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What genetic elements contribute to antibiotic resistance in Staph aureus? - Music/Radio - Nairaland

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What genetic elements contribute to antibiotic resistance in Staph aureus? by seoxpert(m): 11:38pm On Sep 28, 2018
Resistance genes often reside on mobile genetic elements such as plasmids, transposons, and the chromosomal DNA, contributing to the spread of resistance traits, including the mecA gene responsible for methicillin resistance.
Re: What genetic elements contribute to antibiotic resistance in Staph aureus? by seoxpert(m): 9:08am On May 05
Staphylococcus aureus has developed a range of mechanisms to resist the effects of antibiotics, and these mechanisms are often encoded by specific genetic elements within its genome. These genetic elements include genes on the bacterial chromosome, mobile genetic elements like plasmids, transposons, and integrons, and even phages. Here are some key genetic contributors to antibiotic resistance in Staphylococcus aureus:

Methicillin Resistance: mecA gene
The mecA gene is the hallmark of methicillin-resistant Staphylococcus aureus (MRSA). It encodes a penicillin-binding protein (PBP2a) with a low affinity for beta-lactam antibiotics (e.g., methicillin, oxacillin, penicillin). mecA is typically carried on a mobile genetic element called the staphylococcal cassette chromosome mec (SCCmec).

Vancomycin Resistance: vanA and vanB genes
While vancomycin-resistant Staphylococcus aureus (VRSA) is rare, resistance when it occurs is usually due to the acquisition of the vanA or vanB gene clusters, often from enterococci via mobile genetic elements. These genes encode enzymes that alter the peptidoglycan structure in the bacterial cell wall, reducing vancomycin's effectiveness.

Macrolide, Lincosamide, and Streptogramin B Resistance: erm genes
The erm (erythromycin ribosome methylation) genes confer resistance to macrolides, lincosamides, and streptogramin B antibiotics by methylating the ribosome, thus preventing antibiotic binding and inhibiting protein synthesis.

Aminoglycoside Resistance: aac, ant, and aph genes
Genes such as aac (acetyltransferase), ant (nucleotidyltransferase), and aph (phosphotransferase) encode modifying enzymes that inactivate aminoglycosides by acetylation, adenylation, or phosphorylation, respectively.

Tetracycline Resistance: tet genes
The tet genes encode efflux pumps (tet(K), tet(L)) or ribosomal protection proteins (tet(M), tet(O)) that prevent tetracycline from affecting the bacterium.

Fluoroquinolone Resistance: mutations in gyrA and grlA genes
Resistance to fluoroquinolones is often due to chromosomal mutations in the gyrA and grlA genes, which encode subunits of DNA gyrase and topoisomerase IV, respectively. These mutations alter the target sites of fluoroquinolones, reducing their binding affinity.

Beta-lactamase Production: blaZ gene
The blaZ gene encodes beta-lactamase, an enzyme that hydrolyzes the beta-lactam ring found in penicillins and other beta-lactam antibiotics, thereby inactivating these drugs.

The mobility of many resistance genes via plasmids, transposons, and other vectors facilitates their spread among bacterial populations, contributing to the global challenge of antibiotic resistance. In Staphylococcus aureus, the ability to rapidly acquire and disseminate resistance genes has led to it being one of the most formidable pathogens in both hospital and community settings.

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