Radiology's role grows in schistosomiasis mansoni

Schistosomiasis, or bilharziasis, results from infection by one of several species of parasitic flukes of the genus Schistosoma. The World Health Organization describes schistosomiasis as a millenary disease, affecting over 200 million individuals living in 76 different countries across Asia, Africa, and the Americas. It is considered the most important helminthic human disease and constitutes a huge public health problem. The species Schistosoma hematobium was discovered in 1851 by Theodor Bilharz. Just over 50 years later, another species of Schistosoma was discovered and subsequently classified as S mansoni. Schistosomotic patients are affected in many different ways. The majority of infected individuals are asymptomatic carriers of the parasite. At the other end of the spectrum, the hepatosplenic form of schistosomiasis can lead to upper digestive hemorrhage secondary to portal hypertension.1,2 The disease's evolutionary history comprises five major steps. Subjects must first be contaminated with an appreciable quantity of the parasite S mansoni. Live adult worms then affix themselves within the roots of mesenteric veins. Eggs deposited by females and dead worms will migrate toward intrahepatic portal roots in the liver. The resulting inflammatory reactions and scarring constitute Symmers fibrosis. The development of portal hypertension is next. The final stage includes formation of esophageal varices, hypertensive gastropathy and colopathy, and the advent of varices in other organs. While the acute phase of schistosomiasis is usually asymptomatic, clinical signs of varying intensity may occur. Common manifestations include fever, chills, weakness, weight loss, headache, nausea, vomiting, diarrhea, hepatomegaly, splenomegaly, and marked eosinophilia. The toxemic form of schistosomiasis mansoni is regarded as unusual, especially in areas where this parasitosis is endemic. Reports cite patients who developed multiple small papulo-erythematous lesions scattered across the chest, related to systemic vasculitis. Patients with pulmonary involvement, manifested by micronodules disseminated in both lungs as well as a Loffler-like syndrome, have also been observed.3 We have seen acute schistosomiasis mansoni patients presenting with pulmonary involvement that appeared as ground-glass opacities and septal thickening on high-resolution CT (Figure 1). The most common presentation of chronic schistosomiasis is the intestinal form, involving the rectal and sigmoid colons. It usually manifests as bowel irregularity of little relevance. Most colitis caused by schistosomiasis mansoni is asymptomatic or oligosymptomatic. Some patients may present with colonic stenosis (Figure 2) and intestinal obstruction. Development of the hepatointestinal form depends on patients' worm burden and nutritional status as well as immunological factors and treatment choice. Hepatosplenic schistosomiasis, the most severe presentation, is characterized by extensive splenomegaly, periportal fibrosis, portal hypertension, and upper digestive bleeding caused by ruptured esophageal varices. The principal antigenic factor behind hepatic fibrosis is the presence of S mansoni eggs in the portal veins. This causes a granulomatous inflammatory reaction, leading to the formation of fibroid tissue. Subsequent development of an intrahepatic vascular neoformation around the portal ramifications maintains blood flow and preserves hepatic cells. Patients with schistosomiasis consequently do not present with hepatic insufficiency. Development of portal hypertension, regardless of its etiology, is due to increased vascular resistance or increased portal venous flow, or both. The pathophysiology of portal hypertension also frequently displays a systemic hyperdynamic state due to portal shunting of splanchnic vasoactive mediators.4 Periportal fibrosis, also known as Symmers fibrosis (Figure 3), constitutes a pathognomonic lesion of this chronic form.5 The WHO classification of hepatic fibrosis, established in 1993, is based on