INTRODUCTION
The prevalence of non tuburculous mycobacterial cutaneous
infections is small, with an estimated rate of between
0.9 cases per 100,000.1 Many dermatologists will
not see a case of cutaneous mycobacteria during their training
and most will go their entire careers without recognizing a case
of mycobacteria. However, there is data to suggest that cutaneous
mycobacterial infections are more prevalent than previously
recognized.1 Some of the patients with this infection may
also be infected with bacterial organisms and have positive cultures
for bacteria. This can delay the diagnosis and make treatment
difficult. Clinicians should have a high index of suspicion
for atypical mycobacterial infections.
CASE REPORT
A 74 year-old man presented to a dermatology office complaining
of a rash on his arm. The rash had been present for several
weeks and was spreading. He had seen his primary care physician
who began him on an oral antibiotic. The rash spread and
he decided to obtain a dermatologic opinion. The patient was
evaluated and noted to be afebrile and in no acute distress.
Examination revealed an exudative, indurated, erythematous
plaque on the skin overlying his left distal humerus and proximal
ulna (Figure 1).
Review of systems was negative for pulmonary symptoms, fevers,
night sweats, weight loss, or fatigue. He was taking no
medications and had no allergies. The initial clinical opinion
was that he had a methicillin resistant staphylococcus aureus
infection that was resistant to the antibiotics previously utilized.
A culture was taken for bacteria and the patient was begun on
minocycline 100 mg twice a day. After approximately 7 days, he
was evaluated again and found to be no better. The cultures for
bacteria grew staphylococcus aureus, sensitive to minocycline,
ciprofloxacin, and sulfa. Since he had shown no improvement
on the minocycline, his medication was changed to sulfamethoxasole/
trimethoprim. Following two weeks on this drug,
he failed to demonstrate any improvement.
Although the patient had no obvious immunosuppression, consideration
for atypical mycobacterial and deep fungal infections
was entertained. In order to determine what the etiology of the
eruption was, a series of three-millimeter punch biopsies were
performed. These biopsies were processed for histologic evaluation
as well as for culture for atypical mycobacterium and fungal
organisms. Following several weeks of culture, mycobacterium
abscessus was identified by culture as well as by DNA probing.
Susceptibility testing demonstrated that the organism was sensitive
to clarithromycin, linezolid, and ciprofloxacin.
Histopathology revealed suppurative and granulomatous inflammation
with focal acid fast organisms (Figure 2). Higher
power (Figures 3 and 4) showed histiocytes and lymphocytes
with no evidence of eosinophils or organisms. Special stains
for atypical mycobacteria revealed organisms. The patient was
sent for infectious disease consultation.
Treatment with clarithromycin 500 mg twice a day was initiated
and the patient was evaluated on an ongoing basis. After approximately
six weeks, a slight improvement of the erythema and
induration was noted. The patient was seen at monthly intervals
until his six-month visit at which time the eruption had resolved.
DISCUSSION
Mycobacterial infections may present in otherwise healthy
individuals and may be masked by bacterial infections that pre-
