Candida tropicalis in the diabetic urinary tract: Biofilm resistance, genomic plasticity, and public health implications

Abstract

Fungal urinary tract infections (fUTIs) are emerging as a public health concern, notably in South Asia, where a convergence of ecological, genetic, and clinical factors underlies a rising burden of antifungal-resistant disease. This review synthesizes epidemiological, mechanistic, and genetic evidence implicating Candida tropicalis as a dominant uropathogen in South Asia’s diabetic and immunocompromised populations. We examine the shift from Candida albicans to non-albicans Candida (NAC) species, driven by selective antifungal pressure and nosocomial transmission. Emphasis is placed on the virulence and adaptability of C. tropicalis, which forms biofilms, adapts metabolically under glycosuric and hypoxic conditions, and expresses antifungal resistance genes such as ERG11, CDR1, MDR1, and FKS1. Concurrently, South Asian host populations exhibit genetic variants—e.g., in TLR4, CLEC7A, CYP2C19—that impair fungal recognition, immune clearance, and antifungal pharmacokinetics, creating a syndemic landscape. We detail biofilm-mediated resistance mechanisms, epigenetic regulation of virulence genes, and the role of environmental sensing pathways in adaptive pathogenesis. Furthermore, the review delineates clinical challenges posed by biofilm-associated infections, delayed diagnostics, and resistance underestimation. Finally, we propose a suite of public health and clinical recommendations—including biofilm-specific diagnostics, antifungal stewardship programs, pharmacogenomic screening, and national surveillance—to mitigate the escalating burden of drug-resistant candiduria. This integrative perspective bridges molecular pathogenesis and systems-level responses, offering a strategic roadmap for clinicians and policymakers to address C. tropicalis-driven fUTIs in South Asia and other high-risk regions.