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Chapter 17 : Emergence, Spread, and Extinction of Pathogenic Bacterial Clones
Category: Fungi and Fungal Pathogenesis; Bacterial Pathogenesis
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The tremendous genetic diversity observed among pathogenic bacteria mirrors their different lifestyles and physiological versatility; their evolution has enabled them to adapt to specific niches and growth conditions. A remarkable aspect of the major gram-positive community-acquired pathogens infecting humans is the extent of their clonality. A number of factors may influence the emergence, spread, and extinction of clones. These are discussed sequentially for Staphylococcus aureus, Streptococcus pyogenes, and Streptococcus pneumoniae, and the common themes and differences between these organisms are explored. A series of methicillin-susceptible S. aureus isolates of phage type 80/81 isolated between 1962 and 1998, most of which were multilocus sequence type (ST) 30, have been shown to harbor the genes encoding Panton-Valentine Leucocidin (PVL), a common virulence factor among many isolates of contemporary community-associated methicillin-resistant S. aureus (CA-MRSA) strains. Infectious disease epidemiology is characterized by patterns of emergence, spread, and evolution of strains, with phases of reduction and apparent extinction or stabilization of genetic types, and the emergence of new pathogenic or antimicrobial-resistant clones. A major determinant in the stability of bacterial clones is the relative impact of point mutations, DNA rearrangements and horizontal gene transfer, and bacteriophage acquisition, although other factors are undoubtedly important. An expansion in the implementation of sequencing methodologies and clustering algorithms to examine clonal emergence and spread will be important for our continued understanding of how bacteria evolve to become virulent and the response of bacterial populations to antibiotics and vaccines.