Community-Acquired Methicillin-Resistant Staphylococcus Aureus (CA-MRSA): Difference between revisions
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== | ==Origins of MRSA== | ||
<br> | <br>Methicillin was developed by the pharmaceutical company Beecham in 1959 in response to bacteria that were resistant to the drug Penicillin (namely S. aureus). Like Penicillin, and other β-lactam antibiotics that were later developed, Methicillin acts by inhibiting cell-wall synthesis in Gram-positive bacteria. This class of antibiotics binds to the transpeptidase enzyme (also called Penicillin Binding Proteins, or PBPs), which is used by bacteria to cross-link peptidoglycan layers in the cell wall. The β-lactams competitively inhibit these enzymes and prevent these bacteria from successfully undergoing cell division. This ultimately leads to cell death and is a very effective mechanism in dealing with Gram-positive infections. [Wiki Methicillin] | ||
Methicillin was particularly effective upon its introduction into medical use because of its resistance against β-lactamases secreted by bacteria in order to protect against Penicillin. The presence of the ortho-dimethoxyphenyl group on Methicillin prevents enzymatic hydrolysis of the β-lactam ring. However, quickly after its introduction into clinical use, S. aureus began to show resistance to Methicillin. The mechanism of S. aureus resistance to Methicillin is very similar to the mechanism of resistance to Penicillin. Resistance hinges on the presence of the mecA gene in the chromosome. This gene encodes Penicillin Binding Protein 2A, which significantly decreases Methicillin’s affinity to bind to the PBP targets. The mecA gene is a part of the mobile element SCCmec and is easily transferred among S. aureus communities by means of plasmid transfer. [Powerpoint, Evolution of MRSA] | |||
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==Section 2== | ==Section 2== | ||
Revision as of 02:29, 14 April 2009
By: Tom Hardacker
Introduction
Staphylococcus aureus is a circular, anaerobic, Gram-positive bacterium that is prevalent in the nose and skin of most individuals. While the majority of individuals who are colonized by S. aureus are simply carriers, this organism can cause a wide array of illnesses. Infections can range from mild skin irritation to more serious conditions such as endocarditis (inflammation of the inner heart), meningitis, pneumonia and Toxic Shock Syndrome (TSS), among others. Infections by S. aureus can also be prevalent in post-surgical wounds and due to the overuse of antibiotics; certain strains of this organism have become resistant to common treatments. For these reasons, certain strains of this organism have become increasingly problematic in hospitals and healthcare settings, as well as the general community.
Methicillin-Resistant Staphylococcus aureus (MRSA) is a strain of S. aureus that exhibits resistance to the β-lactam antibiotic methicillin (as well as other β-lactams), a common treatment for these infections. MRSA infections can be classified into two major groups: Hospital-acquired MRSA (HA-MRSA) and Community-acquired MRSA (CA-MRSA). HA-MRSA is responsible for post-operative wound infections, or infections resulting from implanted devices such as catheters, that are acquired within the healthcare setting. Typically, patients infected with HA-MRSA are immune-compromised and the resulting infections are generally more invasive. CA-MRSA typically manifests itself as skin infections, such as pimples or boils, and is classified as being acquired outside of any type of healthcare setting. These infections are typically more serious than minor skin irritation and affect otherwise healthy individuals. This article will focus on the latter form of MRSA (an in-depth article regarding HA-MRSA can be found here).
Origins of MRSA
Methicillin was developed by the pharmaceutical company Beecham in 1959 in response to bacteria that were resistant to the drug Penicillin (namely S. aureus). Like Penicillin, and other β-lactam antibiotics that were later developed, Methicillin acts by inhibiting cell-wall synthesis in Gram-positive bacteria. This class of antibiotics binds to the transpeptidase enzyme (also called Penicillin Binding Proteins, or PBPs), which is used by bacteria to cross-link peptidoglycan layers in the cell wall. The β-lactams competitively inhibit these enzymes and prevent these bacteria from successfully undergoing cell division. This ultimately leads to cell death and is a very effective mechanism in dealing with Gram-positive infections. [Wiki Methicillin]
Methicillin was particularly effective upon its introduction into medical use because of its resistance against β-lactamases secreted by bacteria in order to protect against Penicillin. The presence of the ortho-dimethoxyphenyl group on Methicillin prevents enzymatic hydrolysis of the β-lactam ring. However, quickly after its introduction into clinical use, S. aureus began to show resistance to Methicillin. The mechanism of S. aureus resistance to Methicillin is very similar to the mechanism of resistance to Penicillin. Resistance hinges on the presence of the mecA gene in the chromosome. This gene encodes Penicillin Binding Protein 2A, which significantly decreases Methicillin’s affinity to bind to the PBP targets. The mecA gene is a part of the mobile element SCCmec and is easily transferred among S. aureus communities by means of plasmid transfer. [Powerpoint, Evolution of MRSA]
Section 2
Include some current research in each topic, with at least one figure showing data.
Section 3
Include some current research in each topic, with at least one figure showing data.
Conclusion
Overall paper length should be 3,000 words, with at least 3 figures.
References
Edited by student of Joan Slonczewski for BIOL 238 Microbiology, 2009, Kenyon College.
