Transmission

Epidemiology
Hitra Disease appeared in 1977 and occurred for the first time on a large scale in 1979 in fish farms in the Norwegian island of Hitra. Since then, it has devastated fish farms located along the western and northeren Norwegian coast (Egidius et al., 1981). However, single outbreaks have also been reported in Scotland (Bruno et al., 1985, 1986), on the Faroe Islands (Dalsgaard et al., 1988) and in New Brunswick and Nova Scotia, Canada (reference in Sorum et al., 1992).

Epidemiological studies based on plasmid profiles suggest that V. salmonicida was transmitted from cod to Atlantic salmon and vice versa in fish farms in northern Norway (Sorum et al., 1990).

Causative Agent
Vibrio salmonicida is a Gram-negative, peritrichously flagellated, non-spore-forming, curved, rod shaped bacterium. The usual size is 1.5-1.8 µm by 1.0-3 µm. V. salm is a facultative, anaerobic, catalase and oxidase positive bacterium fermenting glucose with production of acid.

The surface layer antigen of V. salm is called the VS-PI antigen. This cell surface product is a single polypeptide, the monomeric form of which has an apparent molecular weight of 40 kD. There are also oligomeric forms with molecular weights in the range 300-700 kD. The antigen contains 6% carbohydrate and several isoelectric forms can be distinguished. Whether VS-P1 is related to the pathogenesis of V. salm is not known, but it is hypothesised that VS-P1 is released from the bacteria and binds specific antibodies, thus saving the bacteria from complement-mediated killing and phagocytosis. Whether plasmidal or chromosomal genes encode the virulence of V. salm or a combination of the two is not known. Some experiments indicate, however, that the virulence is completely or partly plasmid mediated.


Disease reprinted courtesy of OIE Diagnostic Manual for Aquatic Animal Diseases, OIE (World Organisation for Animal Health), Paris, France.