## 1 Introduction  
The occurrence of bacterial pathogens in the food chain is an important cause of foodborne diseases and food poisoning. Both disease states cause severe public health problems and affect well-being in both developed and developing countries [1]. According to annual data from the World Health Organization, almost 1 in 10 people worldwide falls ill because of contaminated food, and nearly one-third of 42,000 food contamination-deaths occur among children under five years of age. In low-income or middle-income countries, losses accounting for up to $10 billion are linked to unsafe food. Due to the high morbidity and mortality rates, foodborne pathogens have gained great attention among researchers. The current antibiotic crisis due to drug resistance and drug tolerance hinders the eradication of pathogens in both the food industry and in patients. Resistance mechanisms such as drug efflux and modification of drug targets are inherited traits attributable to genetic alterations [2]. In contrast, drug tolerance is a property of bacterial persister-cells, which are dormant variants of regular cells arising by non-heritable mechanisms [3]. In 1942, a small fraction within a _Staphylococcus aureus_ population refractory to penicillin treatment was discovered [4], and, in 1944, the term persisters was coined for these cells [5]. Since this first discovery, scientist reported stochastic phenotypic variations conferring drug tolerance in almost every bacterial species [6]. Although a universal definition is lacking, persisters are normally described as transiently antibiotic tolerant phenotypic variants that allow a population to survive antibiotic exposure [7]. It is noteworthy that persisters are not necessarily completely and metabolically inactive. For example, intramacrophage _Salmonella_ persisters secrete certain effectors to diminish host pro-inflammatory immune responses and induce macrophage polarization [8]. Persisters formed either during stress conditions (type I persisters) or are continuously generated during exponential growth (type II persisters), which allows a subpopulation to always be prepared to tolerate future stresses [9]. Clinically, persisters play a role in chronic, recurrent, and antibiotic-resilient infections. In addition, persisters contribute to antibiotic resistance development. For instance, in vitro experiments showed that formation of persisters precedes and promotes the emergence of heritable resistance [10]. [PERSON] et al. [11] reported that _Salmonella_ persisters promote the spread of resistance plasmids in the gut. Therefore, a full understanding of persisters and the stimuli inducing their formation is much desired. The more we know about various persister types and their formation mechanisms, the better we can control this special phenotype to reduce its impact. Due to the low metabolic activity of persister-cells, antibiotics fail to eradicate them. Therefore, new approaches are needed. One possible treatment for persisters is the use of natural or synthetic antimicrobial peptides (AMPs). Natural AMPs are small molecules produced by animals and plants as the first line of defense against a wide spectrum of pathogenic microbes, and by microbes to maintain their environmental niche. Currently, more than 3200 natural AMPs are recorded in The Antimicrobial Peptide Database ([[http://aps.unmc.edu/AP/main.php](http://aps.unmc.edu/AP/main.php)]([http://aps.unmc.edu/AP/main.php](http://aps.unmc.edu/AP/main.php))). Though the synthesis is still costly, it is possible to modify or fully synthesize AMPs to widen the scope of their antimicrobial action as well as to address natural disadvantages such as instability and potential toxicity [12]. Unlike most antibiotics, which target specific cellular metabolic processes, AMPs act via direct interaction with bacterial membranes and, if deployed to combat infections, through interaction with host immunity [13]. Additionally, several AMPs can interact with intracellular targets [14].