Would you like your fish to have their brightest coloration and best possible finnage? Are you interested in the animal’s growth or reproduction? Do you want to keep your fish in excellent health? If you answered yes to any of these questions, then you will be interested in learning about stress and concerned about how it can affect your fish. Why is stress important to understand? Because of the affect it has upon the health, beauty, reproduction, growth, longevity and survival of your prized specimens!

Stress has many consequences to the overall quality of health and longevity of fish. It causes biochemical, physiological and behavioral changes. Stress factors induce the mobilization and reallocation of energy (Barton, et, al. 1988), increase oxygen uptake and transfer, and suppression of immune function (Maule, et, al., 1989. Mock & Peters, 1990. Pickering & Pottinger, 1987b). Any response or adaptation to stress requires the expenditure of energy that would otherwise be utilized for maintaining normal body functions such as growth, digestion, osmoregulation, disease resistance, healing and reproduction. Think of energy as a pie with only so many pieces; stress consumes a portion of the animal’s energy that could be put to better use (Barton & Iwama, 1991. Schreck, 1982).

Fish are more susceptible to stress than many other animals because of a greater dependence upon their surrounding environment (Wedemeyer, 1996a). The delicate surfaces of the gills come into direct contact with chemical toxins that cause stress; this is exacerbated in marine fish by the fact they actually drink large quantities of the water.

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Four important body functions are closely associated with processes in the gills: gas exchange, hydromineral (osmoregulation) control, acid-base balance and nitrogenous waste excretion. These processes are possible because of the close proximity of the blood flowing through the gills to the surrounding water, as well as the differences in the chemical composition of these two fluids (for example, the salt content of fish blood is about 1/3 that of seawater and roughly 100 times that of freshwater).

Adrenaline released during the stress response increases blood flow to the gills to provide for the increased oxygen demands of stress. The release of adrenaline into the blood stream elevates the heart rate, blood flow and blood pressure. This increases the volume of blood in vessels contained within the gills, increasing the surface area of the gills while helping fish absorb more oxygen from the water. The elevated blood flow allows increased oxygen uptake for respiration but also increases the permeability of the gills to water and ions. This is what is known as the osmorespiratory compromise (Folmar & Dickhoff, 1980. Mazeaud, et, al., 1977). In saltwater fish, this leads to accelerated ion influxes and water losses. In freshwater fish, the effects are reversed; it increases water influx and ion losses. Small fish are more susceptible to hydromineral disturbances due, in part, to a higher gill- surface-to-body-mass-ratio than their larger counterparts.

One of the most characteristic aspects of stress in fish is osmoregulatory disturbance, which is related to the effects of both catecholamine and cortisol hormones. The extent of the disturbance following stress depends upon the ionic and osmotic gradients (difference) between the internal fluids of the fish and its surrounding environment (water). If the stress is persistent and of sufficient intensity, changes in the cellular structure of the gills may occur under the influence of cortisol. In this situation, increased death and turnover rates of branchial epithelial cells leads to accelerated aging of the gills. These degenerating and newly-formed gill cells do not function normally, which further limits the fish’s ability to maintain water and ion homeostasis under stressful conditions. Thus, acute stress limits the fish’s capacity to osmoregulate, and prolonged periods of extreme stress may result in osmotic shock and death.

Cortisol released as part of the response to chronic and acute stress affects the digestion of carbohydrates, proteins and lipids. This reduces the useable amount of nutrition animals receive from foods. Stress affects circulating levels of reproductive hormones caused by handling (an acute stressor) and confinement (a chronic stressor) (Safford and Thomas, 1987). Abrupt or drastic temperature changes may weaken fish to the point that latent bacterial infections worsen. Chronic stress can lead to generalized melanosis (discoloration or body darkening), fin fraying and loss of tissue between fin rays (frayed fin syndrome), especially in the pectoral, anal, and caudal fins.

Because stress evokes elevated cortisol blood plasma levels, resulting in suppressed immune function, and drains metabolic energy, the effects of stress are cumulative (Pennell, 1991), reducing the capacity to tolerate subsequent or additional stressors. Stress suppresses the immune response and can predispose fish to disease. Stress reduces antibody production (Pickering and Pottinger 1987b, Pickering, A.D. 1987), slows the body’s response to injury or infection and increases susceptibility to pathogens. This is particularly true with facultative or opportunistic pathogens. Reduced surface mucus production is associated with stress in fish, and since the mucus layer is a major defense barrier to pathogens, less mucus can mean increased susceptibility to infection. A weakened ability to engulf invading bacteria is due to the action of elevated blood cortisol that affects the fluidity of macrophage membranes, but the primary effect is that the macrophage cannot kill the pathogenafter ingesting it.

Sometimes the effects of stress are not immediately apparent. Delayed Mortality Syndrome or disease outbreaks that can take from 2 to 14 days after a stressful event to manifest (Noga, 2000. Stoskopf, 1993). Even slightly elevated levels of cortisol can suppress immune function by decreasing antibody production and slowing the body’s response to injury and infection.

Long-term or chronic stress can slow or stop growth, due in part to cortisol released in response to stress that affects the metabolism of carbohydrates, lipids, and proteins. Stress can prevent reproductive activity while energy that is normally directed toward spawning is diverted to the more immediate needs of homeostasis.

Fish have a limited amount of energy, and stress increases energy demand. Chronic or continuous stress keeps the metabolism running at a faster rate because of this increased energy demand. This consumes energy, oxygen and glucose (Barton and Iwama, 1991). The normal functions of physiological equilibrium such as respiration, tissues repair, locomotion, and hydromineral regulation take priority over the investment activities of reproduction and growth. This means the diversion of energy to deal with an elevated metabolism means that less is available for growth and reproduction.

In order for fish to have a natural adaptive response to stress, they must first sense the presence of a stressor. The sensory cues to stressors can be chemical, hydrodynamic, acoustic, thermal, electrical, mechanical, light or other visual cues. The fish’s abilities to sense a stressor (sensory behavior), recognize that stressor as a threat (stimulus recognition) and respond to the stressor (response capabilities) can all be affected by the duration and severity of stress (Pearson, Miller and Olla, 1980).

A mild stressor that is short in duration causes a correspondingly mild and short stress response. Severe stressors that continue for extended periods have the greatest impact and long-term consequences. The effects of stress on immune function can linger for some time after other physiological changes have returned to pre-stress levels (Maule et al., 1989).


  1. Barton, B.A. & Iwama, G.K. “Physiological Changes in Fish from Stress in Aquaculture with Emphasis on the Response and Effects or Corticosteriods.” Annual Review of Fish Diseases, 1, 3-26, 1991.
  2. Barton, B.A., Schreck, C.B. & Fowler, L.G. “Fasting and Diet Content Affect Stress-induced Changes in Plasma Glucose and Cortisol in Juvenile Chinook Salmon.” Progressive Fish-Culturist, 50, 16-22, 1988.
  3. Folmar, L.C., & Dickhoff, W.W. “The Parr-Smolt Transformation and Seawater Adaptation in Salmonids (review).” Aquaculture, 21, 1-37, 1980.
  4. Maule, A.G., Tripp, R.A., Kaattari, S.L. & Shreck, C.B. “Stress Alters Immune Function and Disease Resistance in Chinook Salmon (Oncorrhynchus tshawytscha).” Journal of Endocrinology, 120, 135-142, 1989.
  5. Mazeaud, M.M. Mazeaud, F. & Donaldson, E.M. “Primary and Secondary Effects of Stress in Fish: Some New Data with a General Review,” Transactions of the American Fisheries Society, 106, 201-12, 1977.
  6. Mock, A., & Peters, G. “Lysozyme Activity in Rainbow Trout, Oncorhynchus mykiss, Stressed by Hnadling, Transport, and Wtare Pollution.” Journal of Fish Biology, 37, 873-885, 1990.
  7. Noga, E.J. “Fish Disease: Diagnosis and Treatment.” Ames, IA: Iowa State University Press, 2000.
  8. Pearson, W.H., Miller, S.E. & Olla, B.L. “Chemoreception in the Food Searching and Feeding Behavior of the Red Hake, Urophycis Chuss. Journal of Experimental Marine Biology and Ecology, 48, 139-150, 1980.
  9. Pennell, W. “Fish Tranportation Handbook.” Province of British Columbia, Ministry of Fisheries, Victoria BC, Canada. 1991.
  10. Pickering, A.D. “Stress Responses and Disease Resistance in Farmed Fish.” In Aqua Nor 87, Conference 3: Fish Diseases – a Threat to the International Fish Farming Industry, pp. 35-49. Norske Fiskeoppdretters Forening, Trondheim. 1987.
  11. Pickering, A.D. & Pottinger, T.G. “Crowding causes Prolonged Leucopenia in Salmonid Fish, Despite Interrenal Acclimation.” Journal of Fish Biology, 32, 701-712, 1987b.
  12. Safford, S.E. & Thomas, P. “Effects of Capture and Handling on Circulatory Levels of Gonadal Steroids and Cortisol in the Spotted Seatrout, Cynoscion nebulosus.” In Procedings of the Third International Symposium on the Reproductive Physiology of Fish. Idler, D.W. Crim, L.W. & Walsh, J.M. (eds.) pp. 312, 1987. Memorial University of Newfoundland, St. John’s.
  13. Schreck, C.B. “Stress and Rearing of Salmoniods.” Aquaculture, 28, 241-249, 1982.
  14. Stoskopf, M.K. “Fish Medicine.” W.B. Saunders Company. Philadelphia, Pennsylvania, 1993.
  15. Wedemeyer, G.A. “Transportation and Handling.” In Principles of Salmonid Culture. Pennell, W. & Barton, B.A. (eds.) pp. 727-758. Elsevier Science B.V. Amsterdam.

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