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Why is Escherichia coli resistant to most veterinary antibiotics in poultry and can we do anything to reverse this?

By John J. Maurer, PhD, and Stephen R. Collett, DVM
Poultry Diagnostic and Research Center, Department of Population Health,
University of Georgia, Athens, GA


Escherichia coli is an important opportunist pathogen of poultry, causing significant economic loss from carcass condemnations, air-sacculitis, septicemia, yolk peritonitis, and cellulitis. Antibiotics had once been effective in treating E. coli infections in poultry. Unfortunately, multidrug-resistant E. coli has rendered these antibiotics ineffective (1, 2) and the most effective class of antibiotic, the fluoroquinolones, have been withdrawn from use in poultry because of human health concerns.

Even if all therapeutic usage of antibiotics were discontinued in poultry medicine today, multi-drug resistant E. coli would persist. Why?

There are several mechanisms behind antibiotic resistance including: drug efflux pumps; enzymes that inactivate the antibiotic; alteration in the target enzyme(s); and enzymes that metabolically by-pass the targeted enzymatic step. Many of these antibiotic resistance genes reside on mobile genetic elements (plasmids, transposons, or integrons) that ferry these genes among bacteria that inhabit the animal gastrointestinal tract or animal manures. In fact, this antibiotic gene pool is quite substantial in poultry litter (3). The conventional wisdom had been that without the selection pressure (antibiotic usage), these mobile genetic elements, most notably plasmids, would place a significant metabolic disadvantage on its bacterial host. However, this is not the case. Most drug-resistant plasmids are highly regulated maintaining copy number to one per bacterial cell and faithfully partition plasmid copies between the daughter cells. More importantly, many of these plasmids contain plasmid-addiction systems that consist of a poison (toxin) and antidote (anti-toxin). Lose the plasmid; lose the antidote; and the bacterial cell dies. Many antibiotic resistance genes are regulated, limiting its metabolic burden on the bacterial cell to only those times when the cell needs it (antibiotic treatment). Worse, these antibiotic genes reside on plasmids that provide its bacterial host with some competitive advantage (bacteriocins, iron-acquisition, etc.). This fortuitous genetic linkage perpetuates antibiotic resistance even in the absence of antibiotic usage. Finally, many antibiotic genes reside on transposons that can ferry these genes between plasmids and chromosomes. Transposon insertion into the chromosome ensures the faithful propagation of the antibiotic gene as the bacterial cell replicates, over and over again. What can we do to ameliorate antibiotic resistance?

One possibility is to displace the antibiotic resistant bacterial population in animal manures or gastrointestinal tract. A bacteriotherapeutic approach was used to determine if prebiotics and probiotics administered to broiler chickens could change the litter microflora and thus reduce antibiotic resistance in the poultry environment. The probiotics and prebiotics, used in this study, did appear to have a significant impact on the species composition of the litter microflora. Unfortunately, there was no effect on antibiotic resistance gene load in poultry litter, and more importantly, there was no change in E. coli’s susceptibility to tetracycline (4). As built-up, top-dressed litter was used, the antibiotic resistance gene load in this environment was so significantly high as to overwhelm the probiotic/prebiotic regimen. It may require complete litter removal and house disinfection before benefits of bacteriotherapeutics on multidrug resistant E. coli can be seen.

Finally, we have avoided this for too long, but it’s time to place more of our research efforts into developing E. coli vaccines. There has been significant work at developing live E. coli vaccine with varied results. Focus on specific E. coli O serogroups may prove short-sighted; as one serogroup is displaced, another will emerge. Alternatively, bacterin, consisting of a cocktail of E. coli strains circulating in a poultry complex, may prove to be the best approach. However, E. coli vaccination will prove to be a revolving door due again to the diversity of E. coli O serogroups circulating in poultry flocks. Obviously, a cross-protective E. coli vaccine is needed. Going back to antibiotics to treat E. coli infections is not an option; especially in today’s regulatory climate and push back on agricultural use of antibiotics.





  1. Zhao S, Maurer JJ, Hubert S, De Villena JF, McDermott PF, Meng J, Ayers S, English L, White DG. 2005. Antimicrobial susceptibility and mo-lecular characterization of avian pathogenic Escherichia coli isolates. Vet Micro-biol 107:215-224.
  2. Bass L, Liebert CA, Lee MD, Summers AO, White DG, Thayer SG, Maurer JJ. 1999. Incidence and characterization of integrons, genetic ele-ments mediating multiple-drug resistance, in avian Escherichia coli. Antimicrob Agents Chemother 43:2925-2929.
  3. Nandi S, Maurer JJ, Hofacre C, Summers AO. 2004. Gram-positive bac-teria are a major reservoir of Class 1 antibiotic resistance integrons in poultry litter. Proc Natl Acad Sci U S A 101:7118-7122.
  4. Pedroso AA, Hurley-Bacon AL, Zedek AS, Kwan TW, Jordan AP, Avellaneda G, Hofacre CL, Oakley BB, Collett SR, Maurer JJ, Lee MD. 2013. Can probiotics improve the environmental microbiome and resistome of commercial poultry production? Int J Environ Res Public Health 10:4534-4559.



Article courtesy of The Poultry Informed Professional
Published by the Department of Population Health, University of Georgia
Editor: Dr Stephen Collett, Associate Professor



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