Researchers then probed one particular genetic element that decides the properties of MRSA—the “staphylococcal cassette chromosome mec” (SCCmec).
Several different versions of this cassette provide bacteria with slightly different properties, according to researchers: healthcare-acquired MRSA have type I, II or III SCCmec elements while community-acquired MRSA have type IV and V elements.
These different cassettes all contain a gene (mecA) that codes for a cell-wall bacteria protein called PBP2a. This specific penicillin binding protein is less sensitive to antibiotics, allowing the bacteria to survive.
Genetically modified MRSA
The researcher team then went on to determine if deleting the mecA gene would affect the toxicity of MRSA, and genetically modified an MRSA strain to delete the mecA gene in the lab.
They then took this strain and a healthcare-acquired MRSA strain, then performed tests on both strains to see how each was able to break up a type of immune cell called a T cell in the laboratory.
The researchers then investigated the ability of both strains to respond to “signaling molecules” that normally cause the bacteria to activate their production of toxins. How virulent the two strains became were then tested on lab mice.
The research team found that deleting the mecA gene caused the MRSA to become more toxic.
This was because the expression of mecA resulted in cell wall changes that interfere with MRSA’s ability to detect or respond to signals to switch on toxin expression.
MRSA with mecA deleted were also found to be more virulent, causing mice to lose weight or die.
Conversely, this meant that the expression of the mecA—the very mechanism that produces the protein that makes MRSA resistant to antibiotic—causes the bacteria to become less toxic.
The researchers then compared healthcare-acquired MRSA with community-acquired MRSA, in terms of PBP2a cell wall protein production, T-cell toxicity and resistance to antibiotics.
They found that typical community-acquired MRSAs had lower resistance to the antibiotic oxacillin, were more toxic to the immune system’s T-cells and expressed less PBP2a.
“This interesting research contributes to our knowledge of MRSA, rather than warning us of an invasion of airborne superbugs,” the NHS said.
Public fears of MRSA began in 2007 when a U.S. study found that MRSA infections were spreading and “posed a major health problem in the United States.”
The study detailed how MRSA, popularly dubbed a “superbug,” is resistant to the antibiotic drug methicillin, as well as to penicillin and other commonly used antibiotics.
It also noted that MRSA can invade tissues and organs, causing blood and bone infections, pneumonia, and inflammation of the heart’s lining and estimated that there were 94,360 invasive MRSA infections in 2005, contributing to 18,650 deaths—more deaths than caused by AIDS in the United States in that year.
But MRSA infections frequently occur in healthcare settings such as hospitals and nursing homes, although infections were said to be increasing in the general community.