Departments of Pathology, Harvard Medical School and Peter Bent Brigham Hospital, Department of Medical Helminthology, London School of Hygiene and Tropical Medicine, Winches Farm Field Station, Boston, Massachusetts 02115, England
Liver changes occurring in mice deprived of their T-cells by a combination of thymectomy and anti-mouse thymocyte serum, and in immunologically intact control mice, were followed during the early stages of heavy Schistosoma mansoni infections. Lesions in both groups began developing by day 38 and were maximal by day 48. Hepatic changes in control mice culminated in large hypersensitivity granulomas, tissue eosinophilia, portal periphlebitis, fibrosis, vascular obstruction, and infarction leading to arterialization and preferential sinusoidal channeling. Deprived mice showed greatly reduced egg reactions composed principally of macrophages, monocytes, and occasional neutrophils, and only minimal alteration of liver architecture; however, focal and disseminated hepatocellular lesions became prominent as the infections progressed, and by day 48 virtually every hepatocyte was affected. Typically, hepatocytes showed microvesicular cytoplasmic damage (steatosis) or ballooning degeneration with accompanying nuclear pyknosis or karyorrhexis. This cellular pathology may be attributed to the direct or indirect effect of eggs or egg products on liver cells. The administration of chronic infection serum obtained from immunocompetent mice to T-cell deprived mice dramatically eliminated the hepatocellular lesions. It also increased eosinophil participation and fibrosis in the egg reactions but did not restore the size and other cellular features typical of egg hypersensitivity granulomas. Serum from uninfected normal mice was found to lack these effects.