From Dormancy to Eradication: Strategies for Controlling Bacterial Persisters in Food Settings

Abstract

Bacterial persistence, a dormant state that enables microorganisms to survive harsh conditions, is a significant concern in food-industry settings, where traditional antimicrobial treatments often fail to eliminate these resilient cells. This article goes beyond conventional review by compiling critical information aimed at providing practical solutions to combat bacterial persisters in food production environments. This review explores the primary mechanisms behind persister cell formation, including toxin-antitoxin systems, the alarmone guanosine tetraphosphate (ppGpp), stochastic processes (in which persistence occurs as a random event), and the SOS response. Given the serious implications for food safety and quality, the authors also report a range of physical, chemical, and biological methods for targeting and eradicating persister cells. The strategies discussed, whether applied individually or in combination, offer varying levels of availability and applicability within the industry and can serve as a guide for implementing microbial contamination control plans. While significant progress has been achieved, further research is crucial to fully understand the complex mechanisms underlying bacterial persistence in food and to develop effective and targeted strategies for its eradication in food-industry settings. Overall, the translation of these insights into practical applications aims to support the food industry in overcoming this persistent challenge, ensuring safer, more sustainable food production.

Keywords: environmental triggers; eradication strategies; food industry; persister cells.

Figure 1

Schematic representation of the modes of action type I and type II TA systems. Figure adaptation from Zhang et al. [27] review.

Figure 2

Production pathways of ppGpp and its activation of the type I TA system of HokB–SokB. An amino acid starvation triggers a stringent response, leading to (p)ppGpp accumulation and the subsequent activation of the HokB–SokB type I TA system. The HokB toxin disrupts membrane potential, contributing to bacterial persistence and survival under stress conditions. The full arrows indicate that it is direct effect. The dotted ones indicate a more indirect effect. In the case of membrane depolarization, the HokB membrane-associated toxin must be activated by the anti-toxin SokB in order to create the pores on the membrane creating the depolarization, which in turn will trigger the increase in persistence.

Figure 3

Representation of bacterial population decay in the presence of an antibiotic. The vertical axis represents the proportion of surviving cells, the horizontal axis represents exposer time (min). In this representation, it is possible to see a steep reduction in bacterial cells (non-persisters susceptible to antibiotic activity) in the first 500 min of exposer and the appearance of a power-law-like tail representing persisters survival. Figure adaptation from Rebelo et al. [10].