Salmonella’s Surprising Weak Spot: A Single Nutrient

Researchers looking for novel pathways to attack Salmonella and treat Salmonellosis, the unpleasant and sometimes deadly intestinal disease that it causes, haven’t focused much attention on nutrient sources. It’s been considered a fairly fruitless exercise: Most bacteria can grow on any of a number of nutrients, so if you get rid of one, they just gobble up another.

But it turns out that Salmonella is a very picky eater. New research from scientists at Ohio State University reveals that a single nutrient, a sugar-amino acid combination called fructose-aspargine (F-asn), is to Salmonella what chicken nuggets are to the average three-year-old—the most divine food source in the world.

“We did a blind genetic screen to find out which genes Salmonella requires most in the gut, and a group of five genes popped up,” says Brian Ahmer, PhD, associate professor of microbiology and the project’s lead investigator. “We were surprised that they were nutrient transporters because we wouldn’t have expected that.”

Previously, University of California-Davis microbiologist Andreas Bäumler, PhD, had found that Salmonella needs to respire using tetrathionate in the gut, and that a select few nutrients are used during that process. Dr. Bäumler identified one, ethanolamine, which confers a growth advantage on the pathogen; F-Asn is the second nutrient identified and is even more important. Without it, Dr. Ahmer’s team found, Salmonella’s “fitness”—its ability to survive, grow and cause damage—dropped by 100 to 10,000 times.

Antibiotics aren’t generally used to treat Salmonellosis, except in very vulnerable groups, because they disrupt gut microbial communities and leave the person susceptible to foodborne diseases. But while F-Asn is an essential nutrient for Salmonella, it doesn’t appear to be important to many of the other microbes in the gut. “You could get rid of Salmonella without having significant off-target effects. That’s the next wave in antibiotics—getting really species-specific drugs so that you don’t disrupt microbial communities,” Dr. Ahmer says. “So one of our next steps will be to identify collaborators for a drug screen for molecules that will inhibit the nutrient utilization system for F-Asn. We’re also looking at ways to incorporate F-Asn into diagnostic media.”


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