“
“Mycobacterium haemophilum is a rare isolate of non-tuberculous Mycobacterium which has been reported to affect immunocompromised

patients. We report a case of a 32-year-old renal transplant patient with M. haemophilum infection initially involving his left sinus which was treated with appropriate antimicrobial therapy for thirteen months. Two weeks after cessation of antibiotics the infection rapidly recurred in his skin and soft tissues of his hands and feet. This case highlights the difficult diagnostic and therapeutic implications of atypical infections in transplant find more patients. To our knowledge this is the first reported case of relapsed M. haemophilum infection in a renal transplant recipient. Non-tuberculous mycobacteria (NTM) infections in Australia occur at a rate of 1.8 cases per 100 000 population, and Mycobacterium haemophilum (MH) is a rare isolate of NTM that has been described with three cases in Victoria and twelve cases in Western Australia.[1] MH is acquired from the environment, especially from water sources and causes ulcerating skin and soft tissue infections and rarer presentations including septicaemia, pneumonitis and osteomyelitis.[2] Though, there are no published reports of human to human transmission, there have been over 120 cases of MH reported, predominantly in immunocompromised hosts with human immunodeficiency virus (HIV) or organ

transplants or immunocompetent children with lymphadenitis.[2, 3] We report a case of a renal transplant selleck products patient with MH infection initially involving his left sinus, and then rapidly recurring in his skin and soft tissues of his hands and feet following cessation of anti-microbial treatment. A 32-year-old Australian man with hypertension, aortic regurgitation and end-stage kidney disease secondary to IgA nephropathy, underwent living-related renal transplantation

in 2007. He received conventional immunosuppression with basiliximab induction followed by maintenance therapy with mycophenolate mofetil (MMF), cyclosporine and oral prednisolone. Carnitine palmitoyltransferase II His postoperative course was complicated by a methicillin-resistant Staphylococcus aureus (MRSA) wound infection which was managed with 6 weeks of oral rifampicin and fusidic acid. Following an allograft biopsy at 10 weeks post transplant that demonstrated histological changes suggestive of calcineurin (CNI) toxicity, cyclosporine was substituted with sirolimus. Repeat allograft biopsy one month later showed changes of acute T-cell-mediated rejection Grade IB with atypical granulomatous inflammation. Immunostaining for bacteria, Mycobacterium and viral inclusion bodies were all negative. Sirolimus was then ceased and tacrolimus introduced as treatment for rejection. He continued on MMF and prednisolone with a serum creatinine of 200–250 μmol/L.