Treatment of MRSA (methicillin-resistant Staphylococcus aureus) with certain antibiotics can potentially make patients sicker, says a new study published in the journal Cell Host & Microbe. These findings could have possible implications for how this “superbug” is managed.
Beta-lactam antibiotics kill normal staph bacteria by inactivating the bacteria’s cell-wall-making enzymes, however one of these enzymes, PBP2A, which is induced when MRSA is exposed to beta-lactam antibiotics, is not rendered inactive by the drugs. This allows the superbug to continue making its cell wall which differs in structure to normal staph.
“This altered cell wall induces a powerful inflammatory response,” said the study’s co-senior author, 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.”
This finding may be potentially problematic for clinicians since beta-lactam antibiotics are often prescribed as first-line therapy when the origin of severe infection is unknown. Because it can take a couple of days to culture MRSA, early diagnosis can be difficult, and treatment with beta-lactam antibiotics may actually worsen the infection.
The research team cautioned that their findings were based on laboratory studies of mice and that the results need to be carefully evaluated in human subjects for validation. “Based on this research, clinical studies are warranted,” said 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.”
1. Mueller S, Wolf AJ, Iliev ID, et al. Cell Host & Microbe, Müller et al.: “Poorly Cross-Linked Peptidoglycan in MRSA Due to mecA Induction Activates the Inflammasome and Exacerbates Immunopathology”dx.doi.org/10.1016/j.chom.2015.10.011
This article originally appeared on MPR