The increased pathogenesis of the Schistosoma mansoni BH strain compared with the SJ strain has been attributed to the number of granulomas formed in experimental infections, which increase the mortality in definitive hosts. The aim of the present study was to investigate the development of granulomas around the eggs of the S. mansoni BH and SJ strains and to determine whether this host reaction was strain specific. Four experimental groups were analyzed. Two groups contained mice inoculated in the caudal vein with eggs from the S. mansoni BH or SJ strains and the other two contained mice that were infected with cercariae of the BH strain prior to being inoculated with eggs. The number of granulomas per tissue area in the lungs and liver, as well as the size of the granulomas, was analyzed to characterize the response to schistosome infection. The largest granulomatous responses were observed around eggs of the BH strain. Granulomas covered a larger area in the lungs of mice that were previously infected with cercariae and subsequently inoculated with eggs of the BH strain. These results indicated that specific granulomatous responses occurred following an infection with the BH and SJ strains of S. mansoni. 1. Introduction Schistosomiasis is considered to be the most notable parasitic disease after malaria due to its wide geographic distribution, the large number of people affected by the disease, its severity, and its association with poor sanitary conditions [1, 2]. The primary pathogenic mediators in schistosomiasis are the trematode eggs. A schistosomal granuloma, the characteristic lesion, forms around mature eggs that have been deposited in the tissues of the definitive host. The distribution of eggs in host tissues, the extent of the granulomatous response, and the degree of infectivity of the parasite strain are key factors in the pathogenesis of schistosomiasis [3]. The diverse behavior of different strains of Schistosoma mansoni [4–11] may account for the regional variation observed in clinical schistosomiasis [12]. The degree of morbidity in human schistosomiasis varies regionally, possibly due to variations in parasite infectivity and fecundity [13]. Previous studies have demonstrated a difference in the development of the BH and SJ strains of S. mansoni in the definitive host [4, 6, 7, 14–16]. More hepatic granulomas were observed in mice infected with the S. mansoni BH strain, and a significantly lower percentage of mice survived in this group than in the group of mice that were infected with the SJ strain. In mice, fewer parasites of the
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