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Similar to scabies, there has been an increase in familial clustering and connubial dermatophytosis with even infants presenting with extensive tinea corporis.3 Hesitancy and embarrassment leads to substantial under-reporting, particularly in women and the underprivileged, and what is being observed is just the tip of the iceberg with many hidden cases in the community that account for the relapse and ongoing transmission of dermatophytosis. Supplementary Material 1 DC Cole, NP Govender, A Chakrabarti, J Sacarlal, DW Denning, Improvement of fungal disease identification and management: combined health systems and public health approaches, Lancet Infect Dis, Vol. 17, 2017, e412-e419 2 S Panda, S Verma, The menace of dermatophytosis in India: the evidence that we need, Indian J Dermatol Venereol Leprol, Vol. 83, 2017, 281-284 3 S Verma, R Madhu, The great Indian epidemic of superficial dermatophytosis: an appraisal, Indian J Dermatol, Vol. 62, 2017, 227-236 4 S Dogra, S Uprety, Indian Dermatol Online J, Vol. 7, 2016, 73-76 5 T Narang, R Mahajan, S Dogra, Dermatophytosis: fighting the challenge: conference proceedings and learning points. September 2-3, 2017, PGIMER, Chandigarh, India, Indian Dermatol Online J, Vol. 8, 2017, 527-533 6 SB Verma, R Vasani, Male genital dermatophytosis-clinical features and the effects of the misuse of topical steroids and steroid combinations-an alarming problem in India, Mycoses, Vol. 59, 2016, 606-614 7 M Schaller, M Friedrich, M Papini, RM Pujol, S Veraldi, Topical antifungal-corticosteroid combination therapy for the treatment of superficial mycoses: conclusions of an expert panel meeting, Mycoses, Vol. 59, 2016, 365-373

Pathogen-related factors, including increased transmission risk, diminished antibiotic response, or accelerated replication, might have contributed to this surge and warrant scrutiny, especially amid the penicillin shortage in specific regions.3 However, when one looks closely at the trends, the rise in syphilis incidence is notably attributable to the stark increase in the number of late latent syphilis compared with other stages.1 The asymptomatic nature of the latent stage means diagnosis is only possible with serological screening tests. The United States Preventive Services Task Force advises routine annual chlamydia and gonorrhoea screening for all sexually active women aged 24 years or younger.4 However, the syphilis screening is targeted for pregnant individuals and non-pregnant individuals at high-risk of syphilis—including males, men who have sex with men (MSM), people with HIV infection, history of incarceration, sex work, military service, and drug use and also considering factors such as local prevalence, socioeconomic determinants, and sexual network characteristics.5 The disproportionate rise in latent stage compared with other stages of syphilis suggests that the absence of routine screening for syphilis could underlie the observed surge, and this suggests the need for incorporating routine serological syphilis screening for all sexually active individuals, even if they are not at high risk and are asymptomatic. Since the trends showed a substantial increase in the incidence of syphilis in people aged 30–44 years, the screening for syphilis should be performed in all sexually active individuals, regardless of the age.1 Given disconcerting trends, especially in congenital syphilis, a comprehensive discussion regarding resource delegation and cost-effectiveness of routine serological syphilis screening is urgently needed, especially regarding the duration of implementation of such screening. [...]the rise in the incidence of syphilis necessitates a coordinated effort.

A 59-year-old man presented with a brown-black lesion on the hard palate. The lesion was associated with pain and caused difficulty eating. The lesion started as a small, black-pigmented area 2 years ago and grew gradually. The patient was a 10-pack-year smoker.

Bullous pemphigoid is an autoimmune blistering disease caused by autoantibodies targeting BP180 and BP230. While deposits of IgG and/or complement along the epidermal basement membrane are typically seen suggesting complement -mediated pathogenesis, several recent lines of evidence point towards complement-independent pathways contributing to tissue damage and subepidermal blister formation. Notable pathways include macropinocytosis of IgG-BP180 complexes resulting in depletion of cellular BP180, direct induction of pro-inflammatory cytokines from keratinocytes, as well as IgE autoantibody- and eosinophil-mediated effects. We review these mechanisms which open new perspectives on novel targeted treatment modalities.

The cutaneous microflora consists of various microorganisms which interact with host epithelial cells and innate and acquired immunity. This microbial milieu and its interaction with host cells prevent the growth of pathogenic organisms and educate host immunity to fight against harmful microorganisms. The microbial composition depends on various intrinsic and extrinsic factors and an imbalance in the cutaneous microflora predisposes the individual to both infectious and non-infectious diseases. Even though probiotics have been extensively studied in various diseases, their efficacy and safety profile are still unclear. A better understanding of the cutaneous microflora is required to develop newer therapeutic targets. In this review, we describe the commensal microbiome and its variation, the current role of the cutaneous microbiome in the pathogenesis of various dermatological diseases, and their therapeutic implications.

A 30-year-old woman presented to us for the treatment of post acne scars. On examination, she was observed to have broad nasal root and unusually large intercanthal distance (dystopia canthorum, figure 1). On closer inspection with a dermatoscope, her irises were found to be multicoloured (brown and blue, figure 2). On enquiry, she admitted to having a white forelock of hair which she had dyed black and had a sister who had done the same. Otorhinolaryngology evaluation for her hearing revealed mild right-sided sensorineural hearing loss (SNHL) with left-sided mild, mixed hearing loss. Apart from heterochromia iridis, ophthalmological examination was unremarkable. Musculoskeletal evaluation revealed no abnormality. Based on the criteria, a diagnosis of Waardenburg syndrome (WS) was furnished. She was explained about her disease but declined undergoing genetic testing due to financial constraints.

The scope of dermatoscopy has now vastly expanded and shows promising use for characterization of both pigmentary and inflammatory dermatoses affecting the skin, nail, and mucosae. Due to concerns of contamination and spread of infection, dermatoscopy has not been widely studied for genital mucosal dermatoses. In this article, we review the dermatoscopic features of nonvenereal dermatosis affecting the genitalia. Although biopsy is required for a definitive diagnosis, dermatoscopy is useful to identify atypical and suspicious pigmentary lesions. For the inflammatory dermatoses and other benign dermatoses, presence of few characteristic findings can aid in the diagnosis.

Recent studies have noticed significant role of interleukin (IL)-17, 22, 23, Foxp3, interferon-gamma (IFN-γ) and Wnt5a in oral and cutaneous lichen planus (LP). This study was undertaken to assess whether similar expression exists in lichen planus pigmentosus (LPP). We recruited 30 patients of treatment-naïve ‘LPP’ (in absence of cutaneous/mucosal LP elsewhere, group 1), 10 patients having active treatment-naïve cutaneous ‘LP’ (group 2), 10 patients having ‘post-LP’ hyperpigmentation (in absence of active LP and off treatment for at least past 3 months, group 3), and 10 controls. Quantitative real-time polymerase chain reaction (qRT-PCR, peripheral blood mononuclear cells [PBMCs] and skin) and immunohistochemistry (IHC, skin) was performed. mRNA expression (in PBMCs) of IL-17A, IL-22, IL-23A, IFN-γ and Foxp3 was significantly decreased in group 1 and 3 as compared to group 2 (p < 0.05). Wnt5a expression was maximal in controls; and while there was no difference between group 1 and 2; whereas expression in group 3 was significantly lesser than group 1 and 2 (p < 0.05). qRT-PCR (skin) and IHC (skin) revealed similar results; and mRNA expression and mean fluorescence intensity of IL-17A, IL-22, IL-23A/R was significantly increased in group 2 and 3 compared to group 1 (p < 0.05). Mean fluorescence intensity and mRNA expression of IFN-γ, Foxp3 and Wnt5a were significantly increased in group 2 compared to group 1 (p < 0.05); whereas the difference between group 1 and 3 was not significant. Mean fluorescence intensity and mRNA expression of IL-17A, 1L-22 and IFN-γ showed no difference between group 2 and 3; whereas that of IL-23A/R, foxp3 and wnt5a were significantly higher in group 2 than group 3 (p < 0.05). Overall, maximal expression of IL-17A, IL-22, IL-23A, IFN-γ and Foxp3 (mRNA PBMCs) was observed in LP. Minimal expression of IL-17A, IL-22, IL-23A/R, IFN-γ and Foxp3 (mRNA skin and IHC skin) was seen in LPP patients. In contrast to LP, LPP lacks the expression of IFN-γ, Foxp3 and the cytokines representing Th17 pathway, and thus seems to have a distinct pathogenesis.