COMPARATIVE PATHOG 1 Sahar M EL-Alfy, 2 Salwa 3* Am 1 Microbiology Section, Botany De 2 U.S.Naval Med 3 Biotechnolog ARTICLE INFO ABST Shiga to for spor several present O114, O present induce sequenc electrop one from the rem enteroh inocula STEC i (6/10) o shared profile. pronoun with dia non-O1 INTRODUCTION Shiga toxin-producing enterohemorrahgic Esche strains of serogroup O157:H7 and non O157:H cause hemorrhagic colitis, which is may be follo uremic syndrome (HUS) and/or acute encepha Paton 2004 and Wani et al., 2003). Shiga toxin, e stx1 or stx2 genes, plays a critical role in the path caused by E. coli O157:H7 (Sheng et al., 20 pathogenesis of these diseases is not well und experimental findings (Fujii et al., 1993), a poss the development of these diseases following an has been proposed: shiga toxin hematogenously the gut to the kidney or the brain (Eijikita et al. tissue damage. E. coli (STEC) or Verotoxigenic V E. coli) is usually acquired by consuming contami although person-to person transmission has not b Mor and Finlay 2006). Most individuals infected from the infection without further complications. patients, primarily children and the elderly, ma complications such as HUS, characterized by thrombocytopenia and hemolytic anemia (Tarr et EHEC is not invasive and is restricted to the lume *Corresponding author: Amira. M. Zakaria Biotechnology institute, Suez Canal University, Ismailia ISSN: 0975-833X Article History: Received 24 th May, 2013 Received in revised form 11 th June, 2013 Accepted 16 th July, 2013 Published online 23 rd August, 2013 Key words: Enterohemorrahgic EHEC Escherichia coli PFGE, Biotype, Serogroup, Virulence Genes, Molecular Profiles, Antibiotic Resistance, Shiga toxin. RESEARCH ARTICLE GENICITY, TOXICITY AND PULSE TYPES NON -O157 Escherichia coli a F. Ahmed, 1 Samy. A. Selim, 1 Mohamed. mira. M. Zakaria, and 2 John. D. Klena epartment, Faculty of Sciences, Suez Canal Univ dical Research Unit No.3 (NAMRU - 3) Cairo, Eg gy institute, Suez Canal University, Ismailia, Egy TRACT oxin producing Escherichia coli (STEC) are recognized as an imp radic cases to serious outbreaks worldwide (Wani et al., 2003). The recent outbreaks due to STEC have highlighted the threat this orga study describes the molecular characterization of STEC expressin O125 and O26) isolated from different sources in Egypt and inv study investigated the ability of each Shiga toxin producing strain disease in vivo using a rat model. STEC strains were identified cing analysis; clonality was determined by comparing pulsetyp phoresis. Ten STEC isolates (three from human stool, four from an m untreated water) were positive for a combination of stx genes; th maining were only positive for stx1. Two of the STEC isolates c hemorrhagic E. coli (EHEC) hemolysin gene, hlyA. All STEC isola ation of STEC bacterial broth or their respective purified toxin to isolates by pulsed-field gel electrophoresis (PFGE) revealed three d of the isolates shared the same PFGE (mrp1) pattern, representing th a second common (mrp II) pattern. Only one strain (10%) show In vivo challenge experiments with O157 and non O157 STE nced epithelial lesions and severe vascular damage. This study ide arrhea, and demonstrated that meats and untreated water available i 157 STEC strains. This finding is of concern due to the potential of t Copyright, IJCR, 2013, erichia coli (STEC) H7 STEC serogroups owed by hemolytic- alopathy (Paton and encoded by either the hogenesis of diarrhea 004). However, the derstood. Based on sible mechanism for n O157:H7 infection y disseminates from ., 2000) resulting in Vero toxin producing inated food or water, been ruled out (Gal- with EHEC recover However, 8–10% of ay go on to develop acute renal failure, al., 2005).Although en of the gut a, Egypt (Acheson et al., 1996) in some circ intestinal tract is able to cross th blood stream. Stx targets the en resulting in intestinal as well as Cleary 2003). Despite progress m the involvement of inflammatory relatively little is known about E intestinal tract and its association define these changes adequately, infection is needed. In rabbits symptoms similar to humans (R absence of renal injury by Stx immunological resources are impo animal model. The ability of S humans is related to the productio (Stx1, Stx2, or variants), which inh leading to cell death (Djordjevi investigation of STEC is complic lack of heterogeneity between c capacity of many methods used to enterohemorrhagic disease is in between clonal members. Ther methods that are highly discrimin context, maximizing the likelihoo amount of variation between stra Available online at http://www.journalcra.com International Journal of Current Research Vol. 5, Issue, 08, pp.2043-2051, August, 2013 I OF O157 AND . H. Abdel Aziz, versity, Ismailia, Egypt gypt ypt portant foodborne pathogen, responsible e morbidity and mortality associated with anism poses to global public health. The ng five different serotypes (O157, O158, vestigates their clonal relationship. The ns with different genetic backgrounds to d and characterized by PCR and DNA pes generated during pulsed field gel nimal stool, two from meat products and hree were positive for both stx1 and stx2, contained eae, whereas one carried the lates exhibited in vivo toxic effects after experimental rats. Subtyping of the ten distinct restriction patterns. Sixty percent he most common profile; and 30% (3/10) wed a distinct and unique mrp III PFGE TEC induced disease in rats, including dentified STEC O157 from human cases in Egypt were contaminated with diverse these organisms to cause human disease. , Academic Journals. All rights reserved. cumstances Stx produced within the he epithelial barrier and enter the ndothelium of susceptible tissues, systemic dysfunction (Ochoa and made during recent years regarding y response in HUS pathogenesis, EHEC-induced local changes in the with systemic disease. In order to , an animal model of EHEC oral s, EHEC induces gastrointestinal Ritchie et al., 2003), however the and the paucity of genetic and ortant limitations for the use of this STEC to cause serious disease in on of one or more Shiga-like toxins hibits protein synthesis of host cells, ic et al., 2003). Epidemiological cated by the ubiquitous nature and clonal strains. The discriminatory o subtype isolates of E. coli causing nsufficient to resolve differences refore phenotypic and genotypic natory are particularly useful in this od of detecting the often minimal ains (Putnam et al., 2004). These INTERNATIONAL JOURNAL OF CURRENT RESEARCH