5/3/2023 0 Comments Vector td unblocked![]() At present, only a handful of loci are known to be necessary for the production of a successful infection in the vector and half of them are regulatory genes. pestis to infect fleas also applies to other aspects of blockage. The lack of knowledge on the “nutritional” mechanisms used by Y. Therefore, blockage boosts plague transmission. The direct consequences of blockage of the proventriculus include (i) the contamination and regurgitation into the dermis of the fresh blood drawn by the infected flea and (ii) an increase in the biting rate as the “blocked” flea starves to death. Ultimately, the consolidated mass causes freshly drawn blood to be blocked in the proventriculus, preventing meal ingestion in the midgut. pestis’ production of an extracellular biofilm that consolidates a soft bactericidal mass produced in the proventriculus and that entraps the bacilli (Fig. In the foregut, these compounds are presumably involved in Y. The nutrients imported by OmpF and the compounds synthesized by RpiAs and Rpe are important for colonization of the proventriculus but not for colonization of the midgut. The only proteins known to be involved in uptake and metabolic are the outer membrane porin OmpF, two ribose phosphate isomerases A (RpiAs) and the ribose phosphate epimerase (Rpe). pestis’ ability to detect, acquire and metabolize nutrients during flea infection is very limited. pestis remains confined to the foregut (proventriculus) and midgut until it is transmitted to a new mammalian host (Fig. The plague agent, Yersinia pestis, is a Gram-negative bacterium that efficiently spreads through mammalian and flea hosts. However, our knowledge is still fragmented with regard to (i) when and how the pathogen takes advantage of ingested nutrients, (ii) the exact source and origin of the nutrients used by the pathogen during an infection, and (iii) the spatial and temporal interplay between a pathogen and its host. Consequently, one can intuitively presume when and where the salvage and biosynthetic pathways for the nutrient of interest are respectively used during an infection. Based on this assumption, one can intuitively deduce the source and origin of the nutrients scavenged by the pathogen during infection. It is generally thought that when a nutrient is available in the environment, the microorganism prefers its salvage pathway to its biosynthetic pathway because the former is more cost-effective. It is therefore not surprising that many microorganisms have both a salvage and a biosynthetic pathway for a given nutrient, in order to survive in fluctuating and sometimes crowded gut environments. In other words, the availability of a nutrient varies throughout the process of gut colonization. Furthermore, the gut lumen is an arena where pathogens compete with the microbiota for nutrient acquisition. Indeed, the lumen content’s composition depends on the host’s diet and absorptive processes in the gut’s various compartments. However, to colonize the host, a pathogen must overcome or circumvent a variety of metabolic issues- even in the lumen of the host’s gut, where microbes are bathed in the nutrients provided by an ingested meal. ![]() Multicellular organisms are a bonanza for those who know how to make the most of them, and pathogens, especially vector-borne pathogens, excel in this profit game. Thus, spatial and temporal factors dictate the bacterium’s lipoylation strategies during an infection, and replenishment of lipoate by digestive proteolysis in the vector might constitute an Achilles’ heel that is exploited by pathogens. ![]() pestis primarily uses lipoate provided by digestive proteolysis (presumably as lipoyl peptides) rather than free lipoate in blood, which is quickly depleted by the vector. Interestingly, the salvage pathway’s lipoate/octanoate ligase LplA enhances the first step in lipoate biosynthesis during foregut colonization but not during midgut colonization. Remarkably, lipoylation of metabolic enzymes, via the biosynthesis and salvage of lipoate, increases the Y. Using Yersinia pestis (the plague bacillus) and its flea vector, we developed a bioluminescence-based approach and employed it to investigate the mechanisms of pathogenesis at an unprecedented level of detail. How these pathogens successfully exploit this environment in time and space has not been extensively characterized. To thrive, vector-borne pathogens must survive in the vector’s gut.
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