These bacteria later 'awaken' when that treatment is over, resuming their work.
It was known that there is a connection between these kind of bacteria and the naturally occurring toxin HipA in the bacteria, but scientists did not know the cellular target of this toxin and how its activity triggers dormancy of the bacteria.
Recently, Hebrew University researchers led by Prof. Gadi Glaser of the Faculty of Medicine and Prof. Nathalie Balaban of the Racah Institute of Physics have been able to demonstrate how this happens. Their research showed that when antibiotics attack these bacteria, the HipA toxin disrupts the chemical “messaging” process necessary for nutrients to build proteins.
This is interpreted by the bacteria as a “hunger signal” and sends them into an inactive state, (dormancy) in which they are able to survive until the antibacterial treatment is over and they can resume their harmful activity.
The research on persistent bacteria has been conducted in Prof. Balaban’s lab for several years, focusing on the development of a biophysical understanding of the phenomenon. It will be combined with other work being done in Prof. Glaser’s laboratory focusing on combating persistent bacteria, in the hope of leading to more effective treatment for bacterial infections.