. While this drug does not kill all of the adult worms, it does prevent infected people from giving the disease to someone else. Lymphedema and elephantiasis are not indications for DEC treatment because most people with lymphedema are not actively infected with the filarial parasite. Physicians can obtain DEC from CDC after lab results confirm infection.

Avoidance of mosquito bites through personal protection measures or community-level vector control is the best option to prevent lymphatic filariasis. Periodic examination of blood for infection and initiation of recommended treatment are also likely to prevent clinical manifestations.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Kalsang Dolma, M.B.B.S.[2]

Lymphatic Filariasis is thought to have affected humans since approximately 1500-4000 years ago and the first documentation of symptoms occurred in the 16th century, when Jan Huygen Linschoten wrote about the disease during the exploration of Goa.

Lymphatic Filariasis is thought to have affected humans since approximately 1500-4000 years ago, though an exact date for its origin is unknown. The first clear reference to the disease occurs in ancient Greek literature, where scholars discuss diagnosis of lymphatic filariasis vs. diagnosis of similar symptoms that can result from leprosy.

The first documentation of symptoms occurred in the 16th century, when Jan Huygen Linschoten wrote about the disease during the exploration of Goa. Soon after, exploration of other parts of Asia and Africa turned up further reports of disease symptoms. It was not until centuries later than an understanding of the disease began to develop.

In 1866, Timothy Lewis, building on the work of Jean-Nicolas Demarquay and Otto Henry Wucherer, made the connection between microfilariae and elephantiasis, establishing the course of research that would ultimately explain the disease. Not long after, in 1876, Joseph Bancroft discovered the adult form of the worm, and finally in 1877 the life cycle involving an arthropod vector was theorized by Patrick Manson, who proceeded to demonstrate the presence of the worms in mosquitoes. Manson incorrectly hypothesized that the disease was transmitted through skin contact with water in which the mosquitoes had laid eggs. In 1900, George Carmichael Low determined the actual transmission method by discovering the presence of the worm in the proboscis of the mosquito vector.^[1]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Kalsang Dolma, M.B.B.S.[2]

Infective larvae are transmitted by infected biting mosquitoes during a blood meal. The larvae migrate to lymphatic vessels and lymph nodes, where they develop into microfilariae-producing adults. The adults dwell in lymphatic vessels and lymph nodes where they can live for several years. The female worms produce microfilariae which circulate in the blood. The microfilariae infect biting mosquitoes. Inside the mosquito, the microfilariae develop in 1 to 2 weeks into infective filariform (third-stage) larvae. During a subsequent blood meal by the mosquito, the larvae infect the vertebrate host. They migrate to the lymphatic vessels and lymph nodes of the human host, where they develop into adults.

Different species of the following genera of mosquitoes are vectors of W. bancrofti filariasis depending on geographical distribution. Among them are: Culex (C. annulirostris, C. bitaeniorhynchus, C. quinquefasciatus, and C. pipiens); Anopheles (A. arabinensis, A. bancroftii, A. farauti, A. funestus, A. gambiae, A. koliensis, A. melas, A. merus, A. punctulatus and A. wellcomei); Aedes (A. aegypti, A. aquasalis, A. bellator, A. cooki, A. darlingi, A. kochi, A. polynesiensis, A. pseudoscutellaris, A. rotumae, A. scapularis, and A. vigilax); Mansonia (M. pseudotitillans, M. uniformis); Coquillettidia (C. juxtamansonia). During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound (1). They develop in adults that commonly reside in the lymphatics (2) . The female worms measure 80 to 100 mm in length and 0.24 to 0.30 mm in diameter, while the males measure about 40 mm by .1 mm. Adults produce microfilariae measuring 244 to 296 μm by 7.5 to 10 μm, which are sheathed and have nocturnal periodicity, except the South Pacific microfilariae which have the absence of marked periodicity. The microfilariae migrate into lymph and blood channels moving actively through lymph and blood (3) . A mosquito ingests the microfilariae during a blood meal (4). After ingestion, the microfilariae lose their sheaths and some of them work their way through the wall of the proventriculus and cardiac portion of the mosquito’s midgut and reach the thoracic muscles (5). There the microfilariae develop into first-stage larvae (6) and subsequently into third-stage infective larvae (7). The third-stage infective larvae migrate through the hemocoel to the mosquito’s prosbocis (8) and can infect another human when the mosquito takes a blood meal (1).

The typical vector for Brugia malayi filariasis are mosquito species from the genera Mansonia and Aedes. During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound (1). They develop into adults that commonly reside in the lymphatics (2). The adult worms resemble those of Wuchereria bancrofti but are smaller. Female worms measure 43 to 55 mm in length by 130 to 170 μm in width, and males measure 13 to 23 mm in length by 70 to 80 μm in width. Adults produce microfilariae, measuring 177 to 230 μm in length and 5 to 7 μm in width, which are sheathed and have nocturnal periodicity. The microfilariae migrate into lymph and enter the blood stream reaching the peripheral blood (3). A mosquito ingests the microfilariae during a blood meal (4). After ingestion, the microfilariae lose their sheaths and work their way through the wall of the proventriculus and cardiac portion of the midgut to reach the thoracic muscles (5). There the microfilariae develop into first-stage larvae (6) and subsequently into third-stage larvae (7). The third-stage larvae migrate through the hemocoel to the mosquito’s prosbocis (8) and can infect another human when the mosquito takes a blood meal (1).

A wide range of mosquitoes can transmit the parasite, depending on the geographic area. In Africa, the most common vector is Anopheles and in the America, it is Culex quinquefasciatus. Aedes and Mansonia can transmit the infection in the Pacific and in Asia.

Shown below is an image of an Anopheles gambiae mosquito taking a blood meal.

Shown below is an image of many species in the genera Anopheles that can transmit the infective larvae that cause lymphatic filariasis.

Shown below is an image of Culex quinquefasciatus, a vector of lymphatic filariasis.

Shown below is an image of Culex that transmits the infective larva of Waucheria bancrofti and brugia malayi.

Shown below is an image of an Aedes aegypti female mosquito taking a blood meal.

Shown below is an image of Aedes that transmits the infective larvae of Waucheria bancrofti and brugia malayi .

Shown below is an image of microfilaria of Wuchereria bancrofti.

Shown below is an image of microfilaria of Brugia malayi.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Kalsang Dolma, M.B.B.S.[2]

Lymphatic Filariasis is caused by nematodes (roundworms) that inhabit the lymphatic vessels and lymph nodes of a human host. Wuchereria bancrofti, Brugia malayi and Brugia timori cause lymphatic filariasis.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Kalsang Dolma, M.B.B.S.[2]

Lymphatic filariasis affects over 120 million people in 80 countries throughout the tropics and sub-tropics of Asia, Africa, the Western Pacific, and parts of the Caribbean and South America. Approximately 66% of those at risk of infection live in the WHO South-East Asia Region and 33% in the African Region.

In the Americas, only four countries are currently known to be endemic: Haiti, the Dominican Republic, Guyana and Brazil.

In the United States, Charleston, South Carolina, was the last known place with lymphatic filariasis. The infection disappeared early in the 20th century. Currently, you can not get infected in the U.S.

Lymphatic filariasis is caused by infection with nematodes of the family Filarioidea: 90% of infections are caused by Wuchereria bancrofti and most of the remainder by Brugia malayi.

Humans are the exclusive host of infection with W. bancrofti. Although certain strains of B. malayi can also infect some animal species (felines and monkeys), the life cycle in these animals generally remains epidemiologically distinct from that in humans.

The major vectors of W. bancrofti are mosquitoes of the genus Culex (in urban and semi-urban areas), Anopheles (in rural areas of Africa and elsewhere) and Aedes (in islands of the Pacific).

The parasites of B. malayi are transmitted by various species of the genus Mansonia; in some areas, anopheline mosquitoes are responsible for transmitting infection. Brugian parasites are confined to areas of east and south Asia, notably India, Indonesia, Malaysia and the Philippines.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Kalsang Dolma, M.B.B.S.[2]

Repeated mosquito bites over several months to years are needed to get lymphatic filariasis. People living for a long time in tropical or sub-tropical areas where the disease is common are at the greatest risk for infection. Short-term tourists have a very low risk.

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