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BIOLOGY, Health Care, Medical

How Can Staphylococcus Aureus Resist Antibiotics?

Antibiotics are a group of drugs that act specifically on bacteria but not other organisms such as viruses, parasites, or prions. However, some bacteria possess advanced mutation mechanisms that enable them to mutate, hence evading the methods antibiotics use to kill them. This case study emphasizes Staphylococcus aureus and how it is able to resist antibiotics, specifically penicillin. It also focuses on the regulations that could have been put in place to prevent antibiotic resistance.

Penicillin stands out as the most prescribed antibiotic owing to the fact that they are broad spectrum. Thus, in the majority of cases, they are the first-line treatment for common bacterial-caused conditions. (An example is an amoxicillin).In terms of their chemical structure, penicillin contains a beta-lactam ring as opposed to other antibiotics. Functionally, penicillin is bactericidal in nature. Penicillin antibiotics destroy the binding to the bacterial cell wall component, D-ALA-D-ALA, and replace it with their own penicillin-binding proteins. These penicillin-binding proteins prevent the action of carboxyl-peptidase that cross-links the components of the cell wall. The beta-lactam ring present in penicillin then makes the cell wall unstable and weak; hence, it can succumb to high osmotic pressure (Yocum, RR et al., 1980). Due to the overuse of penicillin in drugs, even when not necessary, they are able to genetically transfer material amongst each other via transformation and transduction. They transfer the genetic resistance of penicillin binding-proteins gene codons to each other via transposons, chromosomal cassettes and plasmids, and sex pili (Foster, 2017). The resistance then develops very quickly. The end result is that the beta-lactam ring in penicillin is destroyed by the beta-lactamase enzymes, and hence, the antibiotic stops being bactericidal. The most common S. aureus resistant to penicillin are the vancomycin-resistant Staphylococcus aureus and methicillin-resistant Staphylococcus aureus (Lowy, 2003).

Antibiotic resistance could be prevented if governments prevent the issue of antibiotics for non-confirmed bacterial infections. Additionally, some bacterial infections are self-limiting and don’t require medication. The government should also stop the sale of common antibiotics as over-the-counter drugs. This measure certainly would have curbed their resistance. The W.H.O. should also regularly update governments on the findings of antibiotic techniques and how to resolve the issue.

Case Study

A typical mild head cold is caused by non-bacterial pathogens. Mostly, viruses such as rhinovirus and influenza are behind this presentation (U.S. Department of Health & Human Services, 2017). Before seeking treatment with antibiotics, a viral load should be requested to see if the cause is a virus and if the load is higher than in normal infections. However, some bacteria tend to hide behind viruses, and hence antibiotics should be issued when a bacterial culture test is positive.

References

Chambers, H. F., & DeLeo, F. R. (2009, September). Waves of Resistance: Staphylococcus aureus in the Antibiotic Era. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2871281/

Lowy, F. D. (2003, May 1). Antimicrobial resistance: the example of Staphylococcus aureus. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC154455/

TJ, F. (2017, May). Antibiotic resistance in Staphylococcus aureus. Current status and future prospects. – PubMed – NCBI. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/28419231

U.S. Department of Health & Human Services. (2017, December 7). The Development of Antibiotic Resistance Bacteria. Retrieved from https://www.cdc.gov/antibiotic-use/community/about/antibiotic-resistance-faqs.html

Yocum RR, et al. (1980, May). The mechanism of action of penicillin. Penicillin acylates the active site of Bacillus stearothermophilus D-alanine carboxypeptidase. – PubMed – NCBI. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/7372662

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