Opisthorchis viverrini: pathogenesis of infection in immunodeprived hamsters

• Published in: Parasite immunology Vol. 8; no. 5; p. 455
• Main Authors: Flavell, D J, Flavell, S U
• Format: Journal Article
• Language: English
• Published: England 01.09.1986
• Subjects: Alanine Transaminase - blood; Animals; Antibody Formation; Antigens, Helminth - immunology; Aspartate Aminotransferases - blood; Cricetinae; Immunoelectrophoresis; Liver - pathology; Male; Mesocricetus; Opisthorchiasis - etiology; Opisthorchiasis - immunology; Opisthorchiasis - pathology; Opisthorchis - immunology; Organ Size; Parasite Egg Count; Spleen - pathology; T-Lymphocytes - immunology; Thymectomy
• ISSN: 0141-9838
• DOI: 10.1111/j.1365-3024.1986.tb00861.x

Opisthorchis viverrini infections were established in immunologically intact and T cell deprived hamsters. T cell deprivation appeared to have no effect on worm establishment or egg production. Histopathologically, intact and deprived animals showed similar degrees of bile duct hyperplasia and periductular fibrosis, though there was a marked reduction in the intensity of the periportal inflammation in the majority of T cell deprived animals. Serum transaminase levels were significantly raised in intact animals by 25 days after infection, whilst levels remained within normal limits throughout the infection period for the majority of the T cell deprived animals. The antibody response to parasite antigens as determined by immunoelectrophoresis, was impaired in T cell deprived animals. Attempts to correlate the serological picture with transaminase levels at three time points after infection and also with the extent of periductular inflammation seen on killing, proved largely unsuccessful. These results indicate that T cell deprivation of the hamster host ameliorates the periductular inflammatory response provoked by O. viverrini in this species. It is suggested that such inflammatory responses are evoked by parasite antigens which gain access to portal tract and surrounding areas, and that such reactions are immunopathological in their outcome to the host, resulting in liver cell death and subsequent replacement of resolving inflammatory and necrotic areas with fibrotic tissue.