We rely on antibiotics to defend us against common bacterial infections. But a few cells can escape treatment by becoming persisters that allows the infection to come back.
Scientists have now made a key discovery in understanding how a subset of bacterial cells escape being killed by many antibiotics.
Cells become 'persisters' by entering a state in which they stop replicating and are able to tolerate antibiotics.
"Unlike antibiotic resistance, this tolerant phase is only temporary but it may contribute to the later development of resistance," said researchers from the MRC Centre for Molecular Bacteriology and Infection at Imperial College London.
They have succeeded in visualising persister cells in infected tissues for the first time, and have identified signals that lead to their formation, said a new study published in the journal Science.
The team developed a method for tracking single cells using a fluorescent protein produced by the bacteria.
They showed that Salmonella, which causes gastroenteritis and typhoid fever, forms large numbers of non-replicating persisters after being engulfed by immune cells called macrophages.
By adopting this non-replicating mode, Salmonella survives antibiotic treatment and lingers in the host, accounting for its ability to cause recurrent infections.
"Now that we know the molecular pathways and mechanisms that lead to persister formation during infection, we can work on screening for new drugs to coax them out of this state so that they become vulnerable to antibiotics," said lead author Sophie Helaine.
