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Journal of Clinical Microbiology, December 2003, p. 5741, Vol. 41, No. 12
0095-1137/03/$08.00+0 DOI: 10.1128/JCM.41.12.5741.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.
Cystic Fibrosis Unit, Department of Respiratory Medicine, Royal Children's Hospital,1 Department of Respiratory and Sleep Medicine, Monash Medical Centre, Melbourne, Australia2
Received 14 July 2003/ Returned for modification 25 July 2003/ Accepted 27 August 2003
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Case report. A 14-year-old boy with a history of long-segment esophageal atresia repair complicated by long-standing esophageal dysmotility was found by a high-resolution computed tomography scan, at 9 years, to have regional bronchiectasis involving the right middle and lower lobes bilaterally. The bronchiectasis was associated with an increased number of respiratory exacerbations requiring periods of hospitalization for intravenous antibiotic therapy and aggressive chest physiotherapy. At 9 years, his first admission for treatment of a respiratory exacerbation was to a general medical ward. No CF patients were nursed on this ward. He received six more treatment periods on this ward over the next 2 years. Sputum culture grew Streptococcus pneumoniae on one occasion. No other bacterial pathogens were identified. At age 12.3 years, he was admitted to the adolescent ward for a further period of in-hospital treatment. Sputum culture on admission did not grow any bacterial pathogens. During this admission, he was nursed in a six-bed room in which four patients with CF were being nursed. All four CF patients had our epidemic strain of P. aeruginosa in their sputum. He attended physiotherapy with these CF patients. He was readmitted for a further period of in-hospital treatment 6 weeks later. On admission, P. aeruginosa was recovered from his sputum, subsequently shown by bacterial genotyping to be identical to the epidemic strain previously reported in our CF population (1). A sweat test performed was normal, and analysis of his blood for the 17 commonest CF genes found in the Australian population did not identify any CF genes. Since the identification of P. aeruginosa in his sputum, he has struggled to maintain his baseline lung function and respiratory status and has had frequent admissions for intravenous antibiotic therapy and physiotherapy. At his last admission in Feb 2003, his forced expiratory volume in the first second was 23.8% predicted. He is currently being evaluated for lung transplantation.
Implications for patient care. The recent ability to identify, through DNA typing, the passage of bacterial pathogens, in particular P. aeruginosa, between patients with CF has led to a major alteration in clinical practice in many CF centers. Infection control practices have led to cohorting at various clinical levels, including inpatient housing and physiotherapy sessions as well as outpatient-based services such as outpatient clinics and educational sessions. This present report suggests that in centers where epidemic strains of P. aeruginosa may be present, these cohorting practices may need to be extended to include the larger group of respiratory patients with underlying suppurative lung disease. Pediatric respiratory medicine involves the care of patients with chronic lung disease from various causes, such as bronchiectasis from recurrent aspiration and inhalation burns as well as generalized conditions including inherited or medically induced immune suppression states. Traditionally, P. aeruginosa is an uncommon lower airway pathogen in these persons. This present report, however, suggests that cross-infection from P. aeruginosa-positive CF patients to patients with underlying non-CF lung disease can occur in the presence of an epidemic strain of P. aeruginosa.
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