Propionibacterium propionicus infection in chronic granulomatous disease.

Correspondence Propionibacterium propionicus Infection in Chronic Granulomatous Disease Sir—Bourdeaut et al. [1] recently described 2 pediatric patients with chronic granulomatous disease (CGD) who developed chest infections caused by Pro-pionibacterium acnes. We describe a 7-year-old boy with CGD who developed a Propionibacterium propionicus infection. CGD is an inherited disease caused by defects in superoxyde-generating nicotin-amide adenine dinucleotide phosphate oxidase of phagocytes [2]. Impairment of oxygen-dependent intracellular killing mechanisms results in severe infections with catalase-producing Staphylococcus aureus, Burkholderia cepacia, or Aspergil-lus species [3]. In our patient, CGD was diagnosed at 3 months of age after an episode of sup-purative cervical lymphadenitis. X-linked inheritance of CGD was supported by the finding of intermediate values with the ni-troblue-tetrazolium (NBT) test (47% of neutrophils were NBT positive) of a blood sample from the patient's mother. He was given prophylactic cotrimoxazole; he was free of major infections. At 7 years of age, he was admitted to our institute because of chest-wall contusion. At admission he was febrile (temperature, 39ЊC) and tach-ydispneic (respiration rate, 50 breaths/ min). Laboratory values were as follows: erythrocyte sedimentation rate, 84 mm/h; hemoglobin, 147 g/L; WBC count, 52.0 ϫ 10 9 cells/L, with 45.2 ϫ 10 9 neutro-phils/L; C-reactive protein, 237 mg/L (normal range, !10 mg/L). Chest radiography revealed a left-side pleural effu-sion. A thoracic CT scan showed microab-scesses of the left lower lobe. Chest drainage yielded 300 mL of fibrinous ex-udate. Empirical antibiotic treatment with tobramycin and ceftazidime was started. The patient became afebrile 48 h later but pleural effusion persisted, and a thoracot-omy was perfomed 2 weeks later. Pathological examination of the lung tissue specimen revealed microabscesses and granulomatous inflammation. Results of staining for mycobacteria and fungi were negative. Direct Gram staining of pleural fluid and lung biopsy specimens revealed non–acid-fast, gram-positive filamentous rods identified as P. propionicum. Isolates were sensitive to penicillin, cephalospo-rins, and vancomycin. We continued treatment with penicillin, and complete clinical remission was achieved 1 month later. The most common causes of pneu-monitis in patients with CGD are Aspergillus and Nocardia species and Burkholderia cepacia [3]. However, various opportunistic, catalase-producing microbes may infect patients with CGD [2, 3]. P. propionicus is a less common caus-ative agent of a disease similar to actino-mycosis [4]. Thoracic actinomycosis results from aspiration of pieces of infectious material from the teeth and may involve the chest wall, the lungs, or both. Intact mucosa are the first line of defense, because P. propionicus, …