(711b) Development of Synthetic-Hybrid Systems for Enhanced Gene-Expression Control

Development of Gene-Regulatory Control Tools for Salmonella Reduction in Poultry

Brittany Forkus and Yiannis Kaznessis

The development of antibiotic resistance in foodborne pathogens poses a major challenge to current healthcare efforts as it limits our potential treatment options. The rise and spread of these resistant strains is believed to be largely attributed to the overuse of antibiotics, particularly in livestock. Gastrointestinal illnesses caused by these pathogens affect millions and resistant infections yield higher rates of mortality, morbidity, and increased hospital costs when compared to infections caused by antibiotic-sensitive strains. Salmonellainfections, in particular, are primarily derived from poultry sources and yield the highest number of foodborne infections, hospitalizations, and deaths in the U.S, making it a rising concern to limit the number of resistant strains that make their way into food products.

We propose the development of an antibiotic alternative for livestock purposes to reduce Salmonella carriage in poultry. We have re-engineered the probiotic E.coli strain, Nissle 1917, to produce and secrete the antimicrobial peptide, Microcin J25 (Mccj25). Antimicrobial peptides are essentially the antibiotics of the bacterial kingdom and are natively produced by bacteria to ward off competitors and to modulate bacterial populations, but from an engineering standpoint, they serve as an untapped reservoir of antibiotic activity. The engineered Nissle we have developed constitutively produces high titers of Mccj25. In vitro results of this engineered strain demonstrate remarkable antagonistic activity against the leading foodborne strain, Salmonella enteritidis (SE). In our work, we have run pilot studies to observe the effect of our engineered probiotic on young, male turkey poults challenged with SE. We hypothesize that our engineered probiotic could aid in the reduction of SE in turkey poults by an antibiotic-free mechanism.