James Bina, PhD

The Bina lab studies mechanisms of antimicrobial resistance and bacterial pathogenesis in the gram-negative pathogens Vibrio cholerae and Klebsiella pneumoniae. The long-term goal of our studies is to define the underlying processes that allow bacteria use to cause disease and resist antibiotics. There are two ongoing research projects:

I. Function of the RND transporters in V. cholerae pathogenesis. RND efflux systems are ubiquitous transporters in Gram-negative bacteria and have critical functions in antimicrobial resistance. Independent of antimicrobial resistance, RND transporters also effect the expression of diverse phenotypes including virulence, metabolism, and environmental adaptation. Thus, RND transporters fulfil unknown physiological functions in addition to their role in antimicrobial resistance. 

V. cholerae is an important human pathogen that causes ~5 million cases of the epidemic diarrheal disease cholera each year. V. cholerae is also a model enteric pathogen. Like most enteric pathogens, V. cholerae encodes multiple RND transporters that contribute to diverse phenotypes. Our previous studies documented that the RND systems were required for V. cholerae pathogenesis and antimicrobial resistance. Ongoing work is focused on characterizing the molecular mechanisms that link RND-mediated efflux to pathogenesis and identifying novel inhibitors of the RND efflux systems.

II. Antimicrobial resistance in K. pneumoniae. K. pneumoniae is an understudied gram-negative pathogen that causes a multitude of healthcare-associated infections including pneumonia, bloodstream infections, urinary tract infections, wound or surgical site infections, and meningitis. K. pneumoniae has rapidly evolved resistance to all clinically relevant antibiotics. This resulted in K. pneumoniae being identified as a member of the ESKAPE pathogens and included in the World Health Organization’s Priority 1 list of antibiotic-resistant pathogens for which new therapeutics are critically needed. We are working to define and characterize the intrinsic mechanisms that allow K. pneumoniae to resist antibiotics and persist in humans during infection.