• Title of article

    Atlantic salmon bath challenged with Moritella viscosa – Pathogen invasion and host response

  • Author/Authors

    Lّvoll، نويسنده , , M. and Wiik-Nielsen، نويسنده , , C.R. and Tunsjّ، نويسنده , , H.S. and Colquhoun، نويسنده , , D. and Lunder، نويسنده , , T. and Sّrum، نويسنده , , Phillip H. and Grove-White، نويسنده , , S.، نويسنده ,

  • Issue Information
    روزنامه با شماره پیاپی سال 2009
  • Pages
    8
  • From page
    877
  • To page
    884
  • Abstract
    The Gram-negative bacterium Moritella viscosa is considered to be the main causative agent of winter ulcer, a disease that primarily affects salmonid fish in sea water during cold periods. The disease is initially characterised by localised swelling of the skin followed by development of lesions. To gain more knowledge of the role of M. viscosa in the pathogenesis of winter ulcer, 159 Atlantic salmon (80–110 g) were exposed to a bath challenge dose of 7 × 105 cfu ml-1 for 1 h at 8.9 °C. The first mortalities were registered two days post-challenge and the mortality rate increased rapidly. Multi-organ samples were taken throughout the challenge for culture, immunohistochemistry and PCR analysis. real-time PCR, M. viscosa DNA was first detected in the gills of all fish examined 2, 6 and 12 h after challenge. From day 2, the bacterium was detected in the muscle/skin, head kidney, spleen and liver. This was in correlation with positive cultured samples and confirmed systemic infection. The early and consistent detection of M. viscosa DNA in gill samples, and less or not in muscle/skin or intestine, could suggest gills as a port of entry for the bacterium. Immunohistochemical analysis using a polyclonal antiserum against M. viscosa demonstrated generalised staining in the lumen of blood vessels and some positive mononuclear cells. The antigens recognised by the antiserum may have originated from extracellular bacterial products and be part of a bacterial invasion strategy. To better understand the immune response in salmon to M. viscosa infection, the expression profiles of the immune genes IL1β, C3, ISG15 and CD83 were studied. Increased expression of IL1β and C3 was not induced until day 7, which may suggest that M. viscosa might utilize escape mechanisms to evade the hostʹs immune system by suppressing relevant immune responses.
  • Keywords
    Moritella viscosa , Winter ulcer disease , immune response , Bacterial escape mechanisms , PATHOGENESIS
  • Journal title
    Fish and Shellfish Immunology
  • Serial Year
    2009
  • Journal title
    Fish and Shellfish Immunology
  • Record number

    2108573