Notes

Total Genome Series regarding Human Mouth Actinomyces sp. HMT175 Pressure ORNL0102, quite a few the actual Saccharibacterium (TM7) HMT957.
Human infections with the food-borne pathogen Campylobacter jejuni are progressively increasing worldwide and constitute a significant socioeconomic burden to mankind. Intestinal campylobacteriosis in humans is characterized by bloody diarrhea, fever, abdominal pain, and severe malaise. Some individuals develop chronic post-infectious sequelae including neurological and autoimmune diseases such as reactive arthritis and Guillain-Barré syndrome. Studies unraveling the molecular mechanisms underlying campylobacteriosis and post-infectious sequelae have been hampered by the scarcity of appropriate experimental in vivo models. Particularly, conventional laboratory mice are protected from C. jejuni infection due to the physiological colonization resistance exerted by the murine gut microbiota composition. Additionally, as compared to humans, mice are up to 10,000 times more resistant to C. jejuni lipooligosaccharide (LOS) constituting a major pathogenicity factor responsible for the immunopathological host responses during campylobacteriosis. In this chapter, we summarize the recent progress that has been made in overcoming these fundamental obstacles in Campylobacter research in mice. Modification of the murine host-specific gut microbiota composition and sensitization of the mice to C. jejuni LOS by deletion of genes encoding interleukin-10 or a single IL-1 receptor-related molecule as well as by dietary zinc depletion have yielded reliable murine infection models resembling key features of human campylobacteriosis. These substantial improvements pave the way for a better understanding of the molecular mechanisms underlying pathogen-host interactions. The ongoing validation and standardization of these novel murine infection models will provide the basis for the development of innovative treatment and prevention strategies to combat human campylobacteriosis and collateral damages of C. jejuni infections.Campylobacter enteritis is the most common cause of foodborne bacterial diarrhea in humans. Although various studies have been performed to clarify the pathomechanism in Campylobacter infection, the mechanism itself and bacterial virulence factors are yet not completely understood. The purpose of this chapter is to (i) give an overview on Campylobacter-induced diarrheal mechanisms, (ii) illustrate underlying barrier defects, (iii) explain the role of the mucosal immune response and (iv) weigh preventive and therapeutic approaches. Our present knowledge of pathogenetic and diarrheal mechanisms of Campylobacter jejuni is explained in the first part of this chapter. In the second part, the molecular basis for the Campylobacter-induced barrier dysfunction is compared with that of other species in the Campylobacter genus. The bacteria are capable of overcoming the intestinal epithelial barrier. The invasion into the intestinal mucosa is the initial step of the infection, followed by a second step, the epithelial barrier impairment. The extent of the impairment depends on various factors, including tight junction dysregulation and epithelial apoptosis. The disturbed intestinal epithelium leads to a loss of water and solutes, the leak flux type of diarrhea, and facilitates the uptake of harmful antigens, the leaky gut phenomenon. The barrier dysfunction is accompanied by increased pro-inflammatory cytokine secretion, which is partially responsible for the dysfunction. Moreover, cytokines also mediate ion channel dysregulation (e.g., epithelial sodium channel, ENaC), leading to another diarrheal mechanism, which is sodium malabsorption. Future perspectives of Campylobacter research are the clarification of molecular pathomechanisms and the characterization of therapeutic and preventive compounds to combat and prevent Campylobacter infections.Campylobacter jejuni and Campylobacter coli can be frequently isolated from poultry and poultry-derived products, and in combination these two species cause a large portion of human bacterial gastroenteritis cases. While birds are typically colonized by these Campylobacter species without clinical symptoms, in humans they cause (foodborne) infections at high frequencies, estimated to cost billions of dollars worldwide every year. The clinical outcome of Campylobacter infections comprises malaise, diarrhea, abdominal pain and fever. Symptoms may continue for up to two weeks and are generally self-limiting, though occasionally the disease can be more severe or result in post-infection sequelae. The virulence properties of these pathogens have been best-characterized for C. jejuni, and their actions are reviewed here. Various virulence-associated bacterial determinants include the flagellum, numerous flagellar secreted factors, protein adhesins, cytolethal distending toxin (CDT), lipooligosaccharide (LOS), serine protease HtrA and others. These factors are involved in several pathogenicity-linked properties that can be divided into bacterial chemotaxis, motility, attachment, invasion, survival, cellular transmigration and spread to deeper tissue. All of these steps require intimate interactions between bacteria and host cells (including immune cells), enabled by the collection of bacterial and host factors that have already been identified. The assortment of pathogenicity-associated factors now recognized for C. jejuni, their function and the proposed host cell factors that are involved in crucial steps leading to disease are discussed in detail.Human infections by Campylobacter species are among the most reported bacterial gastrointestinal diseases in the European Union and worldwide with severe outcomes in rare cases. Considering the transmission routes and farm animal reservoirs of these zoonotic pathogens, a comprehensive One Health approach will be necessary to reduce human infection rates. Bacteriophages are viruses that specifically infect certain bacterial genera, species, strains or isolates. Multiple studies have demonstrated the general capacity of phage treatments to reduce Campylobacter loads in the chicken intestine. UNC1999 in vitro However, phage treatments are not yet approved for extensive use in the agro-food industry in Europe. Technical inconvenience is mainly related to the efficacy of phages, depending on the optimal choice of phages and their combination, as well as application route, concentration and timing. Additionally, regulatory uncertainties have been a major concern for investment in commercial phage-based products. This review addresses the question as to how phages can be put into practice and can help to solve the issue of human campylobacteriosis in a sustainable One Health approach. By compiling the reported findings from the literature in a standardized manner, we enabled inter-experimental comparisons to increase our understanding of phage infection in Campylobacter spp. and practical on-farm studies. Further, we address some of the hurdles that still must be overcome before this new methodology can be adapted on an industrial scale. We envisage that phage treatment can become an integrated and standardized part of a multi-hurdle anti-bacterial strategy in food production. The last part of this chapter deals with some of the issues raised by legal authorities, bringing together current knowledge on Campylobacter-specific phages and the biosafety requirements for approval of phage treatment in the food industry.Although extensive research has been carried out to describe the transmission pathways of Campylobacter entering livestock farms, the role of livestock farms as source of Campylobacter contamination of the environment is still poorly investigated. It is assumed that Campylobacter-positive livestock farms contribute to an environmental contamination, depending on the animal species on the farm, their Campylobacter status, the housing system, manure management as well as their general farm hygienic and biosecurity management. Different emission sources, like manure, air, water, insects and rodents as well as personnel, including equipment and vehicles, contribute to Campylobacter emission into the environment. Even though Campylobacter are rather fastidious bacteria, they are able to survive in the environment for even a longer period of time, when environmental conditions enable survival in specific niches. We conclude that a significant reduction of Campylobacter emission in the environment can be successfully achieved if various intervention strategies, depending on the farm type, are applied simultaneously, including proper general and personal hygiene, establishing of hygienic barriers, insect controls, manure management and hygienization of stables, barns and exhaust air.Numerous studies point out that at present, a complete elimination of Campylobacter species in the poultry food chain is not feasible. Thus, the current aim should be to establish control measures and intervention strategies to minimize the occurrence of Campylobacter spp. in livestock (esp. poultry flocks) and to reduce the quantitative Campylobacter burden along the food chain in animals and subsequently in foods. The most effective measures to mitigate Campylobacter focus on the primary production stage. Nevertheless, measures applied during slaughter and processing complement the general meat hygiene approaches by reducing fecal contamination during slaughtering and processing and as a consequence help to reduce Campylobacter in poultry meat. Such intervention measures at slaughter and processing level would include general hygienic improvements, technological innovations and/or decontamination measures that are applied at single slaughter or processing steps. In particular, approaches that do not focus on a single intervention measure would need to be based on a thorough process of evaluation, and potential combinatory effects have to be modeled and tested. Finally, the education of all stakeholders (including retailers, food handlers and consumers) is required and will help to increase awareness for the presence of foodborne pathogens in raw meat and meat products and can thus aid in the development of the required good kitchen hygiene.The zoonotic pathogen Campylobacter is the leading cause for bacterial foodborne infections in humans. Campylobacters are most commonly transmitted via the consumption of undercooked poultry meat or raw milk products. The decreasing costs of whole genome sequencing enabled large genome-based analyses of the evolution and population structure of this pathogen, as well as the development of novel high-throughput molecular typing methods. Here, we review the evolutionary development and the population diversity of the two most clinically relevant Campylobacter species; C. jejuni and C. coli. The state-of-the-art phylogenetic studies showed clustering of C. jejuni lineages into host specialists and generalists with coexisting lifestyles in chicken and livestock-associated hosts, as well as the separation of C. coli isolates of riparian origin (waterfowl, water) from C. coli isolated from clinical and farm-related samples. We will give an overview of recombination between both species and the potential impact of horizontal gene transfer on host adaptation in Campylobacter. Additionally, this review briefly places the current knowledge of the population structure of other Campylobacter species such as C. lari, C. concisus and C. upsaliensis into perspective. We also provide an overview of how molecular typing methods such as multilocus sequence typing (MLST) and whole genome MLST have been used to detect and trace Campylobacter outbreaks along the food chain.
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