263
Could farmed salmonids pose a realistic risk to native marine fi sh species?
The data on this topic are confusing. Certainly, marine fi sh larvae have been
infected with Aer. salmonicida subsp. salmonicida, with turbot regarded as being
more susceptible than halibut (Bergh et al. 1997 ). Using co-habitation and injection
challenges, experiments suggested that Aer. salmonicida subsp. salmonicida could
be transmitted rarely from Atlantic salmon to Atlantic cod, halibut and wrasse
(Hjeltnes et al. 1995 ). Interest in turbot has spurred some exciting work on understanding the virulence genes associated with the different stages of the infection
process. Thus, attention focused on the genes known to occur in salmonids, i.e.
vapA, tapA, fl a, ascV, ascC, aexT, satA and aspA , using a PCR and challenge by i.p.
injection and bathing. The result was that the genetic profi le linked to virulence and
challenge by i.p. injection was more frequent in cultures derived from turbot rather
than salmonids or the external environment but it was not possible to predict virulence based solely on the presence of these genes (Lago et al. 2012 ).
Could atypical isolates, which are appearing with increasing frequency in wild
fi sh, pose a threat to cultured salmonids?
Wiklund ( 1995b ) using an atypical isolate from ulcerated fl ounder concluded
that there was not any risk to rainbow trout.
What about the risk of transferring Aer. salmonicida from the freshwater to seawater stage of salmonids?
Eggset et al. ( 1997 ) concluded that the susceptibility of Atlantic salmon to furunculosis in seawater possibly refl ected the overall quality of the smolts.
Pathogenicity – Historical Aspects
Although the factors conferring pathogenicity on Aer. salmonicida strains have been
the subject of speculation since early in the study of the pathogen, it is only relatively recently that the details concerning pathogenesis and virulence have begun to
be elucidated. The initial investigations, carried out in the 1930s, resulted in several
key observations, notably that prolonged laboratory maintenance of Aer. salmonicida isolates was frequently responsible for a loss of virulence, and that histopathological examinations of infected fi sh suggested the occurrence of leucopenia and
proteolysis in certain tissues. Among the fi rst studies concerned with virulence
mechanisms of the organism was the extensive work of the Furunculosis Committee
in the UK (Mackie et al. 1930 , 1933, 1935). This group did not detect any toxin
production by Aer. salmonicida when either ultra-fi ltrates of broth cultures or diseased fi sh tissue was injected into healthy fi sh. Based on their failure to demonstrate
toxin production, they hypothesised as a result of detailed clinical observations that
the pathogenic processes caused by Aer. salmonicida could be explained by the
prolifi c growth in the blood and tissues of its host which, in turn, interfered with
blood supply resulting in anoxic cell necrosis and ultimately death. Additional evidence for a possible contribution to virulence, in the form of a leucocytolytic component, was provided by Blake ( 1935 ), who described the presence of ‘free’ bacteria
and little phagocytosis in the blood of diseased fi sh, with no defi nite leucocytic
Aeromonas salmonicida
Could farmed salmonids pose a realistic risk to native marine fi sh species?
The data on this topic are confusing. Certainly, marine fi sh larvae have been
infected with Aer. salmonicida subsp. salmonicida, with turbot regarded as being
more susceptible than halibut (Bergh et al. 1997 ). Using co-habitation and injection
challenges, experiments suggested that Aer. salmonicida subsp. salmonicida could
be transmitted rarely from Atlantic salmon to Atlantic cod, halibut and wrasse
(Hjeltnes et al. 1995 ). Interest in turbot has spurred some exciting work on understanding the virulence genes associated with the different stages of the infection
process. Thus, attention focused on the genes known to occur in salmonids, i.e.
vapA, tapA, fl a, ascV, ascC, aexT, satA and aspA , using a PCR and challenge by i.p.
injection and bathing. The result was that the genetic profi le linked to virulence and
challenge by i.p. injection was more frequent in cultures derived from turbot rather
than salmonids or the external environment but it was not possible to predict virulence based solely on the presence of these genes (Lago et al. 2012 ).
Could atypical isolates, which are appearing with increasing frequency in wild
fi sh, pose a threat to cultured salmonids?
Wiklund ( 1995b ) using an atypical isolate from ulcerated fl ounder concluded
that there was not any risk to rainbow trout.
What about the risk of transferring Aer. salmonicida from the freshwater to seawater stage of salmonids?
Eggset et al. ( 1997 ) concluded that the susceptibility of Atlantic salmon to furunculosis in seawater possibly refl ected the overall quality of the smolts.
Pathogenicity – Historical Aspects
Although the factors conferring pathogenicity on Aer. salmonicida strains have been
the subject of speculation since early in the study of the pathogen, it is only relatively recently that the details concerning pathogenesis and virulence have begun to
be elucidated. The initial investigations, carried out in the 1930s, resulted in several
key observations, notably that prolonged laboratory maintenance of Aer. salmonicida isolates was frequently responsible for a loss of virulence, and that histopathological examinations of infected fi sh suggested the occurrence of leucopenia and
proteolysis in certain tissues. Among the fi rst studies concerned with virulence
mechanisms of the organism was the extensive work of the Furunculosis Committee
in the UK (Mackie et al. 1930 , 1933, 1935). This group did not detect any toxin
production by Aer. salmonicida when either ultra-fi ltrates of broth cultures or diseased fi sh tissue was injected into healthy fi sh. Based on their failure to demonstrate
toxin production, they hypothesised as a result of detailed clinical observations that
the pathogenic processes caused by Aer. salmonicida could be explained by the
prolifi c growth in the blood and tissues of its host which, in turn, interfered with
blood supply resulting in anoxic cell necrosis and ultimately death. Additional evidence for a possible contribution to virulence, in the form of a leucocytolytic component, was provided by Blake ( 1935 ), who described the presence of ‘free’ bacteria
and little phagocytosis in the blood of diseased fi sh, with no defi nite leucocytic
Aeromonas salmonicida