An Epidemiologic Surveillance of Shiga-like Toxin-producing Escherichia coli Infection in Argentinean Children

López, Eduardo; Contrini, María Marta; Glatstein, Eduardo; Ayala, Silvia González; Santoro, Roberto; Ezcurra, Gustavo; Teplitz, Eduardo; Matsumoto, Yoichi; Sato, Hiroaki; Sakai, Kazuaki; Katsuura, Yasuhiro; Hoshide, S.; Morita, Takuya; Harning, Ronald; Brookman, Sheldon

doi:10.1097/inf.0b013e31822ea6cf

Cited by 47 publications

(50 citation statements)

References 22 publications

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“…However, HUS in each of the patients described in that letter was already resolving (decreasing lactate dehydrogenase and/or rising platelet counts) when eculizumab was started. Several in vitro and animal experiments suggest activation of complement after exposure to Stx/VT (116)(117)(118), but these experiments employed STEC/VTEC concentrations several orders of magnitude higher than the levels that have ever been documented in humans (119). In contrast, a primate model of lethal STEC/ VTEC challenge demonstrated no evidence of complement activation (120).…”

Section: Use Of Plasmapheresis and Eculizumabmentioning

confidence: 92%

Shiga Toxin/Verocytotoxin-Producing Escherichia coli Infections: Practical Clinical Perspectives

2014

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Escherichia coli strains that produce Shiga toxins/verotoxins are rare, but important, causes of human disease. They are responsible for a spectrum of illnesses that range from the asymptomatic to the life-threatening hemolyticuremic syndrome; diseases caused by E. coli belonging to serotype O157:H7 are exceptionally severe. Each illness has a fairly predictable trajectory, and good clinical practice at one phase can be inappropriate at other phases. Early recognition, rapid and definitive microbiology, and strategic selection of tests increase the likelihood of good outcomes. The best management of these infections consists of avoiding antibiotics, antimotility agents, and narcotics and implementing aggressive intravenous volume expansion, especially in the early phases of illness.

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Section: Use Of Plasmapheresis and Eculizumabmentioning

confidence: 92%

Shiga Toxin/Verocytotoxin-Producing Escherichia coli Infections: Practical Clinical Perspectives

2014

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“…IgM antibodies have a 95 and 99 percent sensitivity and specificity respectively [30,31]. However, the accuracy of these findings in patients with similar clinical symptoms, but without positive cultures for E. coli 0157:H7 is unclear.…”

Section: Diagnosismentioning

confidence: 94%

“…Due to the increasing clinical importance of non-O157 Shiga toxin-producing serotypes, the CDC recommends that all samples submitted for acute diarrhoea be tested for non-O157 serotypes including the E. coli O104:H4 outbreak strain (can be cultured on either MacConkey agar or SMAC and can be confirmed as Shiga toxin producers by enzyme immunoassay for the Shiga toxin, or by polymerase chain reaction for the Shiga toxin genes stx1 and stx2). Blood cultures are rarely useful in diagnosing STEC as the patients usually have no bacteraemia even during HUS and the Shiga toxin is detected in the blood only transiently; thus, blood culture is not the proper diagnostic tool [31][32][33][34].…”

Section: Diagnosismentioning

confidence: 99%

“…However, high-risk children to develop HUS have higher levels of prothrombotic factors and endothelial-active cytokines than those with uncomplicated STEC disease [33,34]. Serum angiopoietin-1 (a mediator of endothelial cell quiescence) declines with progressive stages of complicated E. coli O157:H7 infection and can partially discriminate between those children who will have an uncomplicated course of STEC infection and those who will develop HUS [31]. Although none of these markers is sufficiently specific, the combinations of markers may aid in predicting the course of the HUS disease [1].…”

Section: Diagnosismentioning

confidence: 99%

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Hemolytic Uremic Syndrome Caused by Shiga Toxin-Producing Escherichia coli Infections: An Overview

Abdullah¹,

Al-Sultan

Jassim³

et al. 2014

Clon Transgen

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The purpose of this manuscript is to provide a current overview on the Shiga Toxin / verotoxin-producing Escherichia coli (STEC) hemolytic uremic syndrome (HUS) with emphasis on the epidemiology, clinical and laboratory manifestations, pathogenesis, recommended assessment, treatment strategies and prognosis. Hemolytic uremic syndrome (HUS) is a cause of the community-acquired acute renal insufficiency in young children. The outbreak in Germany illustrated both the emerging importance of non-O157 serotypes as agents of human disease and the potential for large-scale methods of food production and distribution to result in widespread disease. Children with STEC-induced HUS typically have a prodromal illness that can rapidly develop severe and multisystem life-threatening complications. STEC infection is acquired through contaminated food or water. Thrombotic microangiopathy is the mechanism of the development of the characteristic pathologic lesion of HUS. Any patient with a recent history of diarrhea and signs of a multi-organ disorder requires a proper assessment for the possible development of HUS. Appropriate laboratory testing for both O157 and non-O157 serotypes, as well as prompt initiation of infection control procedures for confirmed or suspected cases, will facilitate follow-up investigation to identify the source of disease and will help to prevent secondary transmission. Currently, diagnostic test to predict which patients will develop HUS is not available. Supportive care and intravenous fluid replacement are the cornerstones of treatment because of the current lack of safe and specific therapeutic intervention. Culizumab and/or plasma treatment may be considered in patients with severe CNS involvement who have a poor prognosis. None of the multiple therapeutic agents including antithrombotic agents, plasma exchange and/or plasma infusion, tissue-type plasminogen activator, and oral Shiga toxin-binding agent that have been used is recommended. For most patients with uncomplicated STEC-associated gastroenteritis who are treated with supportive care, the prognosis was excellent. Public health interventions are the key to prevent STEC-associated diarrhea and HUS. Researches will improve the care of patients with different HUS types in the years to come. The identification of genetic factors associated with HUS will contribute to a better insight of the pathogenesis of HUS and will have potential therapeutic and preventive implications.

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“…Detecting EHEC in the stools of patients administered antibiotics long after the onset of diarrhea can be challenging because the organisms are typically isolated only from the diarrhea stool tested soon after onset (9,(11)(12)(13)(14). Therefore, alternative laboratory diagnostic methods have been used, such as the detection of Shiga toxin (Stx) protein in the patients' stools or the detection of antibodies against Stx (15) or lipopolysaccharides (LPSs) of E. coli O antigens in the sera of the patients (16)(17)(18). The presence of antibodies to the LPSs of E. coli O antigen in the sera of patients with HUS was first reported by Chart et al (3) in 1991.…”

mentioning

confidence: 99%

Serodiagnosis Using Microagglutination Assay during the Food-Poisoning Outbreak in Japan Caused by Consumption of Raw Beef Contaminated with Enterohemorrhagic Escherichia coli O111 and O157

et al. 2014

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A microagglutination (MA) assay to identify antibodies to Escherichia coli O111 and O157 was conducted in sera collected from 60 patients during a food-poisoning outbreak affecting 181 patients in Japan which was caused by the consumption of contaminated raw beef. Enterohemorrhagic E. coli (EHEC) O111:H8 and/or O157:H7 was isolated from the stools of some of the patients, but the total rate of positivity for antibodies to O111 (45/60, 75.0%) was significantly higher than that for antibodies to O157 (10/60, 16.7%). The MA titers of antibodies to O111 measured in patients with hemolytic-uremic syndrome and bloody diarrhea were higher than those measured in patients with only diarrhea. In patients from whose stool no isolates of E. coli O111 and O157 were obtained, the positive antibody detection rates were 12/19 (63.2%) for O111 and 2/19 (10.5%) for O157, and the MA titers of antibodies to O111 measured were higher than those to O157. Similarly, the MA titers of antibodies to O111 were significantly higher than those to O157, regardless of the other groups, including groups O111, O111 and O157, and O157. These serodiagnosis results suggest that EHEC O111:H8 stx 2 played a primary role in the pathogenesis of this outbreak. Furthermore, our findings suggest that the isolates from the patients' stool specimens were not always the major causative pathogen in patients with multiple EHEC infections, because the sera from patients from whose stools only O157 was isolated were positive for antibodies to O111. Measuring antibodies to E. coli O antigen is helpful especially in cases with multiple EHEC infections, even with a non-O157 serotype.

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An Epidemiologic Surveillance of Shiga-like Toxin-producing Escherichia coli Infection in Argentinean Children

Cited by 47 publications

References 22 publications

Shiga Toxin/Verocytotoxin-Producing Escherichia coli Infections: Practical Clinical Perspectives

Shiga Toxin/Verocytotoxin-Producing Escherichia coli Infections: Practical Clinical Perspectives

Hemolytic Uremic Syndrome Caused by Shiga Toxin-Producing Escherichia coli Infections: An Overview

Serodiagnosis Using Microagglutination Assay during the Food-Poisoning Outbreak in Japan Caused by Consumption of Raw Beef Contaminated with Enterohemorrhagic Escherichia coli O111 and O157

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