Researchers predict increasing severity of Salmonella outbreaks

Future Salmonella outbreaks are likely to become more severe, according to researchers from an Australian university.

The team from the University of Sydney used more than 17,000 Salmonella Typhimurium isolates collected from 2008 to 2016 to demonstrate that genetic networks of Salmonella are linked through a few degrees of separation, likely indicating an increasing severity of infections in future epidemics.

The study demonstrated Salmonella networks operate as “small-worlds,” in which the entire world is linked through a short chain of connections, or degrees. Researchers believe this close degree of pathogen separation could lead to the emergence of an aggressive strain, increasing the chances for a superbug.

Findings published in the journal Nature – Scientific Reports earlier this month challenge the existing view that seasonal epidemics are associated with random sets of co-circulating Salmonella Typhimurium genotypes.

Professor Mikhail Prokopenko, director of Complex Systems Research Group, said the data on Salmonella outbreaks in New South Wales in the past decade highlighted a continuing arms race between pathogens and their human hosts.

“In a classical Darwinian evolution scenario, the pathogens spread over time by initially creating many mutated variants, with the more infectious clones soon becoming the most dominant within their own population,” he said.

Complex Systems researcher Oliver Cliff said there has been little understanding of Salmonella development and how the bacteria has evolved into stronger strains.

“We found there were correlations between the severity of Salmonella epidemics and the pathogen’s genetic diversity. As unpleasant as it sounds, human hosts provide the perfect environment for the bugs to keep evolving. We hope this better understanding of Salmonella will lead to enhanced protection of food sources to reduce instances of illness and death,” Cliff said.

Professor Vitali Sintchenko, a public health microbiologist from the university’s Centre for Infectious Diseases and Microbiology, said the research paper provides an example of how pathogen complexities can be mapped to indicate previously unrecognized pathogenic evolution.

“Our paper was able to identify how the Salmonella pathogen evolves and mutates and can help us better understand what influences it to adapt, change and strengthen. Working alongside pathogen researchers, public health authorities and the fresh food industry, this network mapping will help predict future outbreaks by understanding Salmonella behavior,” Sintchenko said.

Salmonella protection

Meanwhile, another group of researchers has identified a bacterial species that protects mice against Salmonella Typhimurium.

Researchers found the microbiomes of protected mice included bacteria belonging to the species Mucispirillum schaedleri, which were absent from the other groups. Mucispirillum spp. occurs in the gastrointestinal tracts of warm-blooded animals such as mice and humans.

Results from the mice research could, in the long term, lead to development of new strategies to prevent bacterial infections of gastrointestinal tracts.

The team, led by Professor Bärbel Stecher of Ludwig Maximilian University’s Max von Pettenkofer Institute of Public Health, published findings in the journal Cell Host & Microbe.

“We generated two groups of mice, one of which contains Mucispirillum schaedleri, while the other specifically lacks it. We experimentally infected both groups with Salmonella, and were able to confirm that Mucispirillum schaedleri is causally associated with protection against Salmonella infections,” said Stecher, who is also part of the German Center for Infection Research.

Further investigation revealed the protective effect of Mucispirillum schaedleri depends on its ability to successfully compete with Salmonella for certain essential nutrients, such as nitrate. Without adequate amounts of nitrate, Salmonella Typhimurium is unable to express its most important virulence factor, a Type III secretion system so the ability to induce pathogenic changes in the lining of the gut is significantly reduced.