Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Ahmed Elsaiey, MBBCH [2]

Filariasis is a parasitic and infectious tropical disease caused by thread-like parasitic filarial worms called nematodes. These include Wuchereria bancrofti, Brugia malayi, and Brugia timori. They are all transmitted by mosquitoes. The infection occurs when an infected mosquito bites an individual introducing the larvae into the skin. These larvae then spread to various sites such as lymphatic vessels, subcutaneous tissues or serous cavities. The larvae then mature to be adult filariae, then adult worms which produce microfilariae which are carried by another mosquito and the cycle continues. Filariasis is endemic in some Asian, African and South American countries where it affects 120 million individual annually. Screening is important for early detection and the two commonly used tests are dipstick colloidal dye immunoassay and ICT filariasis test kit. If left untreated, patients with filariasis may progress to develop lymphoedema, hydrocele, skin pigmentation, and chyluria. Filariasis has a good prognosis in early cases but the chronic cases may progress to disability. The most common symptom of filariasis is elephantiasis and scrotal swelling. Patients with filariasis present with filarial fever which is self-limited fever. Diagnosis of filariasis is made by identifying microfilariae on a giemsa stained thick blood film. Blood must be drawn at night, since the microfilaria circulate at night. There are also PCR assays available for making the diagnosis. Ultrasound also can help in the diagnosis by detecting the moving living worm which shows filarial dance sign. The recommended treatment for patients with filariasis is albendazole combined with ivermectin. A combination of diethylcarbamazine (DEC) and albendazole is also effective. Prevention of the disease involves wearing appropriate clothing, avoiding outbreaks, use of insecticides, and spatial repellents.

Filariasis is believed to be found since the 16th century when Jan Huygen Linschoten put an overall idea about the disease after his trip to Goa. Moving forward through the 19th century there were many discoveries regarding filariasis, the infective worms, and the arthropod vectors. In 1866, microfilariae were detected in urine and blood. Ten years later in 1876, Joseph Bancroft discovered the adult worm which is responsible for the infection and named it as “Wuchereria bancrofti“. Through the next years till 1900s, more discoveries and description of the life cycles of the worms were made.

Filariasis disease can be classified based on the site of infection. It is caused by different types of roundworms that infect a particular site in the body. A group of these worms infect the lymphatic vessels causing lymphatic filariasis. Others infect serous cavities and subcutaneous tissues.

Filariasis can be also classified into acute and chronic filariasis based on the duration of symptoms.

Filariasis infection occurs when a larva carrying mosquito bites individual skin introducing these larvae into the skin. The larvae then enter the patient’s blood through the skin wound and spread to the different sites such as lymphatic vessels, subcutaneous tissues or the serous cavities. At these sites, the larvae matures in a six to twelve months period into the adult filariae which can live up to fifteen years. Reproduction takes place between the male and female adult worms producing microfilariae which are premature organisms with sheath that circulate the blood in case they are settled in the lymphatic vessels. During another blood meal, the mosquito takes up the microfilariae, then these microfilariae lose their sheath within two weeks to be larvae that enter the human body. When a human is bitten by a mosquito, the cycle restarts again. Pathogenesis of the disease depends on number of factors including immune response of the patient, the number of secondary bacterial infections, the accumulation of the worm antigens, release of Wolbachia bacteria from the worm and the genetic predisposition.

Filariasis is caused by the parasitic organisms nematodes which are round worms or thread worms that infects mainly lymphatic vessels causing lymphatic filariasis. The three main nematodes that cause lymphatic filariasis are Wuchereria bancrofti, Brugia malayi and Brugia timori. Other nematodes include Loa loa (the eye worm), Mansonella streptocerca, and Onchocerca volvulus that cause subcutaneous filariasis. Mansonella perstans and Mansonella ozzardi cause serous cavity filariasis.

Lymphatic filariasis must be differentiated from other causes of lower limb edema, such as chronic venous insufficiency, acute deep venous thrombosis, lipedema, myxedema, cellulitis and causes of generalized edema.

Lymphatic filariasis is widely distributed all over the world and affects as many as 120 million individual worldwide. It is also responsible for disability in about 40 million patient. It affects children below 5 years and the probability of infection increases with age. The causative worms are more found in the tropical areas, Asia and Africa.  

Common risk factors in the development of filariasis are exposure to mosquitoes for long periods of time, getting bitten by them multiple times and people living in tropical areas for long time.

Screening is important especially among the people of Asian countries like Malaysia, China and India. It is important among people who work in agriculture fields. Agriculture fields may be inhabited by the infected mosquitoes and vectors, making these people more vulnerable to getting infected. Two known tests for the screening of filariasis are dipstick colloidal dye immunoassay and Immunochromatographic technique (ICT) filariasis test kit. 

If left untreated, patients with lymphatic filariasis may progress to develop lymphatic dilation and impaired lymphatic drainage. Common complications of filariasis include chronic lymphedema, hydrocele, skin pigmentation, and renal impairment like chyluria. Prognosis is generally good in early cases, but in chronic cases the disease can leave an individual severely disabled with genital damage.

Filariasis can have varied clinical presentations depending on their cause. The most common symptom is elephantiasis. Other symptoms include fever, headache, pruritus, pulmonary symptoms, scrotal and leg swelling.

Filariasis patients appear toxic on presentation due to pain. They present with fever called filarial fever. It is an acute self-limited fever present in the beginning of the disease. Edematous plaques may be observed and it is a sign of acute dermatolymphangioadenitis. In onchocerciasis, blindness occurs and subcutaneous nodules may be found. Genitourinary manifestations also observed in filariasis include hydrocele, chyluria, hematuria and scrotal elephantiasis.

Labarotary findings consistent with the diagnosis of filariasis include identifying microfilariae on thick blood film stained with Giemsa stain. The blood sample is drawn at night as the microfilaria circulate at night. There are also PCR assays available for making the diagnosis.

There are no x ray findings associated with filariasis.

There are no CT scan findings associated with filariasis.

There are no MRI findings associated with filariasis.

Ultrasound can be used to detect the presence of the adult worms in the lymphatics. It is also used in estimating the effectiveness of the medical therapy. Dilated lymphatic channels and living worm movement known as the filarial dance sign are noticed on the ultrasound.

There are no other specific imaging findings for filariasis.

There are no additional diagnostic findings for filariasis.

The mainstay treatment for patients with filariasis is albendazole (a broad spectrum anthelmintic) combined with ivermectin. A combination of diethylcarbamazine (DEC) and albendazole is also effective. All of these treatments are microfilaricides; they have no effect on the adult worms.

Medical therapy is the first-line treatment option for patients with filariasis. Surgery is usually reserved for patients with chronic lymphedema with failure of medical treatment and worsened presentation such as lymphatic venous anastomoses. Hydrocelectomy can also be performed for intractable cases of hydrocele.

There are many primary preventive measures available for filariasis. Wearing appropriate clothing, Avoid outbreaks, insecticides and spatial repellents, bed nets and mass drug treatment programs are effective ways to prevent filariasis.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Ahmed Elsaiey, MBBCH [2]

Jan Huygen Linschoten discovered filariasis in the 16th century after his trip to Goa. In the 19th century there were many discoveries regarding filariasis, the infective worms, and the arthropod vectors. In 1866, microfilariae were detected in urine and blood. Ten years later in 1876, Joseph Bancroft discovered the adult worm which is responsible for the infection and named it as “Wuchereria bancrofti“. More discoveries and description of the life cycles of the worms were made in the 1900s.

• In the 16th century, Jan Huygen Linschoten discovered filariasis during his trip to Goa. After that, more reports of the disease came out from Asia and Africa.^[1]
• In 1866, Timothy Lewis continued what Jean-Nicolas Demarquay and Otto Henry Wucherer started 3 years before him when they detected microfilariae in hydrocele. Timothy made a connection between these microfilariae and the elephantiasis when he discovered the presence of the microfilariae in the blood and urine.
• In 1876, Joseph Bancroft discovered the adult round worm which is responsible for filariasis and was named Wuchereria bancrofti .
• In 1877, Patricj Manson described the life cycle of the arthropod vector causing the disease when he discovered the microfilariae in the mosquitoes. It was also the discovery of arthropod to be the vector.
• In 1900, George Carmichael described how the disease is transmitted when he discovered the presence of the worm in the mosquito vector.
• In 1915. Dr. Rodolfo Robles Valverde conducted a study on patients with river blindness in Guatemala which led to the discovery of O. volvulus as the filaria causing the disease.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Ahmed Elsaiey, MBBCH [2] Omodamola Aje B.Sc, M.D. [3]

Filariasis disease can be classified based on the site of infection. A group of these worms infect the lymphatic vessels causing lymphatic filariasis, others infect serous cavities and subcutaneous tissues.

Filariasis can be also classified into acute and chronic filariasis based on the duration of symptoms.

• Based on the site of infection, filariasis is classified into:^[1]
  • Lymphatic filariasis
  • Subcutaneous filariasis
  • Serous cavities filariasis

• Based on the duration of infection, filariasis is classified into:
  • Acute filariasis
  • Chronic filariasis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Kalsang Dolma, M.B.B.S.[2], Ahmed Elsaiey, MBBCH [3]

Filariasis infection occurs when a larva carrying mosquito bites an individual, introducing these larvae into the skin. The larvae then enters the patient’s blood through the skin wound and spread to the different sites such as lymphatic vessels, subcutaneous tissues or the serous cavities. At these sites, the larvae matures in a six to twelve months period into the adult filariae which can live up to fifteen years. Reproduction takes place between the male and female adult worms producing microfilariae which are premature organisms with sheath that circulate the blood in case they are settled in the lymphatic vessels. During another blood meal, the mosquito takes up the microfilariae, then these microfilariae lose their sheath within two weeks to be larvae that enter the human body. When a human is bitten by a mosquito, the cycle restarts again. Pathogenesis of the disease depends on number of factors including immune response of the patient, the number of secondary bacterial infections, the accumulation of the worm antigens, release of Wolbachia bacteria from the worm and the genetic predisposition.

The pathogenesis of lymphedema and its progression to elephantiasis is controversial. Factors involved in the clinical manifestations of filariasis include:^{[1][2][3][4][5][6]}

• Immune response of the patient
• The number of filarial and bacterial infection
• The accumulation of the worm antigen in the lymphatic vessels
• The release of Wolbachia bacteria following death of the worm

• A mutation in the vascular endothelial growth factor receptor 3 (VEGFR-3) is associated with development of primary lymphedema secondary to dysfunction of the endothelial cells and impaired lymphangiogenesis.^[3][7]
• Mutation in the forkhead transcription factor (FOXC2) also leads to hereditary lymphedema.

In order to understand how filariasis could occur, it is important to know the life cycles of different nematodes causing filariasis. Through this table the important steps in the worms life cycle is discussed as well as the vectors responsible for disease transmission.^{[8][9][10][11]}

Type of filariasis	Causative nematode	Vectors	Life Cycle
Lymphatic filariasis	Wuchereria bancrofti	Culex as C. pipiens Aedes as A. aegypti Anopheles as A. arabinensis Coquillettidia.as C. juxtamansonia
	Brugia timori and Brugia malayi	Mansonia Aedes
Subcutaneous filariasis	Loa loa filaria	Chrysops C. silacea C. dimidiata
	Mansonella streptocerca	Midge (genus Culicoides)
	Mansonella ozzardi	Midge (genus Culicoides)
	Onchocerca volvulus	Blackfly (genus Simulium)
Serous cavity filariasis	Mansonella perstans	Midge (genus Culicoides) Blackfly (genus Simulium)

This video gives a brief explanation on the possible histopathological findings of soft tissue sample of case of filariasis: {{#ev:youtube|67zC7mXigpY}}

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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] Ahmed Elsaiey, MBBCH [3]

Filariasis is caused by the parasitic nematodes which are round worms or thread worms that infects mainly lymphatic vessels causing lymphatic filariasis. The three main nematodes that cause lymphatic filariasis are Wuchereria bancrofti, Brugia malayi and Brugia timori. Other nematodes include Loa loa (the eye worm), Mansonella streptocerca, and Onchocerca volvulus that cause subcutaneous filariasis. Mansonella perstans and Mansonella ozzardi cause serous cavity filariasis.

Filariasis is caused by the following nematodes ^{[1] [2]}

• Wuchereria bancrofti (most common cause)
• Brugia malayi
• Brugia timori

• Loa loa filaria
• Mansonella streptocerca
• Mansonella ozzardi
• Onchocerca volvulus

• Mansonella perstans

• 
  Loa loai, agent of filariasis. Anterior end. Parasite. From Public Health Image Library (PHIL). ^[3]
• 
  Loa loa, posterior end; Agent of filariasis. From Public Health Image Library (PHIL). ^[3]
• 
  Photomicrograph reveals some of the ultrastructural details displayed at the posterior end of the microfilarial-staged nematode, Brugia malayi, one of the organisms responsible for the disease known as lymphatic filariasis. From Public Health Image Library (PHIL). ^[3]
• 
  Photomicrograph reveals some of the ultrastructural details displayed at the posterior end of the microfilarial-staged nematode, Brugia malayi, one of the organisms responsible for the disease known as lymphatic filariasis. From Public Health Image Library (PHIL). ^[3]

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

Lymphatic filariasis must be differentiated from other causes of lower limb edema, such as chronic venous insufficiency, acute deep venous thrombosis, lipedema, myxedema, cellulitis and causes of generalized edema.

Lymphatic filariasis must be differentiated from other causes of lower limb edema like chronic venous insufficiency, acute deep venous thrombosis, lipedema, myxedema, cellulitis and causes of generalized edema.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Ahmed Elsaiey, MBBCH [2]

Lymphatic filariasis is widely distributed all over the world and affects as many as 120 million individuals worldwide. It is also responsible for disability in about 40 million patients. It affects children and the probability of infection increases with age. The causative worms are found predominantly in tropical areas.

• Lymphatic filariasis affects over 120 million people and it has been the leading cause of disability among filariasis patients.^[1]
• It has been reported that 1 billion people are at risk of being infected with the disease.^[2]

• Filariasis causes disability in 40% of the patients affected.^[3]

• Filariasis commonly affects children.
• It affects children before age of 5 but they remain asymptomatic and the symptoms appear after the puberty.^[2]

• Men and women are affected equally by filariasis.

• There is no racial predilection for filariasis.

• Distribution of the different nematodes causing lymphatic filariasis as the following:
  • Wuchereria bancrofti is encountered in tropical areas worldwide.
  • Brugia malayi is limited to Asia.
  • Brugia timori is restricted to some islands of Indonesia.
  • Onchocerca volvulus, which causes river blindness, occurs mainly in Africa with additional foci in Latin America and the Middle East.
  • Loa loa and Mansonella streptocerca are found in Africa.
  • Mansonella perstans occurs in both Africa and South America.
  • Mansonella ozzardi occurs only in the Americas, from Mexico south to South America and in the Caribbean.
• In endemic areas of the world (e.g., Malaipea in Indonesia), up to 54% of the population may have microfilariae in their blood.^[4] In the Americas, only four countries are currently known to be endemic: Haiti, the Dominican Republic, Guyana and Brazil.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Ahmed Elsaiey, MBBCH [2]

Common risk factors in the development of filariasis are exposure to mosquitoes for long time, getting bitten by them multiple times and people living in tropical areas for long time.

Filariasis risk factors include the following:^[1]

• Exposure to mosquitoes for long time and getting bitten by them multiple times.
• People living for a long time in tropical or sub-tropical areas where the disease is common are at the greatest risk for infection.
• People who used to hunt or fish have increase risk of filarial antigenemia.^[2]
• Warm temperature and sweating increase the risk of mosquito bites.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Ahmed Elsaiey, MBBCH [2]

Screening is important especially among the people of Asian countries like Malaysia, China and India. It is important among people who work in agriculture fields. Agriculture fields may be inhabited by the infected mosquitoes and vectors, making these people more vulnerable to getting infected. Two known tests for the screening of filariasis are dipstick colloidal dye immunoassay and Immunochromatographic technique (ICT) filariasis test kit.

• It is recommended to screen for the filariasis among the people who work in agriculture field especially in Asian countries like Malaysia, China and India.
• Screening is important as agriculture fields are an appropriate environment for the mosquitoes and the disease vectors to multiply. People working there are more vulnerable to be infected with filariasis.
• Screening tests include:^[1][2]
  • Dipstick Colloidal dye Immunoassay (DIA):
    • It detects the filarial antigens inside the individual serum and has high sensitivity and specificity for diagnosing lymphatic filariasis.
  • Immunochromatographic technique (ICT) Filariasis test kit:
    • It has specific antibodies for the W. Bancrofti antigens.

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

If left untreated, patients with lymphatic filariasis may progress to develop lymphatic dilation and impaired lymphatic drainage. Common complications of filariasis include chronic lymphedema, hydrocele, skin pigmentation, and renal impairment like chyluria. Prognosis is generally good in early cases, but in chronic cases the disease can leave an individual severely disabled with genital damage.

Lymphatic filariasis can be asymptomatic or symptomatic. Symptoms may include acute adenolymphangitis, filarial fever, and tropical pulmonary eosinophilia. If left untreated, disease can progress to lymphatic dilatation, abnormalities in lymphatic drainage, and microscopic hematuria and proteinuria.

Complications that may develop as a result of lymphatic filariasis include:

• Lymphedema:
  • Lymphedema refers to non-pitting edema in limbs due to chronic inflammation and obstruction of lymphatic vessels.
  • Lymphedema commonly occurs in upper limbs and may involve breasts.
  • Lower limb is a common place for lymphedema that commonly spares genitalia except W.bancrofti endemic areas.^[1]
• Hydrocele:
  • Hydrocele was also reported up to 30 cm in diameter due to lymphedema in the genitalia that may lead to bacterial infection.
  • Some cases of filariasis of the ovary and mesosalpinx were also reported.^[2]
• Renal involvement:
  • Increased intestinal lymph drainage in renal vessels causes loss of lymph fluid in urine giving it milky appearance.^[3]

• Early or mild filariasis, including acute inflammatory episodes, typically responds well to treatment.
• It can be reduced and prevented with simple measures of hygiene, skin care, exercise, and elevation of affected limbs, chronic infection does not.
• Filariasis does not commonly lead to mortality, however, disease can leave an individual severely disabled with genital damage or elephantiasis.
• Lymphatic filariasis is the second leading cause of disability worldwide with 40 million persons suffering from complications that limit occupational activities, educational and employment opportunities, and mobility.^[4]

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