How common superbug causes deadly infections decoded

Scientists have discovered how one of the most common antibiotic resistant bacteria found in hospitals causes life-threatening infections, an advance that will help develop new treatments against the superbug.
Enterococcus faecalis is frequently responsible for causing hospital-acquired infections such as urinary tract infections, heart valve infections and bacteraemia (bacteria in the blood), however scientists currently have a poor understanding of how this happens.
Researchers from University of Sheffield in the UK investigated how E faecalis - bacteria commonly found in the digestive tracts of humans and multi-resistant to antibiotics - can out-compete other microorganisms and cause life- threatening infections.
The team discovered several complex mechanisms controlling the maintenance of the distinctive shape of E faecalis that forms cell pairs or short chains of cells.

The formation of short chains of cells is a crucial factor in stopping bacteria being recognised as a threat by the immune system. This then enables infection to spread, researchers said.
"Our study shows that the formation of short chains of cells by E faecalis is a critical step for causing an infection," said Stephane Mesnage from University of Sheffield.

"Bacteria that form long chains of cells are efficiently recognised and engulfed by the host immune system, whereas short chains of cells can evade host immune cells and spread in the host to cause infection," Mesnage added.
E faecalis is an opportunistic pathogen. It is naturally resistant to a wide range of antibiotics, including synthetic penicillin derivatives.

Following an antibiotic treatment, E faecalis can out- compete other microorganisms to cause infection, researchers said.
"Our work suggests that targeting the mechanisms controlling the formation of short chains of cells could be a novel strategy for developing new treatments to fight E faecalis infections," researchers said.
The study was published in the journal PLOS Pathogens.