4544B Thomas Hall
Jonathan W. Olson
Our lab studies Campylobacter jejuni physiology. C. jejuni is a gram negative spiral bacteria (see figure 1) that is responsible for more cases of bacterial food poisoning than Salmonella, E. coli and Shigella combined. C. jejuni is a normal resident of the GI tract of birds, and its primary route of transmission to humans is through contaminated poultry. This makes C. jejuni eradication of special importance to North Carolina, as the state ranks 1st and 3rd in the nation in turkey and chicken production, respectively. Campylobacteriosis, the term for the disease caused by C. jejuni, is marked by severe diarrhea, typically starting 3-7 days after ingestion of contaminated food. Treatment for infected individuals consists of hydration, patients are not usually hospitalized and antibiotic treatment is not indicated. Symptoms normally resolve in 3-5 days after they start and the infection is usually cleared within two weeks. One important consequence of C. jejuni infection is that about 1 in 1000 people contract the autoimmune disease Guillain-Barre Syndrome (GBS). GBS occurs when the patients antibody response to the infection attacks the myelin sheath of the peripheral nervous system, causing muscle weakness and flacid paralysis. GBS patients also typically recover in 1-2 years, however the case fatality rate is much higher than that for campylobacteriosis.
We have chosen to study metabolic processes that are likely to be required for bacterial persistence in the poultry. The best strategy reducing campylobacteriosis is eliminating C. jejuni contamination in the food supply. We are lucky that complete genome sequence of C. jejuni is available, and we have mined this database to choose our research targets. Once chosen, we use a combination of genomics, proteomics, biochemical assays, gene-directed mutagenesis, and an animal model to characterize each.
Other projects of interest in the lab include characterizing enzymes used to combat oxidative stress, characterizing the proteins induced by stationary phase, and the role of both types of enzymes (oxidative stress and stationary phase) in the controversial "Viable But Non-Culturable" (VBNC) state of C. jejuni. We have also initiated an interdiciplinary project investigating the properties of C. jejuni that trigger GBS.
Jon Olson was born in a suburb of Philadelphia, but began a 23 year residence in Virginia shortly after his third birthday. Jon comes from a family of scientists, and having spent much of his formative years in experimental barnyards and laboratories, a love of scientific inquiry came naturally to him. His early experience with large animal research led him to pursue Biology at the College of William and Mary, where he earned his BS in 1988. Jon's interest in biology turned toward the microbial when he took a job as a laboratory technician in the Biochemistry Department of the Uniformed Services University of the Health Sciences. There Jon spent several years studying Herpes Virus DNA replication as well as a year developing tools for mapping membrane topology of bacterial proteins. In 1992, Jon moved to Baltimore and begin his graduate studies at Johns Hopkins University, studying the biosynthesis of the metal enzyme hydrogenase in the nitrogen fixing soybean symbiont Bradyrhizobium japonicum . During his stay at Johns Hopkins, serendipity introduced him to Helicobacter pylori, which has fascinated him ever since. Jon went on to investigate various aspects of H. pylori physiology as post-doctoral fellow and later an assistant research scientist in Department of Microbiology at the University of Georgia until 2002, when he accepted an offer for an assistant professor position at NC State University.