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There are characteristic gross findings on mucosal surfaces as seen in the oral cavity,
pharynx, trachea, bronchi, esophagus, or vagina. These findings include four appearances:
pseudomembranous candidosis, erythematous candidosis, angular cheilitis, and hyperplastic
candidosis. The most common pseudomembranous form has white, elevated mucosal plaques
that often have a cottage cheese like appearance. Other gross findings include the erythematous
(atrophic) form with flat red patches, the hyperplastic form with partially removable white
plaques, and angular cheilitis with erythema and fissuring at the corners of the mouth. Other
superficial forms of Candida involvement can be seen as paronychia or
onychomycosis.[454,473]
If dissemination occurs to visceral organs, Candida is most likely to produce a pattern
similar to bacterial microabscesses, with small pinpoint to 0.3 cm diameter soft yellow foci,
sometimes surrounded by a small hemorrhagic zone. Organomegaly is infrequent with such
lesions.
Microscopically, Candida microabscesses contain more polymorphonuclear leukocytes
than lymphocytes or macrophages. If the degree of immunosuppression is marked, there may be
little inflammatory reaction, and the pseudohyphae will grow haphazardly throughout the tissues.
In fact, a typical hyphal or pseudohyphal growth pattern exhibits extension across mesothelial-
lined surfaces or into blood vessel walls. Vascular invasion may lead to hemorrhage,
thrombosis, or infarction.
Candida organisms are identified histologically by their 3 to 5 micron size, budding, and
pseudohyphae. The pseudohyphae can be distinguished from Aspergillus hyphae by the lack of
branching, the smaller size, and the frequent absence of true septations in the former. Sometimes
Candida species may also have septate hyphae that can be long, but often of uneven caliber, with
bulbous or pinched portions along their length. Budding cells of Candida are larger than
Histoplasma capsulatum and lack a defined "capsule" with inner nucleus. Candida is smaller
than Cryptococcus neoformans and generally not as pleomorphic. A mucin stain will be
negative with Candida, since there is no surrounding capsule as in C neoformans. Methenamine
silver and PAS stains are most helpful to identify Candida.
Even though Candida occurs in about 40 to 90% of patients with AIDS, death from
Candida infection occurs in less than 5% of cases even when it is present, most often when the
disease is widely disseminated, and usually from pulmonary involvement. In a small number of
AIDS cases, Candida can produce a fatal septicemia. Though disseminated candidiasis and
candidemia are rare in adults with HIV infection, children are more prone to develop these
complications during prolonged hospitalization. Candidemia is more likely to develop as a
community acquired complication in children who are receiving total parenteral nutrition and
intravenous therapy via indwelling central venous lines. The prolonged presence of a central
venous catheter is the most important risk factor for fungemia. Diagnosis of fungemia can be
aided by use of PCR-based assays.[453]
Primary prophylaxis for candidiasis, most often involving oropharynx, esophagus, or
vagina, is usually not indicated, unless recurrences are severe or frequent, since most of these
infections respond well to administered topical or oral antifungal agents, including fluconazole,
ketoconazole or clotrimazole. Fluconazole is more effective for curing oral candidiasis.
Resistance to fluconazole therapy is more frequent when the CD4 lymphocyte count is low.
Though antitretroviral protease inhibitors have theoretical activity against secreted aspartyl
proteinases (SAPs) of Candida, the anti-candidal effect of PIs in vivo has not been uniformly
observed.[473]