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Antibiotic-resistant enterococci are a serious problem for patientsin the hospital, but little is known about how these bacteria areable to escape antibiotics . New discoveries about the ways in which enterococci turn theirresistance to cephalosporin antibiotics on and off are described ina study published November 1 in the online journal mBio®. The new details about resistance could lead to new therapies forpreventing and treating enterococcal infections. Enterococcus faecalis isn't always a deadly pathogen. Normally a friendly resident ofthe gastrointestinal tract, in individuals who are immunecompromised E. faecalis can turn ugly. Infecting the bloodstream, urinary tract, andsurgical sites. Patients who are given cephalosporin antibioticsfor other problems are also prone to opportunistic E. faecalis infection, since the bacterium is naturally resistant to theseantibiotics and flourishes when sensitive bacteria are killed off.Cephalosporins are like a last resort for treating infections thatare resistant to other, less powerful drugs, so a patient treatedwith cephalosporins who acquires an E. faecalis infection essentially goes from the frying pan (their originalinfection) and into the fire ( E. faecalis infection). But how do enterococci overcome cephalosporin antibiotics? Despitethe importance of this pathogen in hospitals, scientists still knowrelatively little about how enterococci skirt cephalosporinattacks. Chris Kristich and his colleagues at the Medical Collegeof Wisconsin have uncovered new details about the bacterium'sability to turn resistance on and off, a development that couldlead to new therapies for enterococcal infections. According to Kristich, the enzyme IreK is involved in resistance tocephalosporins, since enterococci that lack it are much moresensitive to the drugs. IreK is a kinase - an enzyme that carriesphosphate groups. The study coming out in mBio details new findingsabout another aspect of resistance control: an enzyme called IreP,which takes phosphates off of IreK, thus controlling how activeIreK is in the bacterium. "Phosphorylating IreK changes the activity of the kinase - it's away to turn it on and off," says Kristich. "The result of thatactually is to regulate the level of the kinase output - it isreflected by the level of cephalosporin resistance." Kristich says the bacterium probably needs a way to turn resistanceon and off because maintaining the cellular machinery forresistance costs the cell important resources. "We don't knowexactly how [enterococci become resistant to cephalosporins].Whatever the mechanism, it may be costly when there's nocephalosporin around," says Kristich. The problem with enterococcal infections is not going to get betteruntil new therapies and preventive strategies can be developed,says Kristich. Knowing more about how the bacterium can go back andforth from sensitive to resistant and back can help leadresearchers to ways of controlling infections. "There's anopportunity to develop a new strategy by understanding the basisfor cephalosporin resistance," says Kristich. "If we could figureout a way to make enterococci susceptible to cephalosporins, theycould be used to treat or prevent these infections." Additional References Citations. We are high quality suppliers, our products such as Protective Laptop Cases Manufacturer , China Kindle Fire Covers Cases for oversee buyer. To know more, please visits 7 MID UMPC Tablet PC.
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