Journal Article

Molecular Epidemiology and Mechanisms of Carbapenem Resistance in <i>Acinetobacter baumannii</i> Endemic in New York City

John Quale, Simona Bratu, David Landman and Renuka Heddurshetti

in Clinical Infectious Diseases

Published on behalf of Infectious Diseases Society of America

Volume 37, issue 2, pages 214-220
Published in print July 2003 | ISSN: 1058-4838
Published online July 2003 | e-ISSN: 1537-6591 | DOI: http://dx.doi.org/10.1086/375821
Molecular Epidemiology and Mechanisms of Carbapenem Resistance in Acinetobacter baumannii Endemic in New York City

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Multidrug-resistant Acinetobacter baumannii has emerged as a serious nosocomial pathogen in certain areas. In Brooklyn, New York, citywide surveillance revealed that ∼2 of every 3 isolates were resistant to carbapenem antibiotics. Genetic fingerprinting revealed that 2 strains accounted for 82% of these resistant isolates. Compared with carbapenem-susceptible isolates, carbapenem-resistant isolates had reduced expression of 47-, 44-, and 37-kDa outer-membrane proteins. No specific carbapenemase was found; however, carbapenem-resistant isolates expressed greater levels of a class C cephalosporinase. Although expression of penicillin-binding proteins varied among strains, no consistent pattern appeared to account for carbapenem resistance. An efflux pump, present in several strains, did not appear to contribute to carbapenem resistance. Clonal spread of carbapenem-resistant A. baumannii has occurred in hospitals in Brooklyn. The preliminary findings for a small number of strains suggest that diminished production of outer-membrane porins, together with increased expression of a class C cephalosporinase, appear to be important factors leading to carbapenem resistance in this region.

Journal Article.  3728 words.  Illustrated.

Subjects: Infectious Diseases ; Immunology ; Public Health and Epidemiology ; Microbiology

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