Journal of Biosciences

, Volume 33, Issue 5, pp 795–805

Bacterial persistence: some new insights into an old phenomenon



Bigger discovered more than 60 years ago, at the very beginning of the antibiotic era, that populations of antibiotic-sensitive bacteria contained a very small fraction (approximately 10−6) of antibiotic-tolerant cells (persisters). Persisters are different from antibiotic-resistant mutants in that their antibiotic tolerance is non-heritable and reversible. In spite of its importance as an interesting biological phenomenon and in the treatment of infectious diseases, persistence did not attract the attention of the scientific community for more than four decades since its discovery. The main reason for this lack of interest was the difficulty in isolating sufficient numbers of persister cells for experimentation, since the proportion of persisters in a population of wild-type cells is extremely small. However, with the discovery of high-persister (hip) mutants of Escherichia coli by Moyed and his group in the early 1980s, the phenomenon attracted the attention of many groups and significant progress has occurred since then. It is now believed that persistence is the end result of a stochastic switch in the expression of some toxin-antitoxin (TA) modules (of which the hipA and hipB genes could be examples), creating an imbalance in their intracellular levels. There are also models invoking the involvement of the alarmone (p) ppGpp in the generation of persisters. However, the precise mechanisms are still unknown. Bacterial persistence is part of a wider gamut of phenomena variously called as bistability, multistability, phenotypic heterogeneity, stochastic switching processes, etc. It has attracted the attention of not only microbiologists but also a diverse band of researchers such as biofilm researchers, evolutionary biologists, sociobiologists, etc. In this article, I attempt to present a broad overview of bacterial persistence to illustrate its significance and the need for further exploration.


Antibiotics hip BA operon persistence phenotypic switching tolerance toxin-antitoxin 

Abbreviations used


(3′–5′) cyclic dimeric guanosine monophosphate


flavin mononucleotide


green fluorescent protein; glpD, glycerol-3-phosphate dehydrogenase




minimum inhibitory concentration


methicillinresistant Staphylococus aureus


open reading frame


programmed cell death


glycerol-3-phosphate acyl transferase


gunanosine 3′ 5′ bispyrophosphate




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Copyright information

© Indian Academy of Sciences 2008

Authors and Affiliations

  1. 1.Department of Molecular Biology, School of Biological SciencesMadurai Kamaraj UniversityMaduraiIndia

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