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Chapter 22 : Persister Bacteria

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Abstract:

This chapter focuses on persistence in because recent genetic analysis and novel tools for studying persistence in single cells have resulted in new data, but persistence is a ubiquitous phenomenon observed in many different bacterial species. Persistence may be a bet-hedging strategy for survival in fluctuating stressful environments. Still, the identification and characterization of underlying mechanisms responsible for persistence await future studies. The importance of persister bacteria in the recalcitrance of biofilms to antibiotic treatments and the recent observation of genes that enhance type I persistence in biofilms have suggested that biofilm formation may be one of those triggers. Wild-type () seems to generate both types of persister bacteria. The results showed that persisters of differ from both stationary phase cells and exponentially growing cells, that they downregulate chemotaxis genes, and that they overexpress several toxin-antitoxin genes. The chapter provides a mathematical model which gives a framework for the analysis and prediction of the dynamics of persister formation, with and without antibiotics. In the mutants, it has been found that stochastic fluctuations in the number of active HipA proteins underlie the high persistence phenomenon. Bacterial persistence has emerged as a fascinating example of how microorganisms may exploit the inherent noise in the concentrations of molecules in cells and amplify it to face stressful conditions.

Citation: Balaban N. 2011. Persister Bacteria, p 375-382. In Storz G, Hengge R (ed), Bacterial Stress Responses, Second Edition. ASM Press, Washington, DC. doi: 10.1128/9781555816841.ch22

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Figures

Image of Figure 1.
Figure 1.

Persistence in batch cultures is characterized by a biphasic killing curve. Schematic representation of killing curves for different persistence fractions: wild-type persistence (solid line); high persistence (dotted line) with 1,000-fold increased persistence when compared to wild type; and no persistence (dashed lines). Note that the initial killing rate is the same in all curves.

Citation: Balaban N. 2011. Persister Bacteria, p 375-382. In Storz G, Hengge R (ed), Bacterial Stress Responses, Second Edition. ASM Press, Washington, DC. doi: 10.1128/9781555816841.ch22
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Image of Figure 2.
Figure 2.

Persistence at the single cell level. Schematic view of a time lapse experiment of persister bacteria in microfludic devices. Single bacteria (black) are grown in normal growth conditions and divide in the microgrooves (a, b). Exposure to antibiotics kills growing bacteria (c). Stochastic switching of persisters to normal bacteria during the antibiotic treatment might result in killing (d). Only persister bacteria that switch to normal growth after the antibiotics are removed can divide and grow (e).

Citation: Balaban N. 2011. Persister Bacteria, p 375-382. In Storz G, Hengge R (ed), Bacterial Stress Responses, Second Edition. ASM Press, Washington, DC. doi: 10.1128/9781555816841.ch22
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Tables

Generic image for table
Table 1.

Genes related to persistence

Citation: Balaban N. 2011. Persister Bacteria, p 375-382. In Storz G, Hengge R (ed), Bacterial Stress Responses, Second Edition. ASM Press, Washington, DC. doi: 10.1128/9781555816841.ch22
Generic image for table
Table 2.

Equations for the dynamics of normal cells () and persister cells ()

Citation: Balaban N. 2011. Persister Bacteria, p 375-382. In Storz G, Hengge R (ed), Bacterial Stress Responses, Second Edition. ASM Press, Washington, DC. doi: 10.1128/9781555816841.ch22

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