To evaluate the hypothesis that the granuloma cell population in S. haematobium is different from that of S. mansoni infections, a hamaster animal model was established. Infection of hamesters was induced by abdominal skin exposure of male golden hamsters with 300 cercariae. S. haematobium granuloma cell population in the small intestine, urinary bladder, liver and spleen and those of S. mansoni granuloma in the small intestine and liver of infected hamsters were histologically examined between 6 and 12 weeks post-exposure. In both species, the granuloma cell population was fomed of lymphocytes (47%), histiocytes (28%), eosinophils (16%) and polymorphs (8%). As compared to granuloma cell population in S. haematobium; S. mansoni granulomas had: (a) higher population of eosinophils (28% vs. 11%), (b) lower population of polymorphs (4% vs. 10%) and histiocytes (22% vs. 31%) and (c) similar population of lymphocytes (46% vs.47%). The mean diameter of liver granuloma was higher in S. mansoni (175.8 +/- 12.34) than for S. haematobium (125.4 +/- 16.12). As compared to S. haematobium, the numbers of isolated male, female and total worms were significantly higher in S. mansoni (24.5 +/- 2.7 vs. 7.3 +/- 2.3; 6.3 +/- 0.8 vs. 2.2 +/- 0.5; 80 +/- 2.2 vs. 56.3 +/- 3.8, p < .0.05). The heterogeneity of cell population in granuloma suggests the involvement of different immune mechanisms in their development. The cells achieving numerical dominance in the granulomas were in the following order: lymphoyctes > monocytes > eosinophils > polymorphs. The differrence in the granuloma cell population between S. haematobium and S. mansoni may reflect different tissue reactions to the deposited ova.