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Chapter 1 : Impact of Genome Plasticity on Adaptation of during Urinary Bladder Colonization

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Impact of Genome Plasticity on Adaptation of during Urinary Bladder Colonization, Page 1 of 2

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Abstract:

Genome plasticity leads to the generation and selection of fitter mutants via the key processes of Darwinian evolution. Urinary tract infections (UTIs) are considered to be the most common bacterial infection in industrialized countries. Genotypic and phenotypic comparisons of closely related isolates which demonstrated the impact of genome plasticity, i.e., gene acquisition and gene loss, on bacterial evolution as different members of sequence type (ST) 73 represent highly uropathogenic as well as commensal or ABU isolates. Data on genome-wide changes and adaptation during long-term growth of in vitro have started to accumulate only recently. Bacterial adaptation to prolonged in vivo growth in different host backgrounds has been analyzed by comparing the genome structure and virulence- and fitness-related phenotypes of 83972 and three selected reisolates from deliberate human therapeutic urinary bladder colonization. In individual hosts, 83972 used different strategies to optimize proliferation. The observed increased genome plasticity of in vivo-grown reisolates of 83972 relative to control isolates from the in vitro experimental evolution study may in part result from stress-induced increased genome plasticity.

Citation: Dobrindt U, Zdziarski J, Hacker J. 2012. Impact of Genome Plasticity on Adaptation of during Urinary Bladder Colonization, p 1-15. In Hacker J, Dobrindt U, Kurth R (ed), Genome Plasticity and Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555817213.ch1

Key Concept Ranking

Mobile Genetic Elements
0.8827578
Gene Expression and Regulation
0.7894835
Urinary Tract Infections
0.53392553
Bacterial Evolution
0.53014106
Evolutionary Dynamics
0.5204137
Integrative and Conjugative Elements
0.46187532
0.8827578
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FIGURE 1

Impact of genome plasticity on adaptation and evolution of (pathogenic) bacteria. Plasmids, bacteriophages, and genomic islands may encode virulence-associated traits, such as adhesins, toxins, siderophore systems, and capsules. Acquisition of such mobile and accessory DNA elements contributes to the evolution of pathogenic variants by horizontal gene transfer. Genome plasticity can also result in alterations of gene expression or inactivation of virulence factors due to DNA rearrangements, deletions, or point mutations. Altered expression of virulence factors either as a result of active bacterial gene regulation or selection of corresponding mutants arising from genome plasticity can be advantageous for pathogenic bacteria with the ability to cause persistent infection in order to avoid or reduce activation of the host immune response.doi:10.1128/9781555817213.ch01f01

Citation: Dobrindt U, Zdziarski J, Hacker J. 2012. Impact of Genome Plasticity on Adaptation of during Urinary Bladder Colonization, p 1-15. In Hacker J, Dobrindt U, Kurth R (ed), Genome Plasticity and Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555817213.ch1
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FIGURE 2

Competitiveness of in vivo reisolates of 83972 relative to their parent strain in pooled human urine. For growth competition experiments, the chloramphenicol-resistant derivative of parent strain 83972, 83972, and one in vivo reisolate were mixed in the same ratio and cultivated at 37°C for 72 h in pooled human urine. At different time points (6, 24, 48, and 72 h), the ratio of the parent strain 83972to the in vivo reisolate was determined by colony counting on LB agar plates supplemented with chloramphenicol and LB plates, respectively. (A) Results of the control experiment, where the parent strain and its chloramphenicol-resistant variant 83972were cocultured to demonstrate their identical competitiveness. Competitiveness of consecutive reisolates (as indicated by the order of letters) from individual patients P1 to P6 differed between the patients as well as between reisolates from the same patient (B to F). All experiments were performed in triplicate, and the corresponding mean values of the ratio between parent strain and reisolate and standard deviations were plotted.doi:10.1128/9781555817213.ch01f02

Citation: Dobrindt U, Zdziarski J, Hacker J. 2012. Impact of Genome Plasticity on Adaptation of during Urinary Bladder Colonization, p 1-15. In Hacker J, Dobrindt U, Kurth R (ed), Genome Plasticity and Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555817213.ch1
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Tables

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TABLE 1

Examples of in vivo adaptation strategies of uropathogenic during infection

Citation: Dobrindt U, Zdziarski J, Hacker J. 2012. Impact of Genome Plasticity on Adaptation of during Urinary Bladder Colonization, p 1-15. In Hacker J, Dobrindt U, Kurth R (ed), Genome Plasticity and Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555817213.ch1

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