A 23 year-old male with no immunosuppressive diseases, including Cushing syndrome visited Souza Araújo Ambulatory, Fundação Oswaldo Cruz, Reference Center, Brazil, for treatment of leprosy, 3 years after a 12-month standard treatment of multibacillary lepromatous leprosy. He presented with a residual 3+ bacilloscopy index, ulnar nerve neuritis, and an exuberant erythema nodosum leprosum (ENL) reaction, which was not controlled with a previous corticosteroid therapy regimen. No signs of fungal infection were found this time. Therefore, thalidomide regimen was administered at a dose of 200 mg/day with 40 mg/day prednisone; both drugs were gradually reduced at monthly intervals during medical visits, and the treatment was stopped after 3 months. However, 4 months later, the patient presented with new skin lesions (Figure 1A–C), suggesting that ENL had relapsed. Culture samples of the epithelium and nails showed the presence of Trichophyton mentagrophytes and Trichophyton tonsurans (Figure 1D and E). In addition, a skin biopsy showed histopathological features of leprosy activity (logarithmic index of biopsies: 3.8). The recommended treatment was to restart the rifampin, dapsone and clofazimine 12-month WHO/MDT MB scheme after dermatophytosis resolution with oral terbinafine administration.
Globally, Brazil ranks at the top in terms of the number of new leprosy cases. Erythema nodosum leprosum, a leprosy reactional state, has a tendency to occur in multibacillary patients, mainly in those with a lepromatous pole. In most cases, immunosuppressive drugs are necessary to control the reaction, leading to an environment conducive to opportunistic infections, including fungal infections.1
Dermatophytes are fungi causing superficial skin infections; they feed on the keratin present in the corneum skin. Trichophyton mentagrophytes are anamorphic species, that is, they are asexual or imperfect, besides being antrophilic and zoophilic. They are also found in dogs, rodents, and rabbits.2 Furthermore, T. tonsurans are anantrophilic species, more commonly seen in infants and mainly affecting the scalp area; occurrence of this pathogen is also related to poverty.3
This article highlights the importance of dermatophytosis as a late potential iatrogenic effect of corticosteroid therapy; in addition, antifungal immune lymphocyte response in lepromatous leprosy pole is impaired due to Th2/Treg modulation.4 Furthermore, clofazimine can also play a role in dermatophyte dissemination via ichthyosis, its recognized adverse effect, which may also favor fungal proliferation.
Although possible, the association between leprosy and widespread dermatophytosis has rarely been described in the literature5; dermatophytosis can be often misdiagnosed by inexperienced physicians as syphilitic roseola, leprosy reactional states, such as erythema multiforme, or a leprosy relapse; therefore, histopathological and microbiological investigations must be encouraged, whenever possible.
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Salci TP, Salci MA, Marcon SS, Salineiro PHB, Svidzinski TIE, 2011. Trichophyton tonsurans in a family microepidemic. An Bras Dermatol 86: 1003–1006.
Sousa JR, Sotto MN, Quaresma JAS, 2017. Leprosy as a complex infection: breakdown of the Th1 and Th2 immune paradigm in the immunopathogenesis of the disease. Front Immunol 8: 1635.
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