A 17-year-old woman with severe systemic lupus erythematosus and secondary myelodysplastic syndrome received an unrelated T-cell depleted bone marrow transplant. Her conditioning regimen included melphalan, thiotepa, fludarabine, and 2 doses of alemtuzumab. She initially did well posttransplant and was discharged from the hospital Approximately 3 months later, 40–50 tender erythematous papular lesions developed on her extremities. A skin biopsy specimen showed mycobacterial panniculitis. Cultures from skin, blood, and bone marrow grew M. haemophilum after 18–19 days’ incubation. She was successfully treated with rifampin, clarithromycin, and gatifloxacin; however, she died several months later from unrelated complications.
was first described in 1978 when it was isolated from cutaneous lesions of a woman from Israel with Hodgkin disease (6
). M. haemophilum
most often causes joint, cutaneous, and pulmonary infections in immunocompromised patients (7
) and lymphadenitis in immunocompetent children (8
). M. haemophilum
is a fastidious organism that requires media supplemented with ferric ions in the form of hemin, hemoglobin, or ferric ammonium citrate, and incubation at 30°C–32°C for several weeks. On the basis of our experience at Memorial Sloan-Kettering Cancer Center (23 cases of M. haemophilum
infection observed from 1990 through 2000) (9
), the following specimens are routinely set up for culture: blood smear specimens that are positive for acid-fast bacilli, synovial or joint fluids, skin biopsy specimens, cutaneous lesions, ulcers, abscesses, lymph nodes, and lung biopsy specimens. Culture media include Middlebrook 7H11 agar plates with a hemin-containing paper strip (X-factor) placed on the agar surface that are then incubated at 30°C for 6 weeks. Growth of the organism is usually detected within 2 to 3 weeks, and the isolates are usually susceptible in vitro to the quinolones, macrolides, and rifamycins and resistant to several drugs for tuberculosis, including ethambutol, isoniazid, and pyrazinamide (9
Alemtuzumab has been associated with the development of infections caused by a variety of microorganisms. However, mycobacteria have infrequently been the reported cause. In a review of 547 organ transplant recipients who received alemtuzumab treatment, miliary tuberculosis developed in 1 recipient of a kidney transplant, and pulmonary infection with M. kansasii
developed in 2 recipients of lung transplants (5
). There is also a case report of systemic M. bovis
infection developing in a patient with relapsing B chronic lymphocytic leukemia after administration of alemtuzumab (10
Although we believe that alemtuzumab is responsible for the severe immunosuppression that predisposed these patients to M. haemophilum infection, other explanations are plausible. For example, patient 1 had received rituximab and cyclophosamide for 6 months. These drugs, in addition to his underlying disease of chromic lymphocytic leukemia, may have predisposed him to M. haemophilum infection. However, his lesions did not appear until he received alemtuzumab. In patient 2, the immunosuppression associated with his transplant may have predisposed the patient to M. haemophilum infection.
This report identifies M. haemophilum as an opportunistic pathogen in patients who have received alemtuzumab. We recommend that all patients who have received at least 1 dose of alemtuzumab, and who have undiagnosed tender skin lesions located over the extremities, be evaluated by using appropriate techniques to isolate M. haemophilum. Communication with microbiology laboratory staff concerning appropriate methods for detection of the organism is crucial.