Host-parasite interaction in fungal infections

Abstract

The outcome of host-parasite interactions in fungal infections is determined by the balance between pathogenicity of the organism and the adequacy of the host defenses. A wide variety of host defense mechanisms are involved in protection against fungal infections. These include nonspecific mechanisms such as intact skin and mucus membranes, indigenous microbial flora, and the fungicidal activity of neutrophils and monocytes. Such mechanisms constitute the major host defense against opportunistic fungal infections caused by ubiquitous organisms of low virulence. The effective role of immunoglobulins and complement as opsonins varies with the fungal pathogen involved. Specific immune responses of both the humoral and cell-mediated type develop in response to infections by pathogenic fungi. Antibodies, in general, are not of major importance in protection against these infections. Specifically sensitized T lymphocytes produce lymphokines that activate macrophages. Activated macrophages are the major line of defense against systemic fungal pathogens. The type and degree of impairment in immune responses determines the susceptibility and severity of diseases. The type of immune response also determines the tissue reactions in these diseases and sometimes may be involved in the pathogenesis of the disease process. The role of natural killer cell activity, antibody-dependent cellular cytotoxicity, and biological response modifiers in various fungal infections has been described recently. The microbial factors of importance in fungal infections are adherence, invasion, presence of an antiphagocytic capsule, and ability to grow under altered physiological states of the host. The differences in the virulence of fungal strains is of minor importance in determining the outcome in general. The seriousness of the alteration of the host state rather than the pathogenic properties of the fungus determine the severity of the disease.

Aspergillosis

“…These deficiencies are discussed in detail by Khardori and will only be mentioned briefly (19). The most important predisposing factor is prolonged neutropenia, accounting for the high frequency in patients with acute leukemia.…”

Antifungal Proteins

“…Chitin-binding proteins and peptides that have antifungal activity but are not PR proteins have been isolated from a number of sources, including bacteria (13), plants, insects, and crustaceans (19,29,61,76,83,131,136). These non-PR-4 chitin-binding proteins include the tachystatins (75, 135) (horseshoe crab, 6.8 to 7.4 kDa), the penaeidins (31-33) (penaeid shrimp, 5.5 to 6.6 kDa), antifungal protein 1 (AFP1) (13) (Streptomyces tendae, 9.8 kDa), and others.…”

“…Fortunately, only 200 or so species are pathogenic to mammals, although many nonpathogenic fungi cause allergy symptoms (3). The majority of fungal exposures and infections are selflimiting in intact animal hosts (76). However, in patients with compromised immune systems, infections even by fungal organisms with low virulence can be life threatening; for example, systemic fungal infections of leukemia patients account for 50% of fatalities (101,141).…”

Anti-Candida resistance in the mouse brain and effect of intracerebral administration of interleukin 1

“…Although the brain represents an important target organ for C. albicans infections (Lipton et al, 1984;Khardori, 1989), little is known of natural and immune mechanisms active in antifungal resistance in the brain. Using two strains of C. albicans with different pathogenicity, we found that the hosts were more resistant to i.c.…”

“…Conditions leading to systemic or mucocutaneous candidosis include a variety of underlying diseases and/or immunosuppressive regimens (Odds, 1988). In particular, severe mucocutaneous candidosis is often seen in association with defects in T-cell-dependent immunity (Klein et al, 1984;Khardori, 1989;Murphy, 1990).…”