Conjoint Professor Brahm Bhagwandeen

This paper presents the author's experience with hepatic schistosomiasis in an endemic area of S. mansoni in Zambia. The unit of the schistosomal lesion is the pseudo tubercle which develops around the individual eggs. Confluence of these granulomata has a role in the subsequent development of the more severe chronic stages of portal fibrosis. The late stages of pipe stem portal fibrosis of the liver due to schistosomiasis are well documented from the major endemic areas of Schistosoma mansoni in Egypt and South America. Although schistosomal pipe stem portal fibrosis of the liver is now accepted as a pathological entity, there is still some discrepancy in the histopathological descriptions of the liver lesions. This study is an account of the early hepatic lesions produced by S. mansoni and their natural history as observed in liver biopsies. It is an account of the lesions produced by mature, apparently viable eggs of S. mansoni (as judged by the presence of a recognizable miracidium in the egg). Although other factors have been incriminated in the production of hepatic lesions, it is generally accepted that mature, viable eggs of S. mansoni are the main etiologic agents responsible for the subsequent hepatic lesions. Even today there is no unanimity of opinion on this subject but all authors are agreed that the lesions produced by the eggs play a significant role in hepatic schistosomiasis. The following conclusions are drawn. Pipe stem portal fibrosis is the late stage of hepatic schistosomiasis. Hepatic schistosomiasis is a result of S. mansoni infestation. The unit of lesion is the schistosomal pseudotubercle, a reaction around individual schistosome eggs. There is a predominantly eosinophil cellular reaction in the early stages which is later replaced by a fibroblastic reaction in the healing stage. The pseudo tubercles are always located in portal tracts. The severity of the lesions depends on the load of parasitism.