372
transmit Y. ruckeri to recipient fi sh. In fact, it was necessary to stress these carriers,
such as by heat (i.e. a water temperature of 25 °C), in order to enable release and
thus transmission, of the pathogen to other fi sh. Even under these conditions, colonisation of the lower intestine took place in the recipient fi sh without any mortalities. However, the handling of fi sh, which may appear to be extremely healthy, and
crowded conditions causing excess ammonia and metabolic waste products in the
water and, thus, a decrease in oxygen levels, may precipitate outbreaks of clinical
disease (Bullock and Snieszko 1975 ). Nevertheless, outbreaks generally occur only
after the fi sh have been exposed to large numbers of the pathogen (Ross et al. 1966 ).
Mortalities tend to start 5–19 days after exposure, depending on the size of the
inoculum, and last for 30–60 days (Rucker 1966 ; Busch 1973 ). Cumulative losses
due to ERM may account for as much as 30–35 % of the rainbow trout population
(Klontz and Huddleston 1976 ).
There is controversy over some aspects of the ecology of Y. ruckeri, insofar as the
organism has been alternatively considered as well adapted as a normal aquatic
saprophyte (McDaniel 1972 ) and, secondly, as not capable of free-living for any
extended period in water (Klontz and Huddleston 1976 ). Nevertheless, these authors
conceded that survival for up to 2 months was possible in mud. Further experiments
indicated that the pathogen could survive for 4 months in unsupplemented water at
a salinity of 0–20‰; survival being reduced in seawater (salinity = 35‰) (Thorsen
et al. 1992 ). Romalde et al. ( 1994 ) reported survival for 3 months. Therefore, the
implication is that Y. ruckeri is capable of surviving in the (fresh) water column for
a long time after an outbreak of disease has occurred. Survival may be infl uenced by
the ability of virulent cultures to adhere to surfaces, a characteristic linked to the
presence of fl agella. Interestingly, oxolinic acid was better able to inactivate planktonic rather than attached cells of the pathogen (Coquet et al. 2002 ). Perhaps, the
organism is a normal inhabitant of the digestive tract of fi sh or in contaminated
waters. In this respect, Y. ruckeri has been isolated from sewage sludge (Dudley
et al. 1980 ) and a bacteriophage specifi c for Y. ruckeri found in sewage (Stevenson
and Airdrie 1984b ). Moreover, aquatic invertebrates, notably crayfi sh, and even terrestrial mammals, namely muskrats (Stevenson and Daly 1982 ) may harbour large
numbers of the pathogen, thereby serving as a reservoir of infection. It is noteworthy that McArdle and Dooley-Martin ( 1985 ) recovered Y. ruckeri from the digestive
tract of an apparently healthy goldfi sh following inspection of a consignment upon
importation into Ireland. The isolate was subsequently demonstrated to be pathogenic for rainbow trout. Thus it would appear that ornamental fi sh could pose a
reservoir of infection into salmonids. If Dulin et al. ( 1976 ) are correct in asserting
that Y. ruckeri is not ubiquitous in nature, it is puzzling why ERM should be found
in remote fi sh stocks, without prior history or association with the disease (Janeke,
personal communication). Under these conditions, it is doubtful if movement of
infected fi sh could account for the spread of ERM. Yet, isolations have been made
from wild salmonids. In one example, Y. ruckeri type I was recovered from a mature
wild Atlantic salmon in freshwater [in Scotland] (Petrie et al. 1996 ). Whether or not
this suggests a natural reservoir of the pathogen in wild fi sh or refl ects a transfer
from aquaculture remains to be established.
6 Enterobacteriaceae Representatives
transmit Y. ruckeri to recipient fi sh. In fact, it was necessary to stress these carriers,
such as by heat (i.e. a water temperature of 25 °C), in order to enable release and
thus transmission, of the pathogen to other fi sh. Even under these conditions, colonisation of the lower intestine took place in the recipient fi sh without any mortalities. However, the handling of fi sh, which may appear to be extremely healthy, and
crowded conditions causing excess ammonia and metabolic waste products in the
water and, thus, a decrease in oxygen levels, may precipitate outbreaks of clinical
disease (Bullock and Snieszko 1975 ). Nevertheless, outbreaks generally occur only
after the fi sh have been exposed to large numbers of the pathogen (Ross et al. 1966 ).
Mortalities tend to start 5–19 days after exposure, depending on the size of the
inoculum, and last for 30–60 days (Rucker 1966 ; Busch 1973 ). Cumulative losses
due to ERM may account for as much as 30–35 % of the rainbow trout population
(Klontz and Huddleston 1976 ).
There is controversy over some aspects of the ecology of Y. ruckeri, insofar as the
organism has been alternatively considered as well adapted as a normal aquatic
saprophyte (McDaniel 1972 ) and, secondly, as not capable of free-living for any
extended period in water (Klontz and Huddleston 1976 ). Nevertheless, these authors
conceded that survival for up to 2 months was possible in mud. Further experiments
indicated that the pathogen could survive for 4 months in unsupplemented water at
a salinity of 0–20‰; survival being reduced in seawater (salinity = 35‰) (Thorsen
et al. 1992 ). Romalde et al. ( 1994 ) reported survival for 3 months. Therefore, the
implication is that Y. ruckeri is capable of surviving in the (fresh) water column for
a long time after an outbreak of disease has occurred. Survival may be infl uenced by
the ability of virulent cultures to adhere to surfaces, a characteristic linked to the
presence of fl agella. Interestingly, oxolinic acid was better able to inactivate planktonic rather than attached cells of the pathogen (Coquet et al. 2002 ). Perhaps, the
organism is a normal inhabitant of the digestive tract of fi sh or in contaminated
waters. In this respect, Y. ruckeri has been isolated from sewage sludge (Dudley
et al. 1980 ) and a bacteriophage specifi c for Y. ruckeri found in sewage (Stevenson
and Airdrie 1984b ). Moreover, aquatic invertebrates, notably crayfi sh, and even terrestrial mammals, namely muskrats (Stevenson and Daly 1982 ) may harbour large
numbers of the pathogen, thereby serving as a reservoir of infection. It is noteworthy that McArdle and Dooley-Martin ( 1985 ) recovered Y. ruckeri from the digestive
tract of an apparently healthy goldfi sh following inspection of a consignment upon
importation into Ireland. The isolate was subsequently demonstrated to be pathogenic for rainbow trout. Thus it would appear that ornamental fi sh could pose a
reservoir of infection into salmonids. If Dulin et al. ( 1976 ) are correct in asserting
that Y. ruckeri is not ubiquitous in nature, it is puzzling why ERM should be found
in remote fi sh stocks, without prior history or association with the disease (Janeke,
personal communication). Under these conditions, it is doubtful if movement of
infected fi sh could account for the spread of ERM. Yet, isolations have been made
from wild salmonids. In one example, Y. ruckeri type I was recovered from a mature
wild Atlantic salmon in freshwater [in Scotland] (Petrie et al. 1996 ). Whether or not
this suggests a natural reservoir of the pathogen in wild fi sh or refl ects a transfer
from aquaculture remains to be established.
6 Enterobacteriaceae Representatives