Repeated mass treatment of schistosomiasis mansoni: experience in hyperendemic areas of Brazil. 3. Techniques for assessment and surveillance.

Severe morbidity due to schistosomiasis mansoni is now quite rare in Brazil; thus it is proposed that surveillance plus selective and multidisciplinary intervention limited to areas at high risk be the next step. Such a policy has to be carried out periodically and on a state-wide scale, and therefore will have to rely upon cheap and time-saving sampling procedures. Clinical features cannot at present be used as indicators, with the exception of grossly enlarged livers, which are more frequent in areas at high risk. Overall prevalence rates for a county or even city may also be misleading, even if broken down into units of smaller size. Thus, egg counts in the young age groups remain the best indicators for the detection of areas at high risk (i.e., the main foci of transmission). Egg counts performed on pooled specimens adequately reflect the risk rating of a particular neighbourhood, and have a favourable cost-benefit ratio. In addition, it is suggested that field personnel be trained in the empirical recognition of potential foci; such 'screening by suspicion' has been tested and found to be reliable.

T cell phenotype alterations in hepatosplenic schistosomiasis mansoni normalize after chemotherapy.

Peripheral blood T cell phenotypes, CD3-induced mitogenesis and soluble IL 2 receptor and CD8 in sera were studied in intestinal and hepatosplenic Schistosomiasis mansoni before and three to six months after therapy with praziquantel. Fifteen pairs matched for intensity of infection were analyzed and compared with local, non-infected age-matched controls. CD3+ cell counts were lower in untreated hepatosplenic schistosomiasis (median 1040 cells/microliters; 95% confidence interval 608-1269) compared to controls (1534; 1264-1620). This difference was largely accounted for by immature CD1+/CD3-cells circulating in these patients (median 388/microliters, 252-474). The frequency of CD1+ T cells in circulation decreased drastically after chemotherapy. Similar, but less marked, alterations were seen in intestinal schistosomiasis. Lymphocyte proliferation initiated by agonistic anti-CD3 monoclonal antibody was severely impaired in hepatosplenic patients, who had suffered haemorrhagic complications, but not in the cases of incipient hepatomegaly. Soluble CD8 antigen circulated in increased amounts in hepatosplenic schistosomiasis. Remarkably, a negative correlation between CD3-induced mitogenesis and circulating levels of CD8 was noted in these patients. Whereas CD3-induced mitogenesis in hepatosplenic schistosomiasis normalized after therapy, circulating IL 2R and CD8 antigen in hepatosplenic patients still exceeded control levels. The results demonstrate disturbances of CD3 and CD8 expression and/or T cell maturation in hepatosplenic schistosomiasis. Imbalanced CD4/CD8 ratios and an increased IL 2R/CD8 turnover may reflect an inhibitory circuit within the T cell compartment.