Small molecule may stop infectious biofilms growing on medical implants



According to a new study offers a possible solution in the form of a small molecule that blocks the ability of a particularly stubborn and common infectious bacterium to form biofilms.

Biofilms can also develop on the surfaces of devices that are inserted or implanted into the body, such as pacemakers, heart valves, catheters, breast implants, artificial joints, and even contact lenses.

Infections caused by biofilms are more challenging to treat than infections caused by planktonic cells; they are strongly resistant to antibiotics and immune attack, and their occurrence on biomedical surfaces is thought to be a leading cause of death worldwide.

Consequently, there is an urgent need for new methods to tackle biofilm infections in medicine.

The new study concerns the bacterium Staphylococcus aureus, which shows a remarkable ability to form biofilms that are difficult to eradicate – a big factor in helping MRSA infections to spread in the body and resist treatment.

The researchers focused on bonding interactions that occur between certain proteins on the surfaces of the bacterial cells as they aggregate during biofilm formation.

In their paper, they note that there is growing evidence that these interactions contribute to biofilm formation, but the underlying mechanisms are not clear.

They found that one surface protein, in particular, played a dual role. The protein is called SdrC and it promotes adhesion between bacterial cells, as well as attachment of cells to surfaces.

Further investigation revealed that a small molecule (“derived from ß-neurexin”) can block the SdrC interactions between cells, effectively stopping it from recognising other bacterial cells. It can also block interactions between bacterial cells and surfaces to prevent biofilm formation.

The team believes that the findings could lead to new therapies that prevent biofilms forming on medical implants and devices, and that also help the recovery of patients following surgery.

Co-author Dr Joan A. Geoghegan, Trinity College Dublin, said that “This exciting breakthrough will inform the design of new, targeted approaches to prevent biofilm formation by staphylococci and reduce the incidence of medical device-related infection.”