Evolution of Northeastern and Midwestern Borrelia burgdorferi
Recombination is more apparent in Lyme disease foci in the Midwest than in the Northeast. This is likely to be caused by neutral divergence of linkage patterns resulting from small effective population sizes in both regions coupled with gene flow from the Northeast to the Midwest but not in the other direction. Small effective population sizes eliminate most of the linkage combinations in each region such that they are in perfect linkage disequilibrium. Gene flow from the northeastern population then introduces linkage pattern variation into the midwestern population. Linkage patterns unique to the Midwest are absent from the Northeast, suggesting that gene flow from the Midwest to the Northeast is rare.
B. burgdorferi in the Northeast and Midwest share a remarkably similar evolutionary history. Independent evolution of human invasiveness in the 2 regions does not explain the lower human Lyme disease incidence in the Midwest. Other potential causes for the differences in human Lyme disease incidence include differences in human exposure to B. burgdorferi-infected ticks and ecologic differences in the reservoir host community. Lyme disease typically is contracted peridomestically in the Northeast, but similar studies reporting the peridomestic acquisition of B. burgdorferi have not been reported from the Midwest. Human risk for exposure to Lyme disease also may be exaggerated in the Northeast because of the immense suburban populations around the major metropolitan areas. Current ecologic conditions yielding differences in the composition of reservoir host species could alter the prevalence of B. burgdorferi lineages that are particularly invasive in humans. For example, midwestern ticks are rarely infected with ospC genotypes A or B (RST I), 2 of the 4 genotypes that are common in the Northeast and regularly cause human Lyme disease.
This work was supported by National Institute of Health grants AI076342 (D.B.) and GM31912 (D.E.D) and Centers for Diseases Control and Prevention grant U01CK000170 (D.B.).
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