Determinants for the Development of Oropharyngeal Colonization or Infection by Fluconazole-Resistant Candida Strains in HIV-Infected Patients

Masiá, Mar; Rodero, Félix Gutiérrez; Ducasse, Victoria Ortiz de la Tabla; Hernández-Aguado, Ildefonso; González, C. Martín; Sevillano, A. Sánchez; Hidalgo, A.

doi:10.1007/s100960000323

Cited by 41 publications

(10 citation statements)

References 33 publications

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“…The TB burden in South Africa remains high (Wood et al, 2011) and TB further compromises the immune status. In addition, anti-TB therapy may predispose to the development of fluconazoleresistant C. albicans strains (Masiá Canuto et al, 2000). The odds of colonization were five times greater in patients with diabetes in our multivariate analysis, confirming previous findings (Gonçalves et al, 2006).…”

Section: Discussionsupporting

confidence: 82%

Oral Candida colonization in HIV-positive women: associated factors and changes following antiretroviral therapy

Owotade

Patel

Ralephenya

et al. 2013

Journal of Medical Microbiology

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There is a paucity of information about the factors associated with oral colonization with Candida species and the changes associated with antiretroviral (ARV) therapy. This study investigated the role of ARV therapy and other factors in a study population. Relevant clinical and laboratory information was obtained and oral rinse specimens were tested for yeast identification. The findings were compared with previous data from the same clinic before ARV therapy was available. Of 197 patients, 117 (59.4 %) were colonized. Candida albicans was the dominant species (71 %) and Candida dubliniensis was the most frequent non-albicans Candida. The colonized group had a higher rate of concurrent tuberculosis (TB) infection (77.4 % compared with 56 % in the non-colonized patients, P50.03) and a lower median CD4+ count (346.5 cells . Participants not on ARV therapy and those having oral prosthesis were all colonized (P50.003 and P50.022, respectively). The oral Candida count was negatively correlated with the CD4 + count in participants on ARV therapy (P50.006). Associated factors using logistic regression were dental caries (odds ratio51.30; 95 % confidence interval51.07-1.60] and diabetes mellitus (odds ratio55.52; 95 % confidence interval51.68-18.12). The colonization rate was higher (81.3 %) as well as the yeast count before ARV therapy was available, while the prevalence of C. dubliniensis was found to have increased from 6.3 to 11 %. Dental caries, diabetes mellitus, oral prostheses and TB infection were associated with oral colonization. The colonization rate, variety and yeast counts declined with ARV therapy.

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Section: Discussionsupporting

confidence: 82%

Oral Candida colonization in HIV-positive women: associated factors and changes following antiretroviral therapy

Owotade

Patel

Ralephenya

et al. 2013

Journal of Medical Microbiology

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“…C. glabrata has emerged as the second or third most frequently isolated Candida species in the oral flora of persons with diabetes mellitus, advanced cancer, and HIV infection (Masia Canuto et al ., 2000; Davies et al ., 2002; Kadir et al , 2002). In addition to maintaining an intact invasion barrier, oral epithelial cells (OECs) can regulate the inflammatory host response to Candida by releasing a wide array of chemotactic and priming molecules for innate immune effector cells (Dongari-Bagtzoglou and Kashleva, 2003; Dongari-Bagtzoglou et al ., 2005).…”

Section: Introductionmentioning

confidence: 99%

Epithelial GM-CSF Induction by Candida glabrata

Dongari-Bagtzoglou

2009

J Dent Res

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The main cytokine induced by the interaction of oral epithelial cells with C. glabrata is granulocyte monocyte colony-stimulating factor (GM-CSF); however, the mechanisms regulating this response are unknown. Based on previously published information on the interactions of C. albicans with oral epithelial cells, we hypothesized that interaction with viable C. glabrata triggers GM-CSF synthesis via NF-κB activation. We found that C. glabrata-induced GM-CSF synthesis was adhesion-dependent, enhanced by endocytosis, and required fungal viability. NF-κB activation was noted during interaction of epithelial cells with C. glabrata, and pre-treatment with an NF-κB inhibitor partly inhibited GM-CSF synthesis. Blocking TLR4 with anti-TLR4 antibody did not inhibit GM-CSF production. In contrast, an anti-CDw17 antibody triggered significant inhibition of NF-κB activation and GM-CSF synthesis. β-glucans did not stimulate GM-CSF synthesis, suggesting that the CDw17/NF-κB/GM-CSF pathway may be β-glucan-independent. This study provides new insights into the mechanism of GM-CSF induction by C. glabrata.

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“…C. glabrata makes up between 5Y:o and l0%o of all oral isolates recovered from HlV-positive patients who have OPC 1999). OPC can be caused solely by C. glabrata (Hoegl et al, 1998), with one study reporting that up to l4o/o of all oropharyngeal infections were caused by this species (Masia Canuto et al, 2000). It was estimated that approximately 30o/o of patients over 80 years of age were colonized orally with C. glabrata (Lockhart et al,1p99), but the percentage was almost doubled if the patients wore dentures.…”

Section: Candida Speciesmentioning

confidence: 99%