Emergence of Azole Resistant Candida Glabrata as an Important Cause of Hospital Acquired Infection: Its Risk Factors and Impact

Abstract

Candida spp. colonizes the human host and coexists with members of the human microbiome. Candida glabrata are aggressive pathogens, have many virulence factors that lead to serious recurrent candidiasis. Their ability to form a complex biofilm, inability to form hyphae, and inability to secrete hydrolase lead to antifungal resistance. Candidemia is the fourth most common bloodstream infection [1]. Candidemia remains a major source of mortality and morbidity. Mortality among patients with invasive candidiasis is as high as 40%, even when patients receive antifungal therapy [2]. More than 90% of invasive diseases are caused by the 5 most common Candida spp. C. albicans, C. glabrata, C. tropicalis, C. parapsilosis, and C. krusei [3]. The distribution of Candida species has been changing over the last decade, with a decrease in the proportion of C. albicans and an increase in C. glabrata and C. parapsilosis. More than 50% of bloodstream infections are caused by non-albicans Candida [2,4]. The largest proportional increase in the USA is in C. glabrata, which accounts for one third or more of all candidemia isolates [5-7]. C.glabrata are associated with high mortality. Candida glabrata develop acquired resistance following exposure to antifungal agents [8]. 50% of C. glabrata are resistant to fluconazole [9,10]. Furthermore, 9% of C. glabrata that are resistant to fluconazole are also resistant to the echinocandins [8,11].