A new study finds that two subtypes of pathogenic Escherichia coli (E. coli) produce five to 16 times more protective capsular “slime” when Enterococcus faecalis (EF) is present. The finding could lead to targeted therapies for E. coli infections specific to dogs and poultry.

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Source: NIAID

Colorized scanning electron micrograph of Escherichia coli.

The E. coli in question – uropathogenic E. coli (UPEC) and avian pathogenic E. coli (APEC) – cause urinary tract infections in dogs and bloodstream infections in poultry, respectively.

“Urinary tract infections, while not usually fatal to dogs, are extremely common and one of the leading reasons antibiotics are prescribed in small animal medicine,” says Grayson Walker, former DVM/Ph.D. student at North Carolina State University and corresponding author of the study. Walker is currently a veterinary medical officer with the U.S. Department of Agriculture.

“On the other hand, APEC is a leading cause of poultry death worldwide,” Walker says. “And both infections are made more severe when there is a co-infection with EF. Previous studies have shown that part of the reason for this is that EF helps E. coli survive in low-iron environments such as the urinary tract or the bloodstream. We wanted to see what else might be happening.”

Coinfection overcomes low-iron environments 

The research team began by growing different APEC and UPEC strains progressively closer to Enterococcus in an iron-restricted culture system. They identified EF-responsive strains of APEC and UPEC and noted that these strains grew faster and produced more exopolysaccharide, a slimy, protective capsule, when they were in closer proximity to Enterococcus.

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Then they looked at EF-responsive and non-responsive strains in a chicken embryo model of co-infection and found increased mortality in embryos coinfected with EF-responsive strains compared to those coinfected with non-responsive strains or with APEC or EF alone.

They compared the genomes of EF-responsive and non-responsive strains and found that, in addition to iron acquisition genes, responsive strains had genes associated with virulence and capsule production specifically.

“For these infections in dogs and poultry, Enterococcus is acting as E. coli’s armorer,” Walker says. “We already knew that coinfection overcomes low-iron environments. Now we know it also enables E. coli to better protect itself.

“Hopefully this study will lead to the identification of new targets for vaccines or therapeutics against these coinfections of Enterococcus and pathogenic E. coli.”

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