Acute Schistosoma Mansoni Infection Research Articles

Osteopontin Is Upregulated in Human and Murine Acute Schistosomiasis Mansoni.

BackgroundSymptomatic acute schistosomiasis mansoni is a systemic hypersensitivity reaction against the migrating schistosomula and mature eggs after a primary infection. The mechanisms involved in the pathogenesis of acute schistosomiasis are not fully elucidated. Osteopontin has been implicated in granulomatous reactions and in acute hepatic injury. Our aims were to evaluate if osteopontin plays a role in acute Schistosoma mansoni infection in both human and experimentally infected mice and if circulating OPN levels could be a novel biomarker of this infection.Methodology/Principal FindingsSerum/plasma osteopontin levels were measured by ELISA in patients with acute (n = 28), hepatointestinal (n = 26), hepatosplenic (n = 39) schistosomiasis and in uninfected controls (n = 21). Liver osteopontin was assessed by immunohistochemistry in needle biopsies of 5 patients. Sera and hepatic osteopontin were quantified in the murine model of schistosomiasis mansoni during acute (7 and 8 weeks post infection, n = 10) and chronic (30 weeks post infection, n = 8) phase. Circulating osteopontin levels are increased in patients with acute schistosomiasis (p = 0.0001). The highest levels of OPN were observed during the peak of clinical symptoms (7–11 weeks post infection), returning to baseline level once the granulomas were modulated (>12 weeks post infection). The plasma levels in acute schistosomiasis were even higher than in hepatosplenic patients. The murine model mirrored the human disease. Macrophages were the major source of OPN in human and murine acute schistosomiasis, while the ductular reaction maintains OPN production in hepatosplenic disease. Soluble egg antigens from S. mansoni induced OPN expression in primary human kupffer cells.Conclusions/SignificanceS. mansoni egg antigens induce the production of OPN by macrophages in the necrotic-exudative granulomas characteristic of acute schistosomiasis mansoni. Circulating OPN levels are upregulated in human and murine acute schistosomiasis and could be a non-invasive biomarker of this form of disease.

An Outbreak of Acute Schistosomiasis Following a Church Retreat to Mwanza, Tanzania, 2008

Clinical and laboratory findings are described from 77 persons from Nairobi, Kenya, of whom 66 were diagnosed with acute Schistosoma mansoni infection following a trip to Mwanza, Tanzania. Unusual ocular symptoms were observed as a rare manifestation of acute schistosomiasis. The outbreak highlights the risk of swimming in Lake Victoria.

Ultrasound and CT findings in hepatic and pancreatic parenchyma in acute schistosomiasis

A case of acute toxaemic schistosomiasis is presented. Abdominal ultrasound examination revealed hepatosplenomegaly, lymphadenomegaly, heterogeneous hepatic parenchyma and heterogeneous focal lesions in the pancreas. CT confirmed lymph node enlargement and hepatosplenomegaly, and showed multiple small focal nodular lesions in the liver and focal lesions in the pancreas. To our knowledge, this is the first description of pancreatic lesions associated with acute Schistosoma mansoni infection.

Acute schistosoma mansoni infection in the liver

Acute schistosoma mansoni infection in the liver

Ovaries and Adrenals in Murine Schistosomiasis Mansoni

In mice with acute Schistosoma mansoni infection lipoid depletion was found in the zona fasciculata of the adrenal cortex without any other major histological alterations of the adrenals. Schistosomiasis did not influence the weight of the adrenals, or the cortisol level of the blood serum as determined by radioimmunoassay. The changes in morphology and function of the ovaries in the same infected animals reported earlier point to the vulnerability of the gonads in schistosomiasis mansoni, which may be a consequence of partial hypopituitarism.