ÌÇÐÄvlog

Mycobacterium haemophilum typically infects superficial tissues in immunocompromised persons and can lead to systemic illness. Its natural habitat is unknown, although most cases have been reported from cities near large bodies of water.¹ No cases have been previously reported from the northwestern area of the United States. We report 2 cases of M haemophilum infection that demonstrate the broad spectrum of dermatologic manifestations in varied clinical settings; both cases occurred in the state of Washington.

A 59-year-old man with diabetes presented with purulent superficial ulceration involving the scrotum and inguinal folds (Figure 1) that had progressed from a scrotal pustule over a 1-year period. Topical antifungal agents and corticosteroids were ineffective. Biopsy specimens were obtained from the edges of the ulcer. Smears were negative for acid-fast bacilli. Three weeks later, cultures yielded M haemophilum, a finding that was confirmed by gas-liquid and high-performance liquid chromatography. The organism was susceptible to amikacin, ciprofloxacin, clarithromycin, doxycycline, and rifampin. Treatment with ciprofloxacin, rifabutin, and clarithromycin led to clinical improvement during the ensuing months.

A 40-year-old man with human immunodeficiency virus (HIV) infection presented with 4 weeks of eye discomfort as well as pain and swelling of multiple interphalangeal and metacarpophalangeal joints and both knees. Sulfasalazine was prescribed for presumptive reactive arthritis after an initial evaluation revealed no infectious or rheumatologic processes. The patient returned 22 days later with fever, facial papules, and increased joint pain and swelling. Pus aspirated from an interphalangeal joint revealed acid-fast bacilli on smear, and isoniazid, rifabutin, pyrazinamide, clarithromycin and ethambutol therapy was initiated. The regimen was subsequently changed to ethambutol and clarithromycin when blood cultures drawn 20 days earlier yielded acid-fast bacilli, presumptively identified as Mycobacterium avium complex.

Over several weeks, approximately 20 violaceous subcutaneous nodules (1-5 cm) developed on the patient's extremities, head, and trunk (Figure 2), intermittently rupturing with pus. Previous blood and joint acid-fast bacillus isolates were correctly identified as M haemophilum by testing as described in case 1. The susceptibilities were identical to those in case 1. Treatment with rifabutin, ciprofloxacin, and clarithromycin led to initial improvement, but the patient's fever recurred in 9 days, with progression of skin and joint disease and an increase in the CD4 lymphocyte count from 14/µL to 109/µL during antiretroviral therapy. Evaluation was negative for coinfecting pathogens, and immune reconstitution syndrome was diagnosed. Prednisone therapy led to prompt resolution of fever, followed by improvement of the skin and joint disease during the ensuing months.

The cases reported herein demonstrate the dermatologic spectrum of M haemophilum infection, ranging from localized disease to systemic illness with cutaneous dissemination. To our knowledge, case 2 represents the first report of M haemophilum infection causing immune reconstitution syndrome, which was previously reported in cases of Mycobacterium tuberculosis and M avium complex infection in HIV-infected individuals after the initiation of antiretroviral therapy.² Extensive evaluation can be avoided by early recognition of this syndrome, which responds promptly to treatment with corticosteroids.

To our knowledge, our cases are the first reported from the northwestern area of the United States. Because M haemophilum detection depends on the use of iron-supplemented culture media with low temperature incubation,¹ laboratory protocol to culture superficial tissue specimens for this organism is important. Anti-microbial therapy is vital to the eradication of M haemophilum, and empiric clarithromycin, ciprofloxacin, and rifamycin therapy is ideal until susceptibilities return.¹ The duration of therapy is unclear but typically ranges from 6 weeks to 6 months, longer in immunosuppressed individuals, including HIV-infected patients.³ Decreasing immunosuppression may enhance treatment.^1,4 Debridement may be necessary in refractory cases.⁵

Accepted for publication June 29, 2001.

The antimicrobial susceptibilities used in this study were kindly provided by Timothy Kiehn, PhD, Microbiology Laboratory, Memorial Sloan-Kettering Cancer Center, New York, NY.

We thank Sally Andrada and Sean Strother, MD, for contributing the photographs for case 1. We are also indebted to LaDonna Carlson, Harborview Medical Center Microbiology Laboratory, Seattle, Wash, for performing gas-liquid chromatography and to James Kellogg, PhD, Microbiology Laboratory, York Hospital, York, Pa, for performing high-performance liquid chromatography to confirm identification of M haemophilum isolates.

Corresponding author: William M. Geisler, MD, MPH, Department of Medicine, Division of Allergy and Infectious Diseases, University of Washington, Box 356523, HSB BB1223, 1959 NE Pacific St, Seattle WA 98195 (e-mail: wgeisler@u.washington.edu).