Abstract
Methicillin-resistant Staphylococcus aureus (MRSA) and non-aureus staphylococci (MRNAS) cause different infections in animals, including mastitis, in livestock and humans. This study aimed to identify and compare the staphylococcal chromosome cassette mec (SCCmec) types of MRSA or MRNAS isolated from several animal species and humans in different countries. Of 1462 S. aureus and non-aureus staphylococci, 68 grew on Chrom MRSA ID® agar, were phenotypically resistant to cefoxitin and tested positive with the PCR for the mecA gene. These 60 MRSA and 8 MRNAS were isolated in Belgium mainly from cows (livestock-associated (LA) MRS) and humans (community-acquired (CA) MRS) and in Japan from dogs and cats. The SCCmec cassettes were identified by multiplex PCR in 52 MRSA and 7 MRNAS and by whole genome sequencing (WGS) in 8 additional MRSA. The SCCmec types IV and V were the most frequent in Belgian LA-MRS and CA-MRS, while the SCCmec type II was identified in four of the five Japanese MRSA. The remaining isolate was a bovine S. haemolyticus in which no SCCmec was identified. These results confirm the high prevalence of the SCCmec types IV and V in LA-MRS and CA-MRS in Belgium, emphasizing the possible public health hazard of the former, and the absence of SCCmec in some MRNAS.
Highlights
Concentration) test strips and mecA PCR-positive. These 68 mecA-positive staphylococci were isolated from cows, boar, horses, humans, fomites, dogs and cats in Belgium and
The multiplex PCR (mPCR) results gave a perfect match with expected amplification results (Table 2) for 52 methicillin-resistant Staphylococcus aureus (MRSA) and 7 methicillin-resistant non-aureus staphylococci (MRNAS), while the results were equivocal for 8 MRSA and 1 MRNAS
A final identification of the staphylococcal chromosome cassette mec (SCCmec) in these eight MRSA was obtained by Whole Genome Sequencing (WGS) but not in the MRNAS
Summary
The history of methicillin-resistant Staphylococcus aureus (MRSA) began in 1961 following the development and marketing in 1959 of the methicillin antibiotic, a semisynthetic penicillin that is resistant to the activity of the β-lactamase (BlaZ) enzyme from S. aureus (SA) [1]. The mechanism of resistance of these first MRSA was not the production of any mutant Bla enzyme, but the synthesis of a β-lactam-resistant penicillin-binding protein (PBP2a), a transpeptidase involved in the bacterial cell wall formation, encoded by a newly acquired and chromosome-located mec gene [2,3]. The first MRSA were isolated from hospitalized human patients with nosocomial infections (hospital-acquired MRSA or HAMRSA). During the 1990s, community-acquired MRSA strains (CA-MRSA) progressively emerged in humans with no history of hospitalization. Though the first reported animal MRSA was isolated in 1972 from the milk of a cow with mastitis [5], they emerged in the early
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