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J Med Microbiol 55 (2006), 1745-1746; DOI: 10.1099/jmm.0.46795-0
© 2006 Society for General Microbiology
ISSN 1473-5644


Case Report

Mycobacterium kansasii olecranon bursitis

G. S. Barham and D. G. Hargreaves

Department of Trauma and Orthopaedics, Southampton General Hospital, Southampton University NHS Trust, Southampton, UK

Correspondence
G. S. Barham
guybarham1{at}aol.com

Received 23 June 2006
Accepted 27 August 2006


A case is reported of a post-traumatic olecranon bursitis caused by Mycobacterium kansasii following an injury sustained in a public swimming pool. It responded to surgical debridement and combined rifampicin, isoniazid, pyrazinamide and ethambutol antimicrobial therapy. A literature search was performed and a treatment regimen for this uncommon condition is suggested.


    Case report
 TOP
 Case report
 Discussion
 Conclusion
 REFERENCES
 
A 59-year-old male with no pre-existing risk factors for tuberculous disease sustained a 2 cm laceration over his right elbow whilst at a public swimming pool. He developed an olecranon bursitis and was given a course of oral flucloxacillin and subsequently had the bursa aspirated and injected with a steroid. When the bursa ruptured he had a formal surgical excision and the specimen was sent for microbiological and histological assessment.

Two weeks post-operation it was noted that the wound had not healed and had continued to ooze. Histology of the specimen showed an acute and chronic inflammatory infiltrate, focal micro-abscess and granulomas with Langerhans-type multinucleated giant cells, and an acid-fast bacillus was identified on Ziehl–Neelsen stain. An atypical environmental mycobacterium was suspected, so he was started on a 6-month quadruple therapy regimen of rifampicin, isoniazid, pyrazinamide and ethambutol.

Our local mycobacterial reference laboratory (Regional Centre for Tuberculosis Bacteriology, Public Health Laboratory Service, Dulwich, UK) cultured the samples on Lowenstein–Jensen medium incubated at 37 and 25 °C and assessed its photochromogenic properties. The organism was identified as Mycobacterium kansasii.

When reviewed at 1 year, his elbow wound had completely healed and there was no sign of recurrence.


    Discussion
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 Case report
 Discussion
 Conclusion
 REFERENCES
 
The olecranon bursa is a common site for infectious, traumatic and inflammatory bursitis. Staphylococcus aureus is isolated in up to 90 % of infective olecranon bursitis; other organisms encountered include group A streptococci, anaerobes, parasites and mycobacteria (McNab, 2002).

In orthopaedic practice, mycobacteria (atypical and tuberculous) are well known to cause superficial infection, tenosynovitis, synovitis, septic arthritis and osteomyelitis, and can mimic rheumatoid, sarcoid and gout. Several atypical mycobacteria have been associated with olecranon bursitis in man and include Mycobacterium asiaticum, Mycobacterium xenopi, Mycobacterium goodie and Mycobacterium szulgai. The M. asiaticum infection responded to drainage alone, but combined surgical debridement and antimycobacterial was recommended for the M. szulgai and M. goodii bursitis (Dawson et al., 1995; Friedman & Sexton, 2001; Maloney et al., 1987; Rutten et al., 1998).

Atypical mycobacteria surround us in the environment, and inoculation with atypical mycobacteria can follow skin abrasions and lead to both cutaneous and deeper soft-tissue infection. Mycobacterium fortuitum and Mycobacterium chelonae can infect skin and soft tissues after trauma or surgery, and Mycobacterium marinum causes local cutaneous infection following skin trauma in swimming pools or fish tanks: ‘fish fancier's finger’ (Collins et al., 1985). Aquatic habitats as varied as sea water, fresh drinking water and hospital water supplies host atypical mycobacterial species, including M. kansasii, M. marinum, M. xenopi, M. chelonae, M. fortuitum, Mycobacterium avium and Mycobacterium intracellulare, and M. scrofulaceum (Collins et al., 1984).

Systemic or respiratory disease caused by M. kansasii is confined almost exclusively to the immunosuppressed. M. kansasii soft-tissue and joint infection is rare, and also has a higher incidence in the immunosuppressed, with seven of the ten cases of M. kansasii septic arthritis reported in France between 1992 and 1997 being in immunosuppressed patients (Bernard et al., 1999). Joint infection with M. kansasii can cause either a monoarthritis or a destructive polyarthritis (Bouza et al., 1998; DeMerieux et al., 1980; Girard et al., 1973).

There are no treatment guidelines for the treatment of M. kansasii soft-tissue infection in the literature. A review of the literature has shown that both conservative and operative therapies have been used successfully in the management of ‘atypical mycobacterial’ soft-tissue infections. The Sub-committee of the Joint Tuberculosis Committee of the British Thoracic Society (1999) guidelines on M. kansasii suggest that infected lymph nodes should not be aspirated but excised, and 9 to 24 months of rifampicin and ethambutol prescribed with the addition of a macrolide if the condition is not responding to initial treatment. They note that there is insufficient evidence about the management of M. kansasii at other sites, and make no mention of surgical debridement of other soft-tissue M. kansasii infections.

Chow et al. (1987) give more general advice on soft-tissue mycobacterial infections of the hand and wrist. These authors suggest that treatment with drugs alone is appropriate, unless steroids have been injected, in which case they advocate surgical debridement and appropriate antibiotics. Grange & Yates (1986) recommend early contact with the local Health Protection Agency Mycobacterium Reference Unit (formerly the Public Health Laboratory Service) for specialist advice and state that M. kansasii is usually sensitive to a combination of isoniazid, rifampicin and ethambutol for 12 to 24 months. The Sub-committee of the Joint Tuberculosis Committee of the British Thoracic Society (1999) recommends early contact with respiratory physicians, as they are familiar with using and monitoring anti-mycobacterial drugs with their unwanted side-effects.


    Conclusion
 TOP
 Case report
 Discussion
 Conclusion
 REFERENCES
 
M. kansasii is a rare cause of bursitis. There is little evidence on efficacy of treatment regimens in the literature. The case we report responded to thorough surgical debridement and systemic antituberculous chemotherapy. In our practice we request mycobacterial testing in any case that has any suspicious features in history, examination or operative findings. We would recommend both surgical debridement and combined antituberculous medication, with involvement of a respiratory physician and the local Health Protection Agency Mycobacterium Reference Unit, as treatment for M. kansasii bursitis.


    REFERENCES
 TOP
 Case report
 Discussion
 Conclusion
 REFERENCES
 
Bernard, L., Vincent, V., Lortholary, O. & 9 other authors (1999). Mycobacterium kansasii septic arthritis: French retrospective study of 5 years and review. Clin Infect Dis 29, 1455–1460.[CrossRef][Medline]

Bouza, E., Munoz, P., Desai, G. & Mulla, Y. (1998). Osteomyelitis and associated conditions. In Oxford Textbook of Rheumatology, 2nd edn, pp. 879–881. Edited by P. J. Maddison, D. A. Isenberg, P. Woo & D. N. Glass. Oxford: Oxford University Press.

Chow, S. P., Ip, F. K., Lau, J. H. K., Collins, R. J., Luk, K. D., So, Y. C. & Pun, W. K. (1987). Mycobacterium marinum infection of the hand and wrist. J Bone Joint Surg Am 69, 1161–1168.[Abstract/Free Full Text]

Collins, C. H., Grange, J. M. & Yates, M. D. (1984). Mycobacteria in water. J Appl Bacteriol 57, 193–211.[Medline]

Collins, C. H., Noble, W. C. & Yates, M. D. (1985). Mycobacterium marinum infections in man. J Hyg 94, 135–149.

Dawson, D. J., Blacklock, Z. M., Ashdown, L. R. & Bottger, E. C. (1995). Mycobacterium asiaticum as the probable causative agent in a case of olecranon bursitis. J Clin Microbiol 33, 1042–1043.[Abstract]

DeMerieux, P., Keystone, E. C., Hutcheon, M. & Laskin, C. (1980). Polyarthritis due to Mycobacterium kansasii in a patient with rheumatoid arthritis. Ann Rheum Dis 39, 90–94.[Abstract/Free Full Text]

Friedman, N. D. & Sexton, D. J. (2001). Bursitis due to Mycobacterium goodii, a recently described, rapidly growing mycobacterium. J Clin Microbiol 39, 404–405.[Abstract/Free Full Text]

Girard, D. E., Bagby, G. C. & Walsh, J. R. (1973). Destructive polyarthritis secondary to Mycobacterium kansasii. Arthritis Rheum 16, 665–669.[Medline]

Grange, J. M. & Yates, M. D. (1986). Infections caused by opportunistic mycobacteria: a review. J R Soc Med 79, 226–229.[Medline]

Maloney, J. M., Gregg, C. R., Stephens, D. S., Manian, F. A. & Rimland, D. (1987). Infections by Mycobacterium szulgai in humans. Rev Infect Dis 9, 1120–1126.[Medline]

McNab, I. (2002). Bursitis of the elbow. In Oxford Textbook of Orthopaedics and Trauma, pp. 810–814. Edited by C. Bulstrode, J. Buckwalter, A. Carr, L. Mergh, J. Fairbank, J. Wilson-MacDonald & G. Bowden. Oxford: Oxford University Press.

Rutten, M. J., van der Berg, J. C., van der Hoogen, F. H. & Lemmens, J. A. (1998). Non-tuberculous mycobacterial bursitis and arthritis of the shoulder. Skeletal Radiol 27, 33–35.[CrossRef][Medline]

Subcommittee of the Joint Tuberculosis Committee of the British Thoracic Society (1999). Management of opportunistic mycobacterial infections: Joint Tuberculosis Committee guidelines 1999. Thorax 55, 210–218.




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