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ElaKiri Talk!
Superbug Evolves globally with a new Genetic Weapon.
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<blockquote data-quote="imhotep" data-source="post: 30616424" data-attributes="member: 562115"><p><strong>A deadly hospital superbug has evolved into a global force by weaponizing a genetic tool to wipe out its microbial competition.</strong></p><p></p><p>Researchers discovered that vancomycin-resistant Enterococcus faecium (VREfm) developed the ability to produce bacteriocins—natural bacterial toxins—to eliminate rival strains.</p><p>A drug-resistant bacterium commonly found in healthcare settings has evolved over the past several years to gain a powerful advantage: it can now produce an antimicrobial compound that allows it to kill off related strains and rise to dominance. Researchers at the University of Pittsburgh School of Medicine first identified this shift in local hospital data and then confirmed it was happening around the world.</p><p></p><p>Vancomycin-Resistant <em>Enterococcus faecium</em> (VREfm), so-called because it can’t be eradicated with the popular antibiotic vancomycin. VREfm kills about 40% of the people it infects and is a particular plague on immunocompromised and hospitalized patients, who are often taking antibiotics that decrease the diversity of bacteria in their microbiomes, allowing drug-resistant bacteria, such as VREfm, to thrive.</p><p></p><h4>The Weapon: A Bacteriocin</h4><p>The dominant strains had acquired the ability to produce a bacteriocin, which is an antimicrobial that bacteria use to kill or inhibit one another. They’d weaponized this new capability to destroy the other VREfm strains, giving them unfettered access to nutrients for easier reproduction.</p><p></p><p>Once these strains are in an institutional setting – such as a hospital – and are matched up against other strains of VRE in a patient’s gut, they take over. It’s a ‘kill your buddies and eat their food’ scenario.”</p><p></p><p>However, it does not appear that the bacteriocin-wielding VREfm are making patients any sicker than their predecessors did. But it could point to potential avenues for the development of new therapies.</p></blockquote><p></p>
[QUOTE="imhotep, post: 30616424, member: 562115"] [B]A deadly hospital superbug has evolved into a global force by weaponizing a genetic tool to wipe out its microbial competition.[/B] Researchers discovered that vancomycin-resistant Enterococcus faecium (VREfm) developed the ability to produce bacteriocins—natural bacterial toxins—to eliminate rival strains. A drug-resistant bacterium commonly found in healthcare settings has evolved over the past several years to gain a powerful advantage: it can now produce an antimicrobial compound that allows it to kill off related strains and rise to dominance. Researchers at the University of Pittsburgh School of Medicine first identified this shift in local hospital data and then confirmed it was happening around the world. Vancomycin-Resistant [I]Enterococcus faecium[/I] (VREfm), so-called because it can’t be eradicated with the popular antibiotic vancomycin. VREfm kills about 40% of the people it infects and is a particular plague on immunocompromised and hospitalized patients, who are often taking antibiotics that decrease the diversity of bacteria in their microbiomes, allowing drug-resistant bacteria, such as VREfm, to thrive. [HEADING=3]The Weapon: A Bacteriocin[/HEADING] The dominant strains had acquired the ability to produce a bacteriocin, which is an antimicrobial that bacteria use to kill or inhibit one another. They’d weaponized this new capability to destroy the other VREfm strains, giving them unfettered access to nutrients for easier reproduction. Once these strains are in an institutional setting – such as a hospital – and are matched up against other strains of VRE in a patient’s gut, they take over. It’s a ‘kill your buddies and eat their food’ scenario.” However, it does not appear that the bacteriocin-wielding VREfm are making patients any sicker than their predecessors did. But it could point to potential avenues for the development of new therapies. [/QUOTE]
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