Summary The disease burden of chronic‐relapsing and therapy‐refractory superficial dermatophytosis dramatically increased in India within the past 5‐6 years. In order to evaluate the prevalence of this trend, 201 skin scrapings were collected from patients from all parts of India and were tested for dermatophytes using both fungal culture and a PCR‐ELISA directly performed with native skin scrapings. Fungal culture material was identified by genomic Sanger sequencing of the internal transcribed spacer (ITS) region and the translation elongation factor (TEF)‐1α gene. In total, 149 (74.13%) out of the 201 samples showed a dermatophyte‐positive culture result. Out of this, 138 (92.62%) samples were identified as Trichophyton (T.) mentagrophytes and 11 (7.38%) as Trichophyton rubrum. The PCR‐ELISA revealed similar results: 162 out of 201 (80.56%) samples were dermatophyte‐positive showing 151 (93.21%) T mentagrophytes‐ and 11 (6.79%) T rubrum‐positive samples. In this study, we show for the first time a dramatic Indian‐wide switch from T rubrum to T mentagrophytes. Additionally, sequencing revealed a solely occurring T mentagrophytes “Indian ITS genotype” that might be disseminated Indian‐wide due to the widespread abuse of topical clobetasol and other steroid molecules mixed with antifungal and antibacterial agents.

Background An alarming increase in recalcitrant dermatophytosis has been witnessed in India over the past decade. Drug resistance may play a major role in this scenario. Objectives The aim of the present study was to determine the prevalence of in vitro resistance to terbinafine, itraconazole and voriconazole in dermatophytes, and to identify underlying mutations in the fungal squalene epoxidase (SQLE) gene. Patients/Methods We analysed skin samples from 402 patients originating from eight locations in India. Fungi were identified by microbiological and molecular methods, tested for antifungal susceptibility (terbinafine, itraconazole, voriconazole), and investigated for missense mutations in SQLE. Results Trichophyton (T.) mentagrophytes internal transcribed spacer (ITS) Type VIII was found in 314 (78%) samples. Eighteen (5%) samples harboured species identified up to the T interdigitale/mentagrophytes complex, and T rubrum was detected in 19 (5%) samples. 71% of isolates were resistant to terbinafine. The amino acid substitution Phe397Leu in the squalene epoxidase of resistant T mentagrophytes was highly prevalent (91%). Two novel substitutions in resistant Trichophyton strains, Ser395Pro and Ser443Pro, were discovered. The substitution Ala448Thr was found in terbinafine‐sensitive and terbinafine‐resistant isolates but was associated with increased MICs of itraconazole and voriconazole. Conclusions The high frequencies of terbinafine resistance in dermatophytes are worrisome and demand monitoring and further research. Squalene epoxidase substitutions between Leu393 and Ser443 could serve as markers of resistance in the future.

Dermatophytosis has attained unprecedented dimensions in recent years in India. Its clinical presentation is now multifarious, often with atypical morphology, severe forms and unusually extensive disease in all age groups. We hesitate to call it an epidemic owing to the lack of population-based prevalence surveys. In this part of the review, we discuss the epidemiology and clinical features of this contemporary problem. While the epidemiology is marked by a stark increase in the number of chronic, relapsing and recurrent cases, the clinical distribution is marked by a disproportionate rise in the number of cases with tinea corporis and cruris, cases presenting with the involvement of extensive areas, and tinea faciei.

Background Acanthosis nigricans (AN) is a cutaneous disorder characterized by symmetric velvety hyperpigmented plaques on intertriginous areas like axilla, neck, inframammary, and groin. Aims To summarize the pathophysiology and classification of AN, provide an update of diagnostic testing strategies, and describe the current therapeutic options described so far in the literature for this disease. Methods A comprehensive english language literature search across multiple databases (PubMed, EMBASE, MEDLINE, and Cochrane) for keywords (alone and in combination) was performed. MeSH as well as non‐MeSH terms such as “acanthosis nigricans,” “classification,” “pathophysiology,” “diagnosis,” “treatment,” “topical drugs,” “systemic drugs,” “chemical peeling,” and “lasers” were taken into consideration. Results The pathophysiology of AN revolves around a multifactorial stimulation of proliferation of epidermal keratinocytes and dermal fibroblasts. Various types of AN include benign, obesity‐associated, syndromic, malignant, acral, unilateral, medication‐induced, and mixed‐type. Homeostasis model assessment‐insulin resistance (HOMA‐IR) is a good tool for assessment of insulin resistance. Management involves general measures (weight reduction and addressing the underlying cause, if any), topical drugs (retinoids, vitamin D analogs, and keratolytics), oral drugs (retinoids and insulin sensitizers), chemical peels (trichloroacetic acid), and lasers (Long pulsed alexandrite, fractional 1550‐nm erbium fiber, and CO2). Conclusion Acanthosis nigricans is a treatable condition; however, complete cure and disappearance of lesions are difficult to achieve. Weight reduction is the most scientific and practical management strategy. Long‐term studies and further research is warranted in the pathophysiology and treatment of this common condition.