Chapter 15 : Evolution of Plasmids and Evolution of Virulence and Antibiotic-Resistance Plasmids

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Evolution of Plasmids and Evolution of Virulence and Antibiotic-Resistance Plasmids, Page 1 of 2

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This chapter discusses the characteristics and features of plasmids, providing limited but significant and often cited examples of the evolution of natural plasmids. The evolution of plasmid-mediated antibiotic resistance is illustrated through the description of the IncFIme plasmid, a well-studied virulence and resistance plasmid, and of other broad-host-range resistance plasmids. Many natural plasmids are stably maintained at their characteristic copy number within the growing bacterial population. The study of how the evolution of virulence plasmids happens may allow a more complete understanding of how pathogens evolve, and the analysis of those sequences offers the opportunity to compare virulence plasmids from closely related or distant species to better understand the origin of the pathogenic traits. Furthermore, the virulence plasmid might occasionally be replaced or driven away by incoming plasmids of the same Inc group. A model developed to describe the evolution of the iteron-based replication system is that of the IncQ plasmids. Bacterial conjugation is an essential property for plasmid dissemination. Conjugative systems (Tra systems) in gram-negative bacteria support transfer between different genera and kingdoms, regardless of their replication mechanisms. They consist of three components: the transferosome, the relaxosome, and the coupling protein. The presence of multiple physically linked resistance genes on the same plasmid, conferring resistance to different classes of antibiotics, may confer a selective advantage to the bacterial host when several antimicrobials are simultaneously administered. Such synergy between different coexpressed resistance genes would allow the recipient host to be positively selected by each individual class of antibiotics.

Citation: Carattoli A. 2008. Evolution of Plasmids and Evolution of Virulence and Antibiotic-Resistance Plasmids, p 155-165. In Baquero F, Nombela C, Cassell G, Gutiérrez-Fuentes J (ed), Evolutionary Biology of Bacterial and Fungal Pathogens. ASM Press, Washington, DC. doi: 10.1128/9781555815639.ch15
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Image of Figure 1.
Figure 1.

Phylogenetic relationships of RepA proteins and CopA antisense RNA from various virulence plasmids. Genebank numbers are indicated. DNA sequences were aligned using the multiple alignment parameter of gap penalty 7 by the DNA-man software (Lynnon BioSoft, USA).

Citation: Carattoli A. 2008. Evolution of Plasmids and Evolution of Virulence and Antibiotic-Resistance Plasmids, p 155-165. In Baquero F, Nombela C, Cassell G, Gutiérrez-Fuentes J (ed), Evolutionary Biology of Bacterial and Fungal Pathogens. ASM Press, Washington, DC. doi: 10.1128/9781555815639.ch15
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Image of Figure 2.
Figure 2.

(A) Genetic map of pZM3 and IncFI/97 plasmids of the IncFIme group. (B) Genetic map of the S. enterica serotype Typhimurium plasmid pSem (IncL/M), pHCM1 (IncHII), the multidrug resistance locus identified in S. enterica serotype Typhimurium DT193 (chromosomally located) and in S. enterica serotype Enteritidis (located on an IncI plasmid). All IS elements are shown as shaded boxes; resistance genes are shown as white boxes.

Citation: Carattoli A. 2008. Evolution of Plasmids and Evolution of Virulence and Antibiotic-Resistance Plasmids, p 155-165. In Baquero F, Nombela C, Cassell G, Gutiérrez-Fuentes J (ed), Evolutionary Biology of Bacterial and Fungal Pathogens. ASM Press, Washington, DC. doi: 10.1128/9781555815639.ch15
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