Abstract
The success of Salmonella as a foodborne pathogen can probably be attributed to two major features: its remarkable genetic diversity and its extraordinary ability to adapt. Salmonella cells can survive in harsh environments, successfully compete for nutrients, and cause disease once inside the host. Furthermore, they are capable of rapidly reprogramming their metabolism, evolving in a short time from a stress-resistance mode to a growth or virulent mode, or even to express stress resistance and virulence factors at the same time if needed, thanks to a complex and fine-tuned regulatory network. It is nevertheless generally acknowledged that the development of stress resistance usually has a fitness cost for bacterial cells and that induction of stress resistance responses to certain agents can trigger changes in Salmonella virulence. In this review, we summarize and discuss current knowledge concerning the effects that the development of resistance responses to stress conditions encountered in food and food processing environments (including acid, osmotic and oxidative stress, starvation, modified atmospheres, detergents and disinfectants, chilling, heat, and non-thermal technologies) exerts on different aspects of the physiology of non-typhoidal Salmonellae, with special emphasis on virulence and growth fitness.
Highlights
Foodborne pathogens have had to develop resistance mechanisms that enable them to withstand stressful environmental and processing conditions they face along the food chain and just before reaching the gut, such as starvation and acidic stomach conditions [1,2]; they have had to modify and fine-tune their virulence mechanisms in order to evade their host’s defense systems [3,4] in a co-evolutionary process with the latter
Apart from the overexpression of acid shock proteins (ASPs) and of pH homeostasis systems, it is plausible that an increase in the amount of Cyclopropane Fatty Acids (CFA) caused by adaptation to acid shock might impose some fitness cost, since they contribute to membrane rigidification, and, whereas rigid membranes seem to be associated with stress resistance, exponential growth phase cells tend to display membranes that are more fluid, which is normally related to active growing [106,107]
It should be noted these conditions are not comparable to those applied in the previously indicated studies. These results, especially from authors who did not observe any change in the expression of virulence factors, contrast with investigations that studied the effect of osmotic shocks/desiccation on the capability of Salmonella cells to invade CaCo2 cells, such as the study by Lang et al, (2017), who observed that drying increased the invasion capacity of
Summary
Foodborne pathogens have had to develop resistance mechanisms that enable them to withstand stressful environmental and processing conditions they face along the food chain and just before reaching the gut, such as starvation and acidic stomach conditions [1,2]; they have had to modify and fine-tune their virulence mechanisms in order to evade their host’s defense systems [3,4] in a co-evolutionary process with the latter. In this sense, the differences between those two evolutionary adaptation processes (adaptation to environmental stresses and to hosts) are obvious, they have several characteristics in common. It is evident that situations such as these, including growth at pH or aw close to the boundaries, are of utmost relevance for food safety, but would make the discussion too complex for the scope of this review and will not be addressed
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