H Alfizah1, A J Nordiah, W S Rozaidi. 1. Department of Medical Microbiology and Immunology, Faculty of Medicine, National University of Malaysia, Jalan Yaacob Latif, Bandar Tun Razak, 56000 Cheras, Kuala Lumpur, Malaysia. alfizah@mail.hukm.ukm.my
Abstract
INTRODUCTION: Serratia marcescens is a well-known cause of nosocomial infections and outbreaks, particularly in immunocompromised patients with severe underlying disease. An outbreak due to S. marcescens infection was detected from 13 to 22 February 2001 at the intensive care unit (ICU) of our institution. We used pulsed-field gel electrophoresis (PFGE) typing to analyse the outbreak strains involved. METHODS: A total of 25 isolates were included in this study: 12 isolates from infected patients, nine isolates from insulin solution, one isolate from sedative solution (midazolam and morphine infusion) and one isolate from frusemide solution. Two isolates from other wards which were epidemiologically-unrelated were also included. RESULTS: The S. marcescens from patients, insulin solution and sedative solution showed an identical PFGE fingerprint pattern. The isolate from the frusemide solution had a closely-related PFGE pattern to the outbreak strain with one band difference. Attempts were made in the present study to identify the environmental reservoir of S. marcescens during the outbreak. We found that the insulin and sedative solutions used by the patients were contaminated with S. marcescens which was proven to be the source of the outbreak. CONCLUSION: Using PFGE, we showed that the outbreak in the ICU of our hospital was due to the clonal spread of a single strain of S. marcescens.
INTRODUCTION:Serratia marcescens is a well-known cause of nosocomial infections and outbreaks, particularly in immunocompromised patients with severe underlying disease. An outbreak due to S. marcescens infection was detected from 13 to 22 February 2001 at the intensive care unit (ICU) of our institution. We used pulsed-field gel electrophoresis (PFGE) typing to analyse the outbreak strains involved. METHODS: A total of 25 isolates were included in this study: 12 isolates from infectedpatients, nine isolates from insulin solution, one isolate from sedative solution (midazolam and morphine infusion) and one isolate from frusemide solution. Two isolates from other wards which were epidemiologically-unrelated were also included. RESULTS: The S. marcescens from patients, insulin solution and sedative solution showed an identical PFGE fingerprint pattern. The isolate from the frusemide solution had a closely-related PFGE pattern to the outbreak strain with one band difference. Attempts were made in the present study to identify the environmental reservoir of S. marcescens during the outbreak. We found that the insulin and sedative solutions used by the patients were contaminated with S. marcescens which was proven to be the source of the outbreak. CONCLUSION: Using PFGE, we showed that the outbreak in the ICU of our hospital was due to the clonal spread of a single strain of S. marcescens.
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