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Unexplained Fever in the Pediatric Age Group
Published in Benedict Isaac, Serge Kernbaum, Michael Burke, Unexplained Fever, 2019
In recent years, gastrointestinal infections with Campylobacter jejuni and Yersinio enter ocolitica have been responsible for endemic and epidemic diarrhea, which can be accompanied by a multitude of extra-intestinal manifestations. Campylobacter jejuni can cause fever, occasionally up to 40°C, and seizures, in a proportion exceeding that expected in infants and children with fever of other etiologies.24Yersinia enterocolitica gastroenteritis and Yersinia pseudotuberculosis can be preceded or followed by episodes of unexplained fever and arthritis or arthralgia, but prolonged fever may be the only sign.25
Bacteria
Published in Loretta A. Cormier, Pauline E. Jolly, The Primate Zoonoses, 2017
Loretta A. Cormier, Pauline E. Jolly
Thus far, only one study has found Yersinia pseudotuberculosis in wild primates. Here, it was found in several human-habituated lemur species (Bublitz et al. 2015). Outbreaks of both Y. pseudotuberculosis and Y. enterocolitica have been reported in a wide range of captive primates in zoos and laboratory environments, often identified after fatalities occur. Examples of Y. pseudotuberculosis include New World monkeys (Saguinus, Saimiri spp.), Asian monkeys (Macaca spp.), and African monkeys (Cercocebus, Erythocebus, Papio spp.) (Buhles et al. 1981; Bronson et al. 1972; Kageyama et al. 2002; Taffs and Dunn 1983). Examples of Y. enterocolitica include prosimians, New World monkeys (Ateles, Callithrix, Lagothrix, Saguinus, Saimiri spp.), Asian primates (Hylobates, Macaca spp.), and African monkeys (Cercopithecus, Cercocebus spp.) (Iwata et al. 2005; Poelma et al. 1977; Van Damme et al. 1978). These studies suggest that wild primates, at least, are susceptible to enteric forms of Yersinia parasites. In one study of Y. pseudotuberculosis (Kageyama et al. 2002) and one of Y. enterocolitica (Iwata et al. 2005) involving captive primates, the parasite was also isolated from local rodents.
Yersinia pseudotuberculosis YopE prevents uptake by M cells and instigates M cell extrusion in human ileal enteroid-derived monolayers
Published in Gut Microbes, 2021
Alyssa C. Fasciano, Gaya S. Dasanayake, Mary K. Estes, Nicholas C. Zachos, David T. Breault, Ralph R. Isberg, Shumin Tan, Joan Mecsas
Many diverse bacterial and viral pathogens, including enteric Yersinia spp., exploit specialized epithelial microfold (M) cells that reside within the follicular associated epithelium (FAE) above Peyer’s patches (PP) to gain access to deeper tissues.1–3 M cells play a major role in immunosurveillance by taking up and delivering luminal contents to PP and have distinct morphology including apical polarization of β1 integrin and the lack of tightly packed apical microvilli present on neighboring enterocytes.1,4–6 The enteropathogenic bacteria, Yersinia pseudotuberculosis (Yptb) and Y. enterocolitica, are primarily transmitted via ingestion of contaminated food by the fecal-oral route and are psychrotrophs that can grow at temperatures below 4°C.7 Thus, outbreaks have been associated with food stored in the cold such as milk products and vegetables.8–12 After ingestion, Yptb primarily targets to the terminal ileum and gain access to underlying lymph tissues to cause acute intestinal illness and mesenteric lymphadenitis and in rare cases can spread systemically.13 In murine intestinal ligated loop infection models, Yptb has been shown to bind to β1 integrins on M cells using the bacterial adhesin protein invasin.2,14 After breaching the intestinal layer, Yersinia establish infection in PP and form extracellular microcolonies derived from a clonal bacterium.15–18
Inflammatory bactericidal lectin RegIIIβ: Friend or foe for the host?
Published in Gut Microbes, 2018
Tsuyoshi Miki, Nobuhiko Okada, Wolf-Dietrich Hardt
RegIIIβ also plays a protective role against Gram-negative enteropathogens. TLR2-dependent RegIIIβ expression appears to contribute to intestinal clearance of Yersinia pseudotuberculosis.8 However, it remains unknown whether the direct killing of Y. pseudotuberculosis by RegIIIβ can explain for this protective effect, as recombinant RegIIIβ proteins have been shown to lack the bactericidal activity towards Y. pseudotuberculosis.8 Moreover, the absence of RegIIIβ confers susceptibility to salmonellosis upon oral infection with S. Enteritidis.11 In conclusion from these studies, it appears that RegIIIβ protects by inhibiting translocation of the pathogens from the gut lumen into intestinal tissue, rather than by killing the pathogens in the gut lumen.
Quorum sensing pathways in Gram-positive and -negative bacteria: potential of their interruption in abating drug resistance
Published in Journal of Chemotherapy, 2019
Shafiul Haque, Dinesh K. Yadav, Shekhar C. Bisht, Neelam Yadav, Vineeta Singh, Kashyap Kumar Dubey, Arshad Jawed, Mohd Wahid, Sajad Ahmad Dar
Salicylideneaniline is another small peptide virulence factor inhibitor of T3SS in EPEC without influencing motility and expression of flagellin.246 Additionally, micromolar concentrations of INP002 and INP008 can hinder T3SS secretion in Yersinia pseudotuberculosis.247 Though, the exact molecular targets of salicylideneaniline, INP002 and INP008 are equivocal. Molecules targeting the toxin genes by inhibiting its transcription regulators or inhibiting the toxins directly have attracted the attention. For example, virstatin was found to inhibit transcription regulator ToxT in V. cholerae.248 Virstatin ceases the expression of cholera toxin and toxin co-regulated pilus, which are accountable for secretory diaorrhea and attachment of V. cholerae to human intestinal wall.248 Similarly, compound peptide toxin has been shown to bind with cholera toxins.249 Essentially, RNAIII-activating protein controls the expression of α-toxin and serine protease in S. aureus.250 The RNAIII-activating protein is inhibited by RNAIII-activating protein inhibitor peptide (RIP), which also inhibits biofilm formation, α-toxin production and serine protease expression in S. aureus.251 Though, in vivo proteolysis of RIP could confine its potential in the therapeutic application.251 Hamamelitannin is also reported to restrain RNAIII-activating protein,251 however, its biological property in presence of esterases is questionable. Several other small molecules have also been reported to inhibit bacterial virulence factor.252,253