Serum antibodies to Verotoxin-producing Escherichia coli (VTEC) strains in patients with haemolytic uraemic syndrome

Kishore, Kaushal; Rattan, Ashok; Bagga, Arvind; Rn, Srivastava; Nm, Nath; Shriniwas,

doi:10.1099/00222615-37-6-364

Cited by 15 publications

(9 citation statements)

References 18 publications

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“…Overall, the retrospective case-control studies yielded 438 HUS cases and 437 controls (Table). Six studies were conducted in developing countries (11,12,14,17,19,21) and five in developed countries (13,15,16,18,20). …”

Section: Resultsmentioning

confidence: 99%

Haemolytic-Uraemic Syndrome as a Sequela of Diarrhoeal Disease

Walker

Applegate

Black

2012

J Health Popul Nutr

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Haemolytic-uraemic syndrome (HUS) is a serious sequela of diarrhoea and results in a high mortality rate. This systematic review aimed at estimating the proportion of HUS cases that are linked to prior infection due to Shiga toxin-producing Escherichia coli (STEC) or Shigella dysenteriae type 1. A systematic review of the existing literature was done to identify cohort and case-control studies that examined the relationship between STEC and S. dysenteriae type 1 and HUS. After screening 2,516 articles, 11 studies were found that met the inclusion/exclusion criteria. Findings of case-control studies suggest that 60.8% of the HUS cases may be attributable to a previous infection with STEC. In cohort studies, 7.8% of participants with STEC and 8% of participants with S. dysenteriae type 1 developed HUS during follow-up. HUS is linked to diarrhoea due to both STEC and S. dysenteriae type 1. Thus, preventing infections caused by both pathogens is critical for the prevention and control of HUS, especially in areas where timely and effective treatment is not available.

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Section: Resultsmentioning

confidence: 99%

Haemolytic-Uraemic Syndrome as a Sequela of Diarrhoeal Disease

Walker

Applegate

Black

2012

J Health Popul Nutr

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“…Most individuals with Stx-mediated HUS develop antibodies to E. coli LPS [1][2][3]. Moreover, cell culture experiments [8] and experience with a mouse model [9] suggest that both Stx and LPS are important in producing the syndrome.…”

Section: Discussionmentioning

confidence: 99%

“…post-diarrheal) hemolytic uremic syndrome (HUS) is the most common cause of acute renal failure in infants and young children, and is typically preceded by a diarrheal prodrome caused by Stx producing enterohemorrhagic Escherichia coli, such as E. coli O157:H7. There is serological evidence that lipopolysaccharide (LPS) also enters the circulation [1][2][3] and it is assumed that LPS plays a role in the pathogenesis of the disease [4].We have developed a primate (baboon) model of HUS [5] in which the intravenous administration of small amounts (50-200 ng/kg) of LPS-free Stx-1 results in thrombocytopenia, microangiopathic hemolytic anemia and renal thrombotic microangiopathy (TMA). Bypassing the enteric phase of the disease with its associated unpredictable systemic absorption of Stx and LPS provides the opportunity to study the host response in a controlled manner.…”

mentioning

confidence: 99%

Response to Shiga Toxin-1, with and without Lipopolysaccharide, in a Primate Model of Hemolytic Uremic Syndrome

Siegler

Pysher²,

Lou³

et al. 2001

Am J Nephrol

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Shiga toxin (Stx) and lipopolysaccharide (LPS) both participate in the pathogenesis of post-diarrheal hemolytic uremic syndrome (HUS), yet little is known about the factors that modulate the host response to these toxins. We have previously shown that the baboon develops HUS if 100 ng/kg of purified Stx-1 is administered rapidly as a single bolus, but not if it is given as four 25-ng/kg doses every 12 h. We therefore used this baboon model to study the response to small intravenous doses of Stx-1, with and without the co-administration of LPS. The co-administration of two 1-mg/kg doses of LPS (given at 0 and 24 h) and four 25-ng/kg doses of Stx-1 (given at 0, 12, 24, and 36 h) resulted in HUS, but the administration of either toxin separately did not. The development of HUS was associated with a rise in urinary, but not plasma concentrations of TNF, and a rise in both urinary and plasma concentrations of IL-6 and IL-8. We speculate that LPS is not required for disease expression in the human, but that it can augment the response to otherwise subtoxic amounts of Stx and this augmentation may be mediated by LPS-induced cytokine release.

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“…The latter assays are available for a number of EHEC serotypes, such as E. coli O157, O26, O55, O103, O111, and O128 [4,5,6,7,8].…”

Section: Introductionmentioning

confidence: 99%

Antibodies to intimin and Escherichia coli secreted proteins A and B in patients with enterohemorrhagic Escherichia coli infections

Karpman¹,

Békássy²,

Sjögren³

et al. 2002

Pediatr Nephrol

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Enterohemorrhagic Escherichia coli produce an attaching and effacing lesion upon adhering to the intestinal epithelium. Bacterial factors involved in this histopathology include the intimin adhesin and E. coli secreted proteins (Esps) A and B. In this study we investigated the serum antibody responses to recombinant E. coli O157:H7 intimin, EspA, and EspB by immunoblotting. Canadian patients with O157:H7 infection (n=10), Swedish patients with O157:H7 (n=21), non-O157 (n=18), or infection from which the serotype was not available (n=3), and asymptomatic household members (n=25) were studied and compared with Canadian (n=20) and Swedish controls (n=52). In Canadian patients, IgG antibodies to intimin, EspA, and EspB were analyzed, in Swedish patients and their household members IgA, IgG, and IgM antibodies to EspA and EspB were studied. Patients and household members mounted an antibody response to the antigens. Significantly more patients developed an acute response to EspB compared with controls (P<0.01 Canadian patients, P<0.0001 Swedish patients). EspB IgA, IgG, and IgM had a specificity of 100%, 86%, and 86%, positive predictive value of 100%, 83%, and 81%, and sensitivity of 57%, 69%, and 63%, respectively, and appear to be an appropriate assay for the detection of EHEC infection. In cases of hemolytic uremic syndrome or hemorrhagic colitis this assay may be useful when a fecal strain has not been isolated, or in epidemics of non-O157 infection.

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Serum antibodies to Verotoxin-producing Escherichia coli (VTEC) strains in patients with haemolytic uraemic syndrome

Cited by 15 publications

References 18 publications

Haemolytic-Uraemic Syndrome as a Sequela of Diarrhoeal Disease

Haemolytic-Uraemic Syndrome as a Sequela of Diarrhoeal Disease

Response to Shiga Toxin-1, with and without Lipopolysaccharide, in a Primate Model of Hemolytic Uremic Syndrome

Antibodies to intimin and Escherichia coli secreted proteins A and B in patients with enterohemorrhagic Escherichia coli infections

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