Professor(601) 984-1700Email Education PhD, University of Mississippi Medical Center
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Our studies of experimental bacterial keratitis in the rabbit have shown that once bacteria reach a million colony forming units per cornea, the pathogenic processes initiated by bacterial products cannot be reversed by the administration of fortified antibiotics alone or in combination with antiinflammatory drugs. Bacterial toxins and/or enzymes released into the cornea cause damage directly and they stimulate neutrophil infiltration causing more damage. The result of keratitis is irreversible scarring and a loss in visual acuity or even blindness. Thus, there is a need for new therapies designed to arrest damage as antibiotic therapy kills the bacteria, a benefit that no presently available drugs can offer.
The development of such therapy requires a full understanding of the bacterial products that mediate the damage. Underway are bacterial genetic and biochemical studies to identify such reactive molecules and to seek chemotherapeutic or immunological means to arrest their action. These studies are designed to improve therapy of eye infections and the research employs experimental models particularly well suited to detect and analyze new aspects of bacterial virulence. The major ongoing components of this research include:
Our research also includes the study of anti-microbial agents in treating and preventing infections. Important to the antibiotic research are new antibiotics as well as the development of new formulations that better deliver drugs to the eye. Animal models of keratitis suitable for quantifying the effectiveness of antibiotic therapy have been developed for Pseudomonas aeruginosa, Serratia marcescens, Staphylococcus aureus, and Mycobacterium abscessus. A model for studying the benefits of antibiotic prophylaxis has also been developed and used to quantify the value of specific formulations.