Factsheet: Lymphatic filariasis

Etiology

Lymphatic filariasis is a helminth parasitic infection caused by filarial nematode worms belonging to the Wuchereria and Brugia genera. In the Americas, Wuchereria bancrofti is the only species transmitted and Culex spp. (mainly Culex quinquefasciatus) are the most common vectors. Adult worms in the human host are whitish or pinkish, and thin (1.5-2.5mm); they can measure up to 1 meter in length.

Only four countries are endemic to lymphatic filariasis in the American continent: Brazil (State of Pernambuco), Dominican Republic, Guyana and Haiti. It is estimated that up to 11 million individuals are at risk of infection. [1] Costa Rica, Suriname and Trinidad and Tobago have recently interrupted transmission, an achievement that will be probably met soon by Dominican Republic, as transmission is limited to few circumscribed areas. 

Life cycle of the parasite

In order to complete its life cycle, W. bancrofti requires a final host (the man, as there is no significant animal reservoir) and a vector (Culex quinquefasciatus is the main responsible for transmission of lymphatic filariasis in the Americas). Lymphatic filariasis is caught when the third-stage (L3) infective larvae of the worm are deposited on the skin by an infected mosquito vector during a blood meal. The larvae then penetrate the skin at the bite site, migrate to the lymphatic system and in approximately a year mature into adult male and female worms. Adult females release larvae (called microfilariae) that eventually migrate into the general bloodstream through the thoracic duct, and reach a maximal concentration between 10pm and 2am (nocturnal periodicity). Ingestion of circulating microfilariae by another suitable mosquito vector and their development into L3 larvae closes the life-cycle of the parasite and sustains transmission in endemic areas.

Signs and symptoms

Lymphatic filariasis is characterized by a chronic evolution of its clinical picture, which is progressively worsened by episodic, highly-symptomatic acute attacks. The prepatent period (interval between the entry of the L3 larvae and the appearance of detectable microfilaraemia) can last a few months. Presence of microfilariae in the bloodstream may in fact be asymptomatic, while clinical manifestations, if present, can arise from a few months to a few years after infection. They are typically distinguished in acute and chronic. Acute symptoms include recurrent attacks of fever with painful inflammation and swelling of the lymph nodes and lymph ducts. Involvement of the genital tract is common, and orchi-epididymitis (inflammation of the testis and the epididymus) and funiculitis (inflammation of the spermatic cord) are typical findings in male patients. Affected lymph ducts appear dilated and with thickened walls. Such “acute attacks” last a few days and can be attributed to a combination of factors: presence of living adult worms, death of such worms possibly complicated by bacterial super-infection, immunological response to filarial or microfilarial antigens, etc.  

Chronic manifestations stem from repeated inflammatory episodes that can lead to a progressive blockage of the lymph ducts with accumulation of fluid in the interstitial tissues thus resulting in lymphoedema, a condition most frequently affecting the arms and the legs. In male patients, the blockage of the spermatic lymph vessels leads to accumulation of fluid in the scrotal sac (hydrocoele). The increasing fibrosis and sclerosis of the subcutaneous tissues can accelerate the progression of lymphoedema to elephantiasis (skin fold thickening and hardening, epidermal nodules, and pigmentary changes), which is associated with grossly enlarged limbs and disability. Stigma and social exclusion are frequent among such patients.

Diagnosis

A suggestive clinical picture and a high eosinophil count can orientate the diagnosis. The gold standard technique is the direct identification of microfilariae in thick blood smears; blood should be collected near the maximal microfilarial concentration time so as to increase the sensitivity of the test. Immuno-chromatographic card-based tests (ICT) detecting filarial antigens in finger prick blood are independent of microfilarial concentration and have proven sensitive and specific. They are used to map transmission of lymphatic filariasis in community surveys.

Treatment, prevention and control

A combination of diethylcarbamazine (DEC) 6 mg/kg and albendazole (ALB) 400 mg, singe-administration, is the treatment of choice for lymphatic filariasis in the Americas. The combination of DEC and ALB significantly reduces the microfilarial load for periods as long as one year; it has also been shown to have some filaricidal effect on the adult worms. The drug combination is associated with mild and temporary adverse reactions but is generally considered a highly safe treatment. [2,3,4]

The significant effect of DEC+ALB on microfilarial load is the rationale behind the strategy currently recommended by WHO for elimination of lymphatic filariasis: the yearly, large-scale distribution of DEC+ALB to all individuals living in an area where lymphatic filariasis is transmitted (mass drug administration, MDA) is expected to decrease transmission rates. [5] At least five annual rounds are considered necessary to interrupt transmission, which can be accelerated by the implementation of vector control measures directed against the mosquitoes. [4,5]

In individuals who have already developed chronic manifestations such as lymphoedema and elephantiasis, management of the affected limbs is necessary in order to prevent any further deterioration of the situation. This includes elevating and washing the limb, and treating skin infections, all measures that can usually be performed by the patients themselves. Surgery is needed in case of hydrocoele. [4]

Lymphatic filariasis is considered as a “potentially eradicable” disease, [6] and in 1997 the World Health Assembly Resolution WHA50.29 (“Elimination of lymphatic filariasis as a public health problem”) invited Member States to start implementing public health measures against it. [7] In 2009, PAHO’s Directing Council Resolution CD49.R19 (“Elimination of neglected diseases and other poverty-related infections”) urged Member States in our Region to take the final necessary steps and eliminate lymphatic filariasis as a public health problem from the Americas by 2015. [8]

References

1. Pan American Health Organization/World Health Organization. Epidemiological profiles of neglected diseases and other infections related to poverty in Latin America and the Caribbean. Washington: PAHO/WHO, 2009
2. Stuart MC, Kouimtzi M, Hill SR (editors). WHO Model Formulary 2008. Geneva: WHO, 2008
3. World Health Organization. Preventive chemotherapy in human helminthiasis. Coordinated use of anthelminthic drugs in control interventions: a manual for health professionals and programme managers. Geneva: WHO, 2006
4. World Health Organization, Global Programme to Eliminate Lymphatic Filariasis. Lymphatic filariasis: Progress Report 2000-2009 and Strategic Plan 2010-2020. Geneva: WHO, 2010
5. Ottesen E (2000). The Global Programme to Eliminate Lymphatic Filariasis. Tropical Medicine and International Health 5:591-594
6. US Centers for Disease Control and Prevention (1993). Recommendations of the International Task Force for Disease Eradication. Morbidity and Mortality Weekly Report 42:RR-16
7. World Health Organization. Resolution WHA50.29. Elimination of lymphatic filariasis as a public health problem. Geneva: WHO, 1997
8. Pan American Health Organization/World Health Organization. Resolution CD49.R19. Elimination of neglected diseases and other poverty-related infections. Washington DC: PAHO/WHO, 2009