Disease relevance of mecA

• The aim of the present study was to characterize clinical isolates of Staphylococcus epidermidis, one of the bacterial species most often implicated in foreign-body-associated infections, for their ability to form biofilms and for the presence of mecA and IS256 element [1].
• The mecA gene from methicillin-resistant Staphylococcus aureus 27r, which encodes the membrane-bound penicillin-binding protein 2a (PBP 2a), was cloned, sequenced, and expressed in Escherichia coli [2].
• When it was expressed in E. coli, the modified mecA gene from strain 27r encoded a water-soluble form of PBP 2a that was detectable in the cytoplasm of transformants [2].
• The in vivo expression of aap and mecA was high during early but low during late foreign body infections [3].
• SCCmec typing of a collection of 44 methicillin-resistant Staphylococcus epidermidis (MRSE) isolates recovered between 1973 and 1983 from the blood of patients with prosthetic valve endocarditis (PVE) was performed by PCR amplification of key genetic elements (mecA, mecI, IS1272, and ccrAB) [4].

High impact information on mecA

• However, mecA is not involved in the switch of expression phenotype [5].
• SCCmec is a mobile genetic element that carries the gene (mecA) mediating methicillin resistance in staphylococci [4].
• Staphylococci that acquire the mecA gene are usually resistant to beta-lactam antibiotics (methicillin or oxacillin resistance). mecA encodes a penicillin-binding protein (PBP 2a) that has a reduced affinity for beta-lactams [6].
• The discrepant results were (i) eight strains found to be positive by PCR for mecA or ermC but susceptible to the corresponding antibiotic based on disk diffusion and (ii) six strains of S. aureus found to be negative by PCR for mecA or for the four erythromycin resistance genes targeted but resistant to the corresponding antibiotic [7].
• The gyrA probe hybridized to the same SmaI DNA fragment as the mecA probe in all strains tested [8].

Chemical compound and disease context of mecA

• Lack of mecA transcription in slime-negative phase variants of methicillin-resistant Staphylococcus epidermidis [9].
• Phenotypic expression of oxacillin resistance in Staphylococcus epidermidis: roles of mecA transcriptional regulation and resistant-subpopulation selection [10].

Biological context of mecA

• DNA probes consisting of pUC19 containing cloned Staphylococcus aureus chromosomal fragments were constructed from two methicillin-resistant S. aureus strains with different DNA sequences 5' to mecA, the gene that mediates methicillin resistance [11].
• In 1992 and 1993, at The Ohio State University Medical Center, a larger proportion of Staphylococcus epidermidis strains required oxacillin MICs of 1 to 2 micrograms/ml than did Staphylococcus aureus strains. mecA genotype was correlated with antimicrobial susceptibility for selected clinical S. epidermidis strains [12].
• In the present report, we show that the regulation of methicillin resistance occurs primarily at the level of mecA transcription and that in the presence of intact plasmid pI524 or mecR, the gene undergoes negative control [13].
• Genomic diversity of mutation in the mecI gene or mecA promoter/operator region was analyzed for clinical isolates of methicillin-resistant Staphylococcus aureus (MRSA) and Staphylococcus epidermidis (MRSE) [14].
• Cloned mecA or gyrA fragments plus vector sequences each containing a SmaI site were introduced into the chromosome of three isolates each of MRSE and methicillin-resistant S. aureus (MRSA), and the sizes of the generated SmaI fragments were determined by pulsed-field gel electrophoresis [8].

Associations of mecA with chemical compounds

• Correlation between regulation of mecA transcription and expression of methicillin resistance in staphylococci [13].
• Three of 5 strains that required oxacillin MICs of 0.5 microgram/ml and all 18 strains that required oxacillin MICs of > or = 1.0 microgram/ml were resistant by oxacillin disk test and were mecA positive [12].
• The correlation between BBL Crystal MRSA ID and mecA gene PCR was not reliable for CNS (negative predictive value = 68%) [15].
• Quinupristin/dalfopristin and linezolid show good activity against both mecA-positive and -negative CNS [16].
• Both the Velogene and the MRSA Screen assays accurately identified mecA-positive staphylococcal strains and can be successfully used for routine application in clinical microbiology laboratories [17].

Other interactions of mecA

• We have previously shown (G. L. Archer, D. M. Niemeyer, J. A. Thanassi, and M. J. Pucci, Antimicrob. Agents Chemother. 38:447-454, 1994) that some methicillin-resistant staphylococcal isolates contain a partial deletion of the genes (mecR1 and mecI) that regulate the transcription of the methicillin resistance structural gene (mecA) [18].
• Pulsed-field gel electrophoresis (PFGE) of SmaI macrofragments and hybridization of ClaI digests with mecA and murE DNA probes were performed [19].
• In all strains, the mecA gene was detected by polymerase chain reaction (PCR), and penicillin binding protein 2' (PBP2') was detected by the latex agglutination method [20].

Analytical, diagnostic and therapeutic context of mecA

• Site-specific mutagenesis was used to modify the strain 27r mecA gene to permit removal of the region encoding the putative transmembrane region (amino acids 2 to 22) [2].
• In Northern blots of total staphylococcal RNA, the phase variants showed no detectable mecA-specific transcription product, whereas parent strain RP62A revealed a strong signal, indicating that mecA transcription is not the mechanism responsible for the decreased methicillin resistance phenotype of phase variants PV1 to PV5 [9].
• In 164 isolates, the presence of mecA was investigated; 61 strains were mecA-positive and 103 were mecA-negative by Southern blot analysis [21].
• Thirty-five clinical isolates of coagulase-negative staphylococci with decreased glycopeptide sensitivity were examined by a penicillin-binding protein (PBP2') latex agglutination (LA) test and were compared to the detection of the mecA gene by PCR, and oxacillin susceptibility determined minimum inhibitory concentrations [22].

References