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Antibiotics may transform MRSA into a Superbug

Treatment with first-line antibiotics could make MRSA skin infections worse, and that too by activating the body's own pathogen-defense system

Methicillin-resistant Staphylococcus aureus, or MRSA may once have been a controllable health issue but during the last few decades is has transformed into something serious when it comes to public.

Findings of a new study may have significant clinical implications, because many MRSA-infected patients are put at risk by initial inappropriate antibiotic treatment with beta-lactam antibiotics.

Results of this pre-clinical study have been published on November 11 in Cell Host & Microbe.

First-line antibiotics used to treat MRSA could actually worsen the skin infections according to the findings of a pre-clinical research. This takes place when the pathogen defense system of one’s own body gets triggered.

Staphylococcus aureus, also termed as “staph,” is a kind of bacteria usually carried on the skin or inside the nose of healthy people. Data suggests that 25 percent population is colonized with staph, however on an average only 1% is colonized with MRSA. This minority is resistant to methicillin along with a host of other antibiotics.

Co-senior study author George Liu of Cedars-Sinai Medical Center stated that those who are infected with MRSA and are administered a beta-lactam antibiotic could end up being sicker than if they received no treatment at all. He added that their findings underscore the urgent requirement to make awareness of MRSA better along with diagnosing these infections faster to avoid prescribing antibiotics that could put patients’ lives at risk.

The most commonly seen cause of skin and soft tissue infections in the United States are these antibiotic-resistant strains. MRSA is also the reason that leads to very bad illness or death in comparison to methicillin-sensitive S. aureus, however the basic reason behind this is not yet clear.

Liu and co-senior study author David Underhill of Cedars-Sinai Medical Center have done similar studies on this earlier and suspected that the ill effects of MRSA could be a direct result of the gene that leads to antibiotic resistance.

Most bacteria are killed by beta-lactam antibiotics that work by stalling the action of proteins, which are a part of cell wall synthesis. However, MRSA simply avoids the actions of the drug by stimulating a gene called mecA.

This particular gene triggers a back-up route for the synthesis of cell wall. This whole gene alteration permits MRSA to survive antibiotics, however it also ends up changing the structure of the cell wall of bacteria.

Authors of the study caution in extending the interpretation of this preclinical study to humans until further and more detailed study is done.

Source: EurekAlert