Antibiotic Resistance Within Staphylococcus Aureus

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Staphylococcus aureus is a growing issue both within hospitals and communities because of its ability to adjust to different environments. Over the years, S. aureus has become resistant to many different antibiotics including penicillin and methicillin. Today, Staphylococcus aureus remains a growing pandemic because of its increasing antibiotic resistance through different mechanisms including horizontal gene transfer and altering of antibiotics. It continues to cause horrific and sometimes life threatening infections.

Introduction

Staphylococcus aureus is a gram positive bacteria that belongs to the micrococcaceae family and appears in the form of cocci clusters. It differs from other staphylococcus because it appears with gold pigmentation. The bacteria also tests positive for coagulase, mannitol-fermentation, and deoxyribonuclease. Staphylococcus aureus has a thick cell wall made up of peptidoglycan and in this case are 50 percent by weight. The peptidoglycan are made up of both N-acetylglucosamine and N-acetylmuramic acid, which are linked with tetrapeptide chains, found only in S. aureus. It contains prophages, plasmids, and transposons all within a 2800 bp circular chromosome [1]. This is where mechanisms of antibiotic resistance are found. The bacteria was first discovered by Alexander Ogston in 1880 when he became interested in the high post surgery mortality rates, and was later named by Friedrich Julius Rosenbach. More commonly referred to as a “staph infection” or “staph bacteria”, S. aureus is reportedly found in 30% of the population who are asymptomatic nasal carriers, while another large portion carry the bacteria on their skin.[2] S. aureus is transferred through skin to skin contact and more commonly affects persons previously diseased or with weaker immune systems. The most common transfer happens from a health worker who has been in contact with an active strain of it. Other transfers occur from environmental sources or from other carriers of the bacteria. Possible outcomes from staph infections include many hospital originated issues including pneumonia and bloodstream and wound infections. When S. aureus was first identified, and before antibiotics were developed, the bacteria had a mortality rate of 80%. Today, with antibiotic treatment, the mortality rates around the world range from 20-40% [3].

Penicillin Resistance: History and Mechanisms

The first antibiotic introduced to fight S. aureus was penicillin in 1940, which decreased mortality rates significantly. Two years later, resistance to the drug was already being recognized both within communities and hospitals. More than 80% of staphylococcus strains were found to be resistant by the early 1960’s [4]. These strains were found by Bondi and Dietz in 1948 to contain penicillinase, which is a specific type of β-lactamase [5]. β-lactam antibiotics, like penicillin, work by inhibiting the cell enzyme which in this case would be β-lactamase. Inhibiting the cell enzyme slows down cell wall formation which brings down osmotic pressure and eventually kills the cell. β-lactam antibiotics are able to inhibit enzymes with a β-lactam ring, which binds to the enzyme in the bacteria cell. One way in which bacteria become resistant to antibiotics is by hydrolyzing the β-lactam ring. They do this when they contain a blaZ gene, which codes for penicillinase. The gene reorganizes the enzyme and does not allow for it to bind with β-lactam ring. BlaZ gene is located on a transposable part of the large plasmid within the S. aureus bacteria cells. Because of this location, the gene is easily movable to surrounding cells through horizontal gene transfer.

Methicillin: History and Resistance

Include some current research in each topic, with at least one figure showing data.

References

1. Lowy, F. D. (1998). Staphylococcus aureus infections. N Engl J Med, 339(8), 520-532. doi:10.1056/NEJM199808203390806

3. Lowy, Franklin D. “Antimicrobial Resistance: The Example of Staphylococcus Aureus.” Journal of Clinical Investigation 111.9 (2003): 1265–1273. PMC. Web. 26 Feb. 2015.

Edited by (Liza Ach), a student of Nora Sullivan in BIOL168L (Microbiology) in The Keck Science Department of the Claremont Colleges Spring 2014.