filairasis - Wuchereria bancrofti & Brugia malayi


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Wuchereria bancrofti & Brugia malayi



Wuchereria bancrofti and Brugia spp. belong to phylum Nematoda (roundworms). Nematodes are appendageless, cylindrical, non-segmented worms possessing a body cavity and a complete digestive tract with tri-radiate pharynx. The body is covered with a cuticle and has four main longitudinal hypodermal chords. Nematodes have well developed nervous, excretory and reproductive systems, but lack specialized respiratory and circulatory systems. Over 15,000 nematode species have been described and their size ranges from 82 μm over 8 meter in length. Majority of the nematodes are free-living organisms inhabiting water and soil, but a few of them parasitize crops, insects, livestock and human. The first recorded parasitic nematodes were human parasites such as roundworms (Ascaris) and guinea worms (Dracunculus medinensis ). In 1878, Sir Patrick Manson discovered that mosquitoes transmitted nematodes that cause filariasis.

Wuchereria bancrofti taxonomic lineage

cellular organisms - Eukaryota - Fungi/Metazoa group - Metazoa - Eumetazoa - Bilateria - Pseudocoelomata - Nematoda - Chromadorea - Spirurida - Filarioidea - Onchocercidae - Wuchereria - Wuchereria bancrofti

Brugia malayi taxonomic lineage

cellular organisms - Eukaryota - Fungi/Metazoa group - Metazoa - Eumetazoa - Bilateria - Pseudocoelomata - Nematoda - Chromadorea - Spirurida - Filarioidea - Onchocercidae - Brugia - Brugia malayi

Brief facts

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Wuchereria bancrofti life cycle, CDC

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Developmental stages (life cycle)

Life Cycle Stages

The life cycles of nematodes causing lymphatic filariasis are similar. Filarial parasites require two different hosts to complete their life cycle: the vertebrate definitive host where parasites reproduce sexually and the arthropod intermediate host. Adults of human lymphatic filarial nematodes live in the lymphatic system of human. Adult male and female mate and the gravid females viviparously release embryonic larvae (instead of laying eggs) called microfilariae (MF) into the lymphatic system, which migrate to the blood where they become available to biting mosquitoes.

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Wuchereria bancrofti

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, and others); Aedes (A. aegypti, A. aquasalis, and others); Mansonia (M. pseudotitillans, M. uniformis); Coquillettidia (C. juxtamansonia). Among the anophelines, 36 species are capable of both malaria and LF transmission, 26 of which are regarded as major LF vector. species

B. malayi

The typical vector for Brugia malayi filariasis are mosquito species from the genera Mansonia and Aedes.

Bancroftian filariasis and Brugia malayi are unique among the vector-borne parasitic diseases in that larval development can take place in several genera of mosquitoes.

Mosquitoes at MetaPathogen

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Endosymbiotic Wolbachia

Wolbachia of filarial nematodes are Rickettsia-like, matrilineally (from mother) inherited, obligate intracellular alpha-proteobacteria and have some resemblances with insects' Wolbachia endosymbionts. They were first found in hypodermal tissues of lateral chords, uterine wall and in embryos of filarial nematodes. They can be oval, round or rod- shaped and are 0.6-1.5 μm in size. In late 1970s, two groups first identified these endobacteria in filarial worms and speculated that antibiotics could be used to treat filarial infections. All life cycle stages of filarial worms are infected with these bacteria, but the intensity of the infections varies between the life cycle stages, and appears that they have their own developmental life cycle within the worms. Several filarial nematodes have been shown to contain these bacteria. Only a few species (for example: Loa loa, Acanthocheilonema viteae, Setaria equina and Onchocerca flexuosa) do not carry these bacteria. Studies suggest that Wolbachia in filarial nematodes have coexisted for several million years and have not crossed over from their intermediate hosts (mosquitos for example) recently. However, loss of Wolbachia across the nematode family was reported during their evolution. Identification of new molecules in drug discovery research against filarial nematodes was boosted by the observation that Wolbachia can be used as a drug target and thus hold great promise towards therapeutic options available for filariasis treatment.

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Pathogenesis of lymphatic filariasis

The term pathology can be defined as the structural and functional changes that result from a disease process, regardless of whether these changes are clinically apparent or not.

Lymphatic filarial nematodes cause long-term chronic infection with a few infected individuals developing overt disease. One of the most striking features of filarial infection is that individuals with millions of vigorously motile worms often show no obvious clinical signs of disease. Asymptomatic infections are characterized by several immune regulatory processes driven by living parasites, thought to promote their long-term survival. Nevertheless, 40 million people (a third of those infected) have clinical disease, making lymphatic filariasis the second-largest cause of permanent and long-term disability worldwide.

LF is clinically a spectral disease. In 1992, Ottesen suggested that the two polar groups were individuals with chronic pathology and no microfilariae in circulation versus individuals with abundant microfilariae in circulation, but no symptoms.

The pathogenesis of the characteristic lymphatic damage is thought to involve three components:

Lymphatic dilation (lymphangiectasia) is present in all patients who harbor living adult worms. It can remain subclinical for undetermined periods of time, or involve into chronic disease. The death of adult worms can cause episodes of acute filarial lymphangitis (AFL) or may result in subclinical (without complaints from patient) infection. However, lymphangiectasia in the skin (legs arms, penis, scrotum, breasts) further impairs lymphatic function and predisposes to secondary bacterial or/and fungal infections. Recurent infections are an essential cofactor in the development of lymphedema and it progression to elephantiasis (it's why personal hygiene is very important for prevention most severe complications of filarial infection).

Lymphatic filariasis pathogenesis

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Diagnosis of lymphatic filariasis

Diagnosis of filarial infection traditionally relied on detection of motile microfilariae in blood samples (typically taken at night) for lymphatic filariasis. Antigen detection is now the preferred method for diagnosis of bancroftian filariasis.

Also, the identification of the motile adult worms within the lymphatics (termed the "filaria dance sign") using high-frequency ultrasound in conjunction with Doppler has been found quite useful for diagnosis of bancroftian filariasis.

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Control of lymphatic filariasis

Transmission and reservoirs

A non-human reservoir does not exist for W. bancrofti and high human–vector contact is required to maintain transmission, even for the very efficient Culex vectors. Hairston and De Meillon estimated that more than 15,000 infective bites of Culex quinquefasciatus were required to produce a new patient infection. This suggests that transmission can be interrupted by reducing human–vector contact through vector control or an integrated approach combining vector control and mass drug administration (MDA). Vector control can be particularly efficient because transmission of the parasite is very inefficient. There is no multiplication of the parasite in the mosquito vector and only continuous exposure to bites of many infected mosquitoes maintains the infection in humans.

B. malayi can infect not only humans but also monkeys, domestic cats, and forest carnivores, i.e. it has zoonotic reservoir.

Beliefs about disease causality and transmission

The role of mosquitoes in transmitting the parasitic agents of filariasis is poorly appreciated in many endemic communities. In a Malaysian study, only nine of 108 respondents associated filariasis with mosquitoes, while walking barefoot on dirty ground or consuming contaminated food or drink was commonly implicated as the source of infection. In rural Thailand, while schoolchildren indicated correctly that mosquitoes transmit filariasis and that the disease could be prevented by personal protection against mosquito bites, adults maintained that the disease was inherited or resulted from poor blood circulation, carrying heavy loads, prolonged standing, bathing in or drinking swamp water, personal contact with infected individuals or sorcery. Many participants in the Indian survey believed that the disease was inherited. In Papua New Guinea and the United Republic of Tanzania, although most people indicated that mosquitoes spread malaria, few understood that mosquitoes could also spread filariasis. In French Polynesia, despite an intensive community education campaign, most people discounted the idea that mosquitoes played any part in disease transmission and attributed LF to the act of immersing an injured ankle in the sea or consuming contaminated food and drink. A study in rural south India found that only 9% of apparently uninfected people and 20% of patients with chronic filarial pathology knew that filariasis was contracted through mosquito bites. Other causes commonly cited were occupation, polluted drinking water and poor nutrition.

Impact on infected individuals

The chronic manifestations of filariasis can have significant, and often very negative, social impacts. The chronic disabling manifestations of this disease, including lymphedema of the limbs, breasts and external genitalia, have a profoundly detrimental effect on the quality of life of affected individuals. The degree of social disability varies between cultural settings, but the degree of stigmatization appears to be directly correlated with the severity of visible disease.12,13 In conservative contexts, affected individuals avoid seeking treatment for fear of drawing attention to their condition. Failure to treat the disease results in recurrent acute febrile attacks and progressive damage to the lymphatic system. Without access to simple hygiene advice, sufferers are unable to prevent further progression of the outwardly visible complications of LF.

Target for elimination

Lymphatic filariasis is a disease targeted for elimination. The availability of safe, single-dose, two-drug treatment regimens capable of reducing microfilaremia to near-zero levels for 1 year or more, along with remarkable improvements in techniques for diagnosing the infection, resulted in advocacy for a global strategy to eliminate the disease through mass drug administration (MDA). Following the conclusion by an independent International Task Force for Disease Eradication that LF was one of only six infectious diseases considered to be 'eradicable' or ‘potentially eradicable' (, the World Health Assembly in 1997 adopted Resolution WHA50.29, calling for the elimination of LF as a public health problem globally. Out of the 81 countries afflicted with LF, 48 have launched national elimination programs. The WHO, in collaboration with other international agencies in public health and the private sector, formed launched a Global Programme to Eliminate Lymphatic Filariasis (GPELF) by the year 2020.


Drugs to treat filariasis include diethylcarbamazine, ivermectin, and albendazole, which are used mostly in combination to reduce microfilariae in blood and prevent their transmission to their intermediate mosquito hosts.

In addition, filarial endosymbionts Wolbachia that greatly contribute to inflammatory disease pathogenesis especially after release from dead worms are a target for doxycycline therapy, which delivers macrofilaricidal activity, causes long-term sterility of adult worms, improves pathological outcomes, and is effective as monotherapy.

Scale of MDA and GPELF

Since 2000, GPELF has provided more than 1.9 billion treatments with the three antifilarial drugs via mass drug administration to at least 570 million people living in 51 of the 83 initially identified countries with endemic lymphatic filariasis. One study suggests that the GPELF prevented development of lymphatic filariasis in about 6.6 million newborn babies between 2000 and 2007, thus averting nearly 1.4 million cases of hydrocoele, 800,000 cases of lymphedema, and 4.4 million cases of subclinical disease. Similarly, 9.5 million individuals–previously infected but without overt signs of disease–were protected from developing hydrocoele (6.0 million) or lymphedema (3.5 million).

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