Abstract

ObjectiveInvasive infections due to Candida spp. have unique epidemiology, strain distribution, antimicrobial susceptibility, and clinical features. This study aimed to compare and evaluate these characteristic variables between invasive Candida infection and colonization of critically ill patients in local China to potentially improve differential diagnosis and therapy.MethodsA total of 193 critically ill patients were recruited and followed up for the study, and 133 Candida isolates were obtained from invasive Candida-infected or -colonized subjects. The strains were identified to species level through matrix-assisted laser desorption/ionization–time-of-flight mass spectrometry, assisted by DNA sequencing. Candida susceptibility to common antifungals, including azoles, was determined by microbroth ATB Fungus 3 methodology. Azole resistance–related gene sequencing and homologous 3D-structure modeling were employed. Patient demographics and clinical risk factors were documented and comparatively analyzed from the hospital information-management system.ResultsNon–C. albicans Candida (56%) principally caused invasive Candida infections, while C. albicans (55.17%) contributed more to Candida colonization in critically ill patients. Additional risk factors exerted significant impact on both Candida cohorts, primarily including invasive interventions, cancers, and concurrent infections in common. Most colonized Candida spp. harbored relatively higher sensitivity to azoles. ERG11 gene mutations of T348A and A1309G, A395T and C461T, and a novel G1193T to our knowledge were identified in azole-resistant C. albicans, C. tropicalis, and C. parapsilosis respectively, and their corresponding homologous 3D-structure modeling was putatively achieved.ConclusionDistinct epidemiological and clinical characteristics existed between invasive Candida infection and colonization in critically ill patients. Multiple risk factors significantly involved both the Candida cohorts. Colonized Candida exhibited generally higher azole sensitivity than invasively infectious counterparts. ERG11 point mutations had mechanistically potential ties with local Candida resistance to azoles.

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