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.