North Carolina researchers identify important gene in MRSA

University of North Carolina School of Medicine researchers recently pinpointed a gene that allows a drug-resistant bacterial strain to last longer on skin than other strains, which could lead to more effective treatments.

A new strain of methicillin-resistant Staphylococcus aureus known as USA300 spread beyond hospital walls in the last decade, putting others at risk of contracting the dangerous bacterial infection. The researchers identified a gene that makes USA300 resistant to skin compounds called polyamines that are toxic to other forms of MRSA.

By identifying the gene, the researchers have presented a novel target for developing new treatments against MRSA and USA300.

"The problem is by the time you figure out how one strain comes into dominance, it often fades away and a new strain comes in," Anthony Richardson, the senior study author, said. "But because these compounds occur naturally and are so toxic, we still think they can lead to treatments that are effective against all MRSA. We will just have to put in a little extra work to block the gene and make this particular strain of MRSA susceptible to polyamines."

Richardson and his team tested hundreds of MRSA strains against polyamines and found that all were sensitive to the skin compounds except for USA300. The team found that USA300 contained a unique chunk of 34 genes called the arginine catabolic mobile element. The researchers mutated each gene one-by-one until they found that the gene SpeG was the gene that controlled polyamine resistance.

"Previously, the field tried to understand MRSA by focusing on attributes that we already knew were important, such as the amount of toxins or virulence factors a given strain makes," Richardson said. "Those elements may explain why the disease is so bad when you get it, but they don't explain how a particular strain takes over. Our work uncovers the molecular explanation for one strain's rapid and efficient spread to people outside of a crowded hospital setting."

The research, which was published in the journal Cell Host & Microbe, was funded by the National Institute of Allergy and Infectious Diseases.