Schistosomiasis was discovered in Malaysia in 1975 in an autopsy case. Since 1975 autopsies, surveys, and resurveys have been carried out to identify animal hosts, snail intermediate hosts, and reservoir hosts. Seroepidemiologic tests involving enzyme-linked immunosorbent and circumoval precipitin methods have been used to determine the true incidence and prevalence of this protean disease among the Orang Aslis (aborigines) in Malaysia. With the use of better epidemiologic and parasitologic tools, more cases of schistosomiasis are being reported.
In hepatic schistosomiasis, pathology arises when schistosome eggs become lodged in the host liver, evoking an interleukin 4 (IL-4)- and IL-13-mediated dominant CD4(+) Th2 immune response. This response leads to the development of granulomas and fibrosis, with eosinophils, neutrophils, macrophages, hepatic stellate cells, and lymphocytes all identified as major cellular contributors to these events. This review outlines the cellular and molecular mechanisms of hepatic schistosomiasis, with an emphasis on the major cellular components and their release of chemokines. The differences between Schistosoma mansoni- and Schistosoma japonicum-induced hepatic granuloma are also discussed. This comprehensive overview of the processes associated with hepatic schistosomiasis may provide new insights into improved treatment for both schistosomiasis and other granulofibrotic diseases.