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      Hemolytic Uremic Syndrome Associated With Escherichia coli O157 Infection in an Allogenic Stem Cell Transplant Recipient

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          Abstract

          We report the development of a Shiga toxin–producing Escherichia coli O157 gastrointestinal infection associated with hemolytic uremic syndrome in an allogenic stem cell transplant recipient with a history of gastrointestinal graft-vs-host disease receiving long-term immunosuppression.

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          Shiga-toxin-producing Escherichia coli and haemolytic uraemic syndrome.

          Phillip Tarr, Carrie A Gordon, Wayne Chandler (2005)
          Most cases of diarrhoea-associated haemolytic uraemic syndrome (HUS) are caused by Shiga-toxin-producing bacteria; the pathophysiology differs from that of thrombotic thrombocytopenic purpura. Among Shiga-toxin-producing Escherichia coli (STEC), O157:H7 has the strongest association worldwide with HUS. Many different vehicles, in addition to the commonly suspected ground (minced) beef, can transmit this pathogen to people. Antibiotics, antimotility agents, narcotics, and non-steroidal anti-inflammatory drugs should not be given to acutely infected patients, and we advise hospital admission and administration of intravenous fluids. Management of HUS remains supportive; there are no specific therapies to ameliorate the course. The vascular injury leading to HUS is likely to be well under way by the time infected patients seek medical attention for diarrhoea. The best way to prevent HUS is to prevent primary infection with Shiga-toxin-producing bacteria.
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            The risk of the hemolytic-uremic syndrome after antibiotic treatment of Escherichia coli O157:H7 infections.

            C. S. WONG, S Jelacic, R L Habeeb … (2000)
            Children with gastrointestinal infections caused by Escherichia coli O157:H7 are at risk for the hemolytic-uremic syndrome. Whether antibiotics alter this risk is unknown. We conducted a prospective cohort study of 71 children younger than 10 years of age who had diarrhea caused by E. coli O157:H7 to assess whether antibiotic treatment in these children affects the risk of the hemolytic-uremic syndrome and to assess the influence of confounding factors on this outcome. Estimates of relative risks were adjusted for possible confounding effects with the use of logistic-regression analysis. Among the 71 children, 9 (13 percent) received antibiotics and the hemolytic-uremic syndrome developed in 10 (14 percent). Five of these 10 children had received antibiotics. Factors significantly associated with the hemolytic-uremic syndrome were a higher initial white-cell count (relative risk, 1.3; 95 percent confidence interval, 1.1 to 1.5), evaluation with stool culture soon after the onset of illness (relative risk, 0.3; 95 percent confidence interval, 0.2 to 0.8), and treatment with antibiotics (relative risk, 14.3; 95 percent confidence interval, 2.9 to 70.7). The clinical and laboratory characteristics of the 9 children who received antibiotics and the 62 who did not receive antibiotics were similar. In a multivariate analysis that was adjusted for the initial white-cell count and the day of illness on which stool was obtained for culture, antibiotic administration remained a risk factor for the development of the hemolytic uremic syndrome (relative risk, 17.3; 95 percent confidence interval, 2.2 to 137). Antibiotic treatment of children with E. coli O157:H7 infection increases the risk of the hemolytic-uremic syndrome.
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              Graft-versus-host disease disrupts intestinal microbial ecology by inhibiting Paneth cell production of α-defensins.

              Y Eriguchi, Kiminori Nakamura, Hiromi Iwasaki … (2012)
              Allogeneic hematopoietic stem cell transplantation (SCT) is a curative therapy for various hematologic disorders. Graft-versus-host disease (GVHD) and infections are the major complications of SCT, and their close relationship has been suggested. In this study, we evaluated a link between 2 complications in mouse models. The intestinal microbial communities are actively regulated by Paneth cells through their secretion of antimicrobial peptides, α-defensins. We discovered that Paneth cells are targeted by GVHD, resulting in marked reduction in the expression of α-defensins, which selectively kill noncommensals, while preserving commensals. Molecular profiling of intestinal microbial communities showed loss of physiologic diversity among the microflora and the overwhelming expansion of otherwise rare bacteria Escherichia coli, which caused septicemia. These changes occurred only in mice with GVHD, independently on conditioning-induced intestinal injury, and there was a significant correlation between alteration in the intestinal microbiota and GVHD severity. Oral administration of polymyxin B inhibited outgrowth of E coli and ameliorated GVHD. These results reveal the novel mechanism responsible for shift in the gut flora from commensals toward the widespread prevalence of pathogens and the previously unrecognized association between GVHD and infection after allogeneic SCT.
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                Author and article information

                Contributors
                Saad J. Kenderian
                Journal
                Journal ID (nlm-ta): Mayo Clin Proc Innov Qual Outcomes
                Journal ID (iso-abbrev): Mayo Clin Proc Innov Qual Outcomes
                Title: Mayo Clinic Proceedings: Innovations, Quality & Outcomes
                Publisher: Elsevier
                ISSN (Electronic): 2542-4548
                Publication date PMC-release: 15 September 2018
                Publication date Collection: December 2018
                Publication date (Electronic): 15 September 2018
                Volume: 2
                Issue: 4
                Pages: 387-391
                Affiliations
                [a ]Division of Hematology, Mayo Clinic, Rochester, MN
                [b ]Mayo Clinic School of Graduate Medical Education, Mayo Clinic, Rochester, MN
                [c ]Division of Infectious Diseases, Mayo Clinic, Rochester, MN
                [d ]Division of Nephrology, Mayo Clinic, Rochester, MN
                [e ]Department of Immunology, Mayo Clinic, Rochester, MN
                Author notes
                [∗ ] Correspondence: Address to Saad J. Kenderian, MD, Mayo Clinic College of Medicine, 200 First St SW, Rochester, MN 55905 Kenderian.saad@ 123456mayo.edu
                Article
                Publisher ID: S2542-4548(18)30080-8
                DOI: 10.1016/j.mayocpiqo.2018.07.001
                PMC ID: 6260488
                SO-VID: 1fcc0756-f848-41ab-b538-fc82e6d13747
                Copyright © © 2018 Mayo Foundation for Medical Education and Research. Published by Elsevier Inc.
                License:

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                Date received : 8 May 2018
                Date revision received : 9 July 2018
                Date accepted : 13 July 2018
                Categories
                Subject: Case Report

                Keywords: bmt, bone marrow transplant,gvhd, graft-vs-host disease,hus, hemolytic uremic syndrome,ldh, lactate dehydrogenase,stec, shiga toxin–producing escherichia coli,tma, thrombotic microangiopathy
                Data availability:
                Keywords: bmt, bone marrow transplant, gvhd, graft-vs-host disease, hus, hemolytic uremic syndrome, ldh, lactate dehydrogenase, stec, shiga toxin–producing escherichia coli, tma, thrombotic microangiopathy

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