Previous Article | Next Article 
Journal of Clinical Microbiology, March 2004, p. 992-995, Vol. 42, No. 3
0095-1137/04/$08.00+0 DOI: 10.1128/JCM.42.3.992-995.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.
Molecular Epidemiology of Coagulase-Negative Staphylococci Causing Sepsis in a Neonatal Intensive Care Unit over an 11-Year Period
Tannette G. Krediet,1* Ellen M. Mascini,2 Ellen van Rooij,1,2 Judith Vlooswijk,2 Armand Paauw,2 Leo J. Gerards,1 and André Fleer1,2
Department of Neonatology, Wilhelmina Children's Hospital,1
Eijkman-Winkler Institute for Microbiology, Infectious Diseases, and Inflammation, University Medical Center, Utrecht, The Netherlands2
Received 10 March 2003/
Returned for modification 23 April 2003/
Accepted 10 November 2003
Coagulase-negative staphylococci (CoNS) are the major causative microorganisms in neonatal nosocomial sepsis. Previous studies have shown that CoNS sepsis in the neonatal intensive care unit (NICU) is caused by predominant molecular types that are widely distributed among both neonates and staff. Some of these molecular types may persist in the NICU for years. The purpose of the present study was to determine the dynamic behavior of CoNS strains causing sepsis over a prolonged period of time by determining the molecular types of all blood isolates from septicemic infants over a period of 11 years (1991 to 2001). The results show that neonatal CoNS sepsis is increasingly caused by a few predominant molecular clusters. The most striking finding was that in recent years one molecular cluster emerged as the predominant cause of neonatal CoNS sepsis, responsible for no less than 31% (20 of 65) of blood isolates in 2001. Antibiotic resistance, particularly beta-lactam resistance, is probably an important selective force considering the high mecA gene carriage of CoNS blood isolates (70 to 92%). We conclude that neonatal CoNS sepsis is increasingly caused by a limited number of predominant molecular CoNS types and that antibiotic resistance is probably a major selective force.
* Corresponding author. Mailing address: Dept. of Neonatology, Room KE 04.123.1, Wilhelmina Children's Hospital, University Medical Center, P.O. Box 85090, 3508 AB Utrecht, The Netherlands. Phone: 31 30 2504545. Fax: 31 30 2505320. E-mail:
t.krediet{at}wkz.azu.nl.
Journal of Clinical Microbiology, March 2004, p. 992-995, Vol. 42, No. 3
0095-1137/04/$08.00+0 DOI: 10.1128/JCM.42.3.992-995.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.
This article has been cited by other articles:
-
Muldrew, K. L., Tang, Y.-W., Li, H., Stratton, C. W.
(2008). Clonal Dissemination of Staphylococcus epidermidis in an Oncology Ward. J. Clin. Microbiol.
46: 3391-3396
[Abstract]
[Full Text]
-
Wu, Y.-D., Chen, L.-H., Wu, X.-J., Shang, S.-Q., Lou, J.-T., Du, L.-Z., Zhao, Z.-Y.
(2008). Gram Stain-Specific-Probe-Based Real-Time PCR for Diagnosis and Discrimination of Bacterial Neonatal Sepsis. J. Clin. Microbiol.
46: 2613-2619
[Abstract]
[Full Text]
-
Mombach Pinheiro Machado, A. B., Reiter, K. C., Paiva, R. M., Barth, A. L.
(2007). Distribution of staphylococcal cassette chromosome mec (SCCmec) types I, II, III and IV in coagulase-negative staphylococci from patients attending a tertiary hospital in southern Brazil. J Med Microbiol
56: 1328-1333
[Abstract]
[Full Text]
-
Widerstrom, M., Wistrom, J., Ferry, S., Karlsson, C., Monsen, T.
(2007). Molecular Epidemiology of Staphylococcus saprophyticus Isolated from Women with Uncomplicated Community-Acquired Urinary Tract Infection. J. Clin. Microbiol.
45: 1561-1564
[Abstract]
[Full Text]
-
Chaves, F., Garcia-Alvarez, M., Sanz, F., Alba, C., Otero, J. R.
(2005). Nosocomial Spread of a Staphylococcus hominis subsp. novobiosepticus Strain Causing Sepsis in a Neonatal Intensive Care Unit. J. Clin. Microbiol.
43: 4877-4879
[Abstract]
[Full Text]
-
Heikens, E., Fleer, A., Paauw, A., Florijn, A., Fluit, A. C.
(2005). Comparison of Genotypic and Phenotypic Methods for Species-Level Identification of Clinical Isolates of Coagulase-Negative Staphylococci. J. Clin. Microbiol.
43: 2286-2290
[Abstract]
[Full Text]