Chronic cutaneous disease caused by the rapid growers<i>Mycobacterium fortuitum</i>and<i>chelonae</i>
Authors: P.K. Palwade, R.S. Dhurat, U.M. Tendolkar, G.R. Dethe, H.R. Jerajani
Journal: British Journal of Dermatology (2006)

Conflicts of interest: none declared. Sir, Rapidly growing mycobacteria are widely distributed in the environment. Infection by them usually results in a localized pathology. Disseminated cutaneous infection is rarely encountered in clinical practice. We report a case of disseminated Mycobacterium fortuitum and chelonae complex infection that developed out of a postinjection abscess. A 40‐year‐old housewife had developed a postinjection abscess in the right gluteal region 8 years previously. The abscess was drained surgically and she was given antibiotics for a short duration (2 weeks). The abscess healed with a puckered scar in 2 months. Within the next 6 months she started developing discharging nodules in the skin surrounding the scar. Over the next 7 years, the lesions progressed to involve the lower back and abdomen. There was no personal or family history of tuberculosis. On examination, vital parameters were within normal limits. Cutaneous examination revealed multiple erythematous tender nodules of size ranging from 1 × 1 cm to 2 × 1·5 cm situated on the abdomen and extending to the lateral aspects of the trunk (Fig. 1a). Some of these nodules were discharging pus without grains. Multiple scars were seen at the back. A puckered scar of the postinjection abscess was noticeable in the upper quadrant of the right gluteal region. There was no evidence of lymphadenopathy. Laboratory tests showed anaemia (haemoglobin 10 g dL−1) and erythrocyte sedimentation rate 50 mm in the first hour. Serum chemistry, chest X‐ray and abdominal ultrasound were normal. Skin ultrasonography using a 50‐MHz probe showed increased thickness of the mid and deeper dermis with hyperechoeic and hypoechoeic areas (dermal thickness 2·6 mm; normal 1·2 mm). Multiple pus swabs and tissue culture did not yield bacteria or fungi. Skin biopsy from the affected area showed chronic inflammation with suppurative foci; Ziehl–Neelsen staining and Gram staining did not reveal bacteria. Finally, a pus aspirate from one of the active lesions resulted in growth of acid‐fast bacilli (AFB) on Lowenstein–Jensen medium within 7 days in the presence of light. The growth was subcultured on MacConkey's culture medium, which grew similar colonies within 5 days suggestive of rapidly growing mycobacteria. Species identification and antibiotic sensitivity testing could not be done due to lack of facilities, and the growth was identified as M. fortuitum and chelonae complex. Before the confirmation of diagnosis she had received intramuscular injections of amikacin 500 mg once daily and oral trimethoprim–sulfamethoxazole 160/800 mg twice daily for 14 days. The same treatment was continued for the next 7 days. Then the regimen was changed to a combination of oral clarithromycin 500 mg, ciprofloxacin 500 mg and trimethoprim–sulfamethoxazole 160/800 mg twice daily for 8 months. During this period there was progressive improvement: no new lesions appeared and the active lesions healed (Fig. 1b). Skin ultrasonography was repeated after 4 months of the lesion‐free period, which showed a reduction in thickness of the dermis, with uniform normal hyperechoeic dermis (dermal thickness 1·6 mm). Culture of a punch biopsy taken from a healed nodule did not yield growth of AFB. One year after stopping treatment there was no evidence of disease activity.