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Chronic Schistosomiasis

When the illness becomes chronic it is different for each species. In S. haematobium infections urinary symptoms predominate, with hematuria and recurrent urinary infection. Some patients have experienced testicular tenderness and tingling. There may be changes in the ejaculate (presumably when the seminal vesicles or prostate are infected). Patients will notice a decrease in the volume of the ejaculates, which may be watery and yellow. Hematospermia does not always occur, but may be found on microscopy, which will also show schistosomal ova and an increase in the number of polymorphs. There is no decrease in spermatozoal motility. Female partners have been found to be infected, but it seems unlikely that this is transmitted from the male. A common clinical diagnosis is a nongonococcal urethritis. Renal schistosomiasis usually presents clinically because of the obstruction and infection which has affected the lower urinary tract, but an immune complex glomerular nephritis may occur, presenting clinically as albuminuria, hypertension, and a finding of glomerular changes on renal biopsy or autopsy. There is variation in the histopathological findings, which have been classified by the African Association of Nephrology (Barsoum). This type of renal schistosomiasis is the result of longstanding chronic infection, often over 10-15 years. Renal amyloidosis may be the eventual outcome of schistomsomal glomerulopathy. All three major species of schistosome may affect the kidneys.

In S. haematobium infection as well as urinary tract involvement, there may be granulomatous disease of the colon; the latter often occurs in conjunction with mucosal polyps and causes diarrhea, though this varies in extent in different countries and in different people. In S. japonicum infection, the disease may affect the small bowel as well as the colon, liver, and lungs; cerebral infections may cause epilepsy. Infection with S. mansoni, S. japonicum, and S. intercalatum particularly may affect the liver, causing cirrhosis, portal hypertension, and splenomegaly. Espohageal varices develop, with resulting hemorrhage, and pulmonary hypertension may be an added complication. It is necessary to reemphasize that the worms cannot multiply within the body and that most of the clinical manifestations result from dead worms or eggs. Many, perhaps the majority of infected persons, are asymptomatic, often for many years.

The clinical and laboratory investigations for each patient depends on the symptoms. When there is hematuria caused by S. haematobium, ultrasound and subsequently intravenous urography may be indicated. Cystoscopy may show multiple papillomas within the bladder. S. mansoni and S. japonicum infections require barium examination of the bowel and colonoscopy, which may be quite normal even during an active infection. Other patients will show clusters of small, yellow, nodular pseudotubercles or plaques beneath the normal mucosa of the rectum and biopsy will show that these contain eggs. The bowel wall may have only glistening granulation tissue or the reaction may be such that actual polyps are found; sometimes these are quite large and may resemble a neoplasm.

In endemic areas, children are usually exposed to schistosomiasis early in life. Very few children avoid the parasitic onslaught and in some areas infection is almost universal. For instance, in Niger (West Africa) over 80% of children are infected and in rural Zambia the rate is nearly 70%. However, wherever there is a piped water supply, the prevalence decreases considerably. Depending on the severity and constancy of the exposure, on general health and other factors, there may be a latent asymptomatic period of 2-25 years before the portal manifestation of S. mansoni or S. japonicum infections becomes apparent. An enlarging left upper quadrant mass, or gastrointestinal bleeding from esophageal and gastric varices, is frequently the initial complaint causing the patient to seek medical attention. Although the liver is enlarged initially, liver function studies may be nearly normal even at this stage, while hypersplenism and anemia will usually be present. The spleen is often massive; in fact, for centuries this disease was known as "Egyptian splenomegaly" (Fig. 2.9). There is often malnutrition and ascites. The development of esophageal varices is an indication of chronic irreversible liver disease.

The first attack of schistosomiasis may present as a change in intellectual level, particularly in school children: they develop difficulty in concentration. Active schistosomiasis has been shown to affect spatial relationships and numerical ability. Chronic schistosomiasis does not affect growth, physical activity, or the general level of intelligence of children in endemic areas, until it has has progressed to cause significant cirrhosis.

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Fig. 2.9 A,B The sad effect of advanced schistosomiasis in two different children in the tropics. There is hepatomegaly and massive splenomegaly from long-standing presinusoidal cirrhosis and portal hypertension: both children are anemic, malnourished, and suffer from ascites, which is especially marked in the child in A.

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