Abstract

Candida tropicalis is the leading cause of non–C. albicans candidemia in tropical Asia and Latin America. We evaluated isolates from 344 patients with an initial episode of C. tropicalis candidemia. We found that 58 (16.9%) patients were infected by fluconazole-nonsusceptible (FNS) C. tropicalis with cross resistance to itraconazole, voriconazole, and posaconazole; 55.2% (32/58) of patients were azole-naive. Multilocus sequence typing analysis revealed FNS isolates were genetically closely related, but we did not see time- or place-clustering. Among the diploid sequence types (DSTs), we noted DST225, which has been reported from fruit in Taiwan and hospitals in Beijing, China, as well as DST376 and DST505–7, which also were reported from hospitals in Shanghai, China. Our findings suggest cross-boundary expansion of FNS C. tropicalis and highlight the importance of active surveillance of clinical isolates to detect dissemination of this pathogen and explore potential sources in the community.

Highlights

  • Candida tropicalis is the leading cause of non–C. albicans candidemia in tropical Asia and Latin America

  • We conducted a study of 334 patients with C. tropicalis bloodstream infections (BSIs) in Taiwan to examine these relationships in greater detail

  • We determined the genetic relationships of fluconazole-susceptible (FS) and FNS C. tropicalis isolates from blood cultures; compared the relationship of isolates according to time, place, and person; and analyzed the clinical characteristics and outcomes of the patients according to susceptibility to fluconazole and genetic relationship

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Summary

Introduction

Candida tropicalis is the leading cause of non–C. albicans candidemia in tropical Asia and Latin America. C. tropicalis and C. albicans are ascomycetous diploid yeasts, closely related among pathogenic Candida species, and belong in a single Candida clade characterized by the unique translation of CUG codons as serine rather than leucine [6,7]. These pathogens initially were considered to be susceptible to azoles [8,9,10,11,12] with the same clinical. Some studies of the genetic relationship of clinical fluconazole-nonsusceptible (FNS) C. tropicalis isolates have reported clonal diversity [22,23,24], whereas others have demonstrated clonal clusters [20,25,26]. We further explored the potential emergence and spread of FNS C. tropicalis globally

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