Varicella and herpes zoster appearing over sites of tinea corporis, hitherto unreported examples of immunocompromised districts: a case series

Varicella and herpes zoster appearing over sites of tinea corporis, hitherto unreported examples of immunocompromised districts: a case series Dear Editor, Herein we report the development and localization of herpes zoster or varicella over sites of healed superficial dermatophytosis (SD) in three patients (Figs. 1a,b and 2a) and varicella on sites of active SD under treatment in one patient (Fig. 2b,c). The first three cases are examples of Wolf’s isotopic response, that is, development of an unrelated disease over the site of another healed disease. However, the case of varicella localizing to the lesions of active SD under treatment cannot be labeled as Wolf’s isotopic response because the latter has not yet healed, qualifying it to be an example of locus minoris resistentiae instead. We feel it is prudent to use a more inclusive and unifying term like “immunocompromised district” (ICD) that encompasses locus minoris resistentiae, Wolf’s isotopic response, and other related phenomena. ICD is a localized area of skin with altered immunity over which secondary diseases like infections, tumors, or dysimmune reactions develop in an otherwise immunocompetent individual. It can either be because of the increased number of dysfunctional immune cells or their deficiency/absence. The three factors setting the stage for the development of ICD are chronic lymph stasis, herpes-infected sites, and trauma. All the four cases described above are ICDs that are hitherto unmentioned in literature. A literature search yielded just one case of lichen planus developing over healed tinea corporis. All our patients had also applied fixed-dose combination (FDC) creams containing a potent steroid, antifungal, and antibacterial agent for a few days, which are known to cause local immune suppression on sites of SD. It would be difficult, however, to incriminate topical corticosteroids (TCS) solely in causing such a unique presentation of immune dysregulation because innumerable patients use them for prolonged periods in steroid-responsive dermatoses without varicella zoster virus (VZV)-related infections developing and preferentially localizing in areas of TCS application. Varicella localizing to lesions of active dermatophytosis can be explained by the fact that there are specific pathways for migration of cutaneous lymphocyte antigen (CLA+) memory T cells to the skin during immune surveillance, which is markedly increased during active inflammation. Interestingly, VZV shows twofold increased tropism for these T cells. These VZV laden T cells then localize to areas of preexisting cutaneous inflammation. Varicella/herpes zoster appearing at the site of healed dermatophytosis can be explained by the phenomenon of T-cell exhaustion at these sites, which is characterized by a stepwise and progressive loss of T-cell functions. It commonly develops because of antigen persistence and is seen following many chronic viral infections. It is possible that persistent dermatophyte antigens, despite resolution of lesions, may have led to exhaustion of CLA+ T cells in these cases, eventually leading to the affected sites becoming an ICD. TCS application could have additionally contributed in rendering these sites ‘ICDs’. This phenomenon would then qualify to be partly a “pharmacotopic response” and be added to the list of responses found in literature, all of which are known examples of ICD. The epidemic-like situation of SD in India gives us ample opportunities to look for development of secondary diseases appearing over it or SD developing over preexisting diseases. In-depth study of cases of dermatophytosis that have become ICDs may provide some insight into the often recurrent and chronic dermatophytosis, which is largely being fueled by topical corticosteroids.