A team of researchers identified critical factors that allow dangerous bacteria to spread disease by surviving on surfaces in hospitals and kitchens.
The study, published in the journal PLOS Biolog, focuses on the mechanisms that enable the opportunistic human pathogen Pseudomonas aeruginosa to survive on surfaces and could lead to new ways to fight harmful bacteria.
In order to survive outside of their host, pathogenic bacteria must withstand various environmental stresses. One mechanism is the sugar molecule trehalose, which is linked to a number of external stresses, most notably osmotic shock – sudden changes in the concentration of salt around cells.
Researchers at the John Innes Center analyzed how trehalose is metabolized by P aeruginosa to define its role in protecting against external stress. By combining analytical biochemistry and reverse genetics – using mutated bacteria with no key functions – they show that trehalose metabolism in P aeruginosa is related to the biosynthesis of the carbon storage molecule glycogen.
Experiments showed that disruption of the trehalose or glycogen pathways significantly reduced the survivability of P aeruginosa on artificial surfaces such as kitchen or hospital counters.
The study found that both trehalose and glycogen are important for stress tolerance in P aeruginosa, but counteract various stresses: Trehalose helps bacteria survive in conditions with increased salt content; Glycogen helps survive in dry (parched) environments.
The results open up the possibility of targeting the trehalose and glycogen pathways to limit the survival of pathogens on artificial surfaces.
“We showed how a dangerous human pathogen, Pseudomonas aeruginosa, reacts to environmental problems such as salt stress or dehydration. An interruption in the production of certain stress-resistant sugars in this beetle significantly reduces its ability to survive on kitchen and hospital work surfaces,” said the study’s author Dr. Jacob Malone.
One unexpected finding was how the bacteria operate different pathways for different stresses, said Dr. Malone. “Conventional wisdom has it that trehalose was responsible for both phenotypes, but we have shown that trehalose only protects against osmo-stress and that glycogen is needed to protect against dehydration. We were also surprised to see such a marked decrease in surface survival than we bothered the ways in the beetles. “
The next step for research is to understand how trehalose and glycogen metabolic pathways are regulated in P aeruginosa and closely related species. The group also wants to understand how glycogen accumulation enables bacteria to survive in arid environments, and to explain in more detail how and when different parts of the pathways are turned on and off.
P aeruginosa is an important pathogen in both animals and humans. In humans, it mainly affects the immunocompromised, which is a leading cause of pneumonia and hospital-acquired infections. Chronic P-aeruginosa infections occur in 80 percent of adult cystic fibrosis patients, where they are the leading cause of morbidity and mortality.
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