"
Team:Elan Vital South Korea/p background
From 2014hs.igem.org
Jiyongh0204 (Talk | contribs) |
Jiyongh0204 (Talk | contribs) |
||
| Line 134: | Line 134: | ||
</div> | </div> | ||
<div id="article_c"> | <div id="article_c"> | ||
| - | <p>MRSA is an acronym for the pathogen Staphylococcus aureus. MRSA developed resistance to β-lactam antibiotics in a large extent. Currently the methicillin resistance has been widely used as an indication for the β-lactam resistant phenotype of this pathogen. | + | <p class="paragraph"> |
| + | MRSA is an acronym for the pathogen Staphylococcus aureus. MRSA developed resistance to β-lactam antibiotics in a large extent. Currently the methicillin resistance has been widely used as an indication for the β-lactam resistant phenotype of this pathogen. | ||
As a micro-organism in Staphylococcus genus, which are Gram-positive cocci, MRSA is usually found in a skin colonized by bacteria and in nasal passages of many healthy people. They stay as carriage state in healthy people’s skin flora, and there are two predominant species: Staphylococcus epidermidis and S. aureus, which refers to the major pathogens among the staphylococci. | As a micro-organism in Staphylococcus genus, which are Gram-positive cocci, MRSA is usually found in a skin colonized by bacteria and in nasal passages of many healthy people. They stay as carriage state in healthy people’s skin flora, and there are two predominant species: Staphylococcus epidermidis and S. aureus, which refers to the major pathogens among the staphylococci. | ||
| - | MRSA is an ovoid-shaped bacterium with a thick cell wall of peptidoglycan and accessory polymers. It has both complex DNA structure and typical prokaryotic DNA replication machinery enzymes. It complements a large amount of ribosomal proteins in our body. As it grows, they grow in crumps to form a grape-shape. Since it is a gram positive pathogen, it stains purple after Gram-staining. | + | </p> |
| - | MRSA is everywhere. It produces virulence factors by selecting spontaneous mutant variants under external stress, expressing pre-existing genetic resistance determinants, or acquiring resistance elements. These factors allow the MRSA adapt to the harsh environments and stay in a hardy microbial life form. It is an “opportunistic pathogen” which either doesn’t defend or use immunosuppression. MRSA has evolved to carry resistance determinants encoding an additional penicillin-binding protein with low affinity for beta-lactam antibiotics, efflux pumps, beta lactamases, multiresistance factor encoded plasmids, and other resistance factors, regulatory elements, and virulence factors. Therefore people named MRSA as “superbug.” | + | <p class="paragraph"> |
| - | + | MRSA is an ovoid-shaped bacterium with a thick cell wall of peptidoglycan and accessory polymers. It has both complex DNA structure and typical prokaryotic DNA replication machinery enzymes. It complements a large amount of ribosomal proteins in our body. As it grows, they grow in crumps to form a grape-shape. Since it is a gram positive pathogen, it stains purple after Gram-staining. | |
| - | + | </p> | |
| - | Current empirical antibiotic hospital treatment options for MRSA are vancomycin, linezolid, quinupristin, dalfospristin, daptomycin; but there is limit in the use of these antibiotics. | + | <p class="paragraph"> |
| - | </p> | + | MRSA is everywhere. It produces virulence factors by selecting spontaneous mutant variants under external stress, expressing pre-existing genetic resistance determinants, or acquiring resistance elements. These factors allow the MRSA adapt to the harsh environments and stay in a hardy microbial life form. It is an “opportunistic pathogen” which either doesn’t defend or use immunosuppression. MRSA has evolved to carry resistance determinants encoding an additional penicillin-binding protein with low affinity for beta-lactam antibiotics, efflux pumps, beta lactamases, multiresistance factor encoded plasmids, and other resistance factors, regulatory elements, and virulence factors. Therefore people named MRSA as “superbug.” |
| + | </p> | ||
| + | <p class="paragraph"> | ||
| + | The first use of vancomycin in clinics happened during 1958. It has risen as a hope in the treatment of S. aureus strains that produce β-lactamase. However, this new medical technique was soon superseded by the new β-lactams. But as more people discovered and expanded the use of MRSA in clinic, by 1970s, beta-lactams were frequently replaced with vancomycin. | ||
| + | </p> | ||
| + | <p class="paragraph"> | ||
| + | This development, however, lead to another consequence: MRSA showed an increase in vancomycin resistance, especially in the enterococci and eventually in staphylococci. Hence the science had to question whether they should use the ‘right’ agent such as vancomycin, or not to use to prevent the collateral damage resistance. | ||
| + | </p> | ||
| + | <p class="paragraph"> | ||
| + | Current empirical antibiotic hospital treatment options for MRSA are vancomycin, linezolid, quinupristin, dalfospristin, daptomycin; but there is limit in the use of these antibiotics. | ||
| + | </p> | ||
</div> | </div> | ||
</div> | </div> | ||
Revision as of 13:02, 19 May 2014
MRSA is an acronym for the pathogen Staphylococcus aureus. MRSA developed resistance to β-lactam antibiotics in a large extent. Currently the methicillin resistance has been widely used as an indication for the β-lactam resistant phenotype of this pathogen. As a micro-organism in Staphylococcus genus, which are Gram-positive cocci, MRSA is usually found in a skin colonized by bacteria and in nasal passages of many healthy people. They stay as carriage state in healthy people’s skin flora, and there are two predominant species: Staphylococcus epidermidis and S. aureus, which refers to the major pathogens among the staphylococci.
MRSA is an ovoid-shaped bacterium with a thick cell wall of peptidoglycan and accessory polymers. It has both complex DNA structure and typical prokaryotic DNA replication machinery enzymes. It complements a large amount of ribosomal proteins in our body. As it grows, they grow in crumps to form a grape-shape. Since it is a gram positive pathogen, it stains purple after Gram-staining.
MRSA is everywhere. It produces virulence factors by selecting spontaneous mutant variants under external stress, expressing pre-existing genetic resistance determinants, or acquiring resistance elements. These factors allow the MRSA adapt to the harsh environments and stay in a hardy microbial life form. It is an “opportunistic pathogen” which either doesn’t defend or use immunosuppression. MRSA has evolved to carry resistance determinants encoding an additional penicillin-binding protein with low affinity for beta-lactam antibiotics, efflux pumps, beta lactamases, multiresistance factor encoded plasmids, and other resistance factors, regulatory elements, and virulence factors. Therefore people named MRSA as “superbug.”
The first use of vancomycin in clinics happened during 1958. It has risen as a hope in the treatment of S. aureus strains that produce β-lactamase. However, this new medical technique was soon superseded by the new β-lactams. But as more people discovered and expanded the use of MRSA in clinic, by 1970s, beta-lactams were frequently replaced with vancomycin.
This development, however, lead to another consequence: MRSA showed an increase in vancomycin resistance, especially in the enterococci and eventually in staphylococci. Hence the science had to question whether they should use the ‘right’ agent such as vancomycin, or not to use to prevent the collateral damage resistance.
Current empirical antibiotic hospital treatment options for MRSA are vancomycin, linezolid, quinupristin, dalfospristin, daptomycin; but there is limit in the use of these antibiotics.
