Klin Padiatr 2015; 227(04): 232-233
DOI: 10.1055/s-0035-1548748
Short Communication
© Georg Thieme Verlag KG Stuttgart · New York

Purulent Bronchitis Caused by Staphylococcus aureus in an Adolescent Receiving Infliximab for Crohn’s Disease

Eitrige Bronchitis durch Staphylococcus aureus bei einem Jugendlichen unter Infliximab-Therapie eines Morbus Crohn
D. Schöndorf
,
P. Hennes
,
K. Rentz
,
S. L. Becker
,
G. Schneider
,
T. Rohrer
,
L. Gortner
Further Information

Publication History

Publication Date:
14 April 2015 (online)

Case report

We report the clinical course of a boy who was diagnosed with Crohn’s disease (CD) at the age of 10 years, when he presented with complex perianal fistulae and abscesses, diarrhea and failure to thrive. Except for mild atopic dermatitis, the patient’s medical and family history was unremarkable. Abdominal magnetic resonance imaging was performed and revealed a non-stenotic, contrast-enhancing inflammation of the jejunum and the ileum. Gastrointestinal endoscopy showed an ulcerated intestinal mucosa, but no granulomas were seen on histologic examination. After the diagnosis of CD had been established, extensive diagnostic work-up excluded extra-intestinal disease manifestations. Following recommendations for the management of perianal CD (de Zoeten EF et al. Pediatr Gastroenterol Nutr 2013; 57: 401–412), the patient was treated with a single course of prednisolone and subsequent therapy with infliximab (maintenance of remission with one cycle every 8 weeks). No adverse effects were noted and no relapse occurred. However, at the age of 13 years, the patient repeatedly experienced episodes of abdominal pain and diarrhea 2 weeks prior to the next scheduled infusion. Hence, the interval between infliximab infusions was shortened from 8 to 6 weeks.

One year later, when the patient had received a total of 32 infliximab treatment cycles, he developed a productive cough, but no fever. Thoracic imaging studies (X-ray, computed tomography, magnetic resonance) identified a solitary nodule (7 mm in diameter) in the inferior lobe of the right lung ([Fig. 1] [2]). A connection to the bronchial tree was not detected, and there were no further signs of inflammation or lung disease. The initial differential diagnosis included pulmonary tuberculosis, other infectious etiologies, chronic granulomatous disorders and immunoglobulin deficiencies. However, repeated interferon-gamma release assays for the detection of Mycobacterium tuberculosis were negative, chronic granulomatous disorder and immunoglobulin deficiency were excluded. In addition, angiotensin converting enzyme and flow cytometric analysis of the peripheral blood yielded normal results. Iontophoretic sweat test, pulmonary function and echocardiogram were normal. Fecal calprotectin (normal value<50 µg/g) was slightly elevated (631.4 µg/g) compared to the patient’s baseline (500 µg/g), but there were no clinical or sonographic signs of increased intestinal inflammation.

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Fig. 1 Thoracic CT after intravenous application of contrast agent: Solitary nodule marked by arrow.
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Fig. 2 Thoracic MRI (T2 HASTE): Solitary nodule marked by arrow.

Diagnostic bronchoscopy was performed and demonstrated an inflamed mucosa, slightly dilatated bronchi – a preliminary stage of bronchiectasis – and pus in segment 9 of the right inferior pulmonary lobe. Cytologic analysis of bronchoalveolar lavage fluid revealed severe inflammation with a predominance of segmented granulocytes and low lymphocyte and alveolar macrophage counts. Methicillin-sensitive Staphylococcus aureus (MSSA) was isolated from the bronchial specimen. Despite extensive microbiological testing, including several culture techniques and a variety of specific polymerase chain reaction assays, no other bacterial (e. g., Legionella pneumophila), fungal (e. g., Aspergillus spp., Pneumocystis jiroveci), mycobacterial (e. g., M. tuberculosis, atypical mycobacteria), or viral pathogens (e. g., adenovirus, cytomegalovirus) were detected.

Based on the antimicrobial susceptibility pattern, the patient’s purulent bronchitis was treated with intravenous flucloxacillin for 3 weeks, followed by oral administration for another 3 weeks. The infliximab treatment was continued at intervals of 6 weeks due to the continued intestinal remission. Thoracic follow-up imaging confirmed that the development of bronchiectasis could be prevented, while the previously described pulmonary nodule, which was subsequently interpreted as hamartoma, was still present.