Page 106 - AIDSBK23C

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CANDIDA INFECTIONS

Candida as a commensal organism is so ubiquitous in both healthy and ill persons that it
is often difficult to determine just how important it really is when identified in patient specimens.
Candida organisms found on the skin or within the oral cavity are not always presumed to be
pathogens at these sites. Likewise, in AIDS, finding Candida does not always mean that a
pathologic condition is present. In HIV-infected persons, binding of viral gp160 and gp41
envelope proteins enhances the virulence of Candida.[473]
AIDS patients often receive a clinical diagnosis of "oral candidiasis" or "oral candidosis"
or "oral thrush" as a result of finding white creamy patches or plaques on oral mucosal surfaces.
Such mucous membrane involvement is seen in most HIV-infected persons at some point in their
course. [454,473]
Most Candida infections are due to Candida albicans, but non-albicans infections are
increasing. The second most common species isolated Candida glabrata, followed by Candida
tropicalis, and Candida parapsilosis. Much less common species include Candida
guilliermondii, Candida pelliculosa, Candida kefyr, Candida rugosa, and Candida famata.[451]
The progressive depletion and dysregulation of mucosal Langerhans cells from HIV
infection reduces normal processing of Candida antigens, and this, coupled with progressive loss
of CD4 lymphocytes, reduces adaptive immunity to Candida. Depletion of CD4 cells and a shift
in expression from Th1 to Th2 cytokines may reduce anti-candidal activity of phagocytic cells
including macrophages and neutrophils. MHC expression of class I antigens on Langerhans cells
may be partially preserved to allow recruitment of a compensatory protective CD8+ T-cell
response. Innate immune defenses, including intact keratinocytes, intraepithelial T cells,
neutrophils, and calprotectin, remain so that dissemination of Candida is uncommon, but may
appear with bone marrow suppression.[474] There are no specific clinical findings with
disseminated candidiasis, and this manifestation is unlikely to be diagnosed pre mortem.[392]
The most common species isolated in microbiologic cultures include Candida albicans,
Candida tropicalis, and Candida parapsilosis. Candida (formerly Torulopsis) glabrata may
appear clinically and histologically similar to Candida, though they are often of very small 1 to 2
microns size. Except for epidemiologic purposes or antifungal resistance, most of these fungal
species with budding cells are clinically or histologically grouped as "Candida" or "yeast."
Patients are usually colonized with a single strain, and recurrences are usually due to the same
strain.[473] Diagnosis of Candida fungemia may be aided by detection of β-D-glucan (BG), a
unique cell-wall component of many fungi, including Aspergillus, Fusarium, Trichosporon,
Saccharomyces, and Acremonium, but not Cryptococcus or Zygomycetes.[451]
In order to fulfill the definitional criteria for diagnosis of AIDS, Candida must be found
to satisfy specific requirements: there must be invasive esophageal or respiratory tract (trachea,
bronchi, or lungs) candidiasis.[392] Merely finding budding yeasts upon a mucosal surface
without any tissue reaction is not sufficient for diagnosis of AIDS. Candida is seen in the upper
gastrointestinal tract, primarily the esophagus, in many cases in which it is present. The lung is
often involved at autopsy. In a few cases, Candida may be disseminated beyond the respiratory
or gastrointestinal tracts. Other organs are infrequently involved, and in bone marrow, Candida
is rarely identified in AIDS (Table 5). Drug therapies that lead to bone marrow suppression,
corticosteroid therapy, or other immunosuppressive agents may enhance dissemination of
Candida.