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Molecular Epidemiology of Serratia marcescens Outbreaks in Two Neonatal Intensive Care Units

Published online by Cambridge University Press:  02 January 2015

Vladana Milisavljevic ,
Fann Wu ,
Elaine Larson ,
David Rubenstein ,
Barbara Ross ,
Lewis M. Drusin ,
Phyllis Della-Latta  and
Lisa Saiman
Vladana Milisavljevic
Affiliation:
Department of Pediatrics, Columbia University, New York, New York
Fann Wu
Affiliation:
Department of Pathology, Columbia University, New York, New York
Elaine Larson
Affiliation:
School of Nursing, Columbia University, New York, New York
David Rubenstein
Affiliation:
Department of Pediatrics, Columbia University, New York, New York
Barbara Ross
Affiliation:
Department of Epidemiology, New York-Presbyterian Hospital, Weill Cornell Center, New York, New York
Lewis M. Drusin
Affiliation:
Department of Epidemiology, New York-Presbyterian Hospital, Weill Cornell Center, New York, New York Departments of Public Health andMedicine at Cornell University, New York, New York
Phyllis Della-Latta
Affiliation:
Department of Pathology, Columbia University, New York, New York
Lisa Saiman*
Affiliation:
Department of Pediatrics, Columbia University, New York, New York Department of Epidemiology, New York-Presbyterian Medical Center, New York, New York
*
LS5@columbia.edu
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Abstract

Objective:

Serratia marcescens can cause serious infections in patients in neonatal intensive care units (NICUs), including sepsis, pneumonia, urinary tract infection, and conjunctivitis. We report the utility of genetic fingerprinting to identify, investigate, and control two distinct outbreaks of S. marcescens.

Design:

An epidemiologic investigation was performed to control two clusters of S. marcescens infections and to determine possible routes of transmission. Molecular typing by pulsed-field gel electrophoresis determined the relatedness of S. marcescens strains recovered from neonates, the environment, and the hands of healthcare workers (HCWs).

Setting:

Two geographically distinct level III-IV NICUs (NICU A and NICU B) in two university-affiliated teaching hospitals in New York City.

Results:

In NICU A, one major clone, “F,” was detected among isolates recovered from four neonates and the hands of one HCW. A second predominant clone, “A,” was recovered from four sink drains and one rectal surveillance culture from an asymptomatic neonate. In NICU B, four neonates were infected with clone “D,” and three sink drains harbored clone “H.” The attributable mortality rate from bloodstream infections was 60% (3 of 5 infants). The antimicrobial susceptibilities of clone F strains varied for amikacin, cefepime, and piperacillin/tazobactam.

Conclusions:

S. marcescens causes significant morbidity and mortality in preterm neonates. Cross-transmission via transient hand carriage of a HCW appeared to be the probable route of transmission in NICU A. Sinks did not harbor the outbreak strains. Antimicrobial susceptibility patterns did not prove to be an accurate predictor of strain relatedness for S. marcescens.

Type
Original Articles
Information
Infection Control & Hospital Epidemiology , Volume 25 , Issue 9 , September 2004 , pp. 719 - 722
Copyright
Copyright © The Society for Healthcare Epidemiology of America 2004

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