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Journal of Clinical Microbiology, October 2006, p. 3623-3627, Vol. 44, No. 10
0095-1137/06/$08.00+0 doi:10.1128/JCM.00699-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.
Occurrence of Carbapenem-Resistant Acinetobacter baumannii Clones at Multiple Hospitals in London and Southeast England
Juliana M. Coelho,1,
Jane F. Turton,2
Mary E. Kaufmann,2
Judith Glover,2
Neil Woodford,1
Marina Warner,1
Marie-France Palepou,1
Rachel Pike,1
Tyrone L. Pitt,2
Bharat C. Patel,3 and
David M. Livermore1*
Antibiotic Resistance Monitoring and Reference Laboratory,1
Laboratory of Healthcare Associated Infection, Centre for Infections, Health Protection Agency, 61 Colindale Avenue, London NW9 5EQ, United Kingdom,2
Health Protection Agency Collaborating Centre, Microbiology Department, North Middlesex University Hospital, Sterling Way, London N18 1QX, United Kingdom3
Received 3 April 2006/
Returned for modification 29 June 2006/
Accepted 29 July 2006
From late 2003 to the end of 2005, the Health Protection Agency's national reference laboratories received approximately 1,600 referrals of Acinetobacter spp., including 419 and 58 examples, respectively, of two carbapenem-resistant Acinetobacter baumannii lineages, designated OXA-23 clones 1 and 2. Representatives of these clones were obtained from 40 and 8 hospitals, respectively, in London or elsewhere in Southeast England. Both clones had blaOXA-23-like genes, as well as the intrinsic (but downregulated) blaOXA-51-like carbapenemase genes typical of A. baumannii. Both were highly multiresistant: only colistin and tigecycline remained active versus OXA-23 clone 1 isolates; OXA-23 clone 2 isolates were also susceptible to amikacin and minocycline. These lineages increase the burden created by the southeast (SE) clone, a previously reported A. baumannii lineage with variable carbapenem resistance contingent on upregulation of the blaOXA-51-like gene. Known since 2000, the SE clone had been referred from over 40 hospitals by the end of 2005, with 627 representatives received by the reference laboratories. The OXA-23 clone 2 is now in decline, but OXA-23 clone 1 continues to be referred from new sites, as does the SE clone. Their spread is forcing the use of unorthodox therapies, principally colistin and tigecycline, although the optimal regimens remain uncertain.
* Corresponding author. Mailing address: Antibiotic Resistance Monitoring and Reference Laboratory, Centre for Infections, Health Protection Agency, 61 Colindale Ave., London NW9 5HT, United Kingdom. Phone: 44(0)20-8327-7223. Fax: 44(0)20-8327-6264. E-mail:
david.livermore{at}hpa.org.uk.
Present address: National Bacteriology Laboratory, National Blood Service, Colindale Ave., Colindale, London NW9 5BG, United Kingdom.
Journal of Clinical Microbiology, October 2006, p. 3623-3627, Vol. 44, No. 10
0095-1137/06/$08.00+0 doi:10.1128/JCM.00699-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.
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