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Some Antibiotics Make The Superbug MRSA Stronger Instead Of Killing It

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The world is facing the threat of 'superbugs' as these bacteria dubbed as methicillin-resistant Staphylococcus aureus (MRSA) have evolved into one of the most difficult-to-treat pathogens. A new study suggests that treatment with the wrong antibiotic could make MRSA-induced infections worse.

Researchers in the United States unveiled the findings of their study published in the journal Cell Host & Microbe. They discovered that common or first-line antibiotics such as beta-lactam antibiotics can make superbugs stronger and the infection more severe.

"Individuals infected with MRSA who receive a beta-lactam antibiotic--one of the most common types of antibiotics--could end up being sicker than if they received no treatment at all," George Liu of Cedars-Sinai Medical Center and co-senior study author said in a press release.

"Our findings underscore the urgent need to improve awareness of MRSA and rapidly diagnose these infections to avoid prescribing antibiotics that could put patients' lives at risk," he added.

Their study, which was conducted on laboratory mice, claims that MRSA does not only respond to beta-lactam antibiotics, it actually adapts to them, becoming stronger in the process. Apparently, beta-lactam antibiotic's mechanism of action involves neutralizing the enzymes in bacteria that make cell walls.

It inhibits the formation of peptidoglycan cross-links in the bacterial cell wall. Cell wall structural integrity is vital for bacteria and once it is damaged or destroyed, the bacteria will die. However, the researchers discovered that one of these enzymes, PBP2A (penicillin-binding protein 2A), is not neutralized by the antibiotics. Thus, the superbug continue to build its cell wall.

Specifically, MRSA bypasses the action of the drug and stimulates a gene called mecA. This gene activates a back-up pathway for cell wall synthesis. When the researchers further studied if the body's immune system detects structural changes in the cell wall, they found that the exposure of superbugs to first-line antibiotics induced mecA activation rendering the bacteria easier to kill by immune cells.

Cell wall degradation led to fragments being released and at the same time, being detected by the body's immune system. Thus, a harmful inflammatory response happens that worsened skin infections in mice infected with MRSA.

"This altered cell wall induces a powerful inflammatory response. In mice infected with MRSA, induction of PBP2A with methicillin led to more inflammation and pathology," Dr. David Underhill, co-author said.

Researchers reiterated that the pathogenic factor of MRSA is not 'unleashed' unless it is treated or exposed to beta-lactam antibiotics. Thus, MRSA-infected patients are placed at risk because of initial wrong antibiotic treatments.

They recommend health practitioners to know the source of the infection first via laboratory testing before prescribing initial antibiotics. The researchers further clarified that the study was conducted on mice and more research on humans is needed.

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