Why fish die - the treatment and pathophysiology of AGD

Mark D. Powell, Michael Attard, James O. Harris, Shane D. Roberts, Melanie J. Leef

Research output: Book/ReportCommissioned reportpeer-review

Abstract

Prior to this project, the study of amoebic gill disease patho-physiology was confined to using either fish infected by cohabitation or else clinically infected on fish farms under commercial conditions. This project developed a standardised process for acclimating Atlantic salmon smolts to seawater and infecting those salmon with Neoparamoeba sp. in the laboratory. This produced a reliable and repeatable challenge that could re-create AGD in the laboratory within 2-3 weeks. Although it developed more quickly than infections under field conditions, this condensed infection provides a tool with which to study the physiology of the disease and the efficacy of candidate treatments. This project characterised the pathogenesis of AGD under laboratory conditions and supported suggestions that respiratory compromise was a minor cause of mortality in AGD affected salmon. Although the resting metabolic rate of the fish is increased with infection, probably reflecting an increased energetic cost of disease, the main cause of mortality appears to be due to acute cardiovascular compromise. Studies showed that increased vascular resistance (hypertension: high blood pressure) resulted in circulatory failure in AGD affected salmon. This same pathology was not however, seen in less susceptible salmonids such as rainbow trout. The effects of the hypertension could be partially reversed using drugs that lower blood pressure. The role of mucus in AGD was closely studied. Fish affected by AGD showed a reduction in the viscosity of mucus, analogous to a “runny nose” which would slough off the offending Neoparamoeba sp. parasite from the gills. This was reflected in biochemical and histochemical changes in the composition of the mucus both during seawater acclimation and in response to infection in salmonids. The project identified several potential improvements to bathing as a treatment for AGD. The use of softened water enhances mucus sloughing and is more effective at killing Neoparamoeba sp. Similarly, replacement of freshwater with a chloramine-T treatment in seawater may offer an alternative to freshwater bathing, especially as an emergency treatment or for farms that have limited access to freshwater. The use of artificially softened water is now at the point of commercial adoption by the aquaculture industry, and the use of chloramine-T in seawater is close to that point The use of in feed amoebocides or treatments that help to overcome the effects of AGD were also tested. Neoparamoeba sp. are resistant to many families of antiprotozoal drugs, although at least in vitro, Neoparamoeba sp. was sensitive to the drug bithionol. In addition, the use of mucolytic drugs to enhance mucus sloughing and reduced mucus viscosity showed promise in retarding the onset of AGD. Also, the use of nutritional supplements Aquacite and Betabec, maintained feed intake and growth in AGD affected fish under laboratory conditions. In conclusion, this project has identified a primary cause of AGD related mortality and several potential treatment options. This has significantly increased our understanding of the pathophysiology of the disease as well has providing avenues for improvements in the commercial control of the disease.
Original languageEnglish
Place of PublicationLaunceston, TAS
PublisherUniversity of Tasmania
Commissioning bodyAustralian Government - Fisheries Research and Development Corporation
Number of pages112
ISBN (Print)1862952590
Publication statusPublished - Jun 2005
Externally publishedYes

Keywords

  • Amoebic Gill Disease
  • Atlantic salmon
  • treatment

Fingerprint

Dive into the research topics of 'Why fish die - the treatment and pathophysiology of AGD'. Together they form a unique fingerprint.

Cite this