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      Postinfectious Hemolytic Uremic Syndrome

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          Abstract

          Post-infectious hemolytic uremic syndrome (HUS) is caused by specific pathogens in patients with no identifiable HUS-associated genetic mutation or autoantibody. The majority of episodes is due to infections by Shiga toxin (Stx) producing Escherichia coli (STEC). This chapter reviews the epidemiology and pathogenesis of STEC-HUS, including bacterial-derived factors and host responses. STEC disease is characterized by hematological (microangiopathic hemolytic anemia), renal (acute kidney injury) and extrarenal organ involvement. Clinicians should always strive for an etiological diagnosis through the microbiological or molecular identification of Stx-producing bacteria and Stx or, if negative, serological assays. Treatment of STEC-HUS is supportive; more investigations are needed to evaluate the efficacy of putative preventive and therapeutic measures, such as non-phage-inducing antibiotics, volume expansion and anti-complement agents. The outcome of STEC-HUS is generally favorable, but chronic kidney disease, permanent extrarenal, mainly cerebral complication and death (in less than 5 %) occur and long-term follow-up is recommended. The remainder of this chapter highlights rarer forms of (post-infectious) HUS due to S. dysenteriae, S. pneumoniae, influenza A and HIV and discusses potential interactions between these pathogens and the complement system.

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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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            German outbreak of Escherichia coli O104:H4 associated with sprouts.

            A large outbreak of the hemolytic-uremic syndrome caused by Shiga-toxin-producing Escherichia coli O104:H4 occurred in Germany in May 2011. The source of infection was undetermined. We conducted a matched case-control study and a recipe-based restaurant cohort study, along with environmental, trace-back, and trace-forward investigations, to determine the source of infection. The case-control study included 26 case subjects with the hemolytic-uremic syndrome and 81 control subjects. The outbreak of illness was associated with sprout consumption in univariable analysis (matched odds ratio, 5.8; 95% confidence interval [CI], 1.2 to 29) and with sprout and cucumber consumption in multivariable analysis. Among case subjects, 25% reported having eaten sprouts, and 88% reported having eaten cucumbers. The recipe-based study among 10 groups of visitors to restaurant K included 152 persons, among whom bloody diarrhea or diarrhea confirmed to be associated with Shiga-toxin-producing E. coli developed in 31 (20%). Visitors who were served sprouts were significantly more likely to become ill (relative risk, 14.2; 95% CI, 2.6 to ∞). Sprout consumption explained 100% of cases. Trace-back investigation of sprouts from the distributor that supplied restaurant K led to producer A. All 41 case clusters with known trading connections could be explained by producer A. The outbreak strain could not be identified on seeds from the implicated lot. Our investigations identified sprouts as the most likely outbreak vehicle, underlining the need to take into account food items that may be overlooked during subjects' recall of consumption.
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              2009 pandemic influenza A (H1N1): pathology and pathogenesis of 100 fatal cases in the United States.

              In the spring of 2009, a novel influenza A (H1N1) virus emerged in North America and spread worldwide to cause the first influenza pandemic since 1968. During the first 4 months, over 500 deaths in the United States had been associated with confirmed 2009 pandemic influenza A (H1N1) [2009 H1N1] virus infection. Pathological evaluation of respiratory specimens from initial influenza-associated deaths suggested marked differences in viral tropism and tissue damage compared with seasonal influenza and prompted further investigation. Available autopsy tissue samples were obtained from 100 US deaths with laboratory-confirmed 2009 H1N1 virus infection. Demographic and clinical data of these case-patients were collected, and the tissues were evaluated by multiple laboratory methods, including histopathological evaluation, special stains, molecular and immunohistochemical assays, viral culture, and electron microscopy. The most prominent histopathological feature observed was diffuse alveolar damage in the lung in all case-patients examined. Alveolar lining cells, including type I and type II pneumocytes, were the primary infected cells. Bacterial co-infections were identified in >25% of the case-patients. Viral pneumonia and immunolocalization of viral antigen in association with diffuse alveolar damage are prominent features of infection with 2009 pandemic influenza A (H1N1) virus. Underlying medical conditions and bacterial co-infections contributed to the fatal outcome of this infection. More studies are needed to understand the multifactorial pathogenesis of this infection.
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                Author and article information

                Contributors
                +11(416) 813-6283 , Denis.Geary@sickkids.ca
                franz.schaefer@med.uni-heidelberg.de
                martin.bitzan@mcgill.ca
                anne.laure.lapeyraque@umontreal.ca
                Journal
                978-3-662-52972-0
                10.1007/978-3-662-52972-0
                Pediatric Kidney Disease
                Pediatric Kidney Disease
                978-3-662-52970-6
                978-3-662-52972-0
                17 June 2016
                : 653-731
                Affiliations
                [1 ]ISNI 0000 0004 0473 9646, GRID grid.42327.30, Division of Nephrology, , The Hospital for Sick Children, ; Toronto, Ontario Canada
                [2 ]ISNI 0000 0001 2190 4373, GRID grid.7700.0, Division of Pediatric Nephrology, , University of Heidelberg, ; Heidelberg, Germany
                [3 ]ISNI 0000 0001 0350 814X, GRID grid.416084.f, Division of Nehprology, , Montreal Children’s Hospital, ; 1001, Boulevard Decarie, Room B RC.6651, Montreal, H4A 3JI Canada
                [4 ]ISNI 0000 0001 2173 6322, GRID grid.411418.9, Division of Nephrology, , Hopital Sainte Justine, ; 3175 Cote Sainte Catherine, Montreal, H4A 3M7 Canada
                Article
                26
                10.1007/978-3-662-52972-0_26
                7121170
                8e89dec0-31c3-4303-a20d-c126a1ea5c09
                © Springer-Verlag Berlin Heidelberg 2016

                This article is made available via the PMC Open Access Subset for unrestricted research re-use and secondary analysis in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the World Health Organization (WHO) declaration of COVID-19 as a global pandemic.

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                © Springer-Verlag Berlin Heidelberg 2016

                enterohemorrhagic escherichia coli,human immunodeficiency virus,influenza a (h1n1),neuraminidase,streptococcus pneumoniae,shiga toxin,shigella dysenteriae,stec,verocytotoxin

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