CASE REPORT
A 36-year-old Caucasian female initially presented for
evaluation of a chronic rash in 2005. Her past medical
history was significant for persistent asthma requiring
multiple hospitalizations and treatment with systemic corticosteroids
for adequate control. Computerized tomography during
one of her previous admissions revealed hilar lymphadenopathy,
and a presumptive diagnosis of pulmonary sarcoidosis was
made. At her initial presentation to the dermatology department,
she had scattered pink, scaly patches and small plaques on her
scalp and trunk. Biopsy revealed nonspecific granulomatous
dermatitis suggestive of cutaneous sarcoidosis. Minced tissue
culture was negative for bacteria, fungus, or mycobacteria.
The patient was lost to follow-up until 2011. Her rash had
progressed significantly despite intermittent treatment with
topical corticosteroids and oral minocycline (Figure 1). She had
large, pink, indurated plaques on the scalp, neck, trunk, and
extremities and significant alopecia of the scalp. Biopsies revealed
superficial and deep granulomatous dermatitis (Figure
2). Gomori methenamine silver, acid-fast bacilli (AFB), and Fite
stains were negative, as were tissue cultures. Because of the
presumptive diagnosis of an inflammatory condition such as
sarcoidosis, she was started on methotrexate.
Two months into treatment, her rash worsened and she developed
new skin lesions. A fourth biopsy was sent for special
stains and tissue culture. After 7 weeks of incubation, Mycobacterium
avium-intracellulare (MAI) was isolated. She promptly
discontinued the methotrexate and was referred to the infectious
disease service. She was treated with clarithromycin 500
mg twice daily, rifampin 600 mg daily, and ethambutol 1,200
mg daily. As observed in Figure 3, she had an excellent response
after 5 months of treatment; however, she was left with
scarring and areas of atrophy from the chronic inflammation.
DISCUSSION
Nontuberculous mycobacteria (NTM) are slender, nonmotile
AFB that have been implicated in the pathogenesis of cutaneous
disease since the early 1900s. They are ubiquitous in the
environment and can be found in soil, vegetation, water, and
various animals. While hundreds of different NTM have been identified, only a select few appear to be clinically important in
cutaneous disease.1
Of the clinically relevant NTM, MAI most commonly causes
pulmonary disease. Mycobacterium avium and Mycobacterium
intracellulare are typically grouped together as MAI and M
avium complex (MAC), as they are difficult to differentiate and
treatment is the same for each species. They are further classified
as slow-growing, nonphotochromogens.2
Clinically, MAI has been reported to present as scaling or erythematous
plaques, painful subcutaneous nodules, abscesses,
ulcers, and verrucous lesions. Because of this myriad of possible
clinical manifestations, MAI has been reported to be
misdiagnosed as or to mimic other conditions such as lepromatous
leprosy, lupus vulgaris, and sarcoidosis.3-5 Cutaneous
MAI typically occurs in immunosuppressed patients; however,
immunocompetent hosts have also been described.6
Nontuberculous mycobacterial DNA has been isolated from the
cutaneous lesions of sarcoidosis in 16 of 20 patients in previous
studies.7 Given the still-unknown etiology of sarcoidosis
and the reports of NTM resembling sarcoidosis, one must consider
whether NTM species play a role in the pathogenesis of
sarcoidosis. Therefore, in the evaluation of a patient with a his
