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HomeEnvironmentEnterococcus Aids E. coli Defense Mechanisms in Canine and Avian Infections

Enterococcus Aids E. coli Defense Mechanisms in Canine and Avian Infections

A recent study reveals that two strains of harmful Escherichia coli (E. coli) generate five to sixteen times more protective gel-like “slime” when they encounter Enterococcus faecalis (EF). This discovery may pave the way for specific treatments aimed at E. coli infections in dogs and poultry.

A recent study reveals that two strains of harmful Escherichia coli (E. coli) generate five to sixteen times more protective gel-like “slime” when they encounter Enterococcus faecalis (EF). This discovery may pave the way for specific treatments aimed at E. coli infections in dogs and poultry.

The types of E. coli under investigation — uropathogenic E. coli (UPEC) and avian pathogenic E. coli (APEC) — are responsible for urinary tract infections in dogs and blood infections in poultry.

“Urinary tract infections are quite common in dogs, although they are rarely life-threatening, making them a leading reason for antibiotics prescription in small animal medicine,” explains Grayson Walker, who was a DVM/Ph.D. student at North Carolina State University and is the main author of the study. Walker currently works as a veterinary medical officer at the U.S. Department of Agriculture.

“Conversely, APEC is a significant cause of mortality in poultry around the globe,” Walker notes. “Moreover, both types of infections worsen when EF is also present. Earlier research has shown that EF aids E. coli in surviving in low-iron conditions, like the urinary tract or bloodstream. We aimed to explore what other interactions might be occurring.”

The researchers started by cultivating various APEC and UPEC strains closer to Enterococcus in a controlled, iron-deficient environment. They found strains of APEC and UPEC that responded to EF, noting that these strains not only grew more quickly but also produced larger amounts of exopolysaccharide, a thick protective layer, in closer proximity to Enterococcus.

Next, they utilized a chicken embryo model to study both EF-responsive and non-responsive strains during co-infection. The embryos infected with EF-responsive strains showed higher mortality rates compared to those infected with non-responsive strains or when only APEC or EF were present.

Upon comparing the genomes of the EF-responsive and non-responsive strains, the researchers discovered that the responsive strains had additional genes linked to iron acquisition, virulence, and specifically capsule production.

“In these infections affecting dogs and poultry, Enterococcus acts as a protective shield for E. coli,” Walker states. “We had already established that co-infection helps E. coli survive under low-iron conditions; now we understand it also enhances E. coli’s defensive capabilities.”

“We hope this research will assist in uncovering new targets for vaccines or treatments against the co-infections of Enterococcus and pathogenic E. coli.”

This study has been published in PLOS ONE and received support from the U.S. Food and Drug Administration’s GenomeTrakr program (1U18FD00678801) and the U.S. Department of Agriculture’s Animal Plant Health Inspection Service National Bio and Agro-Defense Facility Scientist Training Program. Co-authors from NC State include research specialist Mitsu Suyemoto and professors Megan Jacob and Siddhartha Thakur. Former NC State associate professor Luke Borst also contributed to the study.