A 43-year-old HIV-infected woman presents to the clinic with oral candidiasis that is clinically not responding to fluconazole (Diflucan) 200 mg PO qd. She has advanced immune suppression with a CD4 count of 22 cells/mm3 and HIV RNA of 46,340 copies/ml. She is taking a 5-drug salvage antiretroviral therapy regimen, trimethoprim-sulfamethoxazole (Bactrim, Septra), azithromycin (Zithromax), and fluconazole. She has taken fluconazole on and off for 18 months for recurrent bouts of oropharyngeal candidiasis and the past 3 months she had taken fluconazole 200 mg PO qd. She currently denies any esophageal symptoms.

Which of the following is true regarding fluconazole-resistant oral candidiasis in HIV-infected patients?

A. The most important risk factor identified for the development of fluconazole-resistant oropharyngeal candidiasis is the use of trimethoprim-sulfamethoxazole for longer than 60 days.

B. Fluconazole exerts its effect by inhibiting fungal cell wall synthesis. Fluconazole resistance in Candida species occurs primarily through an increase production in cell wall precursors.

C. More than 95% of Candida albicans isolates from patients with fluconazole-refractory oropharyngeal candidiasis show resistance to itraconazole (Sporonox). Fewer than 5% of patients with fluconazole-refractory oropharyngeal candidiasis will respond to itraconazole solution at a dose of 200 mg per day.

D. Major identified risk factors for the development of fluconazole-resistant candidiasis include low CD4 cell count and cumulative fluconazole use.