Diagram depicting antibiotic resistance through alteration of the antibiotic's target site, modeled after MRSA's resistance to penicillin. Beta-lactam antibiotics permanently inactivate PBP enzymes, which are essential for bacterial life, by permanently binding to their active sites. Some forms of MRSA, however, express a PBP that will not allow the antibiotic into their active site. Acquisition of SCCmec in methicillin-sensitive staphylococcus aureus (MSSA) gives rise to a number of genetically different MRSA lineages. These genetic variations within different MRSA strains possibly explain the variability in virulence and associated MRSA infections.[35] The first MRSA strain, ST250 MRSA-1 originated from SCCmec and ST250-MSSA integration.[35] Historically, major MRSA clones: ST2470-MRSA-I, ST239-MRSA-III, ST5-MRSA-II, and ST5-MRSA-IV were responsible for causing hospitalacquired MRSA (HA-MRSA) infections.[35] ST239-MRSA-III, known as the Brazilian clone, was highly transmissible compared to others and distributed in Argentina, Czech Republic, and Portugal.[35] In the UK, where MRSA is commonly called "Golden Staph", the most common strains of MRSA are EMRSA15 and EMRSA16.[36] EMRSA16 is the best described epidemiologically: it originated in Kettering, England, and the full genomic sequence of this strain has been published.[37] EMRSA16 has been found to be identical to the ST36:USA200 strain, which circulates in the United States, and to carry the SCCmec type II, enterotoxin A and toxic shock syndrome toxin 1 genes.[38] Under the new international typing system, this strain is now called MRSA252. EMRSA 15 is also found to be one of the common MRSA strains in Asia. Other common strains include ST5:USA100 and EMRSA 1.[39] These strains are genetic characteristics of HA-MRSA.[40] It is not entirely certain why some strains are highly transmissible and persistent in healthcare facilities.[35] One explanation is the characteristic pattern of antibiotic susceptibility. Both the EMRSA15 and EMRSA16 strains are resistant to erythromycin and ciprofloxacin. It is known that Staphylococcus aureus can survive intracellularly,[41] for example in the nasal mucosa [42] and in the tonsil tissue.[43] Erythromycin and Ciprofloxacin are precisely the antibiotics that best penetrate intracellularly; it may be that these strains of S. aureus are therefore able to exploit an intracellular niche. Community-acquired MRSA (CA-MRSA) strains emerged in late 1990 to 2000, infecting healthy people who had not been in contact with health care facilities.[40] A later study that analyzed data from more than 300 microbiology labs associated with hospitals all over the United States have found a seven-fold increase, jumping from 3.6% of all MRSA infections to 28.2%, in the proportion of community-associated strains of MRSA between 1999 and 2006.[44] Researchers suggest that CA-MRSA did not evolve from the HA-MRSA.[40] This is further proven by molecular typing of CA-MRSA strains[45] and genome comparison between CA-MRSA and HA-MRSA, which indicate that novel MRSA strains integrated SCCmec into MSSA separately on its own.[40] By mid 2000, CA-MRSA was introduced into the health care systems and distinguishing CA-MRSA from HA-MRSA became a difficult process.[40] Community-acquired MRSA (CA-

MRSA) is more easily treated and more virulent than hospital-acquired MRSA (HA-MRSA).[35] .[40] The genetic mechanism for the enhanced virulence in CA-MRSA remains an active area of research. Especially the Panton-Valentine leukocidin (PVL) genes are of interest because they are a unique feature of CAMRSA.

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