M ethicillin-resistant Staphylococcus aureus (MRSA) is characterized by the mainly clonal structure of bacterial populations and the worldwide spread of a few highly successful lineages, sequence types (STs), and clonal complexes (CCs) that cycle through waves of dominance (1,2). During the late 1990s, the Brazilian endemic clone (BEC), which belongs to the ST239(CC8)-staphylococcal cassette chromosome (SCC) mecIII lineage, comprised ≈80% of MRSA isolates in hospitals in Brazil (3). In the 2000s, isolates of the ST1(CC1)-SCCmecIV lineage supplanted BEC in >2 hospitals in the Rio de Janeiro metropolitan area of Brazil (4). More recent analyses have suggested that CC5 isolates might be increasing in prevalence in Brazil (5).Most studies on the molecular epidemiology of MRSA in Brazil have analyzed a small number of isolates from a limited number of hospitals (5-9). We used molecular and genomic approaches to characterize 600 MRSA isolates collected from 51 hospitals in the Rio de Janeiro metropolitan area and identifi ed a novel MRSA clone of ST105-SCCmecII spa t002 (ST105-SCCmecII-t002), which we termed the Rio de Janeiro (RdJ) clone, as a predominant cause of MRSA bloodstream infections (BSIs).

We analysed the antimicrobial susceptibility, biofilm formation and genotypic profiles of 27 isolates of Staphylococcus haemolyticus obtained from the blood of 19 patients admitted to a hospital in Rio de Janeiro, Brazil. Our analysis revealed a clinical significance of 36.8% and a multi-resistance rate of 92.6% among these isolates. All but one isolate carried the mecA gene. The staphylococcal cassette chromosome mec type I was the most prevalent mec element detected (67%). Nevertheless, the isolates showed clonal diversity based on pulsed-field gel electrophoresis analysis. The ability to form biofilms was detected in 66% of the isolates studied. Surprisingly, no icaAD genes were found among the biofilm-producing isolates.

The extensive geographic spread of MRSA isolates belonging to the Brazilian epidemic clone (BEC) limited the value of pulsed-®eld gel electrophoresis (PFGE) in epidemiological studies of outbreaks caused by these strains. Thus, the discriminatory power of eight different molecular methods was evaluated in an attempt to establish a methodology for genotyping BEC isolates involved in intra-hospital outbreaks. BEC isolates from ®ve hospitals in Teresina City, Piauõ Â State were genotyped by conventional electrophoresis or PFGE of Cla I-or Sma I-digested genomic DNA hybridised with speci®c labelled mecA, Tn554, IS257 and IS256 probes. The combination of PFGE with Cla I/mecA, Cla I/Tn554, Cla I/IS257, Sma I/mecA and Sma I/IS257 probe-®ngerprinting techniques provided a very poor discriminatory power for BEC strains. Although Cla I/ IS256 ®ngerprinting discriminated 17 different polymorphisms among the isolates displaying PFGE A 1 pattern, this strategy was not reproducible. In contrast, the combination of PFGE and Sma I/IS256 polymorphisms differentiated BEC isolates into nine stable polymorphisms. Thus combination of PFGE and hybridisation with IS256 probe may be recommended as a useful means of typing BEC strains involved in intrahospital infections.