Abstract

The processes of spontaneous mutation, sexual recombination and somatic hybridization provide a large array of mechanisms whereby pathogenicity may arise and new combinations of virulence may be generated within individual pathogen populations. Additional variation can also occur through migration from other populations of a pathogen, or through a range of cytological and molecular changes. A detailed understanding of the combined effects of these processes on the genetic architecture of pathogen individuals and their epidemiological and genetical behaviour in field situations will lead to the development of more effective means of controlling the long-term evolution of pathogens.

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