Wound Botulism in Injection Drug Users

To the Editor: Infections are the most frequent and serious wound complications in injection drug users (IDUs). Wound botulism is primarily caused by Clostridium botulinum (1) and was fi rst observed in IDUs in New York in 1982 (2). It results from the introduction of C. botulinum spores into a wound and their multiplication, germination, in situ synthesis, and secretion of toxin under anaerobic conditions. Of 7 designated toxin types, neurotoxins A, B, E, and F result in human disease. During the 1990s, wound botulism cases among IDUs increased in the United States in conjunction with the use of black-tar heroin (3). Since 2000, wound botulism cases in IDUs have been reported in Europe (4). To our knowledge, molecular epidemiologic analyses have not been performed to confi rm suspected outbreaks. Within a 6-week period in October and November 2005, 12 clinical cases were recognized in the metropolitan area of Cologne, Germany (5). Six patients were successfully treated at teaching hospitals of the University of Cologne. On admission, all socially nonrelated patients had signs of bilateral symmetric cranial neuropathies such as ptosis, diplopia, blurred vision, dysphagia, dysarthria associated with symmetrical descending weakness of the upper extremities, and no sensory defi ciencies. Treatment of patients included administration of trivalent A, B, and E antitoxin; antimicrobial drugs such as penicillin G or mezlocillin with metronidazole; and surgical drainage of any existing abscesses. Patient 1, a 31-year-old female IDU, had multiple abscesses on both legs. Four days after her admission, wound botulism was suspected and antitoxin administered. Respiratory failure required mechanical ventilation for 11 weeks. Patient 2, a 51-yearold male IDU, had 1 large abscess on the left lower leg. Antitoxin was administered within 3 days of hospital admission. Mechanical ventilation was required for 5 weeks. Patient 3, a 25-year-old male IDU, had a large abscess on the left forearm. Patient 4, a 43-year-old man who used heroin intramuscularly, had an abscess of moderate size on the left forearm. Antitoxin was administered within 12 hours of admission to patients 3 and 4, and both patients required 2 weeks of respiratory support. Patient 5, a 32year-old male IDU who was positive for hepatitis C virus, had purchased heroin from the same dealer as patient 2. Abscesses were absent. Antitoxin was administered within several hours of admission. Within 10 days, the patient recovered fully without need for mechanical ventilation. Patient 6, a 44year-old male IDU, had several skin lesions at injection sites on his arms, but no abscesses. He received antitoxin treatment within several hours of admission and was discharged with minimal residual neck weakness after 7 days. Serum specimens were obtained from patients 1, 2, 5, and 6. Botulinum toxin detected by the mouse bioassay in serum of patients 1 and 2, but not of patients 5 and 6, was neutralized by polyvalent antitoxin (Novartis Behring, Marburg, Germany). Abscess specimens were available from patients 2, 3, and 4. Anaerobic cultures grew C. botulinum, which was identifi ed by Gram stain, culture morphologic features, Rapid ID 32A (bioMérieux, Marcy l’Etoile, France), and 16S rDNA sequencing. All strains were susceptible to penicillin G and metronidazole, as determined by the E-test (AB Biodisk, Solna, Sweden). PCR assays performed for C. botulinum type A, B, E, and F neurotoxin genes (6,7) identifi ed the single toxin B. Toxin B production was confi rmed by the mouse bioassay. Pulsed-fi eld gel electrophoresis (PFGE) after SmaI, SacII, and XhoI restriction (8) showed indistinguishable strains from patients 2, 3, and 4 (shown for SmaI in the Figure). To our knowledge, this is the fi rst outbreak of wound botulism in IDUs that was confi rmed by molecular epidemiologic typing. PFGE suggests a