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Thomas
S. Whittam, Ph.D.
Hannah Distinguished Professor
Department of Food Science and Human Nutrition
B.A., 1976, Franklin & Marshall College
Ph.D., 1981, University of Arizona
Post-doctoral studies: 1983, University
of Rochester
Address:
National Food Safety and Toxicology Center
194 Food Safety and Toxicology
Michigan State University
East Lansing, MI 48824
Email: whittam@msu.edu
Telephone: (517) 432-3100 Ext.178
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Research
Genetics of Bacterial Populations
Bacteria are a difficult and challenging problem for
population geneticists. The difficulty arises because
in nature bacteria reproduce asexually and recombine
only occasionally through mechanisms of gene transfer.
As a consequence, different species exhibit a range
of population structures from clone mixtures to freely
recombining populations similar to biological species
of higher organisms. Often the amount of recombination
in nature is intermediate - too much for a purely phylogenetic
approach and too little to assume "random assortment."
One of my main research interests has been the study
of the genetic structure of natural populations of bacteria
using molecular polymorphisms and the development of
statistical methods for assessing recombination.
Evolution of pathogenic forms
of E. coli
Although E. coli is normally a harmless organism in
the human gut, certain strains are pathogens that have
caused serious outbreaks of infectious disease. A major
research effort in my laboratory has been the study
of the evolution of pathogenic forms of E. coli associated
with intestinal and extra-intestinal infections. Through
the analysis of molecular polymorphisms, we are testing
evolutionary hypotheses regarding the major genetic
events leading to the origin of new pathogens. In the
course of this work, we have elucidated the ancestry
of a new type of food-borne pathogen, Escherichia coli
O157:H7, which causes hemorrhagic colitis. In addition,
we have investigated, in collaboration with microbiologists
from other countries, the global distribution of bacterial
clones and the dispersion of specific virulence genes
in human populations and animal reservoirs.
Experimental evolution of pathogen
virulence and host resistance
Recently developed evolutionary theory shows that natural
selection can favor intermediate levels of parasite
virulence depending on the relationship between transmissibility
and the parasite’s effect on host mortality. We
are studying the evolution of virulence experimentally
using a microbial host-parasite system. The parasite
is Legionella pneumophila, the bacterium that causes
Legionnaires disease. In nature, Legionella invade and
multiply intracellularly in amoeba and other protozoan
hosts. By propagating host–parasite genotypes
for hundreds of generations we are measuring the direction
and rate of evolution in virulence and changes in host
resistance from the ancestral (original) conditions. |
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