UNEXPLORED HOST GENETIC AND SKIN MICROBIOTA FACTORS IN TINEA IMBRICATA: IMPLICATIONS FOR CLINICALLY PROVEN CURE STRATEGIES

Abstract

Tinea imbricata (ringworm), a tropical fungal infection due to Trichophyton concentricum, is a neglected tropical disease prevalent in indigenous populations of Southeast Asia, Oceania, and Central and South America. Despite more than 50 years of reported endemicity, the reasons underlying its distinct geographical and ethnic distribution remain obscure. We bring together available evidence on host genetics and skin microbiota in tinea imbricata disease, highlighting two key yet underexplored factors. We discuss emerging information about antifungal drug resistance, including the recent identification of terbinafine resistant T. concentricum strains among indigenous Malaysian populations, as well as the latest treatment approaches, including new drugs in the pipeline. Literature was searched via PubMed, ScienceDirect and clinical trial registries up to June 2025. There is evidence for both autosomal dominant and recessive modes of inheritance with candidate genes such as DEFB4 (β-defensin 2) and CLEC7A (dectin-1) associated with susceptibility. Studies focusing on skin microbiome demonstrate decreased commensal bacteria (Cutibacterium acnes, Staphylococcus epidermidis) in populations, implicating microbiome dysbiosis in the development of this condition. Therapeutic outcomes are poor and relapse rates are more than 50% at six months. The growing reports of terbinafine resistance justify revisit to current antifungal algorithms. We advocate for a paradigm incorporating host genetic screening, microbiome and antifungal resistance for clinically cured tinea imbricata. Knowledge gaps include lack of genome-wide association studies, microbiome longitudinal studies and randomized trials in endemic countries