Gottfredsson et al. [1] showed that oropharyngeal colonization by Candida species was strongly associated with plasma human immunodeficiency virus type 1 (HIV-1) RNA and suggested that this probably was due to the suppression of local mucosal immune responses. Klein et al. [2] commented on the report by Gottfredsson et al. [1], pointing out that HIV-1 replication might have a direct effect on the virulence of Candida species and that HIV-1 protease inhibitors (PIs) also might play an important role in colonization of Candida species. In 1992, we evaluated the prevalence of oropharyngeal colonization and infection by Candida albicans in a cohort of 200 HIV-infected persons, by culturing oral swab samples [3]. In January 2000, we once again examined this group of patients: 92 had died, 29 had moved or could not be located, and 9 were excluded (7 because they had been using a new combination of antiretrovirals for <3 months and 2 because they were receiving long-term antifungal prophylaxis for cryptococcosis). We examined the 70 remaining patients, applying both clinical and mycologic criteria, to establish the definitive diagnosis of oral candidiasis. Consequently, we carried out a time-cohort analysis, comparing the frequency of oropharyngeal colonization and infection by C. albicans in these 70 patients in 1992 and 2000 (table 1).
No takes yet. Share an insight, caveat, or question.
Ocampo et al. (2001) studied this question.
Synapse has enriched 4 closely related papers on similar clinical questions. Consider them for comparative context: