Oropharyngeal candidiasis in HIV-infected patients under treatment with protease inhibitors.
OBJECTIVE
Oropharyngeal candidiasis decreased when protease inhibitors were included with other antiretrovirals to treat HIV infection. We tested oral yeast isolates of Brazilian HIV-infected individuals receiving antiretroviral therapy for protease secretion and susceptibility to ritonavir and some antifungals.


METHODS
We collected oral samples and identified yeasts from 19 HIV-infected patients receiving highly active antiretroviral therapy (HAART) and suspected of having oral candidiasis. Ritonavir and its excipients' effects on the isolated yeasts were tested for protease secretion by Rüchel's technique. The yeasts' susceptibility to amphotericin B (AnB), fluorocitosine (5FC), fluconazole (FZL), ketoconazole (KZL), and itraconazole (IZL) was determined by E-test (AB Biodisk). Chi-squared test determined the statistical differences.


RESULTS
Twenty-five different positive isolates were obtained. Sixty-eight percent were C. albicans. Other isolates included C. famata (16%), C. glabrata (4%), C. tropicalis (4%), T. capitatum (4%), and 1 isolate not identified. High protease secretion was observed for most of the isolates (20/25). Ritonavir only altered enzyme secretion in 6/20 of the protease-secreting isolates. All isolates were highly sensitive to both AnB and 5FC. Antifungal activity did not change when ritonavir was added to the culture media. Some isolates were highly resistant to studied antifungals (52.2% KZL, 30.4% FZL, and 26% IZL). Resistance significantly decreased when ritonavir was added to the medium with KZL and IZL (P <.5 by chi-squared). A trend to decreased resistance was also observed with FZL but the results were not statistically significant.


CONCLUSIONS
Candida continues to be the most prevalent fungus in the oral cavity. Although oral candidal isolates secrete protease, ritonavir does not inhibit all protease-secreting oral yeast isolates. There seems to be a synergistic effect between ritonavir and oral antifungals against fungal resistance.
Migliorati
Cesar Augusto
CA
Department of Diagnostic Sciences, NOVA Southeastern University College of Dental Medicine, Fort Lauderdale, Florida 33328-2018, USA. migliora@nova.edu
Birman
Esther Goldenberg
EG
Cury
Arlete Emily
AE
D000163:Acquired Immunodeficiency Syndrome / Q000150:complications* / Q000188:drug therapy; D000328:Adult; D000935:Antifungal Agents / Q000494:pharmacology / Q000627:therapeutic use; D016282:Aspartic Acid Endopeptidases / Q000037:antagonists & inhibitors / Q000378:metabolism; D002175:Candida / Q000187:drug effects* / Q000201:enzymology*; D002180:Candidiasis, Oral / Q000150:complications* / Q000188:drug therapy / Q000201:enzymology; D016009:Chi-Square Distribution; D025141:Drug Resistance, Fungal / Q000187:drug effects*; D004357:Drug Synergism; D005260:Female; D017320:HIV Protease Inhibitors / Q000494:pharmacology* / Q000627:therapeutic use; D006801:Humans; D008297:Male; D008826:Microbial Sensitivity Tests; D008875:Middle Aged; D019438:Ritonavir / Q000494:pharmacology* / Q000627:therapeutic use
D000935:Antifungal Agents; D017320:HIV Protease Inhibitors; D016282:Aspartic Acid Endopeptidases; D019438:Ritonavir