New research published in the journal Nature Communications explains why Methicillin-resistant Staphylococcus aureus (MRSA) contracted outside the hospital are less deadly than those that are hospital-acquired.
Hospital-acquired strains of MRSA, referred to as HA-MRSA, are responsible for most of the 10,000 annual deaths attributed to the antibiotic-resistant disease in the U.S. Comparatively, the community-acquired version (CA-MRSA) is much more prevalent but less deadly. A research team led by NYU Langone Medical Center now believe they know why.
Somewhat paradoxically, the answer lies in how CA-MRSA has additional toxins. MRSA operates by tearing apart red blood cells to get nutrients for its growth. It also emits toxins that can destroy the white blood cells meant to fight off infection. Of these toxins, the research focused on two: the LUK-PV toxin that only the community strain produces, and the LUK-ED toxin that both strains possess.
According to the research, when both toxins are present in the CA-MRSA strain, they exhibit an antagonistic “dueling” effect. In essence, when the two toxins attack the same white blood cell, they end up impeding each other’s efforts. This enables the immune system to mount a better response to the community strain than it can in cases of HA-MRSA, resulting in a less severe infection.
Researchers plan to next study the interactions further to determine the specific biological and chemical interactions that the LUK-PV and LUK-ED toxins operate on, both alone and together. Depending on what is learned, the information can be used to further develop more effective HA-MRSA treatments and potentially a vaccine.
Since the LUK-ED toxin splits red blood cells by using the same attachment point that malaria uses, a separate study is being planned to also see if people with genetic resistance to malaria are also resistant to MRSA.
Sources for Today’s Article:
Yoong, P. and Torres, V.J., “Counter Inhibition between Leukotoxins Attenuates Staphylococcus Aureus Virulence,” Nature Communications September 2015; 6: 8125, doi:10.1038/ncomms9125.