Shiga toxins ELISA Kit

Enterohaemorrhagic Escherichia toff (EHEC) O157:H7 is one of the major foodbome and waterborne pathogens causing severe diseases and outbreaks worldwide. There is scarcity of EHEC O157:H7 data in South Africa. This study was carried out to determine the molecular characteristics and genotypic diversity of EHEC O157:H7 isolates in the Gauteng region, South Africa. Samples were cultured on selective chromogenic media. Antibiotic susceptibility profile of isolates was determined using the VITEK (R)-2 automated system. Isolates were characterised using multiplex PCR assays and the genetic diversity was determined using pulsed-field gel electrophoresis (PFGE) and multilocus sequence typing (MIST). A total of 520 samples of which 270 environmental water samples and 250 stool specimens were collected and analysed. Overall, EHEC O157:H7 was recovered from 2.3% (12/520) of samples collected. Environmental water samples and clinical stool specimens showed a prevalence of 4.07% (11/270) and 0.4% (1/250) respectively. Antibiotic susceptibility profile varied from isolates with full susceptibility to isolates with resistance to multiple antibiotics. Most resistance was detected to the penicillins, specifically ampicillin (7/12). amoxicillin (3/12) and piperacillin/Tazobactam (3/12) followed by one of the folate inhibitors, trimethoprim (3/12) and the carbapenems, imipenem and meropenem (2/12) each. Three isolates harboured a combination of Shiga-toxins (Six)-2, intimin (eae) and enterohaemolysin (hlyA) genes, while two isolates harboured the Stx-1, Slx-2 and hlyA genes. The PFGE performed showed that EHEC O157:H7 isolates were genetically diverse, with two minor pulsotypes and eight singletons. The MIST analysis identified sequence types (STs) (ST10, ST11 and ST1204) that have been previously reported associated with outbreaks. The STs identified in this study pose a potential public health risk to consumers of untreated environmental water and dosed human contacts. There is necessity to enhance surveillance in reducing the propagation of this bacterium which is a public health problem. (C) 2019 Elsevier B.V. All rights reserved.

Shiga toxin-producing Escherichia coli (STEC) are important foodborne pathogens responsible for a wide spectrum of diseases including diarrhea, bloody diarrhea, and hemolytic uremic syndrome (HUS). A considerable number of outbreaks and sporadic cases of HUS have been associated with ingestion of fresh ready-to-eat products. Maintenance and persistence of STEC in the environment and foods can be related to its ability to form biofilm. A non-O157 STEC strain isolated from bovine feces was distinguished by its great ability to form biofilm in abiotic surfaces. In the present study, we aimed to investigate the ability of this strain to adhere to rocket leaves (Eruca sativa). Adherence assays were carried out for 3 h at 28 degrees C and analyzed by scanning electron microscopy. The non-O157 STEC strain adhered to leaf surface and inside the stomata forming several bacterial aggregates. The number of adherent bacteria per square millimeter of leaf was eightfold higher compared with an O157 STEC strain. Deletion of the STEC autotransporter protein contributing to biofilm (Sab) reduced the adherence ability of the non-O157 strain in almost 50%, and deletion of antigen 43 (Ag43) almost abolished this interaction. Very few bacteria were seen on the leaf surface, and these differences were statistically significant, suggesting the role of both proteins and especially Ag43 in the interaction of the non-O157 STEC strain with leaves. The risk posed by non-O157 STEC adherence to leaves on fresh produce contamination should not be neglected, and measures that effectively control adherence should be included in strategies to control non-O157 STEC.

Shiga toxin-producing Escherichia coli is an emergent pathogen that can induce haemolytic uraemic syndrome. The toxin has received considerable attention not only from microbiologists but also in the field of cell biology, where it has become a powerful tool to study intracellular trafficking. In this Review, we summarize the Shiga toxin family members and their structures, receptors, trafficking pathways and cellular targets. We discuss how Shiga toxin affects cells not only by inhibiting protein biosynthesis but also through the induction of signalling cascades that lead to apoptosis. Finally, we discuss how Shiga toxins might be exploited in cancer therapy and immunotherapy.

Shiga toxin (Stx)-producing Escherichia coli (STEC) are food-borne pathogens that cause hemorrhagic colitis and a serious sequela, the hemolytic uremic syndrome (HUS). The largest outbreaks of STEC are due to a single E. coli serotype, O157:H7, although non-O157 serotypes also cause the same diseases. Two immunologically distinct Stxs are found in E. coli, Stx1 and Stx2. The Stxs are AB5 toxins that halt protein synthesis in the host cell, a process that may lead to an apoptotic cell death. Stx-mediated damage to renal glomerular endothelial cells is hypothesized as the precipitating event for HUS. A subset of STEC referred to as the enterohemorrhagic E. coli has the capacity to intimately attach to and efface intestinal epithelial cells, a pathology called the A/E lesion. The A/E lesion is mediated by the adhesin intimin, its bacterially encoded receptor, Tir, and effectors secreted through a type III secretion system. The proteins needed for the A/E lesion are encoded within a large pathogenicity island called the locus of enterocyte effacement or LEE. There are several animal models for STEC infection, but no one model fully represents the spectrum of STEC illness. Currently there is no cure for STEC infection, and therapies are based mainly on alleviating symptoms. However, chimeric or humanized monoclonal antibodies have been developed that neutralize the Stxs, and those therapies may be able to prevent the development of HUS in an STEC-infected patient.