Atlantic salmon bath challenged with Moritella viscosa--pathogen invasion and host response.
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 x 10(5) cfu ml(-1) for 1 h at 8.9 degrees 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. Using 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 IL1 beta, C3, ISG15 and CD83 were studied. Increased expression of IL1 beta and C3 was not induced until day 7, which may suggest that M. viscosa might utilize escape mechanisms to evade the host's immune system by suppressing relevant immune responses.
Løvoll
M
M
National Veterinary Institute, Department of Animal Health, P.O. Box 750 Sentrum, 0106 Oslo, Norway. marie.lovoll@vetinst.no
Wiik-Nielsen
C R
CR
Tunsjø
H S
HS
Colquhoun
D
D
Lunder
T
T
Sørum
H
H
Grove
S
S
D000818:Animals; D015703:Antigens, CD / Q000096:biosynthesis / Q000235:genetics / Q000276:immunology; D003176:Complement C3 / Q000096:biosynthesis / Q000235:genetics / Q000276:immunology; D004269:DNA, Bacterial / Q000235:genetics / Q000378:metabolism; D004797:Enzyme-Linked Immunosorbent Assay / Q000662:veterinary; D005393:Fish Diseases / Q000276:immunology / Q000382:microbiology*; D005880:Gills / Q000276:immunology / Q000382:microbiology; D007136:Immunoglobulins / Q000096:biosynthesis / Q000235:genetics / Q000276:immunology; D007150:Immunohistochemistry / Q000662:veterinary; D053583:Interleukin-1beta / Q000096:biosynthesis / Q000235:genetics / Q000276:immunology; D008562:Membrane Glycoproteins / Q000096:biosynthesis / Q000235:genetics / Q000276:immunology; D034221:Moritella / Q000235:genetics / Q000276:immunology* / Q000472:pathogenicity; D016133:Polymerase Chain Reaction / Q000662:veterinary; D020317:Salmo salar; D014452:Ubiquitins / Q000096:biosynthesis / Q000235:genetics / Q000276:immunology; D014735:Vibrio Infections / Q000276:immunology / Q000382:microbiology / Q000662:veterinary*; D000097802:CD83 Antigen
D015703:Antigens, CD; D003176:Complement C3; D004269:DNA, Bacterial; D007136:Immunoglobulins; D053583:Interleukin-1beta; D008562:Membrane Glycoproteins; D014452:Ubiquitins; D000097802:CD83 Antigen