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Journal of Clinical Microbiology, April 2002, p. 1188-1193, Vol. 40, No. 4
0095-1137/02/$04.00+0 DOI: 10.1128/JCM.40.4.1188-1193.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.
Kathy Hohneker,2 Charlene Carriker,3 Kelly Smith,1 Jonathan Routh,1 John J. LiPuma,4 Robert M. Aris,2 David Weber,2,3,5 and Peter H. Gilligan1,6*
Clinical Microbiology-Immunology Laboratories,1 Department of Hospital Epidemiology, University of North Carolina Hospitals,3 Microbiology-Immunology,6 Medicine,2 Pediatrics, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina,5 Department of Pediatrics and Communicable Diseases, The University of Michigan, Ann Arbor, Michigan4
Received 28 June 2001/ Returned for modification 26 October 2001/ Accepted 24 December 2001
Over a 6-year period, Burkholderia cepacia complex species were isolated from cystic fibrosis (CF) patients receiving care at The University of North Carolina Hospitals (clinic CF patients) and from those referred from other treatment centers. Fifty-six isolates collected from 30 referred patients and 26 clinic CF patients were characterized by pulsed-field gel electrophoresis (PFGE) and were assayed by PCR to detect the cable pilin gene, cblA. PFGE results indicated that six separate clusters (clusters A to F) were present among the 56 isolates and that three clusters (clusters A, B, and E) consisted only of isolates from referred patients infected with B. cepacia complex isolates prior to referral. However, one cluster (cluster C) consisted of isolates from four CF patients, and hospital records indicate that this cluster began with an isolate that came from a referred patient and that spread to three clinic CF patients. Cluster D consisted of two isolates from clinic CF patients, and hospitalization records are consistent with nosocomial, patient-to-patient spread. cblA was present in only 4 of the 56 isolates and included isolates in cluster E from the referred patients. Our results indicate a lack of spread of a previously characterized, transmissible clone from referred patients to our clinic CF population. Only two instances of nosocomial, patient-to-patient spread could be documented over the 6-year period. An additional spread of an isolate (cluster F) from a referred patient to a clinic patient could not be documented as nosocomial and may have been the result of spread in a nonhospitalized setting. The majority (36 of 56) of our B. cepacia complex-infected CF patients harbor isolates with unique genotypes, indicating that a diversity of sources account for infection. These data suggest that CF patients infected with B. cepacia complex and referred for lung transplantation evaluation were not a major source of B. cepacia complex strains that infected our resident CF clinic population.
Present address: Department of Pathology and Area Laboratory Services, Landstuhl Regional Medical Center, Landstuhl, Germany.
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