Schistosomiasis infects

                 One of the oldest diseases known, even today schistosomiasis infects a large part of the world’s population. Both children and adults suffer from this infection. The primary endorgan affected depends on the river fluke involved: Schistosoma japonicum and S. mekongi, primarily Oriental in distribution, affect the liver, S. mansoni involves the liver and rectum, and S. haematobium infestation targets the urinary tract. S. mansoni is found in west central Africa, the Arabic peninsula, some Caribbean Islands, and the Atlantic coast of South America.
                  Fresh water snails serve as an intermediary host for cercariae.Humans are infected through intact skin, the cercariae migrate from peripheral venules to the lungs and heart, and reach the liver where they mature into adult worms. S. japonicum eggs are carried from mesenteric veins into intrahepatic portal vein terminal branches, where extensive fibrosis and a granulomatous reaction lead to presinusoidal portal hypertension.
                   Schistosomiasis can be divided into an acute (Katayama syndrome) and a chronic phase. Early diagnosis during the acute phase is based on clinical and laboratory data, with imaging having no direct role. Eventually these patients develop portal hypertension and esophageal varices. They have a normal hepatic venous pressure gradient due to the presinusoidal nature of their portal hypertension. Hemodynamic studies in patients with hepatic schistosomiasis reveal hyperkinetic systemic and splanchnic circulations.
                  Liver involvement consists of fibrosis and portal hypertension. Some patients progress to cirrhosis and liver failure. In the Middle East, cirrhosis developing in a setting of hepatic schistosomiasis should suggest superimposed hepatitis C virus infection. On the other hand, a Philippines study of prior S. japonicum infection found chronic viral hepatitis to be rare. Patients with chronic liver schistosomiasis are at risk of developing hepatocellular carcinoma.
                 Hepatosplenomegaly and lymphadenopathy are common with acute S. mansoni infection. Left lobe hypertrophy occurs early and is readily detected by US. On a chronic basis the porta hepatis region is usually most extensivelyinvolved, and periportal fibrosis extends intrahepatically for varying lengths. Ultrasonography rather than biopsy is often used in endemic areas to evaluate periportal fibrosis. It reveals widened hyperechoic periportal tracts, a nonspecific finding also seen in some other chronic infections. A relationship exists between the degree of periportal fibrosis as detected by US and the presence of esophageal varices. 
                  Early in the disease MRI shows portal hypertension; then the periportal zones become isodense on T1-weighted images and enhance with contrast. T2-weighted sequences reveal hyperintense periportal regions suggesting inflammation and edema. Patients with S. japonicum infection develop almost pathognomonic turtleback pericapsular and parenchymal calcifications, best identified with CT; US often shows a patchy network pattern. Calcifications are uncommon with S. mansoni and S. haematobium infection.
This is radiology images of Portal hypertension induced by schistosomiasis. T1- (A) and T2-weighted (B) coronal MR images reveal a spleen larger than the normal-sized liver and a dilated portal vein (arrows)
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