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.
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