Mycobacterium asiaticum was isolated from fluid aspirated from an olecranon bursa that had become inflamed following a superficial injury. Other possible causes of the inflammation were excluded. No specific antimycobacterial therapy was given. The infection responded to drainage, regular dressing, and immobilization. Our experience suggests that M. asiaticum is a potential cause of infection of the joints and surrounding tissues. Mycobacterium asiaticum was first described following a study of

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... isolates from the lymph nodes and viscera of healthy monkeys that had been imported from India and kept at a research institute in Hungary (2). Although the organism had been isolated in 1965, the species description was not published until 1971 (7). The first indication that M. asiaticum is a pathogen for humans came from Queensland, Australia, in 1983, when we reported the isolation of M. asiaticum from pulmonary secretions of five patients, two of whom were considered to have mycobacteriosis due to the organism (1). Subsequently, M. asiaticum was reported as the cause of pulmonary disease in a patient from Los Angeles, Calif. (5). Here, we describe a case of olecranon bursitis in which M. asiaticum was the probable causative agent. Clinical summary. In October 1989, a 24-year-old male army officer based in Townsville, Queensland, Australia, presented to the local hospital with a low-grade olecranon bursitis of the left elbow, having incurred a laceration to the same elbow a year earlier while travelling in northern Queensland. The initial treatment was limited to rest and simple analgesia. In late November, when the inflammation had not resolved, straw-colored fluid was aspirated from the bursa, and methylprednisolone was injected. A firm bandage was applied, and the patient's activities were restricted. Two weeks later, when there had been no improvement, a further amount of fluid was aspirated and submitted for routine microbiological analysis. Microscopic examination of the fluid showed many polymorphonuclear leukocytes, but smears and bacterial cultures were negative. A week later, the bursa remained swollen and tender, and a course of flucloxacillin was given. During December, fluid was aspirated on two further occasions, and an aliquot of the aspirate was submitted for mycobacteriological examination. Routine microbiological tests were not repeated. A radiograph of the affected joint showed no bone involvement. A course of a nonsteroidal anti-inflammatory drug was given, but there was no improvement and a sinus had developed by mid-January 1990. The patient transferred to a different hospital (in Victoria, Australia) and received another course of flucloxacillin in February 1990. Again, no improvement was noted, and a new treatment schedule, involving dressings with povidoneiodine and hydrogen peroxide and immobilization in a cast, was commenced. This new approach brought significant improvement. Around this time, mycobacterial culture results indicating the presence of M. asiaticum became known. No specific antimycobacterial therapy was given. When examined in early March, the patient was well, with the affected elbow joint showing an area of induration without any evidence of fluctuance. Routine hematological and biochemical parameters were within normal limits. A radiograph of the joint and a nuclear bone scan showed no evidence of osteomyelitis. A swab of the healing wound was taken for mycobacteriological testing, but no mycobacteria were isolated. The wound subsequently healed, and the patient remains well. Laboratory findings. Approximately 10 ml of cloudy, strawcolored fluid was aspirated from the bursa on 15 December 1989. The cell count showed 525 leukocytes per l, 34 erythrocytes per l, and a leukocyte content of 40% polymorphonuclear leukocytes and 60% lymphocytes. No crystals were seen under polarized microscopy. No organisms were seen in a Gram-stained smear, and all routine cultures for bacteria and fungi were negative. Histologic tests were not performed. The result of a test for rheumatoid factor (RA Test; Ortho Diagnostics) was Ͻ32 IU/ml. The result of a test for C-reactive protein (TDx System; Abbott Laboratories) was 0.02 mg/dl (normal range, Յ1.0 mg/dl). Mycobacteriology. The centrifuged deposit of the aspirate collected on 24 December 1989 was used to prepare a smear for acid-fast microscopy (with Ziehl-Neelsen stain) and was cultured on eight Löwenstein-Jensen slopes (some with sodium pyruvate and ferric ammonium citrate supplements) at 36 or 32ЊC. No acid-fast organisms were seen in the smear. Cultures were examined weekly, and after 4 weeks an acid-fast organism was detected on four slopes (two at 36ЊC and two at 32ЊC). Growth did not appear to be enhanced by the supplements. The isolate was subjected to a panel of standard tests (1) and was identified as M. asiaticum by virtue of the following properties: slow, dysgonic growth at 25 and 36ЊC but no growth at 43ЊC; photochromogenicity (the isolate developed a pale yellow pigment on exposure to light); rapid hydrolysis of Tween 80; a negative nitrate reduction test; negative tests for urease, nicotinamidase, and pyrazinamidase; semiquantitative catalase (Ͼ45 mm of foam); a negative test for ␤-galactosidase activity; and negative tests for arylsulfatase activity. More recently, the