Clinical Manifestations and Pathology

In nature, only humans develop elephantiasis from filarial infection of the lymphatics, so scientists could not easily study the pathogenesis of bancroftian filariasis until the recent development of a cat model. As a result of this and other work, researchers have described the pathogenesis and pathology of bancroftian filariasis more accurately. Filarial disease may not manifest itself for many years despite the presence of microfilaremia. If reexposure to larvae does not occur, infection usually disappears within 8 years. Repeated exposure over many years generally results in clinical disease during adulthood. Newly exposed adults display a different disease pattern and a stronger reaction than do persons who are exposed from childhood. In both cases clinical symptoms occur throughout the body because of widespread disruption of the lymphatics (Beaver et al. 1984).

Once the filarial larva settles in a human lymph channel and begins to mature, it provokes a localized response consisting of lymph vessel dilation and a slowing of lymph flow through that worm-occupied channel. With time the host body responds immunologically, sending eosinophils, plasma cells, and macrophages to the sites of infection. Lymphangitis (inflammation of lymph channels) usually results in swelling, redness, and pain, and, when the lymph vessels become hypertrophied, in varices. Fibrosis of the vessel occurs, trapping and killing the adult worm, which is absorbed or calcified. Obliteration of the lymph vessel forces extravasation of lymph into the tissue space, where it accumulates and causes the typical lymphedema of filarial elephantiasis. The swelling can become quite large, consisting of lymph, fat, and fibrotic tissue under tightly stretched and thickened skin (Beaver et al. 1984; Manson-Bahr and Bell 1987).

The clinical course of bancroftian filariasis can follow one of two paths: In highly endemic areas, people are exposed to repeated filarial infections from a very young age. The microfilariae provoke only a weak local tissue response, and the children show little effect of infection. When the larvae move to and then reside in lymph vessels, their hosts in these highly endemic areas do not react with a strong immunologic response (or display severe symptoms), thus allowing new microfilariae to be discharged through the now dilated lymph channels into the blood. The living worms survive for years, producing microfilariae that circulate in their hosts' blood. These microfilariae soon become part of mosquitoes' meals and are passed on in their larval stage to other human hosts. As the adult worms eventually die in their tolerant human hosts' lymphatics, fibrosis and calcification of these channels disrupt the lymph system. In this chronic phase of filarial infection, as lymph channels become obstructed, typical elephantoid manifestations develop, especially in the groin and lower extremity. People in highly endemic areas are repeatedly infected over the years and so will manifest various stages of filariasis simultaneously.

Uninfected adults newly arrived in an endemic region generally show an inflammatory response to filarial infection. American troops in the Pacific during World War II experienced this problem. Their immune systems reacted quite strongly to the presence of microfilariae in lymphatics, sending a variety of cellular defenders to the affected areas. They surrounded the worms, ultimately causing stenosis of the lymphatics. Many soldiers developed very painful swelling of the scrotum, spermatic cord, and arms or legs, as well as orchitis, lymphangitis, and filarial fever (acute fever with headache and symptoms resembling malaria, recurring sometimes for years). Such a powerful response generally kills the worm, making it impossible for microfilariae to develop and circulate in the blood, but also causing disruption of the lymphatic system and the early development of elephantiasis. Some researchers believe that extreme elephantiasis occurs as a result of secondary infection with streptococcus or other bacteria.

Chronic obstructive filariasis can result in lymph gland enlargement, chyluria (due to obstructed lymph flow to the thoracic duct above the lymphatic branches of the kidney), lymph scrotum (scrotal thickening with lymphatic varicosities), hydrocele, and elephantiasis of the legs, scrotum, labia, arms, or (rarely) breasts (Beaver et al. 1984; Manson-Bahr and Bell 1987; Partono 1987).

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