Fungi cause many diseases, most of which are adequately handled by the immune system of the normal host. However, the increased use of immunosuppressive drugs – the immunosuppression secondary to HIV infection – has raised our awareness of these infections. For example, Candida albicans can cause superficial infections in the normal host and is found throughout the intestinal tract and commonly in the vagina. The organism is usually kept under control by the bacterial flora, but changes in these flora secondary to overuse of anti-biotics or changes in hormone balance will favor a chronic superficial infection. All of this is exacerbated in the immunocompro-mised host.
Another organism that is receiving wide attention is the fungus Pneumocystis carinii (now called Pneumocystis jiroveci), which has a commensal relationship with the lung in the normal host. However, the sudden onset of pneumonia with this organism secondary to HIV infection in a child or adult is often the first sign of an underlying suppressed immune system caused by HIV.
In contrast to the superficial infections of fungi, systemic infections in the immuno-compromised host have a higher mortality rate. This category includes Histoplasma cap-sulatum (pulmonary infection), Coccidiodes immitis (acute pneumonitis), and Crypto-coccus neoformas (meningitis, lung lesions). Such systemic infections may occur in normal individuals, and the cell-mediated immune response is the more important fac-tor in control or prevention of them. How-ever, all of these fungal infections (superfi-cial and systemic) are more likely to occur in immunosuppressed individuals, especially those in which the cell-mediated immune response is compromised.
There are several plausible outcomes to fungal infections. As stated before, an active cellular immune response plus topi-cal antifungal drugs usually handles most superficial infections. Systemic infections, especially in the immunocompromised host, carry a high mortality rate, and even the use of newer prophylactic and thera-peutic agents only partially decreases the mortality.
As with viruses, there is a third possible outcome. If the fungal infection is not elim-inated or causes persistent infection, then the host response may trigger a hypersen-sitivity reaction. As an example, Aspergil-lus fumigatus infections can persist as an aspergilloma in preexisting lung cavities secondary to tuberculosis or bronchiecta-sis following childhood pertussis (whoop-ing cough). Allergic bronchopulmonary aspergillosis may occur and is due to IgE-mediated hypersensitivity to the asper-gillus antigens. Clinically, the condition presents as recurrent episodes of increased wheezing and coughing, fever, and pleu-ritic pain similar to that seen in asthmatics. Another example is farmer’s lung in which antigen-antibody complexes of Micropoly-spora faeni cause a hypersensitivity reaction on the part of the host. The name farmer’s lung indicates that this particular fungus is found in moldy hay.