Elephantiasis in the Americas

ABSTRACT & COMMENTARY

Synopsis: Lymphatic filariasis remains an important public health problem in some areas of the Americas. Asymptomatic infection may be associated with permanent lymphatic damage.

Source: Lymphatic filariasis in the Americas. Epidemiol Bull/PAHO 1997;18:6-7.

In the americas, 6.5 million people live in areas endemic for lymphatic filariasis, and 300,000 are infected with the causative agent in that region, Wuchereria bancrofti. Most cases in the Americas occur in Brazil, Costa Rica, Dominican Republic, Guyana, Haiti, Suriname, and Trinidad and Tobago.

In Brazil, Belem (Para State), Maceio (Alagoas State), and Recife (Pernambuco State) are sites of active transmission of the parasite. (See figure.) In Recife, a city of approximately 1.5 million people, 2.37% of 174, 1224 people examined in 1997 had positive peripheral blood smears. This represented a reversal of the decreasing prevalence of microfilaremia in prior years that was observed in this metropolitan area.

The only nation in the Americas in which lymphatic filariasis is present in most of the country is Haiti, where, in one focus, 30% of residents are microfilaremic, 50% are antigenemic, and approximately 25% of men have hydrocoele. Two percent of relevant mosquitoes trapped in that highly endemic area are infected.

Figure

Map of Brazil*

*Latitude and longitude lines are not exact.

COMMENT BY STAN DERESINSKI, MD, FACP

It is estimated that as many as 100 million people living in tropical regions of Asia, Africa, China, and the Pacific, as well as localized areas of the Americas (including those noted above), are infected with W. bancrofti. While Brugia malayi and Brugia timori also cause lymphatic filariasis, W. bancrofti is much more globally widespread. It is, as a result, a leading cause of permanent and long-term disability.

The results of surveys of the prevalence of microfilaremia, such as those described in the PAHO report, represent significant underestimates of the prevalence of infection. Using a rapid card test for detection of W. bancrofti antigen, Freedman and colleagues found, in an endemic community in Recife, that 17.8% of 847 residents examined were antigenemic (Freedman DO, et al. Lancet 1997;350:1681). Only 24% of those demonstrated to be antigemic had positive stained thick nocturnal blood smears, and 50% were positive on examination of membrane filtered nocturnal blood.

W. bancrofti is transmitted in the Americas by the bite of Culex quinquefasciatus, a mosquito that is distributed as far north as 38°N latitude and as far south as 31°S latitude. The parasite occurs in localized foci with discontinuous distribution, occurring in areas of poor sanitation, generally near large bodies of water. It thrives in developing countries, particularly in areas of rapid unplanned urbanization, since its breeding is confined to domestic habitats such as heavily polluted water in ditches, village ponds, and cesspools. In the areas of high prevalence, lymphatic filariasis is an important cause of long-term, usually permanent, disability.

Microfilaria (first stage larvae) are ingested from the bloodstream of infected humans. The organism develops within mosquitoes into third-stage infective larvae that enter the bloodstream of the definitive (human) host when bitten by the arthropod. The larvae migrate to the nearest proximal lymph node where they take up residence, maturing to the white thread-like adult form within 3-12 months. Lymphatic symptoms occur after an average incubation time of 15 months. The mature adults may survive for as long as 10 years.

Mating of male and female adult W. bancrofti filaria in the lymph nodes results in the vivaparous production of microfilaria (first stage larvae) which leave the lymph node to migrate through the bloodstream and temporarily reside in pulmonary arterioles during the day, emerging once again at night. The periodicity of the nematode is largely determined by the feeding habits of the biting mosquito—Culex species bite at night, a time when it is most likely to encounter microfilaria when it nourishes itself at the expense of the bitten human. Migration of the microfilaria may lead to an IgE antibody response and tropical pulmonary eosinophilia.

The persistence of adult filaria in affected lymph nodes lead to damage to lymphatic vessels either directly or indirectly as a result of the immune response to the organism and to secondary bacterial infection. Resultant repeated episodes of lymphangitis lead to obstruction of lymphatic flow and, in its most spectacular form, elephantiasis.

While most cases of W. bancrofti infection are asymptomatic, subclinical damage to lymph nodes, as demonstrated by lymphoscintigraphy, may commonly be present in microfilaremic patients in the absence of clinical evidence of lymphatic abnormalities (Freedman DO, et al. J Infect Dis 1994;170:927-933; Freedman DO, et al. J Infect Dis 1995;171:997-1001). Scrotal ultrasound examination for the "filarial dance sign," a characteristic peculiar movement of the adult parasite, has demonstrated that the lymphatic vessels of the spermatic cord are an important site of residence of W. bancrofti in asymptomatic microfilaremic men (Noroes J, et al. Trans R Soc Trop Med Hyg 1996;90:55-56).

Studies of the microfilarial nocturnal periodicity of W. bancrofti have uncovered some remarkable findings. Some experiments suggest that it is the result of changes in the venous-arterial oxygen tension differences caused by sleep (McFadzean JS, Hawking F. Trans R Soc Trop Med Hyg 1956;50:543). In fact, switching from nighttime to daytime sleep (as in nightshift workers) may reverse this periodicity. W. bancrofti, after a delay, re-establishes nocturnal periodicity in infected hosts who migrate across multiple time zones (Masuya T. Jpn J Parasitol 1976;25:283). Although the infecting mosquito’s biting habits appear to have the major influence on the periodicity of the parasite, W. bancrofti maintains its nocturnal habits in the new host when transmitted by blood transfusion.

Current recommended methods of control of W. bancrofti infections involve community-wide treatment, combined, if possible, with vector control. The combined administration of single doses of ivermectin (400 mcg/kg) plus diethylcarbamazine (6 mg/kg) results in a 99% reduction of microfilaremia that persists for at least one year. Since man is the definitive host, mass chemotherapy alone, even in the absence of vector control, has the potential for eradicating W. bancrofti.

The lymphoscintigraphic evidence of lymphatic damage in individuals with asymptomatic microfilaremia may provide an incentive to identify such individuals among those potentially exposed to the agents of lymphatic filariasis. Despite the fact that treatment with diethylcarbamazine did not reverse these abnormalities, such treatment may potentially prevent progression of lymphatic destruction (Freedman DO, et al. Am J Trop Med Hyg 1995;52:258-261).

Which of the following is correct?

a. Lymphatic filariasis in the Americas is associated with nocturnal microfilaremia.

b. Man is an accidental host of Wucheria bancrofti.

c. Most cases of lymphatic filaremia in the Americas occur in Mexico.

d. Infection with Wucheria bancrofti is almost always symptomatic.