How superbugs hide from their host
Researchers from the University of Sheffield have discovered how a hospital superbug evades the immune system to cause infection — a breakthrough that could pave the way for new treatments.
The researchers investigated how Enterococcus faecalis, bacteria commonly found in the digestive tracts of humans, cause life-threatening infections. While E. faecalis is harmless in healthy carriers, it is also an opportunistic pathogen that frequently causes hospital-acquired infections such as heart valve infections, urinary tract infections and bacteraemia — the presence of bacteria in the blood. Scientists currently do not fully understand how this happens.
Treatment of E. faecalis infection is difficult as it is highly resistant to several key components of the immune system and resistant to multiple antibiotics. Now, new research led by Dr Stéphane Mesnage has discovered a mechanism used by E. faecalis to hide from the immune system of the host.
Published in the journal PLOS Pathogens, the study revealed that the bacteria changes a component of its cell surface in order to evade the immune system, enabling the spread of infection. The findings could pave the way for novel treatments for infections caused by E. faecalis.
“E. faecalis is an opportunistic pathogen,” said Dr Stéphane Mesnage, a Senior Lecturer in Molecular Biology and Biotechnology. “It is naturally resistant to a wide range of antibiotics, including synthetic penicillin derivatives, and is acquiring resistance to the last resort antibiotic vancomycin. Following an antibiotic treatment, E. faecalis can out-compete other microorganisms to cause an infection.
“Our study shows that this organism modifies its polysaccharide surface, which is essential for causing an infection. Bacteria whose polysaccharides are unmodified are quickly recognised and engulfed by the cells of our immune system, whereas by modifying the polysaccharide, E. faecalis can evade the host immune cells and spread infection.
“Hospital-acquired infections caused by bacteria resistant to last-resort antibiotics are on the rise. Our work suggests that targeting the mechanism that modifies the surface polysaccharides could be a novel strategy for developing new treatments to fight E. faecalis infections.”
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