37. Identification of Putative Ampicillin Resistance Genes of Plesiomonas shigelloides: A Whole Genome Analysis Approach
Session: Posters in the Park: Posters in the Park
Wednesday, October 3, 2018: 5:30 PM
Room: N Hall D Opening Reception and Posters in the Park Area
Posters
  • Villarreal Poster ID Week.pdf (3.2 MB)
  • Background: Plesiomonas shigelloides are water-borne bacterial pathogens, known to cause gastrointestinal infections in humans. Though most infections are mild, in severe cases antimicrobial intervention is warranted. Antimicrobial susceptibility tests of P. shigelloides strains, including the ATCC 14029 type strain, show widespread ampicillin resistance. Generally, ampicillin resistance can be due to modifications in penicillin binding proteins or by the production of beta-lactamase enzymes (inactivating the beta-lactam ring). However, recent data shows that there may be multiple mechanisms of resistance in P. shigelloides. This study aims to elucidate the ampicillin resistance mechanism(s) of P. shigelloides by identifying target resistance genes through genome sequencing.

    Methods: MiSeq NextGen DNA sequencing of the ampicillin-resistant P. shigelloides type strain following DNA extraction and digestion yielded 655,994 reads. Due to the lack of an annotated reference strain, we identified contigs of homology from two P. shigelloides reference genomes. Concurrently, we compiled known ampicillin resistance (beta-lactamase) genes from three genetically similar human pathogens Escherichia coli, Aeromonas hydrophila, and Vibrio cholera and systematically compared the sequences to P. shigelloides contigs using the publically available software, nucleotide BLAST (Basic Local Alignment Search Tool; NCBI). Knowing that P. shigelloides are aquatic, we also compared the contigs to beta-lactamase genes of aquatic Enterobacteriaceae family species Dickeya, Erwinia, Edwardsiella, Cronobacter, Pantoea and Morganella.

    Results: Thirty-five homologous beta-lactamase sequences from ten bacterial species did not show significant regions of overlap with 53 P. shigelloides type strain DNA contigs that had significant homology to our type strain reads.

    Conclusion: Our results could signify that the ampicillin resistance mechanism(s) for P. shigelloides may be novel, although investigation of penicillin binding protein modifications is also required. Elucidation of the mechanism(s) of ampicillin resistance by this pathogen would allow for more targeted therapies for these infections as well as shed light into antibiotic resistance mechanisms of pathogens.

    Carla Villarreal, B.A. and Tracey Taylor, Ph.D., Oakland University William Beaumont SOM, Rochester, MI

    Disclosures:

    C. Villarreal, None

    T. Taylor, None

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