Opportunistic mycoses

'O' Commensal or environmentalfungi that are typically harmless can become invasive mycoses when the host immune defenses are impaired. Host immune suppression and risk for opportunistic mycoses can be broadly classified into three categories:

• Quantitative or qualitative deficits in neutrophil function

• Deficits in cell-mediated immunity

• Disruption of the integument and/or microbiologic barriers

Quantitative defects in neutrophils (neutropenia) resulting from neoplastic diseases, cytotoxic chemotherapy, marrow transplantation, or aplastic anemia are among the most common risk factors for opportunistic mycoses. Qualitative defects may be seen in certain disease states (e.g., advanced diabetes mellitus and chronic granulomatous disease) or with high-dose corticosteroid therapy. Deficits in T-cell-mediated immunity secondary to AIDS, high-dose corticosteroid therapy, cyclosporine or other immunosuppressive drugs, chemotherapy, transplantation, bone marrow failure, and various other disorders have become increasingly common with the prolonged survival of transplant patients on chronic immunosuppressive therapy.

Immune deficits arising from disruption of the integument or GI/genitourinary barriers can also predispose patients to fungal infections. The most common types of integument/barrier disruptions are surgery, use of central venous and urinary catheters, hyperalimentation, and mucositis secondary to cytotoxic chemotherapy. Broad-spectrum antibacterial therapy can also predispose patients to fungal infections through disruption of the microbiologic flora in the gut, which allows overgrowth of Candida species. Successful management of opportunistic fungal pathogens, therefore, requires the reversal or reduction of underlying deficits in the host immune system.

All ofthe opportunistic mycoses are difficult to diagnose and often must be treated empirically before diagnosis is proven. Deciding when to initiate antifungal therapy and what opportunistic pathogens to cover is a decision governed largely by the cumulative immune deficits and clinical status of the host.

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