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pubmed:abstractText |
One hundred and seventy-five isolates of the pathogenic bacterium Listeria monocytogenes recovered from human clinical (blood and cerebrospinal fluid), animal, and environmental sources in Europe, North America, and elsewhere were analyzed electrophoretically for allelic variation at 16 genetic loci encoding metabolic enzymes. Forty-five distinctive allele profiles (electrophoretic types, ETs) were distinguished, among which mean genetic diversity per locus (H) was 0.424. Cluster analysis of a matrix of genetic distances between paired ETs revealed two primary phylogenetic divisions of the species separated at a distance of 0.54. ETs in division I were presented by strains of serotypes 4b, 1/2b, and 4a, whereas strains of ETs in division II were of serotypes 1/2a and 1/2c. Human and animal isolates did not represent distinctive subsets of ETs. The occurrence of linkage disequilibrium between enzyme loci and the widespread distribution of certain ETs indicate that the genetic structure of L. monocytogenes is clonal. One clone, marked by ET1, caused major epidemics of human disease in western Switzerland in the period 1983-1987 and in Los Angeles County, California, in 1985, both of which were attributed to contamination of soft cheese. ET 1 is closely related to the clone (ET7) that caused two large outbreaks of listeriosis in Massachusetts in 1979 and 1983.
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