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Whole-Genome Characterization of Hemolytic Uremic Syndrome-Causing Shiga Toxin-Producing Escherichia Coli in Sweden

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Whole-Genome Characterization of Hemolytic Uremic Syndrome-Causing Shiga Toxin-Producing Escherichia Coli in Sweden Virulence ISSN: (Print) (Online) Journal homepage: https://www.tandfonline.com/loi/kvir20 Whole-genome characterization of hemolytic uremic syndrome-causing Shiga toxin-producing Escherichia coli in Sweden Ying Hua, Milan Chromek, Anne Frykman, Cecilia Jernberg, Valya Georgieva, Sverker Hansson, Ji Zhang, Ann Katrine Marits, Chengsong Wan, Andreas Matussek & Xiangning Bai To cite this article: Ying Hua, Milan Chromek, Anne Frykman, Cecilia Jernberg, Valya Georgieva, Sverker Hansson, Ji Zhang, Ann Katrine Marits, Chengsong Wan, Andreas Matussek & Xiangning Bai (2021) Whole-genome characterization of hemolytic uremic syndrome- causing Shiga toxin-producing Escherichiacoli in Sweden, Virulence, 12:1, 1296-1305, DOI: 10.1080/21505594.2021.1922010 To link to this article: https://doi.org/10.1080/21505594.2021.1922010 © 2021 The Author(s). Published by Informa View supplementary material UK Limited, trading as Taylor & Francis Group. Published online: 03 May 2021. Submit your article to this journal View related articles View Crossmark data Full Terms & Conditions of access and use can be found at https://www.tandfonline.com/action/journalInformation?journalCode=kvir20 VIRULENCE 2021, VOL. 12, NO. 1, 1296–1305 https://doi.org/10.1080/21505594.2021.1922010 RESEARCH PAPER Whole-genome characterization of hemolytic uremic syndrome-causing Shiga toxin-producing Escherichia coli in Sweden Ying Huaa,b, Milan Chromekc, Anne Frykmand,e, Cecilia Jernberg f, Valya Georgievac, Sverker Hanssond,e, Ji Zhangg, Ann Katrine Maritsc, Chengsong Wana, Andreas Matussekb,h,i,j, and Xiangning Baib,k,l aDepartment of Microbiology, School of Public Health, Southern Medical University, Guangzhou, China; bDivision of Clinical Microbiology, Department of Laboratory Medicine, Karolinska Institutet, Huddinge, Sweden; cDivision of Pediatrics, Department of Clinical Science, Intervention and Technology, Karolinska Institutet and Karolinska University Hospital, Stockholm, Sweden; dQueen Silvia Children’s Hospital, Sahlgrenska University Hospital, Gothenburg, Sweden; eDepartment of Pediatrics, Institute of Clinical Sciences, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden; fThe Public Health Agency of Sweden, Solna, Sweden; gMolecular Epidemiology and Public Health Laboratory, School of Veterinary Sciences, Massey University, Palmerston North, New Zealand; hLaboratory Medicine, Jönköping Region County, Department of Clinical and Experimental Medicine, Linköping University, Jönköping, Sweden; iOslo University Hospital, Oslo, Norway; jDivision of Laboratory Medicine, Institute of Clinical Medicine, University of Oslo, Norway; kDivision of Infectious Diseases, Department of Medicine Huddinge, Karolinska Institutet, Huddinge, Sweden; lState Key Laboratory of Infectious Disease Prevention and Control, National Institute for Communicable Disease Control and Prevention, Chinese Center for Disease Control and Prevention, Beijing, China ABSTRACT ARTICLE HISTORY Shiga toxin-producing Escherichia coli, a foodborne bacterial pathogen, has been linked to a broad Received 6 September 2020 spectrum of clinical outcomes ranging from asymptomatic carriage to fatal hemolytic uremic Revised 23 January 2021 syndrome (HUS). Here, we collected clinical data and STEC strains from HUS patients from 1994 Accepted 19 April 2021 through 2018, whole-genome sequencing was performed to molecularly characterize HUS- KEYWORDS associated STEC strains, statistical analysis was conducted to identify bacterial genetic factors Shiga toxin-producing associated with severe outcomes in HUS patients. O157:H7 was the most predominant serotype Escherichia coli; hemolytic (57%) among 54 HUS-associated STEC strains, followed by O121:H19 (19%) and O26:H11 (7%). uremic syndrome; clinical Notably, some non-predominant serotypes such as O59:H17 (2%) and O109:H21 (2%) also caused outcomes; O157:H7; HUS. All O157:H7 strains with one exception belonged to clade 8. During follow-up at a median of virulence genes; whole- 4 years, 41% of the patients had renal sequelae. Fifty-nine virulence genes were found to be genome sequencing statistically associated with severe renal sequelae, these genes encoded type II and type III secretion system effectors, chaperones, and other factors. Notably, virulence genes associated with severe clinical outcomes were significantly more prevalent in O157:H7 strains. In contrast, genes related to mild symptoms were evenly distributed across all serotypes. The whole-genome phylogeny indicated high genomic diversity among HUS-STEC strains. No distinct cluster was found between HUS and non-HUS STEC strains. The current study showed that O157:H7 remains the main cause of STEC-associated HUS, despite the rising importance of other non-O157 serotypes. Besides, O157:H7 is associated with severe renal sequelae in the follow-up, which could be a risk factor for long-term prognosis in HUS patients. Introduction colitis develop HUS, among which, up to 50% of patients need dialysis during the acute phase [4]. Shiga toxin-producing E. coli (STEC) infections can STEC associated-HUS has been described in all age cause a spectrum of clinical manifestations ranging groups but most susceptible to very young children from asymptomatic carriage to the life-threatening below five years and the elderly [5]. Serotype O157: complication hemolytic uremic syndrome (HUS), H7 has been implicated worldwide as the major cause which is characterized by microangiopathic hemolytic of post-diarrhea HUS either during STEC outbreaks or anemia, thrombocytopenia, and acute kidney injury in sporadic cases [1]. Previous study showed that (AKI) [1,2]. Most HUS cases are caused by STEC patients with HUS was significantly more likely to be infection, whereas atypical HUS (aHUS) is associated infected with O157:H7 strains belonging to clade 8 with gene mutations or autoantibodies, which results in lineage, which might acquire critical factors leading to complement dysregulation [3]. It is estimated that more severe disease [6]. It is estimated that up to 15% 6–25% of patients with STEC-related hemorrhagic CONTACT Xiangning Bai [email protected]; Andreas Matussek [email protected] Supplemental data for this article can be accessed here. © 2021 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. VIRULENCE 1297 of STEC-infected children below ten years developed of toxin, which ultimately increases the risk of HUS [1]. Nevertheless, non-O157:H7 STEC strains, HUS [28]. especially those of serogroups O26, O103, O111, and In Sweden, human STEC O157 cases have been O145, are variably present as causes of HUS and diar­ mandatory to report since 1996 and all serotypes since rhea throughout Europe [7–9] and other countries July 2004 [29]. Most STEC infections were sporadic [10,11]. In 2011, an E. coli O104: H4 outbreak resulted cases or smaller family outbreaks, although a few com­ in 4,321 confirmed cases, 852 HUS, and 54 deaths in munity outbreaks have been described [30–32]. In Europe [12–14], highlighting the clinical importance of 2005, a large O157 outbreak occurred on the west non-O157 serotypes. coast of Sweden, 135 cases were recorded totally, The pathophysiology of HUS is thought to be due to including 11 cases of HUS [29]. However, limited the production of bacteriophage-encoded Shiga toxin study had described molecular characteristic of HUS- (Stx), which causes endothelial damage and activates causing STECs of all serotypes in Sweden so far. the complement cascade, leading to thrombotic micro­ Comprehensive analysis is needed to unveil the entire angiopathy that principally affects the kidney. It may molecular picture of HUS-STEC strains, and to identify also involve the central nervous system (CNS), heart, bacterial genetic factors associated with HUS clinical liver, pancreas, and hematopoietic cells [3,4,15]. Stx outcomes. In the current study, we report STEC asso­ comprises two immunologically distinct toxin types, ciated-HUS cases treated in Gothenburg and Stx1 and Stx2, which share 56% amino acid sequence Stockholm in Sweden from 1994 through 2018. By similarity [16]. Strains producing Stx2, especially Stx2a, whole-genome sequencing-based molecular characteri­ Stx2c, or Stx2d subtypes, show a stronger association zation and comparative genomic analysis, we attempt with the development of HUS than other subtypes to ascertain molecular features of highly pathogenic [17,18]. Aside from stx, additional virulence factors HUS-associated STEC strains, and to identify bacterial also contribute to the pathological process. For genetic markers for severe outcomes in HUS patients. instance, eae-encoded intimin, is an important “efface­ ment/adherence” factor in intestinal colonization [19,20], which can induce a strong antibody response Materials and Methods in HUS patients [21]. Several other potential adherence Case definition, collection of isolates and clinical factors, such as ToxB, Saa, Iha, Efa1, and Paa, have also data been described in HUS-STEC strains [22,23]. However, there is no single or combination of genetic markers HUS was characterized by three primary symptoms: that can predict the potential of STEC strains to cause thrombocytopenia, microangiopathic hemolytic ane­ HUS, as various bacterial
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