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Chapter 7 : Host-Parasite Relationships in Microsporidiosis:Animal Models and Immunology

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Abstract:

This chapter describes the host-parasite relationships in animals with microsporidiosis and how they relate to microsporidian infections in humans. The majority of immunologically competent hosts who became infected with microsporidia (e.g., rabbits and mice) developed chronic and persistent infections with few clinical signs of disease. At least three levels or stages of defense mechanisms are expressed to prevent or control infection with most microorganisms. These are innate resistance, early induced responses, and adapted immune responses. The majority of the microsporidian spores appeared to be destroyed after phagocytosis, although some microsporidia taken up by phagocytosis had extruded their polar filaments into the cytoplasm of the macrophage. Microsporidia that infect mammals often persist in the face of innate resistance, early induced response, and adapted immune response mechanisms. The clinical manifestations of microsporidiosis in animals, however, have been highly predictive of the disease in humans, and a competent immune system has been shown to be important in preventing lethal disease. A balanced host-parasite relationship developed in many animals with microsporidiosis that displayed few clinical signs of disease yet carried persistent infections. A better understanding of the immune responses that establish a balanced host-parasite relationship in animals will likely prove beneficial in understanding the immunology of microsporidiosis in humans and in developing immunotherapeutic and chemotherapeutic strategies that can be applied to microsporidiosis.

Citation: Didier E, Bessinger G. 1999. Host-Parasite Relationships in Microsporidiosis:Animal Models and Immunology, p 225-257. In Wittner M, Weiss L (ed), The Microsporidia and Microsporidiosis. ASM Press, Washington, DC. doi: 10.1128/9781555818227.ch7

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Tables

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TABLE 1

Microsporidia of humans

Citation: Didier E, Bessinger G. 1999. Host-Parasite Relationships in Microsporidiosis:Animal Models and Immunology, p 225-257. In Wittner M, Weiss L (ed), The Microsporidia and Microsporidiosis. ASM Press, Washington, DC. doi: 10.1128/9781555818227.ch7

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