Abstract

Schistosomiasis, also commonly known as bilharziasis, is one of the most significant parasitic diseases of humans. A report of World Health Organization in 1996 estimated that over 200 million people were infested worldwide, mainly in rural agricultural and periurban areas. Of these, 20 million suffer severe consequences from the disease and 120 million are symptomatic. Symptoms range from fever, headache and lethargy, to severe sequelae including ascites, hepatosplenomegaly and even death[1]. More than 600 million people in the tropics are at risk for developing schistosomiasis. Schistosomiasis is the major public health problem in rural Egypt, with almost six million Egyptians are infested[2]. Schistosomiasis is caused by digenetic trematodes belong to phylum platyhelminthes, super family schistosmatoida, genus schistosoma. It is usually attributed to three species, subdivided into intestinal Schistosoma mansoni and Schist osoma japonicum or urinary Schistosoma hematobium types, according to the site preferred by the adult worms. In Egypt, the two species of bilharziasis are Schistosoma mansoni and hematobium whose intermediate hosts are fresh s nails, Biomphalaria alexandra, and Bulinus trancatus respectively[3]. In humans, these blood flukes reside in the mesenteric and vesical venules. They have a life span of many years and daily produce large numbers of eggs, which must traverse the gut and bladder tissues on their way to the lumens of the excretory organs. Many of the eggs remain in the host tissues, inducing immunologically mediated granulomatous inflammation and fibrosis. Heavy worm burdens may produce hepatosplenic disease in schistosomiasis mansoni and japonica and urinary tract disease in schistosomiasis hematobia. Because both the schistosomes and the eggs utilize host metabolites, and because the host responses to the parasite are affected by its nutritional status, malnutrition may strongly affect both the parasite and the complex host-parasite relationship[4].

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