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Gewählte Publikation:

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Publikationstyp: Zeitschriftenaufsatz
Dokumentart: Originalarbeit

Publikationsjahr: 2017

AutorInnen: Wöchtl, B; Gunzer, F; Gerner, W; Gasse, H; Koch, M; Bagó, Z; Ganter, M; Weissenböck, H; Dinhopl, N; Coldewey, SM; von Altrock, A; Waldmann, KH; Saalmüller, A; Zimmermann, K; Steinmann, J; Kehrmann, J; Klein-Hitpass, L; Blom, J; Ehricht, R; Engelmann, I; Hennig-Pauka, I

Titel: Comparison of clinical and immunological findings in gnotobiotic piglets infected with Escherichia coli O104:H4 outbreak strain and EHEC O157:H7.

Quelle: Gut Pathog. 2017; 9:30



Autor/innen der Vetmeduni Vienna:

Dinhopl Nora
Gerner Wilhelm
Hennig-Pauka Isabel
Saalmüller Armin
Weissenböck Herbert
Wöchtl Bettina

Beteiligte Vetmed-Organisationseinheiten
Institut für Immunologie
Institut für Pathologie
Universitätsklinik für Schweine


Zugehörige(s) Projekt(e): Bakterielle Therapie der Infektion mit enterohämorrhagschen E. coli im Tiermodell mit gnotobiotischen Ferkeln


Abstract:
Shiga toxin (Stx) producing Escherichia coli (E. coli) (STEC) is the most frequent cause of diarrhoea-positive haemolytic uraemic syndrome (D + HUS) in humans. In 2011, a huge outbreak with an STEC O104:H4 strain in Germany highlighted the limited possibilities for causative treatment of this syndrome. The responsible STEC strain was found to combine Stx production with adherence mechanisms normally found in enteroaggregative E. coli (EAEC). Pathotypes of E. coli evolve and can exhibit different adhesion mechanisms. It has been shown previously that neonatal gnotobiotic piglets are susceptible for infection with STEC, such as STEC O157:H7 as well as for EAEC, which are considered to be the phylogenetic origin of E. coli O104:H4. This study was designed to characterise the host response to infection with the STEC O104:H4 outbreak strain in comparison to an STEC O157:H7 isolate by evaluating clinical parameters (scoring) and markers of organ dysfunction (biochemistry), as well as immunological (flow cytometry, assessment of cytokines/chemokines and acute phase proteins) and histological alterations (light- and electron microscopy) in a gnotobiotic piglet model of haemolytic uraemic syndrome.


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