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Implication of genotypes for prognosis of Candida glabrata bloodstream infections.
Chen, Pao-Yu; Huang, Yu-Shan; Chuang, Yu-Chung; Wang, Jann-Tay; Sheng, Wang-Huei; Chen, Yee-Chun; Chang, Shan-Chwen.
Afiliação
  • Chen PY; Department of Internal Medicine, National Taiwan University Hospital, Taipei City, Taiwan.
  • Huang YS; Graduate Institute of Clinical Medicine, National Taiwan University College of Medicine, Taipei City, Taiwan.
  • Chuang YC; Department of Internal Medicine, National Taiwan University Hospital, Taipei City, Taiwan.
  • Wang JT; Graduate Institute of Clinical Medicine, National Taiwan University College of Medicine, Taipei City, Taiwan.
  • Sheng WH; Department of Internal Medicine, National Taiwan University Hospital, Taipei City, Taiwan.
  • Chen YC; Department of Internal Medicine, National Taiwan University Hospital, Taipei City, Taiwan.
  • Chang SC; National Institute of Infectious Diseases and Vaccinology, National Health Research Institutes, Taipei City, Taiwan.
Article em En | MEDLINE | ID: mdl-38906829
ABSTRACT

BACKGROUND:

Genotyping isolates of a specific pathogen may demonstrate unique patterns of antimicrobial resistance, virulence or outcomes. However, evidence for genotype-outcome association in Candida glabrata is scarce. We aimed to characterize the mycological and clinical relevance of genotypes on C. glabrata bloodstream infections (BSIs).

METHODS:

Non-duplicated C. glabrata blood isolates from hospitalized adults were genotyped by MLST, and further clustered by the unweighted pair group method with arithmetic averages (UPGMA). A clonal complex (CC) was defined by UPGMA similarities of >90%. Antifungal susceptibility testing was performed by a colorimetric microdilution method and interpreted following CLSI criteria.

RESULTS:

Of 48 blood isolates evaluated, 13 STs were identified. CC7 was the leading CC (n = 14; 29.2%), including 13 ST7. The overall fluconazole and echinocandin resistance rates were 6.6% and 0%, respectively. No specific resistance patterns were associated with CC7 or other CCs. Charlson comorbidity index (adjusted OR, 1.49; 95% CI, 1.05-3.11) was the only predictor for CC7. By multivariable Cox regression analyses, CC7 was independently associated with 28 day mortality [adjusted HR (aHR), 3.28; 95% CI, 1.31-8.23], even after considering potential interaction with neutropenia (aHR, 3.41; 95% CI, 1.23-9.42; P for interaction, 0.24) or limited to 34 patients with monomicrobial BSIs (aHR, 2.85; 95% CI, 1.15-7.08). Also, the Kaplan-Meier estimate showed greater mortality with CC7 (P = 0.003). Fluconazole resistance or echinocandin therapy had no significant impact on mortality.

CONCLUSIONS:

Our data suggested comorbid patients were at risk of developing CC7 BSIs. Further, CC7 was independently associated with worse outcomes.

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Idioma: En Revista: J Antimicrob Chemother Ano de publicação: 2024 Tipo de documento: Article País de afiliação: Taiwan

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Idioma: En Revista: J Antimicrob Chemother Ano de publicação: 2024 Tipo de documento: Article País de afiliação: Taiwan