MRSA infections were made worse by antibiotics in mice that were part of the latest study.
The study was conducted by researchers at Cedars-Sinai Medical Center in Los Angeles, CA, and is published in the journal Cell Host & Microbe.
It focuses on the superbug MRSA (methicillin-resistant Staphylococcus aureus), which made the news in October when New York Giants footballer Daniel Fells entered the hospital for treatment against it. After seven surgeries, he managed to escape foot amputation and was released from the hospital at the end of the month.
According to the Centers for Disease Control and Prevention (CDC), MRSA can cause skin and other infections within the community. In a hospital, however, it can cause severe problems such as bloodstream infections, pneumonia and surgical site infections.
Though anybody can get a MRSA infection through direct contact with an infected wound or by sharing personal items that have come in contact with infected skin, people who are in places that involve crowding or skin-to-skin contact are at greater risk.
Examples of such people include athletes, daycare and school kids, military personnel living in barracks and inpatients at hospitals. According to CDC data from 2011, MRSA causes over 80,000 invasive infections and 11,000 related deaths per year.
"It is one of the biggest antibiotic-resistant pathogens in the US," say the researchers.
Beta-lactams made mice with MRSA infections sicker
Given the scale of the MRSA threat, the research team wanted to investigate what makes MRSA so pathogenic. They say though many studies have established that MRSA infections cause more severe diseases compared with normal staph infections, the reason has been unclear.
They found that in laboratory mice, treatment with antibiotics called beta-lactams - which are similar to methicillin - caused the MRSA bacteria to build inflammatory cell walls that damage tissues. Beta-lactam antibiotics kill normal staph by neutralizing their enzymes that make cell walls.
However, the researchers found that one of these enzymes - called PBP2A - is not neutralized by the antibiotics. Furthermore, PBP2A actually enables the superbug to continue building its cell wall.
They also found that the cell wall's structure is different from normal staph, which allows the superbug to proliferate. Co-senior author David Underhill, PhD, further explains:
"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."
The researchers say their take-home message from all of this is that, after introducing the antibiotics to the MRSA-infected mice, they became even sicker.
'Clinical studies are warranted'
Still, the researchers warn that because their findings are based on studies involving laboratory mice, their results need to be carefully assessed in humans.
- About 1 in 3 people carry staph in their nose, usually without illness
- Around 2 in 100 people carry MRSA
- It causes 11,000 related deaths per year.
"Based on this research, clinical studies are warranted," says study author Sabrina Mueller, PhD.
"However, pending the outcome of those studies, physicians should follow current national guidelines set by the Infectious Diseases Society of America for antimicrobial treatment of staph infections," she adds.
She and her colleagues say physicians face a dilemma, in that the effectiveness of beta-lactam antibiotics often makes them the first choice when a severe infection presents itself. Because it takes a couple of days to culture MRSA, early diagnosis of infection type is difficult.
Earlier today, Medical News Today reported on a study that showed how researchers have developed a way of using electrical stimulation in wound dressing that could offer an alternative to antibiotics.