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Editor’s note:  This is the first of a two-part article that is being reprinted with the written permission from the Compendium on Continuing Education For the Practicing Veteri-narian.  This article was originally printed in this journal in November, 2000, Vol 22 (11), pages S160-166

Performing Diagnostic Procedures on Salmonid Fishes

by

Melvin Randall White, DVM, PhD

Aquaculture is a rapidly developing agribusiness.  The culture and harvest of salmonids by private industries for food consumption and exportation represent a $79 million industry in the United States.This article provides guidelines on how to perform diagnostic techniques and properly collect tissue samples from salmonids.  In addition, various diagnostic techniques can help distinguish disease processes unique to salmonids.

DISEASE EVALUATION

Obtaining a Disease History

Important information can be learned about an aquaculture facility by asking the proper questions while compiling a disease history.  Although many questions may be directly related to a particular disease, basic information regarding the facility’s operating procedures should be obtained to reveal possible environmental concerns or problems that are personnel related.

 

  • When was the current disease or problem noticed, and what steps have been taken to correct it?
  • What clinical signs have been noticed?
  • When were new fish last introduced to the system?
  • What changes, if any, have occurred with respect to nutrition?
  • What changes, if any, have occurred with respect to water quality?
  • What changes, if any, have occurred with respect to the physical environment (e.g., tanks, ponds, aeration equipment, feeders)?
  • Have there been any personnel changes?

Environmental Criteria

Water quality is the most important environmental parameter for salmonid producers.  Environmental abnormalities can be categorized into acute and chronic problems.  With acute water problems, at least one of the parameters is severely affected and poses a life-threatening condition to the fish; high mortality will result if the situation is not corrected immediately.  A chronic water problem acts as a stressor and not as the initiating cause of mortality.

Although water-quality parameters vary according to environment and geographic locality, several guidelines are available.2-4 Dissolved oxygen (O2), temperature, ammonia, and nitrite should be monitored at least once or twice daily.  The dissolved O2 of the water must be evaluated onsite using a portable O2 meter or a commercially available test kit.  Parameters that should be evaluated at least once a week include pH, hardness, and alkalinity.

In ponds, dissolved O2 is a critical water-quality parameter.  Usually ponds are aerated, but they also depend on the photosynthetic activity of aquatic plants and algae to produce dissolved O2.  The respiration of these plants consumes dissolved O2, however, potentially resulting in an “O2 debt.”  In artificial aquatic settings (e.g., aquaculture raceways), O2 is added by using mechanical means to agitate the water or by “bubbling” atmospheric gases or purified O2 into the water.  The loss of stratification of ponds or an acute algal bloom die-off can cause the dissolved O2 content of pond water to become acutely lowered.  A vicious cycle occurs whereby the decaying plant life consumes O2 and at the same time the decreased viable algal mass cannot produce as much O2.  In aquatic environments in which mechanical aerators or agitators are used to provide dissolved O2 to the water, equipment failure and/or power outages are common causes of acutely decreased dissolved O2.

Water in ponds commonly stratifies in the late spring and early summer because of temperature fluctuations and the difference between the density of warm and cold water.  As the water temperature increases, and in the absence of water agitation, the pond stratifies by forming an upper layer of warm water (epilimnion) and a deeper layer of cold water (hypolimnion).  Loss of stratification by mechanical agitation or from a severe thunderstorm often results in rapid O2 depletion.  A dilutional effect results as the large volume of O2-poor water in the hypolimnion mixes with the O2-rich surface waters, thereby decreasing the total dissolved O2 content of the pond.

For salmonids raised in raceways, O2 may be added to the aquatic environment when water flows over splashboards.  Raceways are rectangular-shaped tanks; water is commonly added to the tank at one end and drained at the opposite end.  The raceways are usually sloped to enable water to flow over the splashboards, thus creating enough turbulence to increase the dissolved O2 content.  Mechanical failure with the splashboards or the fouling of these devices with extraneous or excessive amounts of organic material can lead to decreased dissolved O2 content.

Ammonia is excreted by both fish and plants2 and rapidly metabolized into nitrite by Nitrosomonas bacteria.  Nitrobacter species then converts the nitrite to nitrate.  Of the three compounds, nitrate is the least toxic to fish.  Ammonia is present in the water in ionized (NH+4) and un-ionized (NH3) forms.  The ratio of ionized and un-ionized ammonia is pH dependent; more acidic water favors the less toxic ionized ammonia, whereas basic water favors the more toxic un-ionized ammonia.  Acute ammonia toxicity can occur from a sudden die-off of fish or plants or if a large amount of fish food is inadvertently introduced into the system.  In these situations, considerable decomposing protein is released into the water, resulting in a concomitant increase of ammonia followed by nitrite.

 Acute ammonia toxicity often occurs when fish are introduced into a new water system with inadequate amounts of Nitrosomonas bacteria to convert the ammonia to nitrite.  In the aquaculture industry, this is known as new tank syndrome.  Fish can also be affected by acute ammonia toxicity with a sudden die-off of Nitrosomonas bacteria in the biofilter of recirculating systems if chemicals that kill these bacteria are introduced into the water system.  Although salmonids were not raised in recirculating systems in the past, these systems are now being used successfully.

The clinical signs of acute ammonia toxicity are nondiagnostic; therefore, careful monitoring of the water quality is needed to prevent it.  Acute ammonia toxicity results in systemic acidosis.  Although ammonia may act as a false neurotransmitter, ammonia toxicity primarily results from inhibition of the citric acid cycle caused by the blockage of oxaloacetate with resultant anaerobic glycolysis.5

Nitrite is another important water-quality parameter that must be constantly monitored.  Acute nitrite toxicosis has been called brown blood disease because of the rapid oxidation of hemoglobin, which occurs when nitrite diffuses across the gill epithelium of fish.  This oxidation results in methemoglobin formation, which causes brown discoloration of the blood.2 Although this condition is observed in catfish raised for production, it is not a common problem in salmonids.

  The pH as well as the hardness and alkalinity of water should be monitored periodically to denote trends or changes in parameters that may result in chronic water problems.  The pH of water is the measurement of the hydrogen ion content expressed as the negative logarithm of the hydrogen ion concentration; thus the pH measures the acidity or alkalinity of water.  The alkalinity is a determination of the buffering capacity of water as measured by the amount of bicarbonate (HCO-3) and/or carbonate (CO-3) in milligrams per liter (mg/l) in the water.  The hardness of water is the measurement of divalent metal cations (e.g., calcium, iron, zinc, magnesium).  The majority of the cations are calcium.  Chronic poor water quality reportedly can diminish the growth, feed efficiency, and feed conversion rates of fish.

(Part two of this article, Diagnostic Techniques and Summary, will be concluded in the next newsletter.)

REFERENCES

  1. U.S. Department of Agriculture: Aqua-culture Outlook, publication Aquaculture 8. Rockville, MD, Economic Research Service, 1998.
  2. Noga EJ: Fish Disease: Diagnosis and    Treatment. St. Louis, Mosby, 1996, pp 3-75.
  3. Collins R: Principles of disease diag-nosis, in Brown L (ed): Aquaculture for Veterinarians, Fish Husbandry and     Medicine. New York, Pergamon Press, 1993, pp 69-89.
  4. U.S. Department of the Interior: Fish     Manual for the Investigation of Fish Kills. Springfield, VA, Fish and Wildlife Service, National Technical Information Service, 1990, p 41.
  5. Osweiler GD, Carson TL, Buck WB, Van Gelder GA (eds): Urea and nonprotein nitrogen, in: Clinical and Diagnostic Veterinary Toxicology (ed 3). Dubuque, IA, Kendall/Hunt Publishing Co, 1985, pp 160-166.
  6. Noga EJ, Levine JF, Townsend K, et al: Kidney biopsy: A non-lethal method for      diagnosing Yersinia ruckeri infection (enteric red mouth disease) in rainbow trout (Salmo gairdneri). Am J Vet Res 49:363-365, 1988.
  7. White MR, Albregts SR, Wu CC, et al: The use of kidney biopsy of broodstock steelhead trout (Oncorhyncus mykiss) to determine the status of bacterial kidney       disease infection. J Vet Diagn Invest 8:519-522, 1996.
  8. Hille S: A literature review of the blood chemistry of rainbow trout, Salmo gairdneri   Richardson. J Fish Biol 20:535-569, 1982.
  9. Hoffman R, Lommel  R: Haema-tological studies in proliferative kidney disease of rainbow trout, Salmo gairdneri. Richardson. J Fish Dis 7:323-326, 1984.
  10. Miller WR, Hendricks AC, Cairns Jr J: Normal ranges for diagnostically important hematological and blood chemistry characteristics of rainbow trout (Salmo gairdneri) Can J Fish Aquatic Sci 40:420-425, 1983.
  11. Smith LS, Bell GR: A Practical Guide to the Anatomy and Physiology of Pacific     Salmon.  Ottawa Department of the Environment, Fisheries and Marine Service. 1976, p 11.
  12. Yasutake WT, Wales JH: Microscopic Anatomy of Salmonids: An Atlas. Research publication 150, Washington, DC, U.S. Depatment of the Interior, 1983, p 44.
  13. Sundararaj BI: Reproductive Phy-siology of Teleost Fishes. A Review of Present Knowledge and Needs for Future Research. Rome, United Nations Development Programme, 1981, p 15.

 

 

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