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odynophagia and/or dysphagia. For use of candidiasis as a presumptive clinical diagnosis for
definition of AIDS, there must be:[392]

a. Recent onset of retrosternal pain on swallowing; AND
b. Oral candidiasis diagnosed by the gross appearance of white patches or plaques on an
erythematous base or by the microscopic appearance of fungal mycelial filaments in an
uncultured specimen scraped from the oral mucosa.

Oral candidiasis can appear in multiple sites or on large areas of oral mucosa. There are
four clinical variants. Thrush, or pseudomembranous candidiasis (PC), is characterized by
yellow-white plaques that can be removed by scraping. Removal leaves an erythematous and
slightly hemorrhagic surface. This variant most often affects the tongue. Angular cheilosis (AC)
is the next most common form and characterized by erythematous fissuring at one or both
corners of the mouth, and other organisms such as staphylococci or streptococci may contribute
to the findings. Erythematous candidiasis (EC) is marked by erythematous macular mucosal
patches due to increased vascularity with or without epithelial atrophy. The number of CD4 cells
in the inflammatory response appears diminished in both PC and EC. Hyperplastic candidiasis
(HC) is the least common variant and is marked by hyperkeratotic white plaques that cannot be
removed by scraping, and it is located most often on the buccal mucosa. These variants have no
significance in terms of patient prognosis.[473,666]
Diagnosis of oral candidiasis may be made microscopically by finding typical budding
yeasts with pseudohyphae. A scraping with smear stained with potassium hydroxide (KOH) may
aid in finding the organisms. Acute inflammatory cells are often present. On biopsy, the
organisms may invade superficially. Though visible with routine H&E staining, the periodic
acid-Schiff (PAS) stain aids in demonstrating the organisms, particularly when extensive
inflammation and necrosis is present. An overlying pseudomembrane of neutrophils, fibrin, and
parakeratotic debris can be present. The squamous epithelium often shows acanthosis, though in
the hyperplastic pattern there may also be hyperkeratosis with dysplastic changes.[667]
The esophageal plaques of Candida are often adherent to the underlying mucosa and may
bleed when removed. Biopsy (or scraping of oral mucosa for cytologic examination) may show
budding yeasts and pseudohyphae on the epithelial surface. There may be superficial invasion of
the submucosa. Invasive, inflamed lesions may have irregular ulceration, but deeply invasive
lesions with perforation do not occur. Candida is typically not a cause for diarrhea in persons
with AIDS.[473,487]
Radiologic findings in association with esophageal candidiasis include discrete linear or
irregular longitudinally oriented filling defects that represent the heaped-up mucosal plaques.
Esophagography may reveal a markedly irregular, shaggy mucosal appearance with more
advanced esophageal disease.[416]
Though no primary prophylaxis is indicated, persons with frequent oral candidiasis may
benefit from clotrimazole troches or topical nystatin to prevent progression to esophageal
infection. For further treatment of recurrent oral or for esophageal candidiasis, fluconazole or
ketoconazole are given.[208] Treatment of dental caries may be useful to help control oral
candidiasis, since dentinal carious lesions provide a location for Candida colonization.[668]
The fungi Cryptococcus neoformans, Histoplasma capsulatum, and Coccidioides immitis
may produce focal inflammation. The GI tract is usually involved only when there is widespread
dissemination. These organisms are most likely to be found in the submucosa or on the mucosa.