We’ve discovered how the superbug E. faecalis prevents chronic wounds from healing. It’s not a toxin. It’s metabolism. The bacteria use extracellular electron transport (EET) to electrochemically generate ROS, effectively "freezing" skin cells in place. doi.org/10.1126/sciadv.aeb5297

Most bacteria generate ROS inside their cell but E. faecalis generates ROS outside its cell. Our study shows this process generates hydrogen peroxide at the wound interface. This oxidative stress triggers the unfolded protein response (UPR) in the host skin cells, stopping them from migrating.

The evidence is in the movement (or lack thereof). 👇 Left: Uninfected cells closing the wound. Middle: Infected cells paralyzed by the bacteria. Right ΔEET): Mutant bacteria that cannot produce the ROS. Note how the wound closes just like the healthy control!

Crucially, we found that we can reverse this paralysis. By adding antioxidants (like catalase) to the wound, we neutralized the ROS and restarted the healing process. This could be a new blueprint for treating chronic diabetic ulcers when combined with topical antimicrobials.