has a low ß-lactam binding affinity. Therefore, it can mediate cell wall synthesis even in the presence of ß-lactam drugs (5).
mecA Homolog mecC gene
Recently, mec C gene was found to confer ß-lactam resistance in SCCmecXI-carrying S. aureus. The mec C gene was found to share 70% similarity to mec A. Where as mec C encoded PBP2A homolog PBP2C, shares only 63% identity with PBP2A protein. In order to prove its role in Methicillin resistance, a knockout strain was generated.These stains have shown considerably reduced Oxacillin and Cefoxitin MICs in comparison with the wild type MRSA strain. Despite the fact that mecA and mecC were of different clonal heredities and independent of the strain foundation, mecC showed similar Oxacillin and Cefoxitin …show more content…
Rational administration of antibiotics based on rapid and reliable laboratory test results will help reducing cases of treatment failure. Antibiotics such as Tetracyclin with 18-82% resistance, Trimethoprim with 16-65% resistance are broad spectrum antibiotics and may be used for treating MRSA infections. But drugs such as Vancomycin with 0-5% resistance, Linezolid with 0-1% resistance, Tigecyclin and Daptomycin with 0% resistance are the preferred drugs of choice …show more content…
This combination has apparently repressed MRSA development in Kinetic growth curve assay. As an aftereffect of this synergistic cooperation, MIC of Ampicillin against MRSA was decreased to 0.78mg/L from a beginning value of 50mg/L. Western blot analysis proposed hindrance of PBP2A in MRSA cultures developed in synergistic combination treatment in which no PBP2A band was expressed.
Bioactive fraction F-10 posesses antimicrobial activity, and anti MRSA evaluation shows the fraction working synergistically with Ampicillin in hindering bacterial growth.The ability of F-10 to attenuate PBP2A production is postulated to restore MRSAs susceptibility to Ampicillin.
The study seem promising in repressing MRSA, yet resulting investigations necessary to concentrate on the pharmacokinetic properties of the fraction and its association with Ampicillin in an in-vivo model. Aside from this, the communications of F-10 with the regulatory genes, mecI-mecRI-mecR2 and their resultant protein prompting the inhibition phenomenon stays to be unsolved and requires furthur testing (8).
mecA Homolog mecC gene
Recently, mec C gene was found to confer ß-lactam resistance in SCCmecXI-carrying S. aureus. The mec C gene was found to share 70% similarity to mec A. Where as mec C encoded PBP2A homolog PBP2C, shares only 63% identity with PBP2A protein. In order to prove its role in Methicillin resistance, a knockout strain was generated.These stains have shown considerably reduced Oxacillin and Cefoxitin MICs in comparison with the wild type MRSA strain. Despite the fact that mecA and mecC were of different clonal heredities and independent of the strain foundation, mecC showed similar Oxacillin and Cefoxitin …show more content…
Rational administration of antibiotics based on rapid and reliable laboratory test results will help reducing cases of treatment failure. Antibiotics such as Tetracyclin with 18-82% resistance, Trimethoprim with 16-65% resistance are broad spectrum antibiotics and may be used for treating MRSA infections. But drugs such as Vancomycin with 0-5% resistance, Linezolid with 0-1% resistance, Tigecyclin and Daptomycin with 0% resistance are the preferred drugs of choice …show more content…
This combination has apparently repressed MRSA development in Kinetic growth curve assay. As an aftereffect of this synergistic cooperation, MIC of Ampicillin against MRSA was decreased to 0.78mg/L from a beginning value of 50mg/L. Western blot analysis proposed hindrance of PBP2A in MRSA cultures developed in synergistic combination treatment in which no PBP2A band was expressed.
Bioactive fraction F-10 posesses antimicrobial activity, and anti MRSA evaluation shows the fraction working synergistically with Ampicillin in hindering bacterial growth.The ability of F-10 to attenuate PBP2A production is postulated to restore MRSAs susceptibility to Ampicillin.
The study seem promising in repressing MRSA, yet resulting investigations necessary to concentrate on the pharmacokinetic properties of the fraction and its association with Ampicillin in an in-vivo model. Aside from this, the communications of F-10 with the regulatory genes, mecI-mecRI-mecR2 and their resultant protein prompting the inhibition phenomenon stays to be unsolved and requires furthur testing (8).