Report On Antibiotic Resistance
Antibiotic resistance occurs when there is a gain or change in the DNA of the bacterial organism. Most mechanisms of antibiotic resistance are associated with plasmid-mediated transfer of genetic information; using transposons facilitates the transfer of information, and in fact many common modes of resistance are associated with transposons such as beta – lactamases, tetracycline resistance and aminoglycoside resistance (Microbiology, 2007 pg. 64-65). Resistance is accomplished by one of three mechanisms (Microbiology, 2007 pg.65): Report On Antibiotic Resistance
- Decreased uptake
- Alteration of target site: A change in the penicillin binding site of certain bacterial cell walls leads to less binding. This method explains the mechanism of resistance of streptococcus pneumonia to penicillin.
- Ability to destroy or modify the antibiotic:
- Beta – lactamases inactivates penicillin
- Esterases hydrolyze the lactone ring of macrolide
Resistance to MRSA is mediated by penicillin binding protein – 2A (PBP-2A) encoded by the mecA gene located on a transposon called the staphylococcal chromosome cassette (SCCmec) (Anderson, 2013). This leads to resistance to methicillin and other β – lactam antibiotics. Vancomycin is the treatment of choice for invasive MRSA infections, but other antibiotics can be considered if the patient develops adverse reactions to vancomycin, or the infection is not susceptible to it. Other antibiotics used for treatment include, daptomycin, linezolid, ceftaroline, and quinupristin – dalfopristin (Lowy, 2012). Active surveillance in hospital patients is the most useful in the setting of hospital outbreaks (Harris, 2013). Report On Antibiotic Resistance