Schistosomiasis( Blood Fluke Infection )

SCHISTOSOMIASIS( BLOOD FLUKE INFECTION )

EPIDEMIOLOGY

The widespread distribution and extensive morbidity of schistosomiasis makes it the single most important helminthic infection in the world today. Currently, more than 200 million individuals in 74 countries are infected. The continued presence of the parasite depends on the disposal of infected human excrement into fresh water, the availability of appropriate snail hosts, and the exposure of humans to water infected with cercariae. The construction of modern sanitation and water purification facilities would break this cycle of transmission but exceeds the economic resources of most endemic nations. Paradoxi-cally, several massive land irrigation projects launched over the past two decades for the express purpose of speeding economic development have resulted in the dispersion of infected humans and snails to previously uninvolved areas. S. mansoni, the most widespread of the blood flukes, is the only one present in the Western Hemisphere. Origi-nally thought to have been introduced by African slaves, it is now found in Venezuela, Brazil, Surinam, Puerto Rico, the Dominican Republic, St. Lucia, and several other Caribbean islands.

Because a suitable snail host is lacking, transmission does not occur within the conti-nental United States; however, nearly half a million individuals residing there have acquired schistosomiasis elsewhere. Puerto Rican, Yemenite, and Southeast Asian popula-tions are those predominantly involved. In the Eastern Hemisphere, the prevalence of S. mansoni infection is highest in the Nile Delta and the tropical section of Africa.Isolated foci are also found in East and South Africa, Yemen, Saudi Arabia, and Israel.

S. haematobium is largely confined to Africa and the Middle East, where its distribu-tion overlaps that of S. mansoni. Schistosoma japonicum affects the agricultural popula-tions of several Far Eastern countries, including Japan, China, the Philippines, and the Celebes. The closely related S. mekongi is found in the Mekong and Mun River valleys of Vietnam, Thailand, Cambodia, and Laos.

Within endemic areas, there are wide variations in both infection rates and worm loads. In general, both peak in the second decade of life and then decrease with advancing age. This finding has been explained in part by changes in the intensity of water exposure and in part by the slow development of IgE-mediated immunity. Most infected patients carry fewer than 10 pairs of worms in the vascular system and, accordingly, lack clinical manifestations of disease. Individuals who develop much heavier loads as a result of repeated infections may experience serious morbidity or mortality. Patients with concomitant S. mansoni and human immunodeficiency virus infections excrete substantially fewer eggs in their stool.

PATHOGENESIS

There are three major clinicopathologic stages in schistosomiasis. The first stage is initi-ated by the penetration and migration of the schistosomula. The second or intermediate stage begins with oviposition and is associated with a complex of clinical manifestations. The third or chronic stage is characterized by granuloma formation and scarring around retained eggs.

IMMUNITY

The major clinicopathologic manifestations of schistosomiasis result from the host’s cell-mediated immune response to the presence of retained eggs. With time, the intensity of this reaction is muted; granulomas formed in the later stages of infection are smaller and less damaging than those formed early. The mechanisms responsible for this modulation are not fully understood. Present evidence suggests that both suppressor T lymphocyte ac-tivity and antibody blockade are involved. The correlation in humans between HLA types A1 and B5 and the development of hepatosplenomegaly suggests that the extent of the im-munoregulation is influenced, at least in part, by the genetic background of the host.

As evidenced by their prolonged survival, the adult worms are remarkably well toler-ated by their hosts. In part, this tolerance may be attributable to the formation of IgG4 blocking antibodies early in the course of infection. Tolerance may also reflect the ability of the developing parasites to disguise themselves by adsorbing host molecules, including immunoglobulins, blood group glycolipids, and histocompatibility complex antigens. Nevertheless, as mentioned earlier, the prevalence and intensity of human infection be-gins to abate during adolescence, despite continuing exposure to infective cercariae. It has been suggested that schistosomula penetrating the skin after the primary infection are coated with specific antibody, bound to eosinophils, and destroyed before they can reach the portal system. Although protection is not complete, the 60 to 80% kill rate is highly effective in controlling the intensity of parasitism. This condition, in which adult worms from a primary infection can survive in a host resistant to reinfection, has been termed concomitant immunity. Eventually, production of blocking antibodies wanes and that of protective IgE antibodies active against adult worms increases, leading to a decrease in the host’s total worm population.