Studies of proliferative kidney disease in salmonid fishes
Sequential clinical and pathological changes were studied in 277 naturally-infected rainbow trout. Infection was histologically detectable at the beginning of June; gross pathology developed from the beginning of July; clinical signs, principally abdominal distension, were evident from mid-July. The...
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| Format: | Doctoral or Postdoctoral Thesis |
| Language: | English |
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University of Stirling
1986
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| Online Access: | http://hdl.handle.net/1893/31449 http://dspace.stir.ac.uk/bitstream/1893/31449/1/Clifton-Hadley_Thesis.pdf |
| Summary: | Sequential clinical and pathological changes were studied in 277 naturally-infected rainbow trout. Infection was histologically detectable at the beginning of June; gross pathology developed from the beginning of July; clinical signs, principally abdominal distension, were evident from mid-July. The main changes were associated with the kidney. Renal haemopoietic hyperplasia preceded the development of vascular lesions and intravascular haemoglobin crystallization. Diffuse inflammation disrupted nephrons and caused renal enlargement. A grading system was elaborated to assess disease severity. Haematological changes were studied in 181 naturally-infected rainbow trout. A hypoplastic anaemia developed, exacerbated in some by hydraemia. The infective period at the experimental site was shown to be between May and September when maximum water temperatures exceeded 10°C. Fish infected from the end of July did not become clinically affected. In subclinically-infected fish held in the laboratory at temperatures between 9°C and 18°C, PKD was delayed at the lower temperatures although the causative organism persisted in fish held at 9°C for several months. In clinically-affected fish held at 7°C to 21°C the rate of recovery was enhanced at the lower temperatures. Resistance to PKD was assessed. Rainbow trout appeared more susceptible than Atlantic salmon and brown trout. Previously unexposed 0+ and 1+ rainbow trout were equally susceptible to the disease. Fish recovering from subclinical infection without renal swelling remained susceptible. Survivors of clinical disease could be re-infected but remained clinically unaffected when re-challenged. Fry from broodstock surviving clinical disease were susceptible. PKD was transmitted using infected rainbow trout renal tissue by inoculation of rainbow trout via the peritoneal and subcutaneous routes, and by inoculation of brown trout via the peritoneal route. In rainbow trout, challenges via gill, skin and stomach were unsuccessful. No direct transmission was demonstrated from ... |
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