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Professional Version

Environmental Diseases of Aquatic Animals in Aquatic Systems


Ruth Francis-Floyd

, DVM, DACZM, Department of Large Animal Clinical Sciences, College of Veterinary Medicine, University of Florida;

Roy P. E. Yanong

, VMD, Tropical Aquaculture Laboratory, Institute of Food and Agricultural Sciences, University of Florida;

Barbara D. Petty

, DVM, Department of Large Animal Clinical Sciences, College of Veterinary Medicine, University of Florida

Reviewed/Revised May 2023 | Modified Jun 2023
Topic Resources

Because poor water quality is the most common cause of environmentally induced diseases, assessing water quality is essential. Inexpensive test kits are easy to use and provide reasonably accurate information. Professional aquaculturists or advanced tropical fish hobbyists should be encouraged to purchase and use their own water-testing equipment. Pet fish owners often rely on pet stores to do the water testing; however, many pet stores have very limited capabilities in this area, use less accurate tests, and may be unable to accurately interpret results.

Veterinarians practicing fish medicine should have a comprehensive understanding of the dynamics and management of water quality, including general guidelines for acceptable water quality parameters ( see Table: “Normal” Reference Ranges for Routine Water Quality Analysis “Normal” Reference Ranges for Routine Water Quality Analysis “Normal” Reference Ranges for Routine Water Quality Analysis ). Including temperature, basic parameters of water quality can be grouped into six major categories:

The significance of water quality parameters varies with the type of system, species, and stocking density. Low dissolved oxygen and high ammonia are the two water quality parameters most likely to directly kill fish. Water quality interactions are dynamic and complex. Indirect relationships can lead to toxicity from other parameters, such as the effect of rising pH on (increased) ammonia toxicity, or there can be indirect relationships between water quality and certain infectious agents. For example, low or inappropriate temperature can be associated with fungal diseases of fish. A classic example is Fusarium solani infection of bonnethead sharks, which can be managed by raising the environmental temperature to > 80°F (27°C).


See table: Common Environmental Hazards for Fish Common Environmental Hazards for Fish Common Environmental Hazards for Fish for an overview of common environmental diseases of fish.


Chlorine, Chloramine, and Other Toxicants as a Cause of Environmental Disease in Aquatic Systems

Aquatic organisms are sensitive to a wide variety of toxicants, particularly chlorine and chloramine, which are common additives to municipal water. Chlorine is also used to disinfect tanks and equipment. Chloramine is a form of chlorine that has been stabilized by amination. When treated for removal of the chlorine molecule, ammonia is released into the system. Both compounds are highly toxic to fish, with adverse effects occurring at chlorine concentrations as low as 0.02 mg/L and mortality at 0.04 mg/L.

A simple colorimetric test is available to measure chlorine and chloramine in aquatic systems. No chlorine or chloramine should be detected at any time live animals are present. Water samples for chlorine testing should be tested onsite; however, if that is not possible, they may be transported in glass bottles. The chemical can be transient and difficult to detect, so a negative test result may not completely exclude some contamination in the system being evaluated.

To test for chlorine and/or chloramine, kits are available that measure both free and total chlorine. Free chlorine measures hypochlorous acid (HOCl) and the hypochlorite ion (OCl), which is the active chemical in bleach. Total chlorine measures free chlorine plus chlorine that is tied up as chloramine. Water treated with chloramines alone will test negative for free chlorine but have high amounts of total chlorine detectable; therefore, testing for both is important. When chloramines are treated with sodium thiosulfate to eliminate the chlorine, ammonia is released into the system. In such an instance, repeated water changes (each of which requires dechlorination, releasing additional ammonia) can result in high ammonia levels that also may be toxic.

A properly conditioned biofilter should be able to metabolize the ammonia as it is released; however, a new or damaged bacterial bed will not be able to manage the influx of ammonia from repeated deamination of chloramines. This problem can be overcome by using a dechlorinator specifically designed to deal with chloramines by also binding the ammonia byproduct. Effective use of dechlorination products requires testing water for both free and total chlorine before and after use. Following label instructions on products sold from pet stores usually effectively removes these chemicals; however, in rare instances more chlorine/chloramine than expected may be present in municipal water supplies. Treatment of water supplies will vary, and boluses of chlorine or chloramine may be sent through water lines as part of maintenance protocols in some circumstances. Further, inaccurate calculation of the volume to be treated can also lead to poor performance or failure of dechlorination products.

Chronic exposure to sublethal concentrations of chlorine is a surprisingly frequent problem, even for experienced aquarists. Veterinarians should test water for chlorine (free and total) every time a sample is submitted from a tank that uses a municipal water supply as source water. Clinical indications of sublethal chlorine exposure are nonspecific; however, they may include ragged fins, excess mucus on skin and gills, cloudy corneas, clinical signs such as lethargy or irritation, and sometimes a history of low chlorine level and chronic mortality.

Other toxicants include hydrogen sulfide and heavy metals. Hydrogen sulfide usually is a problem in poorly maintained tanks or ponds in which the sediments are not cleaned frequently enough, allowing anoxic areas to develop. Cleaning or other disturbance of these areas can release hydrogen sulfide into the water column, resulting in acute and catastrophic mortality. Another common source of hydrogen sulfide is well water; if this is the case, a distinctive “rotten egg” smell can sometimes be detected. Hydrogen sulfide is volatile and transient, so unless a water sample is collected at the time of the problem, a confirmed diagnosis may not be possible. Acute mortality has been reported at concentrations of 0.5 mg/L; however, any detectable hydrogen sulfide should be considered a major problem.

Heavy metals in water can result in acute, or more often, chronic mortality. If household plumbing includes copper piping, some copper may leach into the water. If released in sufficient volume, this may result in fish death. Problems are most likely when water has been allowed to stand in pipes. A copper test of suspect water should confirm the problem. Solutions include running the water before it is placed into the aquarium, or special filtration (eg, activated carbon) to remove metals.

Zinc toxicity Zinc Toxicosis in Animals In small animals, zinc toxicosis is usually a result of ingestion of objects that contain or are coated with zinc, most commonly US pennies. In large animals, the main causes are contaminated... read more Zinc Toxicosis in Animals has been associated with use of stainless steel vessels to house fish. It has also been reported rarely from public exhibits in which coins were allowed to collect on the substrate or to be ingested by fish.

Dissolved Gases as a Cause of Environmental Disease in Aquatic Systems

Oxygen is the most important of the dissolved gases. In outdoor production ponds, the primary source of oxygen is photosynthesis by algae. As photosynthesis occurs during daylight hours, oxygen levels rise and CO2 levels fall. During the night, respiration results in a decrease in dissolved oxygen and an increase in CO2. A dissolved oxygen concentration > 5 mg/L is optimal for most finfish. Fish experience stress at levels < 5 mg/L. Depending on species, size, and duration of exposure, a fish kill may result in response to low dissolved oxygen. Clinical signs of a fish kill caused by hypoxia include sudden, significant mortality, usually noticed early in the morning (when oxygen levels are lowest); often, large fish are affected more than small fish. Fish that are hypoxic often school near the surface of the water and may try to gulp air, a behavior referred to as “piping.” Differential diagnoses for piping includes low dissolved oxygen, high nitrite, and gill disease.

Although low dissolved oxygen is most common early in the morning in outdoor ponds, it can occur at any time. Other common causes of low dissolved oxygen in ponds are cloudy weather (decreased light intensity), death of an algal bloom, excessive feeding, overstocking, "old" ponds which have not been cleaned, and pond turnover.

Unrecognized overstocking can occur in koi ponds if fish spawn successfully and offspring are retained in the system. Pond turnover is a common cause of catastrophic mortality in pond fish. It occurs most frequently in deep ponds (> 6 ft) and involves a phenomenon referred to as stratification. Water at the bottom of the pond cools, and a temperature gradient, called a thermocline, develops between warm surface water and cool bottom water. Due to density differences associated with water temperature, surface water, which is where oxygen enters the system, does not mix with the cooler bottom layer. Existing oxygen near the bottom is depleted over time due to degradation of organic material, resulting in a biologic oxygen demand. When the pond is mixed, or “turns over,” dissolved oxygen is removed from the water column as the biologic oxygen demand is satisfied. This sudden removal of oxygen can result in oxygen depletion and a fish kill.

The most common cause of pond turnover in the southern US is a summer thunderstorm, in which energy released from cold rain coupled with wind and wave action is sufficient to mix the pond. Fish kills in Florida are common after hurricanes and have been attributed to pond turnover. Pond turnover can also be caused by seining, aeration, and other management practices that result in mixing of the epilimnion and hypolimnion. Fish kills caused by pond turnover can be avoided by doing a weekly oxygen profile during periods of greatest risk (usually during hot, summer weather). If stratification is detected, the pond should be aerated or mixed to break down stratified layers before a hypoxic layer can develop.

Turnover events resulting in localized areas of low dissolved oxygen are common causes of wild fish kills during the summer in lakes, ponds, and even rivers in the southern US. Although rare, stratification-related phenomenon can occur in aquariums and other aquatic systems. Under some conditions, flow rate, current patterns (related to tank design), and oxygen demand can cause layering (ie, stratification) and consequent focal areas of anoxia.

When assessing dissolved oxygen and aeration in indoor systems or exhibits in which the primary source of dissolved oxygen is an aeration device, and water is clear, the percent saturation should be considered along with the total dissolved oxygen reading. The amount of oxygen that water can hold in saturation varies with water temperature, salinity, and altitude. Of these three factors, water temperature is the most important. As any of these variables increase, the amount of oxygen in solution at saturation decreases. Saturation tables are available to determine percent saturation for a given dissolved oxygen if temperature, salinity, and altitude are known. Many modestly priced oxygen meters now provide data on the concentration of dissolved oxygen(mg/L) as well as the percent saturation. If oxygen saturation is < 100%, it may indicate inadequate aeration for the bioload or sanitation problems (development of anoxic, organic-rich areas within the system). In either case, an inability to maintain a system at, or very near, 100% oxygen saturation requires correction. Most fish do well if dissolved oxygen is > 5 mg/L; however, the percent saturation should be considered an indicator of the system’s health.

Gas bubble disease is caused by supersaturation of water with dissolved gases. Although oxygen and/or CO2 can contribute to supersaturation, the predominant gas contributing to the problem is usually nitrogen. Gas bubble disease can result in acute catastrophic or chronic mortality. It may occur transiently and can be difficult to confirm. Supersaturation should be considered when unexplained mortality is encountered in an aquarium setting.

One common source of supersaturation is the use of well water that contains high concentrations of nitrogen (gas) or CO2. This problem is easily remedied by aerating the water before it comes into contact with the fish. Common causes of gas bubble disease in public aquaria include the use of cavitating pumps, leaks in plumbing on the intake side (allow for gas to enter and be forced under pressure through the pump), and sometimes excessive turbulence in cold water exhibits. In these cases, the supersaturation is caused by atmospheric nitrogen gas. Gas bubble disease is manifest by exophthalmos and the presence of tiny gas emboli within fins, corneas, or other tissue. The presence of gas emboli within gill capillaries is diagnostic.

Treatment of gas bubble disease is vigorous aeration to volatilize excess gas and correction of underlying mechanical problems. Confirming a case of supersaturation can be extremely difficult, especially if mortality was acute and gas emboli cannot be detected in tissue. Sometimes, tiny gas bubbles may be visible on the inside of the glass in an aquarium, suggesting a lot of gas is in the water column. A saturometer will measure all dissolved gases and is the best tool for direct detection of the condition. If dissolved oxygen of the system is known, this equipment can be used to calculate the concentration of nitrogen gas present. Permanent correction of the problem includes identification and correction of the source of the excess gas.

CO2 can be toxic to fish at concentrations > 12 mg/L (aka hypercarbia). The concentration of CO2 in solution in ground water is typically < 10 mg/L. Water from affected systems often is acidic (pH < 7); in some cases, however, it may have pH > 7 but lower than the pH of the original, aerated source water, which should be used for baseline comparison.

A quick field test for excessive CO2 involves vigorous aeration (using an aeration device or airstone) of a bucket of suspect water for 1 hour. A notable increase in pH (ie, > 1 unit) over the hour is indicative of excess CO2.

Fish exposed to high concentrations of CO2 may be quite lethargic and even disoriented. Hybrid striped bass exposed to toxic levels of CO2 (~40 mg/L) were observed congregating at the surface with their backs out of the water. These fish reacted dramatically to salt added to the affected tank by trying to jump out of the water. When CO2 is high in the water column, fish are not able to release it from the bloodstream, resulting in hypercarbia and acidemia. The condition is exacerbated by low concentrations of DO. Nephrocalcinosis and visceral granuloma were reported in salmonids exposed to a high level of CO2 in the water, leading to metabolic acidosis and urinary and tissue precipitation of calcium, around which extensive granulomas developed.

Treatment for CO2 toxicity is increased, vigorous aeration. Stocking density should be assessed and may need to be decreased. In systems which routinely must add pure oxygen to meet consumption needs by high density culture, hypercarbia is a common issue that must be monitored and managed.

Nitrogenous Compounds as a Cause of Environmental Disease in Aquatic Systems

Fish foods typically are very high in protein. Fish metabolize protein and excrete ammonia directly from the blood stream, across the gill epithelium, and into the water column by passive diffusion. This is method of excretion requires little to no metabolic energy but relies on a concentration gradient between the ammonia in the bloodstream and the ammonia in the water column to work effectively. Ammonia released from the fish is metabolized by environmental bacteria (natural or supplied by use of a biofilter) and enters the nitrogen cycle. The ammonia is oxidized to nitrite and eventually nitrate by aerobic bacterial processes. Nitrate is eliminated from the system by water changes, anaerobic bacterial activity, or live plants.

In large, commercial systems, discharge of salt water to municipal water supplies is not allowed, and nitrate accumulates because of the inability to discharge salt water. Nitrate may also be a problem in freshwater recirculating systems that are stocked with high densities of fish and that have limited water exchanges. Toxicity of each of these parameters is discussed below.

Ammonia is released directly from the fish. Once it enters the water column an equilibrium is formed, that is affected by both pH and water temperature. Most water quality test kits measure Total Ammonia Nitrogen (TAN) which includes both toxic (unionized) ammonia (NH3) and less toxic ammonium (NH4+). The percentage of Total Ammonia Nitrogen that is present in the toxic, unionized form (NH3) increases as pH and temperature increase. Of these, pH has more influence than temperature. In most home aquariums, a TAN reading of 1.0 is not a huge concern unless pH exceeds 8.5. Calculations should always be done though to ensure the practitioner appreciates the role detectable ammonia may be playing in the disease process. A calculated NH3 concentration of 0.05 mg/L is high enough to cause histologic changes to gill tissue and is considered harmful to fish.

When NH3 levels exceed 0.05 mg/L, histopathologic evaluation has demonstrated damage to gill tissue, including hyperplasia of epithelial and chloride cells, hypertrophy of chloride cells, and lamellar fusion. Unionized ammonia concentrations of 2 mg/L are lethal for many fish. Fish exposed to ammonia may be lethargic and have poor appetites. Acute toxicity may be suggested by neurologic clinical signs such as spinning, disorientation, and convulsions.

Overfeeding or malfunction (death) of a biologic filter are common causes of increased NH3. If possible, a water change (≥50%) should be done as soon as high NH3 levels are detected. When changing water to alleviate NH3 toxicity, it is imperative to consider whether source water contains ammonia or chloramines. If these are present in source water, water changes can contribute to ammonia in the system, either directly (ammonia in source water) or indirectly (ammonia released from chloramines during dechlorination). If TAN is extremely high (ie, > 5 mg/L) and pH is acidic (ie, < 7), fish should be moved to a clean system (tempered for pH and temperature) to avoid a sudden shift from NH4+ to NH3 as the pH rises during the water change. Feeding should be discontinued or substantially reduced until the problem has been corrected.

Two conditions encountered in pet fish medicine are characterized by high NH3 concentrations; these are aptly called "new tank syndrome" and "old tank syndrome".

New tank syndrome occurs when NH3 levels rise during the first 2–3 weeks after a new system is set up, and/or when NO2 levels rise subsequently, because the microbial population of the biofilter has not had time to develop. In this situation, the NH3 and/or NO2 concentration will be increased; however, all other parameters should be within normal limits. Beginning aquarists are likely to overstock and overfeed new systems, resulting in significant NH3 or NO2 spikes and, subsequently, sick or dying fish. Daily monitoring of TAN and NO2 coupled with frequent water changes to manage NH3 and NO2 will be necessary until the biofilter cycles. Maturation of the biofilter will be indicated when TAN and NO2 have peaked and dropped, followed by a rise in NO3. Damage to a biofilter can be caused by use of antimicrobials or other chemicals and result in damage to bacteria in the biofilter. It usually takes ~6 weeks for a new biofilter to become completely established. When this time frame is extended, there may be complications attributed to poor design, use of chemicals, or lack of adequate oxygen and carbonate (alkalinity) in the filter bed.

To prevent new tank syndrome, aquarists use several “tricks” to get biofilters started. These include purchasing commercially available nitrifying bacteria from a reputable source, “feeding” the bacteria with fish food or ammonium chloride before adding fish, or adding fish slowly to the new system.

Old tank syndrome is less frequently recognized. It is characterized by extremely high NH3 levels (TAN may be > 20 mg/L), extremely low pH (usually < 6, may be < 5 in severe cases), and alkalinity significantly lower than what is present in source water. Inadequate water changes typically precede this condition which is caused by an accumulation of organic acids, and consequent depletion of the buffering system (alkalinity).

Over time, the biofilter bacteria acidify the water via the nitrification process and bicarbonates/carbonates are used as a carbon source by the biofilter bacteria. As buffering capacity is depleted, PH falls and the nitrification process is disrupted leading to a rise in TAN. Aggressive water changes will correct the situation but neutralizing the ammonia (using over the counter products) is recommended to avoid a sudden shift of NH4+ to NH3. The biofilter will have to be re-established and the system should be managed accordingly for about 6 weeks, or until nitrifying bacteria have re-established themselves.

The second breakdown product in the nitrogen cycle is nitrite (NO2), which is also toxic to fish and which can contribute to "new tank syndrome" issues. Most test kits actually measure nitrite-nitrogen rather than nitrite. A conversion factor of 3.3 can be used to calculate the actual nitrite concentration (3.3 × mg/L NO2−N = mg/L NO2). NO2 forms methemoglobin when absorbed into the fish's bloodstream, a condition referred to as brown blood disease.

As in other species, RBCs containing methemoglobin do not release oxygen to tissues, creating a hypoxic state regardless of water quality conditions. Marine fish were thought to be protected from NO2 toxicity by salts in their environment; however, red drum have developed brown blood disease in the presence of NO2. A tentative diagnosis of brown blood disease can be made by observing the characteristic chocolate brown color of the gills, although this change is not detectable until methemoglobin levels are substantial. In severe cases, the color of blood samples will also be abnormally dark. Methemoglobin concentrations in the blood can be determined, although this is not necessary for clinical management. Behaviorally, fish affected by nitrite toxicity will seek oxygen, congregating in oxygen rich areas or piping at the surface. The presence of nitrite can be confirmed using a standard water quality test kit.

NO2 toxicity can be rapidly corrected by a water change, but this may not be practical for large ponds. Increasing chloride (Cl) concentration in fresh water systems is another solution: Cl serves as an antagonist for NO2 at the gill epithelium. Many ornamental ponds and aquaria are maintained with residual chloride levels because of the addition of salt (1–3 ppt) as a relatively permanent treatment. In these cases, NO2 toxicity is less likely to be a problem, because chloride levels are increased by the residual salt concentration and competitively block NO2 absorption. In freshwater production ponds for channel catfish, low concentrations of salt can be used to provide sufficient environmental chloride to mitigate the risk of methemoglobinem is caused by sudden increases in NO2.

There are species-specific sensitivities to nitrite. Channel catfish are recognized as very sensitive to nitrite, and in commercial ponds with high stocking and feeding rates, nitrite can rise rapidly under some environmental conditions. In contrast, centrarchids (bass and bluegill), seem to be resistant to nitrite and it is not often a concern in recreational fishing ponds. Nitrite toxicity should be considered if channel catfish are exhibiting signs of hypoxia, such as piping, but largemouth bass in the same pond appear unaffected.

In aquariums and garden ponds, a water change and filter maintenance are recommended to correct nitrite problems; however, salt may still be used to halt mortality during a sudden increase in NO2 exposure for many freshwater fish. Any underlying problems, such as biofilter failure, should be addressed. Production ponds will self-correct over time as bacterial populations return to a healthy condition.

Although considered less toxic than ammonia or nitrite, chronic exposure to nitrate has been associated with development of goiter in some species of elasmobranchs. As for nitrite test kits, most test kits for nitrate actually measure NO3−N. To convert to the actual NO3 concentration, this number must be multiplied by a correction factor of 4.4. Veterinarians should read the literature carefully to distinguish reports of NO3-N versus NO3 concentrations.

Goiter is a complex disease, and there seem to be species-specific differences in susceptibility that are not well understood. Contributing factors include inadequate dietary iodine or environmental iodide, ozonation, and nitrate exposure.

Goiter is characterized by a ventral midline swelling in the cervical region of elasmobranchs. Diagnosis can be confirmed by measuring T4. In healthy (no clinical or histologic evidence of goiter), captive, white spotted bamboo sharks housed in a natural seawater system, T4 was 14.77 ng/mL (range of 9.57–30.50 ng/mL in five animals). Lower levels have been reported in sharks with visual evidence of goiter. If post-mortem examination is done, thyroid tissue can be evaluated histologically to confirm the diagnosis. Nitrate is well recognized as a goitrogenic compound and may be present in fairly high concentrations (> 70 mg/L NO3-N) in recirculating aquarium and aquaculture systems. Nitrate blocks the uptake of iodine by the thyroid gland, resulting in an inability to produce thyroid hormone and constant stimulation of the glandular tissue. Fish and elasmobranchs absorb micronutrients, including iodine, from the water column. In an ozonated system, the problem is exacerbated because iodine is converted to iodate (IO3), which is not biologically available. Dietary supplementation of iodine at 10–30 mg/kg per week is recommended for elasmobranchs to prevent development of goiter. Environmental iodine should be maintained with concentrations of 0.15 mcM (0.01–0.02 mg/L) iodide (I). Potassium iodide (Lugol's solution) has been used to increase environmental iodide concentrations in public aquaria. Goiter occurs in teleosts and other aquatic species although it is not as easily recognized. In some teleosts, enlarged masses around the gills may be observed (due to the disseminated nature of thyroid tissue). The body shape of many elasmobranchs allows for easy recognition of the problem during a visual examination.

pH and Carbonate Compounds as a Cause of Environmental Disease in Aquatic Systems

The carbonate cycle is an important concept in water quality management, and its complexity is reflected in the dynamic interactions between CO2, pH, total alkalinity, and total hardness. In aquatic systems containing algae or plants, CO2 fluctuates on a diurnal basis, similar but opposite to fluctuations in DO. As CO2 concentration changes, the pH of the water also changes. In outdoor ponds with phytoplankton blooms, photosynthesis drives changes in CO2 during daylight hours. CO2 decreases when photosynthesis is taking place, resulting in rising pH throughout daylight hours. Conversely, respiration dominates overnight and CO2 increases, resulting in a decline in pH.

Most freshwater fish can tolerate reasonable fluctuations in pH, and the lethal limits for many species are approximately 4 and 10. Marine fish are much less tolerant of pH fluctuations; the marine environment is much more stable, with a pH of 8.2–8.3. For marine tanks, a pH in the range of 7.8–8.5 is usually considered normal.

CO2 released into an aquatic system enters the carbonate cycle: H2O + CO2 ↔ H2CO3 ↔ H+ + HCO3 ↔ 2H+ + CO32–. The process is driven by the presence of carbonate (CO32–) in the system, which is measured by testing the total alkalinity (TA), a measure of bases (OH, CO3, and HCO3). For most fish, water should be of moderate alkalinity (100–250 mg/L). When TA is < 50 mg/L, water is considered low in alkalinity, and buffering ability will not be adequate to prevent major pH fluctuations. Toxicity of copper sulfate, an algicide and effective parasiticide, is closely associated with TA when it is used in freshwater systems, and the compound is contraindicated if TA is < 50 mg/L. To raise alkalinity, dolomite (CaCO3 and MgCO3) or agricultural limestone (CaCO3) may be added to the system. Dolomite is most convenient for small systems and can be purchased in 50-lb bags and used to effect. Baking soda (NaHCO3) can also be used to increase alkalinity in small systems.

Although fish kills caused by improper pH are rare, hydrated lime (Ca[OH]2) is sometimes added to freshwater ponds by mistake. Ca(OH)2 will rapidly increase the pH to > 10, killing all fish present. To raise alkalinity in outdoor ponds, agricultural limestone is commonly used; the method is similar to “liming” a pasture. Soil samples can be tested to determine how much agricultural limestone needs to be added; however, in general, 1–2 tons per surface acre works well. The limestone should be unloaded on the bank of the pond and then moved into the water using a shovel and boat. It does not need to be distributed throughout the entire surface area of the pond; however, it takes several weeks to get into solution. Consequently, the alkalinity will change slowly, so it should be monitored for several weeks after the addition of these compounds. Lack of alkalinity can impair biologic filtration, resulting in accumulation of ammonia in a system. Alkalinity should be ≥ 100 mg/L in freshwater systems and ≥ 250 mg/L in saltwater systems.

Total hardness (TH) should not be confused with TA. Both TH and TA are reported as mg/L of CaCO3. The difference is that the test for TA measures the HCO3, OH, and CO32– fraction, and the test for TH measures the calcium (Ca2+) fraction. The test for TH also measures other divalent cations in the system, including magnesium, manganese, iron, and zinc. TH is important in determining the amount of calcium available to young fish. Calcium chloride, dolomite, or agricultural limestone can be added to water to increase calcium concentration. For channel catfish, TH > 20 mg/L is required for normal skeletal growth and development. Fish absorb minerals from the water column; therefore, use of water with very low TH, which can be caused by use of deionized water, can result in poor growth and mortality.

Salinity as a Cause of Environmental Disease in Aquatic Systems

Sea water is a complex mixture of ions, and consequently, adjusting salinity in marine systems requires the use of natural sea water or an artificial sea salt product. In contrast, salinity adjustments to freshwater systems can be accomplished using simple NaCl. Table salt or water softening salt are both acceptable. Adjustments to salinity can enhance parasite control protocols and are also valuable for osmoregulatory enhancement, which may be indicated by disease or handling/ transport. Salinity is measured using a clinical refractometer or an inexpensive hydrometer, the latter of which can be purchased from a pet store. Almost all water quality parameters are reported a parts per million (ppm) which is mg/L, however salinity is reported as parts per thousand (ppt) which is g/L.

The easiest way to calculate the amount of salt needed to increase salinity is to calculate the total volume in liters (3.8 L = 1 gal.), remembering that 1 g/L = 1 part per thousand (ppt). Alternatively, if volume in gallons is known, multiply the total gallons by 3.8 and that will indicate how many grams of salt need to be added to increase salinity 1 ppt in the system. Most non-pond freshwater systems can be maintained with a residual salinity of 1–3 ppt, whereas most saltwater systems will have a salinity of 30–33 ppt. Some freshwater species (eg, wild-caught Amazonian fish, elephantnose, and related mormyrids) may not tolerate permanent exposure to the low levels of salt mentioned above.

Temperature as a Cause of Environmental Disease in Aquatic Systems

Environmental temperature is extremely important to the health and well-being of fish and other aquatic species. As poikilotherms, fish have a very limited ability to control body temperature, and physiologic systems are designed to work optimally at species-specific temperature ranges. Sudden changes in temperature, of even just a few degrees, can result in compromise of immunity and increased pathogenicity of some infectious agents.

Some fish (eg, channel catfish or koi) are very tolerant of a wide range of environmental temperatures; however, this does not imply that drastic temperature fluctuations are acceptable even for these species. Others, such as discus, thrive in only a very narrow temperature window. When evaluating housing and husbandry, veterinarians should know the temperature at which animals are being housed and confirm that it is appropriate for the species. Suboptimal environmental temperature is an important component in some fungal infections.

Some parasitic infestations, eg, Ichthyophthirius, are more common when temperature fluctuations or change of seasons occur. Many infectious agents, especially viruses, have specific temperature windows at which they cause clinical disease and mortality. Fish infected but maintained at temperatures above or below these optimal ranges are more likely to survive infection; however, they may become carriers. When handling or transporting fish, moderating temperature change is essential. A general rule is 1°F, or even 1°C, per hour as a maximum change. Some fish may tolerate more or less of a change over time.

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