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Mycobacterium chelonae finger infection associated with Raynaud’s phenomenon
  1. H Sari-Kouzel1,
  2. P R Chadwick2,
  3. L T S W Muir3,
  4. A L Herrick1,
  5. D W Denning4
  1. 1University of Manchester Rheumatic Diseases Centre, Hope Hospital, Salford M6 8HD, UK
  2. 2Department of Microbiology, Hope Hospital, Salford M6 8HD, UK
  3. 3Department of Orthopaedic Surgery, Hope Hospital, Salford M6 8HD, UK
  4. 4Research and Teaching Block, University of Manchester, Wythenshawe Hospital, Southmoor Rd, Manchester M29 9LT, UK
  1. Correspondence to:
    Dr H Sari-Kouzel
    Department of Rheumatology, Basildon and Thurrock University Hospital, Nethermayne, Basildon, Essex SS16 5NL, UK;

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Mycobacterium chelonae infections are uncommon and have not been reported as a complication of Raynaud’s phenomenon previously. We describe a patient with this problem who responded well to treatment.


A 21 year old female telephonist was referred with a 1 week history of swollen right index and middle fingers. There was no history of trauma but she had had Raynaud’s phenomenon since the age of 12. There was no history of recent travel abroad or of unusual hobbies.

On examination she was apyrexial, she had diffuse swelling but no discolouration of the right index and middle fingers. She had no blisters or ulceration and the fingers were not tender to touch. Nine days later, despite flucloxacillin orally and a non-steroidal anti-inflammatory agent, all her fingers were cold and bluish, and the right index and right middle fingers remained diffusely swollen. She was admitted for intravenous prostacyclin because of worsening of her Raynaud’s phenomenon.

Her baseline investigations were normal, including erythrocyte sedimentation rate and C reactive protein. A hand x ray examination showed no bony abnormality. Blood cultures were negative. Her immunoglobulin levels were normal, and cryoglobulins were not detected. Her autoantibody profile was negative except for raised IgG cardiolipin antibodies at 46 GPLU (reference range 0–13).

As she finished the 72 hour intravenous prostacyclin infusion, a pustule appeared on the pulp of the right index finger, and intravenous ceftriaxone was started. Two days later a second pustule appeared on the other finger (fig 1). Microscopy of a needle aspiration showed acid fast bacilli. Antibiotics were changed to clarithromycin 500 mg twice daily and ciprofloxacin 750 mg twice daily. Both lesions were incised and drained, and histology of the material showed an abscess wall with no granulomata.

Figure 1

 Pustules on the index and middle fingers of the right hand.

M chelonae was cultured from pus and was susceptible in vitro to azithromycin and clarithromycin, but resistant to other antituberculous agents, as well as to ciprofloxacin. As her lesions were healing at the time these results became available (14 days later) her antibiotics were not changed. She continued the combination for a total of 5 weeks and her fingers healed completely.


M chelonae is associated with a variety of infections. Cutaneous lesions occur secondary to wound infections after surgery, accidental trauma, or needle injections.1,2M chelonae isolates are susceptible in vitro to clarithromycin, but generally resistant to ciprofloxacin. The use of at least two drugs (one of which should be clarithromycin) is recommended for treatment of M chelonae infection, as the emergence of resistance is a risk associated with monotherapy.3,4 Treatment is usually given for 4–6 months, but our patient responded to combination therapy within weeks. A case has been reported of postoperative infection at a donor vein graft site that healed after 2 months of clarithromycin treatment, combined with heat treatment.5 Thus shorter courses of treatment may be appropriate in non-immunosuppressed patients.

Isolates of M chelonae have optimal growth at 28–30°C,6 unlike the standard 35°C for most organisms. Our patient had severe Raynaud’s disease before the infection, so the coldness of her hands may have promoted the growth of this unusual organism. We are not aware of any previous reports of M chelonae infection in a patient with Raynaud’s phenomenon. A significant portion of the 100 patients with M chelonae infections reported by Wallace et al7 were receiving corticosteroids or immunosuppressant drugs, or both. In their series 35 patients had a localised cutaneous infection and only five had no history of trauma, of whom three had an underlying immunosuppressive condition.

Our patient had no history of trauma, she was immunocompetent, but had a history of Raynaud’s phenomenon. Because there were no systemic features during the acute phase of her illness, an atypical infection was suspected and acid fast bacilli were specifically looked for. In conclusion, unusual presentations have unusual explanations and should raise suspicion of atypical infections.


Mycobacterial identification and susceptibility tests were performed at Newcastle Public Health Laboratory, Newcastle, UK. We thank John Magee of Newcastle PHL for helpful discussions of this case.