Researchers have discovered a concerning mechanism in dogs that may lead to ineffective antibiotic treatment for E. coli infections, which are a significant cause of antimicrobial resistance-related deaths worldwide.
A study to be published on July 16 in the journal Applied and Environmental Microbiology sheds light on potential treatment avenues for both animals and humans, emphasizing clinical infections in dogs as a means of monitoring public health.
Through analyzing over 1,000 genomes of antimicrobial-resistant E. coli strains from sick dogs, researchers identified a group of genes that were losing functionality and adapting to trap antibiotics within the bacteria’s cell membrane, making them ineffective. This unexpected adaptation could render multiple classes of antibiotics ineffective.
Laura Goodman, the senior author of the paper and an assistant professor at Cornell University, described the genetic changes as a fortuitous evolutionary event, repurposing specific genes to hinder antibiotic effectiveness.
This research not only benefits canine health but also underscores the role of dogs as a valuable model for human health studies. Dogs commonly share E. coli strains with their owners and are often treated with the same antibiotics, including critically important ones like third generation cephalosporins and quinolones identified by the World Health Organization.
The study suggests that interventions targeting the E. coli cell membrane’s pore function could enhance antibiotic efficacy, potentially unveiling new treatment options.
By leveraging leftover clinical samples from dogs, researchers have filled crucial knowledge gaps in understanding antibiotic resistance and surveillance of human E. coli infections. The collaboration with the U.S. Food and Drug Administration’s Veterinary Laboratory and Response Network provided essential support for this study.
