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      Shiga Toxin-Associated Hemolytic Uremic Syndrome: A Narrative Review

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          Abstract

          The severity of human infection by one of the many Shiga toxin-producing Escherichia coli (STEC) is determined by a number of factors: the bacterial genome, the capacity of human societies to prevent foodborne epidemics, the medical condition of infected patients (in particular their hydration status, often compromised by severe diarrhea), and by our capacity to devise new therapeutic approaches, most specifically to combat the bacterial virulence factors, as opposed to our current strategies that essentially aim to palliate organ deficiencies. The last major outbreak in 2011 in Germany, which killed more than 50 people in Europe, was evidence that an effective treatment was still lacking. Herein, we review the current knowledge of STEC virulence, how societies organize the prevention of human disease, and how physicians treat (and, hopefully, will treat) its potentially fatal complications. In particular, we focus on STEC-induced hemolytic and uremic syndrome (HUS), where the intrusion of toxins inside endothelial cells results in massive cell death, activation of the coagulation within capillaries, and eventually organ failure.

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          Most cited references 368

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

          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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            Atypical hemolytic-uremic syndrome.

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              Syndromes of thrombotic microangiopathy.

              This review article covers the diverse pathophysiological pathways that can lead to microangiopathic hemolytic anemia and a procoagulant state with or without damage to the kidneys and other organs.
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                Author and article information

                Journal
                Toxins (Basel)
                Toxins (Basel)
                toxins
                Toxins
                MDPI
                2072-6651
                21 January 2020
                February 2020
                : 12
                : 2
                Affiliations
                [1 ]Department of Nephrology, AP-HP, Hôpital Tenon, F-75020 Paris, France; adrien.joseph@ 123456hotmail.fr (A.J.); cedric.rafat@ 123456aphp.fr (C.R.)
                [2 ]Department of Microbiology, AP-HP, Hôpital Robert Debré, F-75019 Paris, France; aurelie.cointe@ 123456aphp.fr (A.C.); patricia.mariani@ 123456aphp.fr (P.M.K.)
                [3 ]Department of Renal Transplantation, Sorbonne Université, AP-HP, Hôpital Pitié Salpêtrière, F-75013 Paris, France
                Author notes
                Article
                toxins-12-00067
                10.3390/toxins12020067
                7076748
                31973203
                © 2020 by the authors.

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

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