J. Lindsay Oaks , Thomas E. Besser, Seth T. Walk, David M. Gordon, Kimberlee B. Beckmen, Kathy A. Burek, Gary J. Haldorson, Dan S. Bradway, Lindsey Ouellette, Fred R. Rurangirwa, Margaret A. Davis, Greg Dobbin, and Thomas S. Whittam1
Author affiliations: Washington State University, Pullman, Washington, USA (J.L. Oaks, T.E. Besser, G.J. Haldorson, D.S. Bradway, F.R. Rurangirwa, M.A. Davis); University of Michigan Health System, Ann Arbor, Michigan, USA (S.T. Walk); The Australian National University, Canberra, Australian Capital Territory, Australia (D.M. Gordon); Alaska Department of Fish and Game, Fairbanks, Alaska, USA (K.B. Beckmen); Alaska Veterinary Pathology Services, Eagle River, Alaska, USA (K.A. Burek); Michigan State University, East Lansing, Michigan, USA (L. Ouellette, T.S. Whittam); University of Prince Edward Island, Charlottetown, Prince Edward Island, Canada (G. Dobbin); 1Deceased.
Figure 3. Dendrogram (unweighted pair group method with arithmetic mean) of Escherichia albertii isolates from birds, based on pulsed-field gel electrophoresis band profiles. Isolates from disease outbreaks in Alaska and Scotland form clonal groups, indicating that these outbreaks are associated with expansion of a single clone. The profiles for the other isolates indicate that the bird and human E. albertii isolates are heterogeneous and do not segregate on the basis of host, geographic origin, or disease status. Scale bar indicates percent similarity.
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