262
ogy of Aer. salmonicida diseases in aquatic environments other than freshwater,
again, as in so many other aspects of the pathogen, demands additional attention to
unravel it complexities.
Aeromonas salmonicida – The Summary In summary, although substantial
efforts have been made to reach an understanding of the natural disease cycle in the
environment, there still remain many issues to be resolved. Some of the data provide partial answers, some are contradictory. Lack of appropriate methodology
appears to constitute a major hindrance to progress. In the face of the several unresolved questions concerning Aer. salmonicida epizootiology, McCarthy ( 1980 ) has
valiantly put forth several hypotheses aimed at deriving an overall view of Aer.
salmonicida epizootiology. The fi rst of these is that furunculosis is introduced to a
fi sh farm by importation of healthy carrier fi sh or that non-carrier resident fi sh may
be infected from a water supply contaminated by wild or imported carrier fi sh.
Accordingly, if contact with carriers of Aer. salmonicida can be prevented, furunculosis should not arise in the population. The second hypothesis McCarthy ( 1980 )
advanced is that the mechanisms by which carriers disseminate the disease to noncarriers is dependent upon environmental parameters at a given fi sh farm site. He
postulated that if stressful conditions are absent, resident fi sh may become carriers
without developing clinical signs of disease, and that under such conditions a high
carrier rate could be maintained without clinical evidence of furunculosis. This, in
the opinion of other workers, would be an arguable premise, as some believe all
carriers will eventually succumb to the disease. It is reasonable to suppose that once
carrier fi sh are present on a fi sh farm they are responsible for initiation of epizootics,
although infection also occurs by the water-borne route. The third hypothesis is that
the bacterium in the carrier state provides a measure of protection to the fi sh in
return for shelter from the ravages of the aquatic environment. Were this the case,
the observation by McCarthy ( 1980 ) that non-carrier and carrier fi sh exhibit marked
differences in their susceptibility to furunculosis would be explained.
Finally, it is our opinion that while a fi rm understanding of the interactions of the
pathogen in its milieu and in its fi sh host is lacking, fi sheries scientists will remain
at a serious disadvantage when tackling the problems of infectious diseases of Aer.
salmonicida aetiology that currently beset fi sh cultivation.
Pathogenicity
The Spread of the Pathogen
Historically, Aer. salmonicida was regarded as a risk primarily to salmonids (e.g.
Mackie et al. 1930 , 1933, 1935). Then, cyprinids followed by other freshwater and
marine fi sh became recognised to be vulnerable to infection (e.g. Herman 1968 ;
Austin et al. 1998 ).
5 Aeromonadaceae Representative (Aeromonas salmonicida)
ogy of Aer. salmonicida diseases in aquatic environments other than freshwater,
again, as in so many other aspects of the pathogen, demands additional attention to
unravel it complexities.
Aeromonas salmonicida – The Summary In summary, although substantial
efforts have been made to reach an understanding of the natural disease cycle in the
environment, there still remain many issues to be resolved. Some of the data provide partial answers, some are contradictory. Lack of appropriate methodology
appears to constitute a major hindrance to progress. In the face of the several unresolved questions concerning Aer. salmonicida epizootiology, McCarthy ( 1980 ) has
valiantly put forth several hypotheses aimed at deriving an overall view of Aer.
salmonicida epizootiology. The fi rst of these is that furunculosis is introduced to a
fi sh farm by importation of healthy carrier fi sh or that non-carrier resident fi sh may
be infected from a water supply contaminated by wild or imported carrier fi sh.
Accordingly, if contact with carriers of Aer. salmonicida can be prevented, furunculosis should not arise in the population. The second hypothesis McCarthy ( 1980 )
advanced is that the mechanisms by which carriers disseminate the disease to noncarriers is dependent upon environmental parameters at a given fi sh farm site. He
postulated that if stressful conditions are absent, resident fi sh may become carriers
without developing clinical signs of disease, and that under such conditions a high
carrier rate could be maintained without clinical evidence of furunculosis. This, in
the opinion of other workers, would be an arguable premise, as some believe all
carriers will eventually succumb to the disease. It is reasonable to suppose that once
carrier fi sh are present on a fi sh farm they are responsible for initiation of epizootics,
although infection also occurs by the water-borne route. The third hypothesis is that
the bacterium in the carrier state provides a measure of protection to the fi sh in
return for shelter from the ravages of the aquatic environment. Were this the case,
the observation by McCarthy ( 1980 ) that non-carrier and carrier fi sh exhibit marked
differences in their susceptibility to furunculosis would be explained.
Finally, it is our opinion that while a fi rm understanding of the interactions of the
pathogen in its milieu and in its fi sh host is lacking, fi sheries scientists will remain
at a serious disadvantage when tackling the problems of infectious diseases of Aer.
salmonicida aetiology that currently beset fi sh cultivation.
Pathogenicity
The Spread of the Pathogen
Historically, Aer. salmonicida was regarded as a risk primarily to salmonids (e.g.
Mackie et al. 1930 , 1933, 1935). Then, cyprinids followed by other freshwater and
marine fi sh became recognised to be vulnerable to infection (e.g. Herman 1968 ;
Austin et al. 1998 ).
5 Aeromonadaceae Representative (Aeromonas salmonicida)