A recently published study proposes that viruses capable of infecting bacteria, called bacteriophages, may be responsible for accelerating the evolution and increasing the impact of Pseudomonas aeruginosa, a bacterial species that causes chronic lung infections in cystic fibrosis (CF) patients.
‘Temperate phages both mediate and drive adaptive evolution in pathogen biofilms,” published in the Proceedings of the National Academy of Sciences, was a collaborative effort by researchers at three U.K.-based universities: University of Liverpool, University of Salford, and University of York.
Disease-causing bacteria that establish chronic lung infections often adapt quickly and become more infectious to the patient and resistant to antibiotic treatment, but how the evolution occurs is not well understood. In chronic lung infections, bacteriophages coexist with bacteria, and can even be found at higher levels than the bacteria they infect. The bacteriophages can modulate the physiology of the bacteria they infect, including physiological traits that influence the ability of the bacterium to cause disease in humans.
In the study, researchers examined whether bacteriophages contribute to the rapid evolution, and increased infectivity, of bacteria that cause chronic lung infections in CF patients. Specifically, bacteriophages known to coexist with Pseudomonas aeruginosa.
Using artificial sputum that mimics the patient sputum, researchers compared the rate of evolution of bacteriophage-infected bacteria to uninfected bacteria. Rate of evolution was determined by sequencing the entire genome of populations of Pseudomonas aeruginosa in each condition.
When infected with bacteriophages, the Pseudomonas aeruginosa showed increased genetic diversity in traits that are known to affect the establishment and infection of bacterium – specifically bacterial mobility, antibiotic resistance, and metabolism were enriched. The findings indicated that, in the laboratory setting, bacteriophage infection drives the positive selection of bacterial traits that enhance infection-dependent processes.
The data suggested that bacteriophage infection facilitates the evolution of Pseudomonas aeruginosa in CF patients.
If supported with clinical evidence, finding could reveal exactly how the bacteria rapidly evolves and could lead to better treatment options.
“To design better treatments and preserve our antibiotics, we urgently need to better understand how bacteria evolve in infections. These new results suggest that bacteriophages may play a much bigger role than previously thought, by turbo-charging evolutionary adaptation,” said a study author, Michael Brockhurst, of the University of York, in a press release.