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Zoonoses are diseases transmitted from animals to humans, posing a great threat to the health and life of people all over the world. According to WHO estimations, 600 million cases of diseases caused by contaminated food were noted in 2010, including almost 350 million caused by pathogenic bacteria. Campylobacter, Salmonella, as well as Yersinia enterocolitica and Listeria monocytogenes may dwell in livestock (poultry, cattle, and swine) but are also found in wild animals, pets, fish, and rodents. Animals, often being asymptomatic carriers of pathogens, excrete them with faeces, thus delivering them to the environment. Therefore, pathogens may invade new individuals, as well as reside on vegetables and fruits. Pathogenic bacteria also penetrate food production areas and may remain there in the form of a biofilm covering the surfaces of machines and equipment. A common occurrence of microbes in food products, as well as their improper or careless processing, leads to common poisonings. Symptoms of foodborne infections may be mild, sometimes flu-like, but they also may be accompanied by severe complications, some even fatal. The aim of the paper is to summarize and provide information on campylobacteriosis, salmonellosis, yersiniosis, and listeriosis and the aetiological factors of those diseases, along with the general characteristics of pathogens, virulence factors, and reservoirs.

Enteric redmouth disease (ERM) is a serious septicemic bacterial disease of salmonid fish species. It is caused by Yersinia ruckeri , a Gram-negative rod-shaped enterobacterium. It has a wide host range, broad geographical distribution, and causes significant economic losses in the fish aquaculture industry. The disease gets its name from the subcutaneous hemorrhages, it can cause at the corners of the mouth and in gums and tongue. Other clinical signs include exophthalmia, darkening of the skin, splenomegaly and inflammation of the lower intestine with accumulation of thick yellow fluid. The bacterium enters the fish via the secondary gill lamellae and from there it spreads to the blood and internal organs. Y. ruckeri can be detected by conventional biochemical, serological and molecular methods. Its genome is 3.7 Mb with 3406–3530 coding sequences. Several important virulence factors of Y. ruckeri have been discovered, including haemolyin YhlA and metalloprotease Yrp1. Both non-specific and specific immune responses of fish during the course of Y. ruckeri infection have been well characterized. Several methods of vaccination have been developed for controlling both biotype 1 and biotype 2 Y. ruckeri strains in fish. This review summarizes the current state of knowledge regarding enteric redmouth disease and Y. ruckeri : diagnosis, genome, virulence factors, interaction with the host immune responses, and the development of vaccines against this pathogen.

Background Yersiniosis is one of the most significant intestinal disorders caused by Yersinia enterocolitica and affects both humans and animals. This study aimed to investigate the prevalence of Y. enterocolitica in New Valley Governorate, Egypt in animals, humans, fresh milk and dried milk. Additionally, this study analyzed the presence of virulence genes, including ail and Yst in tested isolates and conducted a phylogenetic analysis to determine the genetic similarity between human, and animal Y. enterocolitica isolates. Finally, the antimicrobial resistance patterns of the isolates were examined. Results Among the 982 samples examined, the prevalence of Y. enterocolitica based on ISO10273-2017 was 11.7% in animal samples including 12.8% of animal faeces, and 10.4% in milk samples. Moreover, the prevalence of Y. enterocolitica was 13.2% in human stool, and 9.5% in dried milk samples. The molecular characterization of the six randomly selected isolates showed that the 16S rRNA, ail and Yst genes were found in 50, 33.3 and 100% of the examined Y. enterocolitica isolates , respectively. Phylogenetic analysis of animal and human isolates based on the 16S rRNA gene revealed a high degree of similarity between the isolates. All the tested animal and human Y. enterocolitica isolates (100%) were resistant to ampicillin and cefotaxime, but highly sensitive to norfloxacin. Conclusions The high prevalence of Y. enterocolitica in animal and human samples with high degrees of genetic similarity poses a threat to public and animal health. Animal faeces, milk and milk powder represent the main sources of Y. enterocolitica infection in humans. Additionally, high levels of antibiotic resistance of Y. enterocolitica can cause public health hazards by leading to the failure of disease prevention and treatment programs in humans and animals.

Cell death and inflammation are intimately linked during Yersinia infection. Pathogenic Yersinia inhibits the MAP kinase TGFβ-activated kinase 1 (TAK1) via the effector YopJ, thereby silencing cytokine expression while activating caspase-8–mediated cell death. Here, using Yersinia pseudotuberculosis in corroboration with costimulation of lipopolysaccharide and (5Z)-7-Oxozeaenol, a small-molecule inhibitor of TAK1, we show that caspase-8 activation during TAK1 inhibition results in cleavage of both gas-dermin D (GSDMD) and gasdermin E (GSDME) in murine macrophages, resulting in pyroptosis. Loss of GsdmD delays membrane rupture, reverting the cell-death morphology to apoptosis. We found that the Yersinia-driven IL-1 response arises from asynchrony of macrophage death during bulk infections in which two cellular populations are required to provide signal 1 and signal 2 for IL-1α/β release. Furthermore, we found that human macrophages are resistant to YopJ-mediated pyroptosis, with dampened IL-1β production. Our results uncover a form of caspase-8–mediated pyroptosis and suggest a hypothesis for the increased sensitivity of humans to Yersinia infection compared with the rodent reservoir.

Data on enteric yersinioses in Central America are limited. Genomic characterization of 78 Yersinia enterocolitica isolates from Costa Rica indicated persistent infection-source circulation between animal reservoirs and humans, as well as unusual antimicrobial resistance levels. Our study highlights the importance of genomic surveillance to monitor Yersinia-caused infections in Costa Rica.

Background Pure Eurasian wild boars and/or hybrids with domestic pigs are present in the wild on most continents. These wild pigs have been demonstrated to carry a large number of zoonotic and epizootic pathogens such as Salmonella spp., Yersinia enterocolitica and Y . pseudotuberculosis . Wild boar populations throughout Europe are growing and more and more wild boar meat is being consumed, the majority within the homes of hunters without having passed a veterinary inspection. The aim of this study was to investigate if factors such as population density, level of artificial feeding, time since establishment of a given population, and the handling of animal by-products from slaughtered animals could influence the presence of these pathogens in the wild boar. Results In total, 90 wild boars from 30 different populations in Sweden were sampled and analysed using a protocol combining pre-cultivation and PCR-detection. The results showed that 27% of the sampled wild boars were positive for Salmonella spp., 31% were positive for Y. enterocolitica and 22% were positive for Y. pseudotuberculosis . In 80% of the sampled populations, at least one wild boar was positive for one of these enteropathogens and in total, 60% of the animals carried at least one of the investigated enteropathogens. The presumptive risk factors were analysed using a case–control approach, however, no significant associations were found. Conclusion Human enteropathogens are commonly carried by wild boars, mainly in the tonsils, and can thus constitute a risk for contamination of the carcass and meat during slaughter. Based on the present results, the effect of reducing population densities and number of artificial feeding places might be limited.

Tissue-resident memory T cells (T RM cells) provide rapid frontline protection from reinfection. Bergsbaken and Bevan identify a gut T RM cell population generated via an unconventional pathway that is protective against a natural mouse intestinal pathogen. We report that oral infection with Yersinia pseudotuberculosis results in the development of two distinct populations of pathogen-specific CD8 + tissue-resident memory T cells (T RM cells) in the lamina propria. CD103 − T cells did not require transforming growth factor-β (TGF-β) signaling but were true resident memory cells. Unlike CD103 + CD8 + T cells, which were TGF-β dependent and were scattered in the tissue, CD103 − CD8 + T cells clustered with CD4 + T cells and CX3CR1 + macrophages and/or dendritic cells around areas of bacterial infection. CXCR3-dependent recruitment of cells to inflamed areas was critical for development of the CD103 − population and pathogen clearance. Our studies have identified the 'preferential' development of CD103 − T RM cells in inflammatory microenvironments within the lamina propria and suggest that this subset has a critical role in controlling infection.

Various pathogens systematically reprogram gene expression in macrophages, but the underlying mechanisms are largely unknown. We investigated whether the enteropathogen Yersinia enterocolitica alters chromatin states to reprogram gene expression in primary human macrophages. Genome-wide chromatin immunoprecipitation (ChIP) seq analyses showed that pathogen-associated molecular patterns (PAMPs) induced up- or down-regulation of histone modifications (HMod) at approximately 14500 loci in promoters and enhancers. Effectors of Y . enterocolitica reorganized about half of these dynamic HMod, with the effector YopP being responsible for about half of these modulatory activities. The reorganized HMod were associated with genes involved in immune response and metabolism. Remarkably, the altered HMod also associated with 61% of all 534 known Rho GTPase pathway genes, revealing a new level in Rho GTPase regulation and a new aspect of bacterial pathogenicity. Changes in HMod were associated to varying degrees with corresponding gene expression, e. g. depending on chromatin localization and cooperation of the HMod. In summary, infection with Y . enterocolitica remodels HMod in human macrophages to modulate key gene expression programs of the innate immune response.

Receptor-interacting protein kinase-1 (RIPK1), a master regulator of cell fate decisions, was identified as a direct substrate of MAPKAP kinase-2 (MK2) by phosphoproteomic screens using LPS-treated macrophages and stress-stimulated embryonic fibroblasts. p38 /MK2 interact with RIPK1 in a cytoplasmic complex and MK2 phosphorylates mouse RIPK1 at Ser321/336 in response to pro-inflammatory stimuli, such as TNF and LPS, and infection with the pathogen Yersinia enterocolitica. MK2 phosphorylation inhibits RIPK1 autophosphorylation, curtails RIPK1 integration into cytoplasmic cytotoxic complexes, and suppresses RIPK1-dependent apoptosis and necroptosis. In Yersinia-infected macrophages, RIPK1 phosphorylation by MK2 protects against infection-induced apoptosis, a process targeted by Yersinia outer protein P (YopP). YopP suppresses p38 /MK2 activation to increase Yersinia-driven apoptosis. Hence, MK2 phosphorylation of RIPK1 is a crucial checkpoint for cell fate in inflammation and infection that determines the outcome of bacteria-host cell interaction.

Yersinia enterocolitica causes yersiniosis, the third most common gastrointestinal infection in humans throughout Europe. The emergence of multidrug resistance and the lack of effective new antibiotics have drawn attention to phage therapy as a treatment option. Here, we report the complete genome sequence of phage fMtkYen3-01, which infects Y. enterocolitica serotype O:3 strains. This phage has a genome 40,415 bp in length with 45.1% GC content and 49 predicted genes. fMtkYen3-01 infected 9.5% of the 42 Y. enterocolitica strains tested and showed stability at 25–40 °C, as well as pH 5.0–10.0. These results suggest the therapeutic potential of this phage.