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Plasmid Analysis of Simultaneous Nosocomial Outbreaks of Methicillin-Resistant Staphylococcus aureus

Published online by Cambridge University Press:  02 January 2015

Phyllis E. Kozarsky ,
David Rimland ,
Pamela M. Terry  and
Kaye Wachsmuth
Phyllis E. Kozarsky
Affiliation:
Division of Infectious Diseases, Department of Medicine, Emory University School of Medicine; Medical Service, Veterans Administration Medical Center; Biotechnology Branch, Center for Infectious Diseases, Centers for Disease Control, Atlanta, Georgia
David Rimland*
Affiliation:
Division of Infectious Diseases, Department of Medicine, Emory University School of Medicine; Medical Service, Veterans Administration Medical Center; Biotechnology Branch, Center for Infectious Diseases, Centers for Disease Control, Atlanta, Georgia
Pamela M. Terry
Affiliation:
Division of Infectious Diseases, Department of Medicine, Emory University School of Medicine; Medical Service, Veterans Administration Medical Center; Biotechnology Branch, Center for Infectious Diseases, Centers for Disease Control, Atlanta, Georgia
Kaye Wachsmuth
Affiliation:
Division of Infectious Diseases, Department of Medicine, Emory University School of Medicine; Medical Service, Veterans Administration Medical Center; Biotechnology Branch, Center for Infectious Diseases, Centers for Disease Control, Atlanta, Georgia
*
Medical Service, V.A. Medical Center, 1670 Clairmont Road, Decatur, GA 30033
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Abstract

A large outbreak of infections caused by methicillin and aminoglycoside resistant Staphylococcus aureus provided the opportunity to evaluate mechanisms of resistance and compare the usefulness of typing systems. Between January 1979 and December 1980, 63 patients developed infections with S aureus resistant to multiple antibiotics, including methicillin and tobramycin. All isolates had an identical antibiogram and were phage type 47/54/75/77/83A. Beginning in January 1981, a superimposed outbreak caused by S aureus of the same phage type but with a resistance pattern now including gentamicin occurred. The two strains contained different aminoglycoside inactivating enzymes. The initial strain contained a single plasmid of 21.5 mDa molecular weight, whereas the subsequent strain which had acquired gentamicin resistance contained this plasmid plus a heavier one of 33 mDa. Plasmid analysis complements the analysis of antibiograms and phage types and aids in defining epidemiologic patterns of transmission.

Type
Original Articles
Information
Infection Control & Hospital Epidemiology , Volume 7 , Issue 12 , December 1986 , pp. 577 - 581
Copyright
Copyright © The Society for Healthcare Epidemiology of America 1986

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