epithelial cells from impairment, thus maintaining epithelial homeostasis. These results suggest that the lipid-related active component present in the ATCC 9790 cell wall, lipoteichoic acid, is crucial for this effect. This study demonstrates that E. hirae is a potential probiotic bacterium in the human intestine.15 The long-term goal of this project is to compare “wild” enterococci isolates with human infection isolates and potentially find novel methods to discriminate between environmental and clinical enterococci. It is important to know more about enterococci in the environment because little research has been done in this area. Future investigation could further indicate the presence and characteristics of pathogenic strains that occur in environmental settings. In future studies, it will be of interest to identify more of my enterococcal isolates to the species level, as well as to determine the antibiotic susceptibilities and resistances of these isolates.
Acknowledgments This research was funded by The University of Texas System Louis Stokes Alliance for Minority Participation summer research internship, NSF Grant #HRD-1202008. I especially would like to thank my mentor, Dr. Kelli Palmer, whose guidance, help and support on this project were invaluable. I would like to thank Dr. Juan E. González for his help and support during this internship. I would also like to thank members of the Palmer lab, especially Valerie Price, for their guidance, assistance and support.
References 1. Mark Huycke, Daniel F. Sahm, and Michael S. Gilmore, “Multiple-Drug Resistant Enterococci: The Nature of the Problem and an Agenda for the Future,” Emerging Infectious Diseases 4, no. 2 (1998): 239–249. 2. Ben Ridwan et al., “What Action Should be Taken to Prevent Spread of Vancomycin Resistant Enterococci in European Hospitals?” British Medical Journal 324, no. 7338 (2002): 666–668. 3. Kelli L. Palmer and Michael S. Gilmore, “MultidrugResistant Enterococci Lack CRISPR-cas,” mBio 1, no. 4 (2010): e00227–10. 4. Huycke, Sahm, and Gilmore.
5. Becton, Dickinson and Co. “BBL™ Enterococcosel™ Agar.” Quality Control Procedures. http://www.bd.com/ds/technicalCenter/inserts/L007376(08)(0406).pdf (accessed February 14, 2014). 6. Sylvie Dutka-Malen, Srefan Evers, and Patrice Courvalin, “Detection of Glycopeptide Resistance Genotypes and Identification to the Species Level of Clinically Relevant Enterococci by PCR,” Journal of Clinical Microbiology 33, no. 1 (1995): 24–27. 7. G.C. Baker, J.J. Smith, and D.A. Cowan, “Review and Re-analysis of Domain-specific 16S Primers,” Journal of Microbiological Methods 55, no. 3 (2003): 541–555. 8. J. Michael Janda and Sharon L. Abbott, “16S rRNA Gene Sequencing for Bacterial Identification in the Diagnostic Laboratory: Pluses, Perils and Pitfalls,” Journal of Clinical Microbiology 45, no. 9 (2007): 2761–2764. 9. “Ribosomes and Ribosomal RNA: (rRNA),”Ribosomal RNA. http://serc.carleton.edu/microbelife/research_methods/ genomics/ribosome.html (accessed February 14, 2014). 10. S.A. Anderson, S.J. Turner, and G.D. Lewis, “Enterococci in the New Zealand Environment: Implications for Water Quality Monitoring,” Water Science and Technology 35, no. 11 (1997): 325–331. 11. Baker, Smith, and Cowan. 12. John A.E. Farrow and Matthew D. Collins, “Enterococcus Hirae, a New Species that Includes Amino Acid Assay Strain NCDO 1258 and Strains Causing Growth Depression in Young Chickens,” International Journal of Systematic and Evolutionary Microbiology 35, no. 1 (1985): 73–75. 13. L.A. Devriese et al., “Differentiation and Identification of Enterococcus Durans, E. Hirae and E. Villorum,” Journal of Applied Microbiology 92, no. 5 (2002): 821–827. 14. Farrow and Collins. 15. E. Miyauchi et al., “Cell Wall Fraction of Enterococcus Hirae Ameliorates TNF-α-induced Barrier Impairment in the Human Epithelial Tight Junction,” Letters in Applied Microbiology 46, no. 4 (2008): 469–476.
Spring 2014
The Exley
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