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Philip M Sherman - One of the best experts on this subject based on the ideXlab platform.

Olga Kovbasnjuk - One of the best experts on this subject based on the ideXlab platform.

Masatoshi Honda - One of the best experts on this subject based on the ideXlab platform.

  • Hemolytic Uremic Syndrome Following Hemorrhagic Colitis Caused by Verotoxin-producing Escherichia coli 0157:H7 : Early Signs of Hemolytic Uremic Syndrome
    The Keio journal of medicine, 1996
    Co-Authors: Atsutoshi Tsuji, Michiko Sasaki, Takefumi Kanemitsu, Norio Uehara, Hiroshi Ito, Masatoshi Honda
    Abstract:

    Ten cases of hemolytic uremic syndrome (HUS) following Hemorrhagic Colitis caused by verotoxin T2-producing Escherichia coli O157:H7 (VTEC) occurred in a Kindergarten. Slight changes in results of peripheral blood and blood chemistry studies an average of 4 days after onset suggested HUS, and within the following 12 hours platelet counts and levels of haptoglobin and lactic dehydrogenase decreased. Treatment was mainly directed toward the management of renal failure and included supportive therapy and anticoagulant and antiplatelet treatment. Although neurological complications occurred in some cases, all patients eventually recovered completely.

Dana J. Philpott - One of the best experts on this subject based on the ideXlab platform.

Edgar C. Boedeker - One of the best experts on this subject based on the ideXlab platform.

  • EnteroHemorrhagic Escherichia coli infection stimulates Shiga toxin 1 macropinocytosis and transcytosis across intestinal epithelial cells
    American journal of physiology. Cell physiology, 2011
    Co-Authors: Valeriy Lukyanenko, Chengru Zhu, Edgar C. Boedeker, Irina Malyukova, Ann L. Hubbard, Michael Delannoy, Liudmila Cebotaru, Olga Kovbasnjuk
    Abstract:

    Gastrointestinal infection with Shiga toxins producing enteroHemorrhagic Escherichia coli causes the spectrum of gastrointestinal and systemic complications, including Hemorrhagic Colitis and hemol...

  • Protection against Hemorrhagic Colitis in an Animal Model by Oral Immunization with Isogeneic Rabbit Enteropathogenic Escherichia coli Attenuated by Truncating Intimin
    Infection and immunity, 2005
    Co-Authors: Tonia S. Agin, Chengru Zhu, Laura A. Johnson, Timothy E. Thate, Zhuolu Yang, Edgar C. Boedeker
    Abstract:

    Strains of Shiga toxin (Stx)-producing Escherichia coli, also called enteroHemorrhagic E. coli (EHEC), are important food-borne pathogens for humans. Most EHEC strains intimately adhere to the intestinal mucosa in a characteristic attaching and effacing (A/E) pattern, which is mediated by the bacterial adhesin intimin. Subsequent release of Stx1 and/or Stx2 leads to the frequent development of Hemorrhagic Colitis and, less commonly, to hemolytic-uremic syndrome. The aim of the present study was to develop an attenuated A/E E. coli strain for use as a vaccine against EHEC infection encoding a truncated intimin lacking adhesive capacity, but which would still express somatic antigens, other products of the locus of enterocyte effacement pathogenicity island, and an immunogenic remnant of the intimin molecule. A single-nucleotide deletion was generated in the eae gene in the prototype rabbit A/E E. coli strain RDEC-1 (O15:H−), which resulted in truncation of intimin by 81 C-terminal residues (860 to 939 amino acids) containing a disulfide loop. Inoculation of rabbits with large doses of the truncated intimin mutant (RDEC-1Δeae860-939) was well tolerated, as observed by the absence of clinical signs of disease or evidence of intestinal A/E lesions. The efficacy of RDEC-1Δeae860-939 as a vaccine was evaluated by orogastric inoculation of rabbits with RDEC-1Δeae860-939 followed by challenge with the virulent strain RDEC-H19A, an Stx1-producing derivative of wild-type RDEC-1 capable of inducing Hemorrhagic Colitis in rabbits. Following RDEC-H19A challenge, nonimmunized control rabbits exhibited characteristic weight loss with watery to bloody diarrhea and demonstrated intimate bacterial attachment, effacement of microvilli, submucosal edema, mucosal heterophile infiltrates, and Shiga toxin-induced vascular lesions. In contrast, the RDEC-1Δeae860-939-immunized rabbits showed no clinical signs of disease, maintained normal weight gain, had reduced fecal shedding of challenge organisms, and showed an absence of gross or microscopic lesions in the intestinal mucosa. Serum antibodies specific to intimin were detected among rabbits immunized with RDEC-1Δeae860-939, indicating that truncation of the intimin functional domain not only attenuated bacterial virulence, but also retained at least some of the immunogenicity of native intimin. Although it is not possible to gauge the exact contribution of residual intimin immunity to protection, this attenuation strategy for A/E E. coli strains shows promise for the development of effective vaccines to prevent EHEC infection in humans and animals.