Clinical experiences in Sakai City Hospital during the massive outbreak of enterohemorrhagic Escherichia coli O157 infections in Sakai City, 1996

Fukushima, Hisao; Hashizume, Takao; Morita, Yoshiharu; Tanaka, Junko; Azuma, Katsumi; Mizumoto, Yuki; Kaneno, Masako; Matsu-Ura, Moto-O; Kitani, Kazushi Konma And Teruo

doi:10.1046/j.1442-200x.1999.4121041.x

Cited by 101 publications

(69 citation statements)

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“…Clade 3 consists of seven genotypes and includes the genome strain EDL-933 (30) (SG-12) from the first human O157 outbreak in 1982 linked to hamburgers sold at a chain of fast food restaurant outlets in Michigan and Oregon (36). Although these outbreaks representing clades 1, 2, and 3 affected Ϸ12,000 people combined, the rate of HUS and hospitalization was low for each (4,14,15,36) compared with the average rates for 350 North American outbreaks (3) ( Table 1). Clade 8, in contrast, consists of five SGs that include O157 strains from multistate outbreaks linked to contaminated spinach (37) and lettuce (7) (SG-30) in North America.…”

Section: Figmentioning

confidence: 99%

“…The 1993 outbreak in western North America (4) and the large 1996 outbreak in Japan (13) had low rates of hospitalization and HUS (14,15), whereas the 2006 North American spinach outbreak (8) had high rates of both hospitalization (Ͼ50%) and HUS (Ͼ10%). One hypothesis is that outbreak strains differ in virulence as a result of variation in the presence and expression of different Shiga toxin (Stx) gene combinations (16)(17)(18)(19).…”

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Variation in virulence among clades of Escherichia coli O157:H7 associated with disease outbreaks

Manning

Motiwala

Springman

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

411

612

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Escherichia coli O157:H7, a toxin-producing food and waterborne bacterial pathogen, has been linked to large outbreaks of gastrointestinal illness for more than two decades. E. coli O157 causes a wide range of clinical illness that varies by outbreak, although factors that contribute to variation in disease severity are poorly understood. Several recent outbreaks involving O157 contamination of fresh produce (e.g., spinach) were associated with more severe disease, as defined by higher hemolytic uremic syndrome and hospitalization frequencies, suggesting that increased virulence has evolved. To test this hypothesis, we developed a system that detects SNPs in 96 loci and applied it to >500 E. coli O157 clinical strains. Phylogenetic analyses identified 39 SNP genotypes that differ at 20% of SNP loci and are separated into nine distinct clades. Differences were observed between clades in the frequency and distribution of Shiga toxin genes and in the type of clinical disease reported. Patients with hemolytic uremic syndrome were significantly more likely to be infected with clade 8 strains, which have increased in frequency over the past 5 years. Genome sequencing of a spinach outbreak strain, a member of clade 8, also revealed substantial genomic differences. These findings suggest that an emergent subpopulation of the clade 8 lineage has acquired critical factors that contribute to more severe disease. The ability to detect and rapidly genotype O157 strains belonging to such lineages is important and will have a significant impact on both disease diagnosis and treatment guidelines.pathogens ͉ polymorphisms ͉ population genetics E nterohemorrhagic Escherichia coli (EHEC) includes a diverse population of Shiga toxin-producing E. coli that causes outbreaks of food and waterborne disease (1-3). EHEC often resides in bovine reservoirs and is transmitted via many food vehicles including cooked meat, such as hamburger (4) and salami (5), and raw vegetables, such as lettuce (6, 7) and spinach (8). In North America, E. coli O157:H7 is the most common EHEC serotype contributing to Ͼ75,000 human infections (9) and 17 outbreaks (3) per year.It is not clear why outbreaks of EHEC O157 vary dramatically in the severity of illness and the frequency of the most serious complication, hemolytic uremic syndrome (HUS) (10-12). The 1993 outbreak in western North America (4) and the large 1996 outbreak in Japan (13) had low rates of hospitalization and HUS (14, 15), whereas the 2006 North American spinach outbreak (8) had high rates of both hospitalization (Ͼ50%) and HUS (Ͼ10%). One hypothesis is that outbreak strains differ in virulence as a result of variation in the presence and expression of different Shiga toxin (Stx) gene combinations (16)(17)(18)(19).To assess the genetic diversity and variability in virulence among E. coli O157 strains, we developed a real-time PCR system for identifying synonymous and nonsynonymous mutations as SNPs (20-23). Although molecular subtyping methods, such as pulsedfield gel electrophoresis (PFGE), ...

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Section: Figmentioning

confidence: 99%

mentioning

confidence: 99%

Variation in virulence among clades of Escherichia coli O157:H7 associated with disease outbreaks

Manning

Motiwala

Springman

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

411

612

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“…Another notable outbreak, which occurred in 1996 in Sakai, Japan, was associated with contaminated radish sprouts, and over 5000 individuals (mostly children) were reportedly affected (Fukushima et al, 1999;Higami et al, 1998;Ikeda et al, 1999;Michino et al, 1999). While both outbreaks were severe, recent genomic sequencing and genotyping data have demonstrated that the two O157 : H7 strains [TW14359, Spinach; and RIMD0509952, Sakai (Hayashi et al, 2001)] implicated in the outbreaks represent divergent phylogenetic lineages (Laing et al, 2009;Leopold et al, 2009;Manning et al, 2008).…”

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confidence: 99%

Differences in adherence and virulence gene expression between two outbreak strains of enterohaemorrhagic Escherichia coli O157 : H7

et al. 2010

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The Escherichia coli O157 : H7 TW14359 strain was implicated in a multi-state outbreak in North America in 2006, which resulted in high rates of severe disease. Similarly, the O157 : H7 RIMD0509952 (Sakai) strain caused the largest O157 : H7 outbreak to date. Both strains were shown to represent divergent phylogenetic lineages. Here we compared global gene expression patterns before and after epithelial cell exposure, as well as the ability to adhere to and invade epithelial cells, between the two outbreak strains. Epithelial cell assays demonstrated a 2.5-fold greater adherence of the TW14359 strain relative to Sakai, while whole-genome microarrays detected significant differential expression of 914 genes, 206 of which had a fold change ≥1.5. Interestingly, most locus of enterocyte effacement (LEE) genes were upregulated in TW14359, whereas flagellar and chemotaxis genes were primarily upregulated in Sakai, suggesting discordant expression of these genes between the two strains. The Shiga toxin 2 genes were also upregulated in the TW14359 strain, as were several pO157-encoded genes that promote adherence, including type II secretion genes and their effectors stcE and adfO. Quantitative RT-PCR confirmed the expression differences detected in the microarray analysis, and expression levels were lower for a subset of LEE genes before versus after exposure to epithelial cells. In all, this study demonstrated the upregulation of major and ancillary virulence genes in TW14359 and of flagellar and chemotaxis genes in Sakai, under conditions that precede intimate bacterial attachment to epithelial cells. Differences in the level of adherence to epithelial cells were also observed, implying that these two phylogenetically divergent O157 : H7 outbreak strains vary in their ability to colonize, or initiate the disease process.

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“…However, a large outbreak (.4000 cases) of gastroenteritis and HUS belonging to an unusual (O104:H4), non-O157 STEC strain, predominantly affecting adults (89%), recently occurred in Germany (7). More than 25% of cases developed HUS, a proportion that is much higher than in previous outbreaks (8)(9)(10). The E. coli O104:H4 strain combines virulence potentials of enteroaggregative E. coli with a characteristic "stacked-brick" pattern of adherence to intestinal epithelial cells and of typical Stx-producing enterohemorrhagic E. coli (11).…”

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Lack of the Lectin-like Domain of Thrombomodulin Worsens Shiga Toxin-Associated Hemolytic Uremic Syndrome in Mice

Zoja

Locatelli

Pagani

et al. 2012

The Journal of Immunology

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Shiga toxin (Stx)-producing Escherichia coli is a primary cause of diarrhea-associated hemolytic uremic syndrome (HUS), a disorder of thrombocytopenia, microangiopathic hemolytic anemia, and acute renal failure. The pathophysiology of renal microvascular thrombosis in Stx-HUS is still ill-defined. Based on evidence that abnormalities in thrombomodulin (TM), an anticoagulant endothelial glycoprotein that modulates complement and inflammation, predispose to atypical HUS, we assessed whether impaired TM function may adversely affect evolution of Stx-HUS. Disease was induced by coinjection of Stx2/LPS in wild-type mice (TMwt/wt) and mice that lack the lectin-like domain of TM (TMLeD/LeD), which is critical for its anti-inflammatory and cytoprotective properties. After Stx2/LPS, TMLeD/LeD mice exhibited more severe thrombocytopenia and renal dysfunction than TMwt/wt mice. Lack of lectin-like domain of TM resulted in a stronger inflammatory reaction after Stx2/LPS with more neutrophils and monocytes/macrophages infiltrating the kidney, associated with PECAM-1 and chemokine upregulation. After Stx2/LPS, intraglomerular fibrin(ogen) deposits were detected earlier in TMLeD/LeD than in TMwt/wt mice. More abundant fibrin(ogen) deposits were also found in brain and lungs. Under basal conditions, TMLeD/LeD mice exhibited excess glomerular C3 deposits, indicating impaired complement regulation in the kidney that could lead to local accumulation of proinflammatory products. TMLeD/LeD mice with HUS had a higher mortality rate than TMwt/wt mice. If applicable to humans, these findings raise the possibility that genetic or acquired TM defects might have an impact on the severity of microangiopathic lesions after exposure to Stx-producing E. coli infections and raise the potential for using soluble TM in the treatment of Stx-HUS.

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Clinical experiences in Sakai City Hospital during the massive outbreak of enterohemorrhagic Escherichia coli O157 infections in Sakai City, 1996

Cited by 101 publications

References 1 publication

Variation in virulence among clades of Escherichia coli O157:H7 associated with disease outbreaks

Variation in virulence among clades of Escherichia coli O157:H7 associated with disease outbreaks

Differences in adherence and virulence gene expression between two outbreak strains of enterohaemorrhagic Escherichia coli O157 : H7

Lack of the Lectin-like Domain of Thrombomodulin Worsens Shiga Toxin-Associated Hemolytic Uremic Syndrome in Mice

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