Although Schistosoma japonicum egg granulomas are generally considered to be similar to those of S. mansoni (which are largely immunologic reactions of the delayed hypersensitivity type) there are suggestions that the histopathology and perhaps the etiology of the lesions are different. In mice with light S. japonicum infections, at 5 weeks after infection (2 weeks after egg production began), the livers contained 36,000 eggs each, but there was no reaction to the eggs, nor any evidence of hepatosplenic disease. By 6 weeks, large abscesses replete with cosinophils occurred around some of the eggs, and there was periportal inflammation consisting predominantly of plasma cells. From this time on, major lesions occurred mainly around large aggregates of eggs, and there was hepatosplenomegaly and portal hypertension. Living S. japonicum eggs injected into the pulmonary microvasculature of mice did not evoke significant granulomatous reactions on either primary or secondary exposure. Even when the eggs were injected into the lungs of infected animals, which had large granulomas around egg aggregates in the liver, little or no inflammatory reaction was seen around the eggs distributed singly throughout the pulmonary vessels. When the priming dose of eggs or soluble egg antigens was injected subcutaneously with or without complete Freund's adjuvant, significant granuloma formation occurred around eggs subsequently injected into the lungs. On the basis, therefore, of differences in the parasite factor (eggs) and host factors (histopathology and responses to routes of injection) it is suggested that the immunologic factors responsible for granuloma formation around S. mansoni and S. japonicum eggs may differ significantly.