The AIDS epidemic has resoundingly illustrated this principle: the immunodeficiency of many HIV-infected patients permits the development of life-threatening fungal infections of the lung, blood, and brain. Other than the capsule of C. neoformans, specific fungal antigens involved in tissue invasion are not well characterized. Both fungal and protozoal pathogens undergo morphologic changes to spread within a host. Yeast-cell forms of C. albicans transform into hyphal forms when invading deeper tissues. Malarial parasites grow in liver cells as merozoites and are released into the blood to invade erythrocytes and become trophozoites. . | Chapter 114. Molecular Mechanisms of Microbial Pathogenesis Part 9 Fungal pathogens almost always take advantage of host immunocompromise to spread hematogenously to deeper tissues. The AIDS epidemic has resoundingly illustrated this principle the immunodeficiency of many HIV-infected patients permits the development of life-threatening fungal infections of the lung blood and brain. Other than the capsule of C. neoformans specific fungal antigens involved in tissue invasion are not well characterized. Both fungal and protozoal pathogens undergo morphologic changes to spread within a host. Yeast-cell forms of C. albicans transform into hyphal forms when invading deeper tissues. Malarial parasites grow in liver cells as merozoites and are released into the blood to invade erythrocytes and become trophozoites. E. histolytica is found as both a cyst and a trophozoite in the intestinal lumen through which this pathogen enters the host but only the trophozoite form can spread systemically to cause amebic liver abscesses. Other protozoal pathogens such as T. gondii Giardia lamblia and Cryptosporidium also undergo extensive morphologic changes after initial infection to spread to other tissues. Tissue Damage and Disease Disease is a complex phenomenon resulting from tissue invasion and destruction toxin elaboration and host response. Viruses cause much of their damage by exerting a cytopathic effect on host cells and inhibiting host defenses. The growth of bacterial fungal and protozoal parasites in tissue which may or may not be accompanied by toxin elaboration can also compromise tissue function and lead to disease. For some bacterial and possibly some fungal pathogens toxin production is one of the best-characterized molecular mechanisms of pathogenesis while host factors such as IL-1 TNF-a kinins inflammatory proteins products of complement activation and mediators derived from arachidonic acid metabolites leukotrienes and cellular degranulation histamines readily .
