Disseminated Mycobacterium Chelonae Mimicking Erythema Nodosum in a Patient With Gout

Abstract Mycobacterial chelonae (M.chelonae) is a rapidly growing non-tuberculosis mycobacteria that can present in a variety of ways such as disseminated cutaneous infection, pulmonary disease, musculoskeletal disease in immunosuppressed patients. The presentation of cutaneous findings is initially difficult to differentiate from the autoimmune process, thus presenting a conundrum between infection and inflammation, especially in setting of systemic disease. We present the case of a 74-year-old male with past medical history of heart failure, atrial fibrillation, and gout who was recently placed on prednisone taper for gout flare and presented to the hospital for new subcutaneous nodules and polyarthralgia of the bilateral ankles, and left knee, and big toe. Exam findings were remarkable for discrete erythematous nodules with hyperpigmented papular rash of the upper and lower extremities initially concerning for erythema nodosum. Initial labs remarkable for uric acid 10.4, elevated ESR and CRP, WBC of 4.9, ANA panel unremarkable (1:80) as well as ANCA, HLA-B27 and Rheumatoid Factor, with bone scan showing concerns for possible inflammatory arthritis. Nonetheless, given concerns for possible autoimmune etiology, such as atypical gout or sarcoidosis, the patient was started on prednisone taper. However, the patient's rash worsened concerning for infectious etiology and the steroids were discontinued. The hospital course was complicated by worsening respiratory and renal failure requiring ICU level of care, with concerns for possible worsening sepsis. Given worsening respiratory decline the patient underwent bronchoalveolar lavage that was largely unremarkable. Full thickness skin biopsy was notable for acid-fast bacilli, with Karius testing showing M.chelonae and so the patient was transitioned to intravenous antibiotics (imipenem, azithromycin, and doxycycline) with improvement of his condition. Interestingly, the patient's initial QuantiFERON-TB gold was negative, and it was later found that the patient had visited a foot spa immediately prior to his presentation. Our case highlights the need to consider NTM as a possible opportunistic infection in the setting of gout patients. Prior studies have found that M.chelonae usually occurs in the setting of corticosteroid therapy and is often disseminated. Furthermore, the case highlights that clinicians should realize that gout can also predispose patients to opportunistic infections due to innate immune dysregulation due to the effects of uric acid.