Cutaneous reactions due to rifampicin (RPM) are uncommon and amongst these fixed drug eruption (FDE) is especially rare. There have been only three reports of FDE to RPM in the literature so far. 1-3 In 1985, Naik et al. first repOlted a peculiar urticarial type of FDE due to RFM . Here, we describe a second such case with a similar unusual cutaneous drug eruption. Case reportA 24-year-old soldier suffering from borderline tuberculoid leprosy (BT) was admitted to the Leprosy Center, Base Hospital, Lucknow for supervised institutional therapy. He was put on cap RPM 600 mg once a month and dapsone 100 mg daily. The patient developed a solitary itchy erythematous urticarial lesion of 3.5 cm diameter with typical peau d'orange appear ance (Figure 1), on the right side of the chest wall about 1 h after the second monthly dose of RFM. The lesion subsided on its own within 1 h without any residual hyperpigmentation. A similar lesion at the same site was observed following the third monthly dose of RPM which also subsided within 1 h without treatment. At this stage, a clinical diagnosis of FDE was made and all drugs were discontinued. Two days later, the patient was subjected to a provocation test with 600 mg of RFM, following which he developed an urticarial lesion at the same site. The provocation test to dapsone did not evoke any cutaneous reaction. Skin biopsy of the lesion revealed slight dermal oedema and sparse eosinophilic infiltration. Interestingly, this cutaneous response to RFM ceased after the fifth dose of RPM.In our patient, recurrence of a wheal at exactly the same site following administration of RPM is highly suggestive of FDE. Though FDE can be urticarial, the residual hyper pigmentation that follows a classical FDE was not seen. Moreover, the histopathology was

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Necrotizing fasciitis is a life-threatening soft tissue infection that results in rapid local tissue destruction. Type 1 necrotizing fasciitis is characterized by polymicrobial, synergistic infections that are caused by non-Group A Streptococci, aerobic and anaerobic organisms. Type 2 necrotizing fasciitis involves Group A Streptococcus (GAS) with or without a coexisting staphylococcal infection. If not treated precociously and in an adequate manner the mortality rate can reach up to 74%. [1] Here we present a case of 37years old male with tuberculous necrotising fasciitis presenting with signs of acute inflammation. The tissue was debrided (sent for histopatological examination) and pus drained (sent for routine culture and AFB culture). The histopatological report of the underlying muscle and fascia was suggestive of tuberculous inflamation (dense neutrophilic infiltration with caseous necrosis) while the pus culture and AFB culture was negative for Mycobacteium species.

Buruli ulcer is a chronic, indolent, necrotizing disease of the skin and soft tissue. Buruli ulcer is the third most common mycobacterial disease of immunocompetent hosts, after tuberculosis and leprosy, and is caused by toxin-producing mycobacteria named Mycobacterium ulcerans. Over the last 2 decades, a re-emergence of cases has occurred, leading to the 1998 World Health Organization (WHO) Buruli Ulcer Initiative and the Fifty-Seventh World Health Assembly Resolution on Buruli Ulcer, which have stimulated ongoing research into diagnosis, pathogenesis, and effective treatment.