Attribute of dominant MRSA strain enables it to persist on skin and spread in community
In the last decade, a new strain of MRSA has emerged that can spread beyond hospital walls, putting everyone at risk of contracting the dangerous bacterial infection. This particular strain of MRSA - known as USA300 - contains a chunk of genes not shared by any other strains, though it is unclear how this unique genetic material enables the bacteria to survive and persist in the community.
Now, research from the University of North Carolina School of Medicine has pinpointed a gene that causes the infection to linger on the skin longer than other strains, allowing it to be passed more readily from one person to the next.
The gene makes this strain of MRSA resistant to specific compounds on the skin called polyamines that are toxic to other forms of the bacteria. In uncovering this property, researchers have identified a novel target for developing new treatments against methicillin-resistant Staphylococcus aureus, particularly the USA300 strain that accounts for the vast majority of MRSA skin and soft tissue infections seen in emergency rooms.
"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. 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," said senior study author Anthony Richardson, PhD, assistant professor of microbiology and immunology at the UNC School of Medicine.
The UNC study, published Jan. 16, 2013, in the journal Cell Host & Microbe, follows an attribute of MRSA previously unexplored by other scientists -- its sensitivity to the naturally occurring compounds called polyamines.
Polyamines are critical to wound repair because they are anti-inflammatory and promote tissue regeneration. Scientists first observed that MRSA infections were killed by polyamines in the 1950s, but no one followed up until recently, when Richardson decided to twist this scientific observation into a treatment option.