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Query: UMLS:C0017160 (gastroenteritis)
 11,398 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Shiga toxin (Stx)-producing Escherichia coli strains of serogroup O111 are the most frequently isolated non-O157 strains causing outbreaks of gastroenteritis with hemolytic-uremic syndrome. The O111 O-antigen gene cluster had been cloned and about half of it has been sequenced; we have now sequenced the remainder of the gene cluster, which is 12.5 kb in length and which comprises 11 genes. On the basis of sequence similarity, we have identified all the O-antigen genes expected, including five sugar biosynthetic pathway genes, three transferase genes, the O-unit flippase gene, and the O-antigen polymerase gene. By PCR testing with E. coli strains representing all 166 O-antigen forms, some randomly selected gram-negative bacteria, and Salmonella enterica serovar Adelaide, we showed that four O-antigen genes are highly specific to O111. This work provides the basis for a sensitive test for the rapid detection of E. coli O111. This is important both for decisions related to patient care, because early treatment may reduce the risk of life-threatening complications, and for the detection of sources of contamination.
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PMID:Sequencing of Escherichia coli O111 O-antigen gene cluster and identification of O111-specific genes. 977 62

Shiga toxin-producing Escherichia coli strains of serogroup O111 are the most frequently isolated non-O157 strains causing outbreaks of gastroenteritis with haemolytic uraemic syndrome (HUS). O antigen is a major antigen in Gram-negative bacteria, and it has been shown that O111 is a protective antigen. Attenuated Salmonella enterica sv Typhimurium aroA strain STM-1 was used as a live carrier to express the E. coli O111 O antigen. Mice immunized intraperitoneally produced serum immunoglobulin G, and mice immunized orally produced serum immunoglobulin G and secretory immunoglobulin A in the intestine against E. coli O111 cells as determined by enzyme-linked immunosorbent assays.
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PMID:Immunization of mice with live oral vaccine based on a Salmonella enterica (sv Typhimurium) aroA strain expressing the Escherichia coli O111 O antigen. 1037 9

The aim of this study was to investigate the association between Shiga toxin-producing Escherichia coli (STEC) O157 and the simultaneous presence of the virulence genes stx2 and eae in STEC from patients with gastroenteritis. In Germany, the proportion of serogroup O157 is substantially higher among STEC isolates from patients with haemolytic uraemic syndrome (HUS) than among STEC isolates from patients with gastroenteritis. The reason for this is unknown. Independent of serogroup, the virulence genes stx2 and eae have been associated with severe disease. Data collected in 2000-2001 from a Germany-wide laboratory-based surveillance system for STEC-associated gastroenteritis in patients <15 years were analysed. Overall, 18% of the STEC isolates belonged to serogroup O157. Compared with non-O157 strains, 0157 isolates were strongly associated with the simultaneous presence of both an stx2 gene and the eae gene (OR, 76; 95%CI, 27-230). Within the subset of STEC isolates that carried both virulence genes, 60% belonged to serogroup O157, a proportion similar to that found in STEC isolates from pediatric patients with HUS in Germany and Austria (67%, P=0.35). These data suggest that the more frequent carriage of both virulence genes, i.e. stx2 and eae, forms the basis of why STEC O157 predominates in patients with HUS.
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PMID:Strong association between shiga toxin-producing Escherichia coli O157 and virulence genes stx2 and eae as possible explanation for predominance of serogroup O157 in patients with haemolytic uraemic syndrome. 1461 96

We studied the effect of the supernatants of 2 to 5 samples of one of the following serotypes of EPC: 026:H, 086:H34, 0111:H-, 0119:H6, 0126:H21, 0128ab:H35 and 0142:H-, isolated from the stools of infants with gastroenteritis. We also studied 3 samples of the serotype 0157:HNT, that produces the Shiga-like toxin. The following control solutions were selected 1-SC1 (glucose-saline solution); 2-SC2 (TSB broth culture solution); 3-SC3 (E.coli K12 711 culture supernatant, a non enterotoxigenic serotype). These solutions were perfused in the small intestine of rats "in vivo" and sodium transport was determined. The comparison among the 3 control solutions revealed that there was always sodium absorption, but there was a difference in the intensity of the transport (SC1 >SC2 and SC3). The serotypes 0111:H-, 026:H-, 0126:H21, and 0142:H2, as well as the serotype 0157:HNT, induced sodium secretion and these values were significantly different in comparison with the 3 control solutions. On the other hand, the serotypes 0128ab:H35 and 0119:H6 induced sodium secretion but the differences were only significant in comparison with the SC1 and SC2, and SC1, respectively. The supernatants of the serotypes investigated provoked an important derangement in sodium transport probably due to the presence of an enterotoxin.
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PMID:[The effect of the supernatants of enteropathogenic Escherichia coli strains on the intestinal transport of sodium in rats "in vivo"]. 1468 81

Ruminants are a major reservoir of enterohaemorrhagic Escherichia coli (EHEC), which cause acute gastroenteritis in humans with potentially life-threatening sequelae. The mechanisms underlying EHEC persistence in ruminant hosts are poorly understood. EHEC produce several cytotoxins that inhibit the proliferation of bovine lymphocytes in vitro and influence EHEC persistence in calves, suggesting that bacterial suppression of mucosal inflammation may be important in vivo. In order to address this hypothesis, intraepithelial lymphocytes (IEL) obtained from ligated intestinal loops of five 9-14 day old calves were characterized 12 h after inoculation with E. coli strains. Loops were inoculated with an EHEC O103 : H2 strain, an isogenic Deltastx1 mutant incapable of producing Shiga toxin 1 (Stx1) and a porcine non-pathogenic E. coli strain. The IEL mainly comprised activated CD2(+) CD3(+) CD6(+) CD8alpha(+) T cells and resembled IEL obtained from the intestinal mucosa of orally challenged calves. Forty per cent of all IEL were potentially sensitive to Stx1 in that they expressed the receptor for Stx1. Nevertheless, analysis of IEL from inoculated loops failed to detect a significant effect of the different E. coli strains on proliferative capacity, natural killer cell activity or the cytokine mRNA profile. However, the EHEC wild-type strain reduced the percentage of CD8alpha(+) T cells in the ileal mucosa compared with loops inoculated with the Deltastx1 mutant. This shift in IEL composition was not associated with inhibition of IEL proliferation in situ, since the majority of the IEL from all loops were in the G(0)/G(1) phase of the cell cycle. These studies indicate that the ligated ileal loop model will be a useful tool to dissect the mechanisms underlying suppression of mucosal inflammation by EHEC in the reservoir host.
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PMID:Phenotypic and functional characterization of intraepithelial lymphocytes in a bovine ligated intestinal loop model of enterohaemorrhagic Escherichia coli infection. 1515 Mar 40

In 2003, OzFoodNet conducted enhanced surveillance of foodborne diseases across Australia, which covered all states and territories. During 2003, there were 23,250 notifications of eight potentially foodborne diseases, of which 67 per cent and 30 per cent were due to Campylobacter and Salmonella infections respectively. The most common Salmonella serotype was Typhimurium, as in previous years. Most S. Enteritidis were acquired overseas, except for Queensland where 52 per cent of infections were acquired locally. Locally acquired S. Enteritidis infections in Australia were predominantly due to phage type 26. The most common serotype of Shiga toxin producing E. coli was O157, although for 49 per cent of notified infections serotype was unknown due to the use of polymerase chain reaction based screening tests. There were 12 materno-foetal listeriosis infections in 2003, which was an increase compared to recent years. During 2003, there were 444 outbreaks of gastroenteritis and foodborne disease recorded. Ninety-nine of these were of foodborne origin affecting 1,686 persons, hospitalising 105 and causing six deaths. A wide range of agents and foods caused these outbreaks, with Salmonella Typhimurium being the most common pathogen. Outbreaks associated with fish and seafood dishes, poultry meat, and Asian style and imported foods were common. Four outbreaks with international implications were reported: an outbreak of Salmonella in Montevideo involving contaminated tahini from the Middle East and three outbreaks of norovirus infection associated with imported Japanese oysters. Outbreak data indicated a need to monitor food safety in aged care settings, restaurants and catering. Eighty-nine investigations into clusters of gastrointestinal illness where a source could not be identified were conducted, including multi-state outbreaks of salmonellosis. One multistate investigation of antibiotic resistant Salmonella Paratyphi b Java identified 18 cases who had recent exposure to tropical fish aquariums. Ninety-seven per cent of Salmonella notifications on state and territory surveillance databases have complete information on serotype and phage type. In 2003, OzFoodNet demonstrated the benefits of national collaboration to control food borne disease.
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PMID:Foodborne disease investigation across Australia: annual report of the OzFoodNet network, 2003. 1557 61

In this study we analyzed the symptoms of gastroenteritis or food-borne disease caused by the 10 most prevalent pathogens: Norovirus, Salmonella, Vibrio parahaemolyticus, Campylobacter jejuni, Clostridium perfringens, Shiga toxin-producing Escherichia coli (STEC), enterotoxigenic E. coli (ETEC), Shigella sonnei/flexneri (Shigella), Staphylococcus aureus, and emetic-type Bacillus cereus. The symptoms diarrhea, vomiting, fever, abdominal pain, and headache, and the incubation period in 646 cases in 10 districts of Kyushu between January 2000 and December 2004 were recorded. The pathogen with the shortest mean incubation period was B. cereus (0.8 h), and was followed by S. aureus (3.3 h), C. perfringens (10.7 h) and V. parahaemolyticus (16.4 h). All the patients infected with B. cereus and S. aureus developed symptoms within 6 hours, and those infected with V. parahaemolyticus and C. perfringens developed symptoms within 24 hours. Bloody diarrhea was associated with STEC and Shigella, but rare with other pathogens. Vomiting was associated with almost all cases of S. aureus and B. cereus infection, and occurred in 71.5% of the Norovirus cases and 56.1% of the V. parahaemolyticus cases. Vomiting was less common in the C. perfringens (22.0%) and the ETEC and STEC (both about 5%). Bloody diarrhea, abdominal pain, and vomiting were statistically significantly more common with STEC 0157 infection than with STEC non-0157 infection. Since the cases analyzed in this study included all degrees of illness, mild to severe, and a wide range of ages, the information obtained will serve as a good reference material for administrative and laboratory work when an outbreak takes place.
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PMID:[Symptoms of food-borne diseases and gastroenteritis in Kyushu, Japan]. 1636 57

Hemolytic uremic syndrome is caused primarily by Shiga toxin-producing Escherichia coli O157:H7. The most common cause of acute renal failure in children, hemolytic uremic syndrome also can occur in adults. Characteristic features of the syndrome are microangiopathic anemia, thrombotic thrombocytopenia, and renal failure. Although the presentation of this syndrome is diverse, the classic prodromal illness is bloody diarrhea following ingestion of hamburger meat contaminated with E. coli O157:H7, the most common mode of infection in the United States. Children with hemolytic uremic syndrome generally present with gastroenteritis complaints (e.g., abdominal pain or tenderness, nausea or vomiting, fever, anemia); affected adults may be asymptomatic. Complications from hemolytic uremic syndrome can include intussusception, chronic renal failure, and seizures in severe cases. Because an incubation period of approximately one week occurs between the start of diarrhea and the onset of hemolytic uremic syndrome, physicians should maintain a high index of suspicion; early laboratory testing is important to diagnose and manage this syndrome. Obtaining a complete blood count and stool culture and performing Shiga toxin testing are the first of a series of tests that may help diagnose hemolytic uremic syndrome.
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PMID:Hemolytic uremic syndrome: an emerging health risk. 1700 34

Escherichia coli O157:H7 and other strains of E. coli that produce Shiga toxin are collectively known as Shiga toxin-producing E. coli (STEC). The current outbreak of STEC O157 infections associated with eating fresh spinach illustrates the importance of obtaining isolates to identify the source of the infections. Laboratory methods that do not require bacterial culture of stool specimens to identify STEC are being used increasingly by clinical diagnostic laboratories, sometimes without subsequent confirmation of a strain by isolating it in culture. This report describes findings from outbreaks of gastroenteritis in 2005 in New York and North Carolina in which clinical diagnostic laboratories initially used only non-culture methods to detect Shiga toxin (Stx). The findings highlight the importance of confirmation of Stx-positive stool specimens by bacterial culture for timely and reliable identification of STEC infections, including E. coli O157 and non-O157 STEC, to enable implementation of appropriate public health actions. An important part of that identification is determining the serotype of all STEC isolates and the subtype of STEC O157 strains so that outbreaks can be detected and traced back to sources.
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PMID:Importance of culture confirmation of shiga toxin-producing Escherichia coli infection as illustrated by outbreaks of gastroenteritis--New York and North Carolina, 2005. 1700 67

In 2005, OzFoodNet sites recorded 25,779 notifications of seven potentially foodborne diseases, which was 12.5 per cent higher than the mean for the previous five years. Diseases with significant increases in 2005, when compared to historical reports include: Shiga toxin-producing Escherichia coli, shigellosis, haemolytic uraemic syndrome, salmonellosis and campylobacteriosis. The most significant increases were those due to Salmonella (13.1%) and Campylobacter (5.1%) because of the frequency of these infections. Reports of listeriosis were lower than previous years and there were only four materno-foetal infections compared to seven in 2004. Sites reported 624 outbreaks of gastroenteritis and foodborne disease in 2005. One hundred and two of these were foodborne and affected 1,926 persons, hospitalised 187 and caused four deaths. Among foodborne outbreaks, Salmonella Typhimurium was the most common pathogen and restaurants were the most common place where food implicated in outbreaks was prepared. Outbreaks associated with fish, poultry meat, and mixed meat dishes were common. There were several large outbreaks of salmonellosis, including one associated with dips at a Turkish restaurant, one with alfalfa sprouts, and two due to egg-based dishes. In addition, there were several multi-state investigations of Salmonella infection during 2005, including one large outbreak of S. Typhimurium 135 implicating poultry meat from retail supermarkets. Sites identified a source of infection for 39 per cent (41/104) of investigations into clusters of salmonellosis. Overall, 97.4 per cent of Salmonella notifications on state and territory surveillance databases recorded complete information about serotype and phage type. This report highlights the considerable burden of disease from food sources in Australia and the need to continue to improve food safety.
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PMID:Burden and causes of foodborne disease in Australia: Annual report of the OzFoodNet network, 2005. 1712 Apr 83


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