Amy Kirby

Postdoctoral Research Associate

B.S.A., University of Georgia, 1997.

Ph. D., University of Buffalo, SUNY, 2003.

M.P.H., Emory University, 2011.

Over the past 50 years, agriculture has evolved from a modest-scale, local or regional enterprise into an industrial-scale, world-wide business.  Unfortunately, this has also driven the scale of food-borne infections toward widespread epidemics.  It is clear that the dynamics of these infections have changed to cope with/take advantage of industrial agriculture.  We now think of single farms or processing plants as reservoirs for pathogens and animals as the breeding grounds for new strains.  Indeed, E. coli O157:H7 would likely not be the problem that it currently is without the environment provided in concentrated animal feeding operations.  Adding to the problem is the use of antibiotics, both as therapeutics and prophylactics, and the resulting drug resistance.

Like Pandora’s box, it is impossible to force industrial agriculture back to its roots, however, we must address the unintended synergy that this production scale has with pathogens.  Generally, the response has been the sledgehammer approach.  For farmers, it means more antibiotics.  For processors, it means more chemicals.  Neither of these solutions works and, even if they produce microbiologically-safe food, will anyone want to eat it?  My goal is to approach the problem from a different perspective and, hopefully, develop better solutions.  The population biology techniques used in the Levin lab will complement my background in molecular microbiology, epidemiology and agriculture to enable me to examine the microbiological environment created by industrial agriculture at a variety of levels, from molecules to populations (both of bacteria and consumers).

Currently, I am characterizing the interaction of bacteriophage with host bacteria residing in biofilms.  Past work, in this lab and others, has elucidated the dynamics of phage-host interactions in planktonic cultures.  However, the jury is still out on the efficiency of phage replication in biofilms, which are the predominant developmental state of bacteria outside the laboratory (and probably inside the lab, too).  Using both lab-adapted and wild-caught phage, I am trying to determine the characteristics which enable a phage to replicate in biofilms of either E. coli or S. aureus.  Though this work is descriptive in nature, it is necessary for the rational design of phage as therapy and/or surface treatment.

I am also interested in the role of persistence (i.e. non-genetic resistance) in antibiotic therapy and the influence of subtherapeutic treatments on subsequent therapies.   

Publications

Kirby, A. E., D. J. Metzger, E. R. Murphy and T. D. Connell. 2001. Heme utilization in Bordetella avium is regulated by RhuI, a heme-responsive extracytoplasmic function sigma factor. Infect. Immun. 69: 6951-6961. [PDF]

Kirby, A. E., N. D. King and T. D. Connell. 2004. RhuR, an extracytoplasmic function sigma factor activator, is essential for heme-dependent expression of the outer membrane heme and hemoprotein receptor of Bordetella avium. Infect. Immun. 72:896-907.[PDF]

King, N. D., A. E. Kirby, and T. D. Connell. 2005. Transcriptional control of the rhuIR-bhuRSTUV heme acquisition locus in Bordetella avium. Infect. Immun. 73: 1613-1624.[PDF]