Experimental Schistosoma bovis Infections in Goats Studies on the Host-Parasite Relationship with Special Reference to Immunoregulatory Effects and Immunopathology

The ruminant trematode Schistosoma bovis occurs endemically mainly in Africa and the Middle East, where a considerable negative impact of infection on production has been appraised. The pathological effects in schistosomosis are due to immune responses of the host to the eggs of the parasite, leading to intestinal and hepatic granulomatous disease and hepatic fibrosis. Ruminant schistosomosis is most often chronic under natural transmission conditions, and development of an acquired resistance has been proven in cattle and goats. Several aspects of chronic S. bovis infection such as duration of resistance to challenge infection, and effects of anthelmintic treatment on immunoregulatory events and regression of infection with increasing time after treatment, have not been explored previously. Although perioval granulomas are key factors in disease caused by schistosome infections, knowledge on the immunopathology of granulomatous inflammation in ruminant S. bovis infection is very limited. The overall aim of this thesis was to gain further knowledge on the host-parasite relationship in ruminant schistosomosis by use of the S. bovis/West African Dwarf goat model. Parasitological data from experimental infections revealed that resistance to both primary and challenge infection persisted in long-standing infection, with suppression of the female worm fecundity as the key effector mechanism. Furthermore, resistance to challenge was not abolished by anthelmintic elimination of the primary infection. The fact that host immune responses, as reflected by humoral anti-worm antibodies and histopathological immune cell reactions, persisted both in very late primary infection and after treatment, may explain the sustained anti-fecundity effect observed. Quantification of cytokine gene expressions suggested a role for the Th1 type cytokines IFN-γ, IL-2 and TNFα in the inflammation of the intestine at 13 weeks of infection, and indicated that IFN-γ may be produced by cells in the S. bovis egg granuloma.