Some level of mortality (1-3%) is expected shortly after smolt transfer - and there are often buyer-seller arrangements to cover these losses. Fish health consultants frequently deal with resolving the causes of unexpected post-
transfer mortality spikes. As well, protracted patterns of low-level mortality persisting for weeks or months after transfer are a common concern. Determining whether these reflect hatchery problems, events which occurred during transfer itself, or mismanagement by sea-cage operators can be a difficult task.
Acute post-transfer losses due to severe seawater intolerance do occur, and are more common with fall transfers (Bettencourt and Anderson, 1990). Bouck and Smith (1979) showed that skin damage markedly reduced the success of coho salmon transfers to seawater. This highlights the care needed during the transfer process. An additional problem are 'slinks', those fish not adapting to saltwater. Slinks fail to start feeding after transfer, and gradually die from starvation. They are typified by poor body condition and dark colouring, atrophy of many visceral organs, distended gall bladder, serous atrophy of fat stores, and increased stores of melanin and lipofuscin pigments. The latter reflects catabolism. These fish become problems for a number of reasons. In their debilitated state they are particularly vulnerable to pathogens and then become an important source of infective agents. A more subtle problem is that during disease outbreak investigations, slinks are much easier to capture than their pen mates. Unfortunately, their disease status is quite often a poor reflection on the disease status of the pen as a whole, thus introducing a bias into the disease investigation.
The smolt transfer period presents several opportunities for preventing pathogen transfer between companies, and between environments. For example, post-transfer outbreaks of furunculosis are assumed to reflect recrudescence of this bacterial pathogen in carrier smolt, which are stressed by the transfer process. Although generally regarded to be a freshwater protozoal disease, costiasis is also reported in post-transfer smolt (Fig. 12.15) (Ellis and Wooten, 1978; Urawa, 1993). Accordingly, programmes of health checks, stress tests (with cortisol and temperature elevation), saltwater challenges, chemical baths and vaccinations, are used to uncover, treat, or prevent diseases which could affect fish post-transfer. Paradoxically, multiple management events close to the smolt window may not always be beneficial. Treatment chemicals may have increased toxicity (either immediate effects or affecting ability to accommodate seawater challenge) to salmonids during the smolt window because of changes to gill physiology. For example, presmoltification changes such as the increased numbers and enlarged apical surface area of chloride cells, along with the development of accessory cells with ion-permeable junctions (Pisam et al., 1988; Laurent and Perry, 1991), could result in unexpected gill damage following chemotherapeutic exposure. Smith et al. (1987), however, have shown that repeated formalin treatment at 167 p.p.m. (one hour baths) performed up to the time of transfer did not affect seawater survival of fall release chinook salmon. Also, effects on the Na+-K+ ATPase enzyme activity were inconsistent and regarded as biologically unimportant. Data from work with Atlantic salmon smolt concurs (Powell et al., 1996). In contrast, Bouck and Johnson (1979) earlier had shown that coho salmon smolt transfer success was inhibited when either formalin, nifurpurinol, copper sulphate, Hyamine 1622, potassium permanganate, or malachite green treatments were administered
shortly before transfer, but not if a delay of four days was allowed. Copper's effects on cellular tight junctions and the gill Na+-K+ ATPase enzyme, mediated through its affinity to sulphydryl groups (Lauren and McDonald, 1986) suggest avoiding copper sulphate treatment before smolt transfer.
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