Less than 10% of patients infected with Schistosoma mansoni develop severe hepatosplenic symptomatology. As an approach to understanding the immunological events associated with progression to severe forms of the disease, blastogenic responses of peripheral blood mononuclear cells to different parasite antigens were measured in patients with hepatosplenic (46 subjects), hepatointestinal (40) and chronic intestinal (39) schistosomiasis and compared with 16 patients with the acute form of the disease. It was found that although essentially all patients are highly responsive to soluble egg antigen (SEA) soon after initial infection, 75% of chronic intestinal patients suppress response to SEA. This result indicates successful regulation of the potentially harmful anti-egg response.

In contrast, many patients who had entered the hepatointestinal or ambulatory hepatosplenic phases of the disease again responded strongly to the egg antigen. However, among the most severe hospital cases of hepatosplenic disease were found a high proportion which were non-responders to SEA. This lack of response was suggested to be due to a non-specific, possibly anergic, suppression of responsiveness resulting from the pathology of the disease. Thus, although there is clearly a degree of correlation between intensity of infection and hepatosplenism, these studies also indicate that failure to regulate adequately immune responsiveness to egg antigens may also be a contributory factor and that this and other possible interactive facets of both host and parasite may combine to lead to severe disease.newline˜A.J.G. SimpsonADDITIONAL ABSTRACT:The peripheral blood mononuclear cell responses were measured upon exposure to schistosomal egg antigens (SEA), adult worm antigens (SWAP) and a cercarial antigenic preparation (CERC), in 34 patients with hepatosplenic Schistosoma mansoni infection (group 1) treated in hospital in Brazil, 12 ambulatory patients with early hepatosplenic schistosomiasis not under treatment (group 2), 40 subjects with hepato/intestinal schistosomiasis (group 3) and 39 with chronic intestinal infection (group 4). In each group of patients some failed to respond to some or all of the antigens. The responders were divided into high and moderate responders (on levels of incorporation of tritiated thymidine). The proportions of high responders were 20% (to SEA), 32% (to SWAP) and 21% (to CERC) in group 1. These values were 67%, 34% and 42% resp. in group 2, 40%, 23% and 23% in group 3 and 23%, 31% and 26% in group 4. Previous studies have shown that 94% of patients with acute early schistosomiasis were high responders and that none were non-responders. 100% of cured patients were also high responders to SEA. It is suggested that during acute infection all patients express a vigorous response to SEA which is modulated in continuing infections. The relationships between progressive development of clinical forms of schistosomiasis and responsiveness to SEA are discussed.