Study finds that antibiotics can make Superbug MRSA stronger

The infection came into focus last month when Daniel Fells, the football player for NY Giants received treatment for this ailment. Thus, a risky inflammatory reaction occurs that worsened skin diseases in mice infected with MRSA. In a hospital, however, it can cause severe problems such as bloodstream infections, pneumonia and surgical site infections.

Researchers conducted this new study for investigating the factors that make the superbug so pathogenic. Beta-lactam antibiotics kill normal staph by neutralizing their enzymes that make cell walls.

They also found that the cell wall’s structure is different from normal staph, which allows the superbug to proliferate. Therefore, MRSA is able to continue building cell walls.

Researchers reiterated that the pathogenic factor of MRSA is not “unleashed” unless it is treated or exposed to beta-lactam antibiotics. If left untreated, it can be life threatening. In addition, it results in the death of more than 11,000 people around the world each year.

Scientists at Cedars-Sinai Medical Center in Los Angeles, California, used a mouse model to show that beta-lactams promote increased inflammation by inducing the resistance gene mecA. Eventually, the person becomes much sicker and the infection possibly stronger.

Beta lactam antibiotics are most commonly used among antibiotics. For this study, researchers examined the effects of using first-line antibiotics – beta-lactam antibiotics (i.e. penicillin, amoxicillin and carbapenem) – on MRSA skin infections in rats.

This kind of bacteria is so common that it’s usually carried on the skin or in the nose of people who are healthy. The typical treatment is beta-lactam.

The researchers hope that their study’s findings will help doctors make safer medical decisions when it comes to treating MRSA skin infections. Then, they administered beta lactam antibiotics to treat the infection. In turn, this made the mice get even sicker after being treated with antibiotics.

However, the researchers found that one of these enzymes – called PBP2A – is not neutralized by the antibiotics. “How that translates to human infection is less clear”. Beta-lactam antibiotics kill the bacteria by inhibiting these proteins. This activates a component of the innate immune system, prompting the release of high concentrations of the cytokine interleukin (IL)-beta.

“In situations where there is a lot of infection, this highly aggressive response can cause extensive inflammation and tissue damage, effectively making the consequences of the infection worse”, Liu said.

They recommend health practitioners to know the source of the infection first via laboratory testing before prescribing initial antibiotics. According to David Underhill, PhD, associate director of the Division of Immunology Research in the Cedars-Sinai Department of Biomedical Sciences and the Janet and William Wetsman Family Chair in Inflammatory Bowel Disease, “In mice infected with MRSA, induction of PBP2A with methicillin led to more inflammation and pathology”. The study authors doo, indeed, warrant the extension of the study results to humans until more research can be done.