New research from the Imperial College of London now offers a promising novel approach in the fight against methicillin-resistant Staphylococcus aureus (MRSA), and their findings are decidedly salty.
Fighting Staphylococcus aureus in its most antibiotic-resistant form has been a priority for the healthcare community since the strain began defying drug treatment in recent decades. New research from the Imperial College of London (ICL) now offers a promising novel approach in the fight against methicillin-resistant Staphylococcus aureus (MRSA), and their weapon is salt.
In the same way that brining food keeps it preserved and prevents bacterial growth, high salt environments can be unfriendly and deadly to pathogens. Some bacteria such as S. aureus have remained impervious to the pickle jar approach to blocking bacteria though, and the scientists at the ICL have figured out why. In their new study published in the journal Science Signaling, ICL professor and study author Angelika Gründling and her research team explain their findings on how S. aureus regulates its sale uptake.
The bacteria are highly resistant to osmotic stresses high-salt concentration environments, in a way that has eluded the medical and science community until now. The study authors knew that to survive an increase in osmolarity, the S. aureus bacteria immediately take up potassium ions and small organic compounds known as compatible solutes. In studying cells of MRSA, the researchers found that the bacteria regulate these salt levels through a signaling molecule called cyclic di-AMP that is key to the bacteria’s survival mechanism. Cyclic di-AMP can detect when the bacteria are exposed to high salinity, and the molecule then sends a signal to transporter proteins. The protein’s response acts to pull another molecule into the cell that protects the bacteria cell from taking in too much salt and losing water. This molecule essentially acts as a sponge, moving into the cell and soaking up the water in a protective maneuver, while also blocking salt from entering the cell.
By disrupting the mechanism by which S. aureus regulates its salt intake, the researchers believed that the bacteria would either absorb too much salt from surroundings or lose too much water, a process that would cause it to dehydrate and die. Working on the MRSA cells, they increased the signal to the transporter protein. This greatly reduced the number of protective sponge molecules entering the cell, thereby exposing the MRSA cells to the higher salt levels and interrupting the protective process.
The implications of this research offer the potential for an alternate approach to battling MRSA infections. The “superbug” remains impervious to antibiotic drug treatment and the medical community has been in need of a new weapon against this healthcare associated infection.
According to the Centers for Disease Control and Prevention, two in 100 people carry MRSA and those who carry the bacteria can do so without having any signs of infection. It is spread in healthcare settings through direct contact with an infected wound or from contaminated hands, often from healthcare providers. The drug-resistant bacteria can cause a range of difficult-to-treat infections, such as sepsis, pneumonia, skin infections and blood infections. Symptoms of MRSA pneumonia include cough, fever and difficulty breathing and can be more severe due to the antibiotic resistance of the bacteria.
To prevent a MRSA infection, the CDC recommends good hygiene practices such as washing your hands regularly and disinfecting frequently touched surfaces. While MRSA infections have fallen in recent years thanks to more stringent precautions in health care settings, new research can lead to novel treatments to further reduce the threat of this superbug.