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Journal of Clinical Microbiology, February 2007, p. 529-535, Vol. 45, No. 2
0095-1137/07/$08.00+0 doi:10.1128/JCM.01444-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.
Therapeutic Development Network Core Laboratory for Cystic Fibrosis Microbiology,1 Microbiology Laboratory, Department of Laboratories and Pathology, Children's Hospital and Regional Medical Center,2 Division of Infectious Diseases, Immunology and Rheumatology, Department of Pediatrics,3 Department of Laboratory Medicine, University of Washington School of Medicine, Seattle, Washington4
Received 12 July 2006/ Returned for modification 11 September 2006/ Accepted 15 November 2006
Cystic fibrosis (CF) patients are predisposed to chronic respiratory infection by nonfermentative gram-negative bacilli, including Stenotrophomonas maltophilia. S. maltophilia is highly resistant to most antibiotics, with the exception of sulfamethoxazole-trimethoprim (SXT). SXT-resistant S. maltophilia has been reported, but the mechanism of resistance is not well defined. Repeated findings of suspected small-colony-variant (SCV) S. maltophilia isolates from the sputa of five CF patients were confirmed by partial 16S rRNA gene sequencing. The SCV S. maltophilia isolates were the only S. maltophilia isolates in these cultures, and none were clonally related. DNA fingerprint analysis confirmed that once established, the SCV S. maltophilia strains persisted. Nutritional studies of SCV S. maltophilia have suggested auxotrophy in hemin, methionine, and thymidine associated with resistance to multiple antibiotics, including SXT. The phenotypic switch from wild-type to SCV S. maltophilia was reproducible in vitro by exposure to SXT, suggesting that prolonged exposure to antibiotics may select for both the SCV S. maltophilia phenotype and SXT resistance by interference with the dihydrofolate reductase pathway. Recovery of SCV S. maltophilia from the sputum of CF patients has implications for both laboratory testing and patient management.
Published ahead of print on 29 November 2006.
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