Antibiotic Resistance Within Staphylococcus Aureus: Difference between revisions
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==Introduction== | ==Introduction== | ||
<i>Staphylococcus aureus</i> is a gram positive bacteria that belongs to the [http://en.wikipedia.org/wiki/Micrococcaceae 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 [http://en.wikipedia.org/wiki/Coagulase coagulase], [http://en.wikipedia.org/wiki/Mannitol_salt_agar mannitol-fermentation], and [http://en.wikipedia.org/wiki/Deoxyribonuclease deoxyribonuclease]. 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”, <i>S. aureus</i> is reportedly found in 30% of the population who are asymptomatic nasal carriers, while another large portion carry the bacteria on their skin.[http://www.nejm.org/doi/full/10.1056/NEJM199808203390806] <i>S. aureus</i> 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 <i>S. aureus</i> 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%.The first antibiotic introduced to fight <i>S. aureus</i> was penicillin in 1940 which decreased mortality rates significantly. By 1942, 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. In short, resistance to penicillin is facilitated by the blaZ gene. This gene codes for [http://en.wikipedia.org/wiki/Beta-lactamase β-lactamase] which is the enzyme that renders β-lactam antibiotics inactive. β-lactam antibiotics contain a β-lactam ring which works by binding to the enzyme within the cell, stopping cell wall formation and thus destroying the <i>S. aureus</i> bacteria. When the bacteria contains the blaZ gene, β-lactamase is able to break down the ring that would normally inhibit cell wall formation. The blaZ gene is located on a transposable part of the large plasmid. Through horizontal gene transfer, other bacteria cells accumulated this resistance mechanism and therefore <i>S. aureus</i> continues to be resistant to penicillin. [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC154455/] | <i>Staphylococcus aureus</i> is a gram positive bacteria that belongs to the [http://en.wikipedia.org/wiki/Micrococcaceae 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 [http://en.wikipedia.org/wiki/Coagulase coagulase], [http://en.wikipedia.org/wiki/Mannitol_salt_agar mannitol-fermentation], and [http://en.wikipedia.org/wiki/Deoxyribonuclease deoxyribonuclease]. 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”, <i>S. aureus</i> is reportedly found in 30% of the population who are asymptomatic nasal carriers, while another large portion carry the bacteria on their skin.[http://www.nejm.org/doi/full/10.1056/NEJM199808203390806] <i>S. aureus</i> 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 <i>S. aureus</i> 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%.The first antibiotic introduced to fight <i>S. aureus</i> was penicillin in 1940 which decreased mortality rates significantly. By 1942, 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. In short, resistance to penicillin is facilitated by the blaZ gene. This gene codes for [http://en.wikipedia.org/wiki/Beta-lactamase β-lactamase] which is the enzyme that renders β-lactam antibiotics inactive. β-lactam antibiotics contain a β-lactam ring which works by binding to the enzyme within the cell, stopping cell wall formation and thus destroying the <i>S. aureus</i> bacteria. When the bacteria contains the blaZ gene, β-lactamase is able to break down the ring that would normally inhibit cell wall formation. The blaZ gene is located on a [http://en.wikipedia.org/wiki/Transposable_element transposable] part of the large plasmid. Through [http://en.wikipedia.org/wiki/Horizontal_gene_transfer horizontal gene transfer], other bacteria cells accumulated this resistance mechanism and therefore <i>S. aureus</i> continues to be resistant to penicillin. [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC154455/] | ||
==Cell Structure and Mechanisms== | ==Cell Structure and Mechanisms== | ||
Revision as of 07:10, 24 March 2015
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 . Methicillin antibiotics were introduced to combat the bacteria. Today, Staphylococcus aureus becomes increasingly resistant to this particular antibiotic through different mechanisms including horizontal gene transfer and altering of antibiotics.
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. 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.[1] 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%.The first antibiotic introduced to fight S. aureus was penicillin in 1940 which decreased mortality rates significantly. By 1942, 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. In short, resistance to penicillin is facilitated by the blaZ gene. This gene codes for β-lactamase which is the enzyme that renders β-lactam antibiotics inactive. β-lactam antibiotics contain a β-lactam ring which works by binding to the enzyme within the cell, stopping cell wall formation and thus destroying the S. aureus bacteria. When the bacteria contains the blaZ gene, β-lactamase is able to break down the ring that would normally inhibit cell wall formation. The blaZ gene is located on a transposable part of the large plasmid. Through horizontal gene transfer, other bacteria cells accumulated this resistance mechanism and therefore S. aureus continues to be resistant to penicillin. [2]
Cell Structure and Mechanisms
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.
Further Reading
[Sample link] Ebola Hemorrhagic Fever—Centers for Disease Control and Prevention, Special Pathogens Branch
References
Edited by (your name here), a student of Nora Sullivan in BIOL168L (Microbiology) in The Keck Science Department of the Claremont Colleges Spring 2014.
