Lymphatic filariasis currently infects about 120 million individuals in Africa, Latin Amer-ica, the Pacific Islands, and Asia; more than 75% of these cases are concentrated in Asia. W. bancrofti, transmitted primarily by mosquitoes of the genera Anopheles or Culex, isthe more cosmopolitan of the two species; it is found in patchy distribution throughout the poorly sanitated, densely crowded urban areas of all three continents. A small en-demic focus once existed near Charleston, South Carolina, but died out in the 1920s. Moreover, some 15,000 W. bancrofti infections were acquired by American servicemen during World War II. The same infection has recently been found in approximately 7% of Haitian refugees to the United States.
B. malayi, transmitted by mosquitoes of the genus Mansonia, is confined to the ruralcoastal areas of Asia and the South Pacific. Strains with an unusual periodicity have been found in animals. Humans are the only known vertebrate hosts for most strains of B.malayi and for W. bancrofti. In the eastern Indonesian archipelago, a closely relatedspecies, B. timori, is transmitted by night-feeding anopheline mosquitoes.
Pathologic changes, which are confined primarily to the lymphatic system, can be divided into acute and chronic lesions. In acute disease, the presence of molting adolescent worms and dead or dying adults stimulates dilatation of the lymphatics, hyperplastic changes in the vessel endothelium, infiltration by lymphocytes, plasma cells, and eosinophils, and thrombus formation (ie, acute lymphangitis). These developments are followed by granuloma formation, fibrosis, and permanent lymphatic obstruction. Re-peated infections eventually result in massive lymphatic blockade. The skin and subcuta-neous tissues become edematous, thickened, and fibrotic. Dilated vessels may rupture, spilling lymph into the tissues or body cavities. Bacterial and fungal superinfections of the skin often supervene and contribute to tissue damage.
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