%0 Journal Article
%T Oriental schistosomiasis with neurological complications: case report
%A Yuesheng Li
%A Allen G Ross
%A Xunya Hou
%A Zhaoyang Lou
%A Donald P McManus
%J Annals of Clinical Microbiology and Antimicrobials
%D 2011
%I BioMed Central
%R 10.1186/1476-0711-10-5
%X Although not commonly reported in western countries, schistosomiasis is, after malaria, the second most prevalent tropical disease, affecting over 200 million people [1]. It is an intravascular disease, caused by dioecious parasitic trematode worms of the genus Schistosoma. Eggs released by adult female worms cause the majority of lesions in schistosomiasis when they embolize in the liver, spleen, lungs, or urino-genital or cerebrospinal systems [1-3]. Egg secretions provoke eosinophilic inflammatory and granulomatous reactions which are progressively replaced by fibrotic deposits [1,2]. Schistosomiasis is thus associated with chronic liver and intestinal or genitourinary tract fibrosis. Neurological complications can also develop, and neuroschistosomiasis is the most severe clinical outcome associated with schistosome infection [1,2]. Neurological complications during the early course of infection are thought to occur through in situ egg deposition following aberrant migration of adult worms to the brain or spinal cord [1,2]. The presence of eggs in the central nervous system (CNS) induces a Th2 driven periovular granuloma reaction [1]. The mass effect of thousands of eggs and the large granulomas concentrated within the brain or spinal cord explain the signs and symptoms of increased intracranial pressure, focal neuropathy and subsequent clinical sequel associated with neuroschistosomiasis [1].The Asian schistosome species (S. japonicum; S. mekongi) lay up to 3000 eggs daily with the resulting morbidity being more severe than with the African forms (S. mansoni; S. haematobium; S. intercalatum), which produce ten times fewer eggs per day [1,2]. Myelopathy (acute transverse myelitis and subacute myeloradiculopathy) of the lumbosacral region is the most common neurological manifestation of S. mansoni or S. haematobium infection, whereas acute encephalophalitis of the cortex, subcortex, basal ganglia or internal capsule is typical of S. japonicum [1,2].Only a minority
%U http://www.ann-clinmicrob.com/content/10/1/5