Hospital-acquired Methicillin Resistant Staphylococcus Aureus (MRSA)

From MicrobeWiki, the student-edited microbiology resource

By: Anthony Alexander

Introduction


Staphylococcus aureus is a spherical microbe and a member of the bacteria domain. This bacterium can be found naturally on the skin and in the mucus membranes of humans most importantly. In fact, Staphylococcus aureus can be found in the nostrils of up to 30% of people (1). The bacteria is spread most commonly through human contact be it hand-to-hand, from a wound secretion or mucus. The spherical bacteria is gram-positive (contains a peptidoglycan layer in its cell wall) and forms colonies that grow in two planes (2). Staphylococcus aureus however lacks flagella and as a result is immotile. The genome of Staphylococcus aureus was first sequenced and mapped by Peter A. Pattee for the strain NCTC 8325 (2). This strain had a circular genome containing approximately 2,900 open reading frames, 61 tRNA genes, 3 structural RNAs and 5 complete ribosomal RNA operons (2). The aspect of Staphylococcus aureus and its genome that is most concerning revolves around the plasmids that are incorporated/associated with this bacterium’s genome. The plasmids that this bacterium contains often code some type of antibiotic resistance. Over time, Staphylococcus aureus was able to acquire antibiotic resistance through conjugation (horizontal gene transfer) of a plasmid containing a transposon, Tn 1546 (2). The transposon Tn 1546 contains the gene mecA which encodes a modified penicillin-binding protein granting Staphylococcus aureus methicillin, and more broadly, penicillin resistance. Methicillin is a beta-lactam antibiotic similar to penicillin. Beta-lactam antibiotics target penicillin-binding proteins. Once bound to the protein, the antibiotic prevents proper peptidoglycan and cell wall formation so that cells will eventually burst as the bacteria attempt to grow larger (3). Penicillin and similar beta-lactam ring antibiotic resistance can be achieved in two main ways; first bacteria can acquire a gene (through horizontal gene transfer) encoding beta-lactamase enzyme which cleaves the critical ring structure of this particular type of antibiotics preventing them from binding the penicillin-binding proteins and disrupting cell wall formation. Second, some bacteria can produce a modified penicillin-binding protein that no longer actually binds the antibiotic which again prevents the desired effects of the antibiotic (3). Methicillin is frequently used to fight bacteria that produce beta-lactamase but is still susceptible to the second form of bacterial resistance to beta-lactam antibiotics. Bacteria like methicillin resistant Staphylococcus aureus are currently of special interest, especially in hospitals, because very few drugs (antibiotics) are still effective against them.

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Section 3

Conclusions

References