also been reported Sanders et al 1978 At low temperatures the effect was the

Also been reported sanders et al 1978 at low

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also been reported (Sanders et al., 1978). At low temperatures, the effect was the continual loss of small numbers offish (Snieszko and Griffin, 1955). This is quite a feat for a supposedly unreactive organism! BKD has been diagnosed in fish 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 sal- monids in the oceanic environment (Fryer and Sanders, 1981). Data obtained with ELISA have shown that Ren. salmoninarum occurs com- monly, in the absence of pathological signs of BKD, in wild fish, i.e. Artie charr and brown trout in Iceland (Jonsdottir et al, 1998). Thus, the route of transmission to aquaculture may be from wild fish. 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 fish (Paterson et al, 1981). Subsequent experiments in which fish were administered diets rich in trace elements resulted in reduced incidences of BKD. This theme should be exploited further for control purposes. In fish 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 hypoth- esis that the organism is a normal resident of some fish, 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, poss- ibly 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 fish, 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 fish? This remains a possibiHty. However, there are other equally plausible
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242 Bacterial Fish Pathogens 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 fish 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 fish, and require repair before being able to produce colonies. This parallels the problem of
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