100
found that BKD occurred over a wide range of water temperatures from 8 to
18 °C. Most epizootics occurred in the autumn and winter, i.e. during periods of
declining water temperatures. However, most mortalities occurred at higher temperatures, a conclusion which has been echoed by Austin ( 1985 ), although the
reverse has also been reported (Sanders et al. 1978 ). At low temperatures, the effect
was the continual loss of small numbers of fi sh (Snieszko and Griffi n 1955 ). This is
quite a feat for a supposedly unreactive organism!
BKD has been diagnosed in fi sh following movement from fresh to seawater
(Earp et al. 1953 ; Bell 1961 ). Indeed, the disease may be of paramount importance
in the ability to acclimatize to seawater (Frantsi et al. 1975 ) and the survival of salmonids in the oceanic environment (Fryer and Sanders 1981 ).
Data obtained with ELISA have shown that Ren. salmoninarum occurs commonly, in the absence of pathological signs of BKD, in wild fi sh, i.e. Arctic charr
and brown trout in Iceland (Jónsdóttir et al. 1998 ). Thus, the route of transmission
to aquaculture may be from wild fi sh.
The effect of nutritional (dietary) status on the development of BKD is only partially understood. Some diets, notably those containing corn gluten (Wedemeyer
and Ross 1973 ) or lipid (Austin 1985 ), enhanced the disease. Nutritional studies
with Atlantic salmon have shown that levels of vitamin A, iron and zinc are lowered
in BKD infected fi sh (Paterson et al. 1981 ). Subsequent experiments in which fi sh
were administered diets rich in trace elements resulted in reduced incidences of
BKD. This theme should be exploited further for control purposes.
In fi sh culture, Ren. salmoninarum appears to be a most unaggressive organism,
generally devoid of much production of exoenzymes (exotoxins). Yet, it causes such
a severe problem in salmonids. With lack of evidence to the contrary, it is our
hypothesis that the organism is a normal resident of some fi sh, in (or on) which it
exists, probably in fairly low numbers. Conceivably, it may be a normal resident of
kidney tissue, forming a synergistic or controlled parasitic relationship with the
host, possibly in the macrophages. Alternatively, it may be a normal resident of the
digestive tract (Austin 1986 ). To continue the scenario, we postulate that at times of
stress to the host, such as sub-clinical infections, damage to the digestive tract, starvation, kidney damage or temperature shock, the organism is able to migrate to the
kidney (if not already there) and multiply. This would lead ultimately to the condition known as BKD. The problems with recovery of the organism, particularly from
asymptomatic fi sh, may be explained within the realms of this concept. Evelyn and
co-workers (Evelyn 1978 ; Evelyn et al. 1981 ) have considered the presence of
inhibitors in the kidney that suppress the development of Renibacterium on solid
medium. Could these unnamed compounds control the growth and development of
the organism in healthy fi sh? This remains a possibility. However, there are other
equally plausible explanations, namely dormancy, damage, or the presence of
altered - osmotically fragile - cells. The renibacteria may normally be in a dormant
or altered phase within the fi sh and, thus, would require to be triggered back into
activity in order to produce colonies. Alternatively, renibacteria may be in some
way damaged in the fi sh, and require repair before being able to produce colonies.
This parallels the problem of damaged coliform bacteria in the aquatic environment
3 Aerobic Gram-Positive Rods and Cocci
found that BKD occurred over a wide range of water temperatures from 8 to
18 °C. Most epizootics occurred in the autumn and winter, i.e. during periods of
declining water temperatures. However, most mortalities occurred at higher temperatures, a conclusion which has been echoed by Austin ( 1985 ), although the
reverse has also been reported (Sanders et al. 1978 ). At low temperatures, the effect
was the continual loss of small numbers of fi sh (Snieszko and Griffi n 1955 ). This is
quite a feat for a supposedly unreactive organism!
BKD has been diagnosed in fi sh following movement from fresh to seawater
(Earp et al. 1953 ; Bell 1961 ). Indeed, the disease may be of paramount importance
in the ability to acclimatize to seawater (Frantsi et al. 1975 ) and the survival of salmonids in the oceanic environment (Fryer and Sanders 1981 ).
Data obtained with ELISA have shown that Ren. salmoninarum occurs commonly, in the absence of pathological signs of BKD, in wild fi sh, i.e. Arctic charr
and brown trout in Iceland (Jónsdóttir et al. 1998 ). Thus, the route of transmission
to aquaculture may be from wild fi sh.
The effect of nutritional (dietary) status on the development of BKD is only partially understood. Some diets, notably those containing corn gluten (Wedemeyer
and Ross 1973 ) or lipid (Austin 1985 ), enhanced the disease. Nutritional studies
with Atlantic salmon have shown that levels of vitamin A, iron and zinc are lowered
in BKD infected fi sh (Paterson et al. 1981 ). Subsequent experiments in which fi sh
were administered diets rich in trace elements resulted in reduced incidences of
BKD. This theme should be exploited further for control purposes.
In fi sh culture, Ren. salmoninarum appears to be a most unaggressive organism,
generally devoid of much production of exoenzymes (exotoxins). Yet, it causes such
a severe problem in salmonids. With lack of evidence to the contrary, it is our
hypothesis that the organism is a normal resident of some fi sh, in (or on) which it
exists, probably in fairly low numbers. Conceivably, it may be a normal resident of
kidney tissue, forming a synergistic or controlled parasitic relationship with the
host, possibly in the macrophages. Alternatively, it may be a normal resident of the
digestive tract (Austin 1986 ). To continue the scenario, we postulate that at times of
stress to the host, such as sub-clinical infections, damage to the digestive tract, starvation, kidney damage or temperature shock, the organism is able to migrate to the
kidney (if not already there) and multiply. This would lead ultimately to the condition known as BKD. The problems with recovery of the organism, particularly from
asymptomatic fi sh, may be explained within the realms of this concept. Evelyn and
co-workers (Evelyn 1978 ; Evelyn et al. 1981 ) have considered the presence of
inhibitors in the kidney that suppress the development of Renibacterium on solid
medium. Could these unnamed compounds control the growth and development of
the organism in healthy fi sh? This remains a possibility. However, there are other
equally plausible explanations, namely dormancy, damage, or the presence of
altered - osmotically fragile - cells. The renibacteria may normally be in a dormant
or altered phase within the fi sh and, thus, would require to be triggered back into
activity in order to produce colonies. Alternatively, renibacteria may be in some
way damaged in the fi sh, and require repair before being able to produce colonies.
This parallels the problem of damaged coliform bacteria in the aquatic environment
3 Aerobic Gram-Positive Rods and Cocci