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Clin Microbiol Infect. 1997 Aug;3(4):414-422.

Increasing incidence and widespread dissemination of methicillin-resistant Staphylococcus aureus (MRSA) in hospitals in central Europe, with special reference to German hospitals.

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1
Robert Koch Institute, Wernigerode Branch, Wernigerode, and.

Abstract

OBJECTIVE:

to present data on prevalence and interregional spread of methicillin-resistant Staphylococcus aureus (MRSA) in Germany.

METHODS:

A nationwide collection of MRSA isolates from nosocomial infections in 143 hospitals was established from isolates (n=4368) sent to a microbiological reference center during 1993--95. As chosen by distinguishable resistance phenotypes at each time of occurrence during the study period, 1830 isolates were subjected to molecular typing by means of Smal macrorestriction patterns, PCR for RNA gene spacer patterns, and PCR for patterns of DNA stretches flanked by the ERIC-2 sequence and flanked by Tn916 and ribosomal binding site. In addition, data from a multicenter study on the incidence of antibiotic resistance have been analyzed (32 centers, 637 S. aureus isolates).

RESULTS:

In 1995 the prevalence of MRSA among S. aureus isolates was 8.7% overall in central Europe (including Germany), in comparison to 1.7% in 1990. From 1993 until now, a continuous interregional dissemination of six epidemic strains, which were identified by molecular typing, was recorded. Besides these epidemic strains, 15 MRSA strains were identified which could not be allocated to the epidemic MRSA or to the known clonal groups of the species S. aureus. MRSA from three cases of sporadic nosocomial infections exhibited characteristics of the clonal group of S. aureus with the capacity for toxic shock syndrome formation. The pattern of one MRSA corresponded to those of the S. aureus group exhibiting phage pattern 94,96.

CONCLUSIONS:

The prevalence of MRSA has increased in central Europe (and Germany) during the last 5 years, to 8.7%. The main source of infection with MRSA is obviously interregional dissemination of epidemic strains. At the same time, the mecA gene has been acquired by strains previously sensitive to methicillin.

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