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Original Research: CYSTIC FIBROSIS |

Infection With Burkholderia cepacia Complex Bacteria and Pulmonary Exacerbations of Cystic Fibrosis*

Melissa St. Denis, BSc; Karam Ramotar, PhD; Katherine Vandemheen, BScN; Elizabeth Tullis, MD, FCCP; Wendy Ferris, MSc; Francis Chan, PhD; Craig Lee, MD; Robert Slinger, MD; Shawn D. Aaron, MD
Author and Funding Information

*From the University of Ottawa (Ms. St. Denis, Ms. Ferris, Dr. Chan, and Dr. Slinger), Ottawa, ON, Canada; The Ottawa Health Research Institute (Dr. Ramotar, Ms. Vandemheen, and Dr. Lee), Ottawa, ON, Canada; St. Michael’s Hospital (Dr. Tullis), Toronto, ON, Canada; and The Woolcock Research Institute (Dr. Aaron), Sydney, NSW, Australia.

Correspondence to: Shawn Aaron, MD, The Ottawa Hospital, General Campus, 501 Smyth Rd, Ottawa, ON, Canada, K1H 8L6; e-mail: saaron@ohri.ca



Chest. 2007;131(4):1188-1196. doi:10.1378/chest.06-2611
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Background: Studies have shown that cystic fibrosis (CF) patients who are chronically infected with Burkholderia cepacia complex bacteria may potentially acquire new strains of B cepacia. Our objective was to determine whether pulmonary exacerbations of CF are associated with acquisition of new B cepacia strains or with B cepacia strain replacement.

Methods: Thirty-six patients from seven centers who were chronically infected with B cepacia complex bacteria were prospectively followed up over a 38-month period. Patients had sputum cultures performed every 3 months while clinically stable and at the time of a pulmonary exacerbation. Each B cepacia complex isolate was speciated by polymerase chain reaction amplification of the recA gene to determine species status and was genotyped by pulsed-field gel electrophoresis to determine strain type.

Results: Thirty-five of 36 patients (97%) had chronic infection with Burkholderia cenocepacia III-A during clinical stability. All 36 patients maintained the same species and strain of B cepacia complex at the time of exacerbation as was found during clinical stability. B cepacia complex isolates retrieved during exacerbations were significantly less susceptible to ciprofloxacin, chloramphenicol, piperacillin, meropenem, and tobramycin compared to isolates retrieved from the same patients during clinical stability.

Conclusion: Adult CF patients infected with B cenocepacia maintain the same strain of B cenocepacia during exacerbations; pulmonary exacerbations are not caused by acquisition of a new B cepacia species or strain. B cepacia isolates retrieved during exacerbations may be more resistant to antibiotics.

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