Vibrio spp., known human foodborne pathogens, thrive in freshwater, estuaries, and marine settings, causing vibriosis upon ingestion. The rising global vibriosis cases due to climate change necessitate a deeper understanding of Vibrio epidemiology and human transmission. This review delves into Vibrio contamination in seafood, scrutinizing its sources and pathways. We comprehensively assess the contamination of human‐pathogenic Vibrio in the seafood chain, covering raw materials to processed products. A “ Farm‐to‐Fork” approach, aligned with the One Health concept, is essential for grasping the complex nature of Vibrio contamination. Vibrio ’s widespread presence in natural and farmed aquatic environments establishes them as potential entry points into the seafood chain. Environmental factors, including climate, human activities, and wildlife, influence contamination sources and routes, underscoring the need to understand the origin and transmission of pathogens in raw seafood. Once within the seafood chain, the formation of protective biofilms on various surfaces in production and processing poses significant food safety risks, necessitating proper cleaning and disinfection to prevent microbial residue. In addition, inadequate seafood handling, from inappropriate processing procedures to cross‐contamination via pests or seafood handlers, significantly contributes to Vibrio food contamination, thus warranting attention to reduce risks. Information presented here support the imperative for proactive measures, robust research, and interdisciplinary collaboration in order to effectively mitigate the risks posed by human pathogenic Vibrio contamination, safeguarding public health and global food security. This review serves as a crucial resource for researchers, industrials, and policymakers, equipping them with the knowledge to develop biosecurity measures associated with Vibrio ‐contaminated seafood.

The food-borne pathogen Listeria monocytogenes is a problem for food processors and consumers alike, as the organism is resistant to harsh environmental conditions and inimical barriers implemented to prevent the survival and/or growth of harmful bacteria. One mechanism by which listeriae mediate survival is through the accumulation of compatible solutes, such as proline, betaine and carnitine. In other bacteria, including Escherichia coli , the synthesis and accumulation of another compatible solute, trehalose, are known to aid in the survival of stressed cells. The objective of this research was to investigate trehalose metabolism in L. monocytogenes , where the sugar is thought to be transferred across the cytoplasmic membrane via a specific phosphoenolpyruvate phosphotransferase system and phosphorylation to trehalose-6-phosphate (T6P). The latter is subsequently broken down into glucose and glucose-6-phosphate by α,α-(1,1) phosphotrehalase, the putative product of the treA gene. Here we report on an isogenic treA mutant of L. monocytogenes 568 (568:ΔTreA) which, relative to the wild-type strain, displays increased tolerances to multiple stressors, including heat, high osmolarity, and desiccation. This is the first study to examine the putative trehalose operon in L. monocytogenes , and we demonstrate that lmo1254 ( tre A ) in L. monocytogenes 568 indeed encodes a phosphotrehalase required for the hydrolysis of T6P. Disruption of the treA gene results in the accumulation of T6P which is subsequently dephosphorylated to trehalose in the cytosol, thereby contributing to the stress hardiness observed in the treA mutant. This study highlights the importance of compatible solutes for microbial survival in adverse environments.