Presentation
D.P. is a 59-year-old white Hispanic woman with a 12-year history of type 2 diabetes treated with a thiazolidindione and multiple daily injections of insulin. She presented to the outpatient clinic with a 10-week history of painful skin lesions on her abdomen that had been increasing in size. The lesions developed at the site of insulin injections. She was injecting in the abdomen, using a new needle each time. She had received a 14-day course of levofloxacin 7 weeks before the clinic visit and had been instructed to change the insulin bottles and to use her arms for injection. The skin lesions did not seem to improve, but she did not developed new lesions. She denied fever or other constitutional symptoms.
Her medical history was significant for severe asthma requiring chronic oral steroids and hypertension. Her medications included rosiglitazone;irbesartan; prednisone, 20 mg daily; bronchodilators; and glargine and aspart insulins. Her glycemic control was poor, with a hemoglobin A1cresult of 13.2%.
On physical examination, she had Cushingoid features and did not appear ill. Her blood pressure was 120/60 mmHg, heart rate 84 bpm, respiratory rate 16 rpm, and temperature 98.4° F. On her abdomen, she had multiple tender,red, indurated, hemorrhagic crusted papules and nodules, 0.5-2 cm in size in the periumbilical region bilaterally(Figure 1). There was no peripheral edema, and there were no lesions elsewhere on her body.
Pink nodules and pink, crusted, scaly papules coalescing into plaques on the right mid-abdomen.
Pink nodules and pink, crusted, scaly papules coalescing into plaques on the right mid-abdomen.
Routine laboratory tests, including leukocyte count with differential,platelets, electrolytes, creatinine, and liver enzymes, were within normal ranges.
A skin biopsy was performed from one of the nodules and was sent for histopathology and culture.
Questions
What is the microorganism involved in this patient's skin infection?
How was the insulin bottle contaminated with the etiologic agent?
Commentary
The biopsy demonstrated numerous acid fast bacilli in the inflamed dermis(Figure 2). Unfortunately, due to lab error, a culture was not performed.
Multiple acid fast bacilli in the dermis (original magnification 100×)
In this patient, the insulin bottle was the culprit. After she changed it,she did not develop new lesions. Upon further questioning, she admitted that there was water dripping in the refrigerator where she kept the insulin bottle, as a possible explanation of how the bottle was contaminated with the environmental pathogen.
D.P. was treated with clarithromycin for 3 months with resolution of the lesions and only mild residual hyperpigmentation in the area.
Occasionally, mycobacteria are isolated from nodular skin lesions of immunosuppressed patients. Many cases are linked to injections, and diabetic patients are at especially high risk. The skin infections are usually due to M. abcessus, M. chelonea, M. fortuitum, and M. kansasii.
Nontuberculous mycobacteria grow slowly. Even the rapid growers may take 3-7 days to form visible colonies on media, whereas slow-growing mycobacteria take weeks or do not grow at all. The slow growth complicates antibiotic susceptibility testing. Antibiotics may be degraded during prolonged incubation.
These mycobacteria are notoriously resistant to most antituberculosis drugs. Debridement is best combined with two or three antibiotic drugs. Most commonly used antibiotics are clarithromycin, clofazimine, amikacin,rifabutin, and sulfonamide.
It is important to consider the possibility of mycobacterial infection in cases that do not respond to standard antibiotic therapy. It is essential to perform skin biopsy and cultures to evaluate the lesions in order to guide therapy.
Clinical Pearls
It is important to keep in mind the rare but potential skin infection with atypical mycobacteria in diabetic patients who do not respond to antibiotic therapy for common skin pathogens.
When suspected, it is imperative to inform the lab technician to use special media for atypical mycobacterium isolation. Skin biopsy and cultures are essential to guide the therapy.
Irma Gazeroglu, MD, is a fellow at the University of Miami, Division of Endocrinology, Diabetes, and Metabolism; Michael Borenstein, MD,PhD, is a resident at the University of Miami, Department of Dermatology; and Maria P. Solano, MD, is an assistant professor of medicine at the University of Miami,Division of Endocrinology, Diabetes, and Metabolism in Miami, Fla.