Because poor water quality is the most common cause of environmentally induced diseases, some means of assessing water quality is essential. Inexpensive test kits are easy to use and provide information that is reasonably accurate. Professional aquaculturists or advanced tropical fish hobbyists should be encouraged to purchase and use their own water-testing equipment. Veterinarians practicing fish medicine should have a comprehensive understanding of the dynamics and management of water quality.
Basic parameters of water quality can be grouped into 4 major categories: dissolved gases, nitrogenous compounds, carbonate compounds, and salinity (see Aquaculture Systems). The significance of these parameters varies with the type of system, species, and stocking density; however, low dissolved oxygen and high ammonia are the 2 water quality parameters most likely to kill fish directly.
Chlorine and Other Toxicants
In addition to the water quality problems discussed below, aquatic organisms are sensitive to a wide variety of toxicants. One toxicant worthy of special mention is chlorine, a common additive to city water that is sometimes used to disinfect tanks or equipment. It is highly toxic to fish, with adverse effects seen at concentrations of 0.02 mg/L and deaths occurring at 0.04 mg/L. A simple, colormetric test is available to measure chlorine in aquatic systems. No chlorine should be present at any time live animals are present. Most kits measure both free and total chlorine. Results from both tests should be zero or nondetectable. Free chlorine measures hypochlorous acid (HOCl) and the hypochlorite ion (OCI–), which is the active property in bleach. Total chlorine measures free chlorine, plus chlorine that is tied up as chloramines. Many municipalities aminate chlorine as a means of stabilizing the molecule. Water from these sources may show no free chlorine but have high amounts of total chlorine, indicating the presence of chloramines. 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, but a new or damaged bacterial bed will not be able to manage the influx of ammonia from deamination of chloramines. This problem can be overcome by using a dechlorinator that is specifically designed to deal with chloramines. Completely safe use of dechlorination chemicals involves testing water for chlorine before and after dechlorination. Following labels on products sold from pet stores is usually effective; however, in rare instances more chlorine than expected may be present in city water. Inaccurate calculation of the volume to be treated can also lead to poor performance or failure of the products.
Chronic exposure to sublethal concentrations of chlorine is a frequent problem, even with experienced aquarists. Veterinarians should test water for chlorine every time a sample is submitted from a tank that uses a municipal water supply as source water. Clinical indications of chlorine exposure are nonspecific but may include ragged fins, excess mucus on skin and gills, cloudy corneas, behavioral signs such as lethargy or irritation, and sometimes a history of low level and chronic mortality.
Other toxicants include hydrogen sulfide and heavy metals. Hydrogen sulfide usually is a problem in poorly maintained tanks 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 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, but any detectable hydrogen sulfide should be considered a significant 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 cause a fish kill. 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 water before it is placed into the aquarium, or special filtration (eg, activated carbon) to remove metals.
Of the dissolved gases, oxygen is the most important. In ponds, photosynthesis by algae is the primary source of oxygen. A diurnal cycle is established, which coincides with photosynthetic activity. During daylight hours, when photosynthesis occurs, oxygen levels rise and carbon dioxide levels fall. At night, respiration is the driving force, resulting in a decrease in dissolved oxygen (DO) and an increase in carbon dioxide. Most finfish thrive when the DO concentration is >5 mg/L. When DO is <5 mg/L, fish become stressed; depending on species, size, and duration of exposure, a fish kill may result. Cardinal 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 be seen trying to gulp air, a behavior referred to as “piping.” Differential diagnoses for piping include low DO, high nitrite, and gill disease.
Although low DO is most common early in the morning in outdoor ponds, it can occur at any time. The most common causes in ponds are cloudy weather, death of an algal bloom, and pond turnover. 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. The thermocline acts as a physical barrier between the surface water (epilimnion) and bottom water (hypolimnion). Because photosynthesis, and hence oxygen production, occurs at the surface, the hypolimnion becomes hypoxic and develops a biologic oxygen demand. When the pond is mixed, or “turns over,” the oxygen is removed as the biologic oxygen demand of the hypolimnion 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 USA 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 have occurred following hurricanes and have been attributed to pond turnover. Pond turnover can also be caused by seining, aeration, or other management practices that result in mixing of the epilimnion and hypolimnion. Fish kills caused by pond turnover can be avoided by performing 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 significant oxygen demand layer can develop.
When assessing dissolved oxygen and aeration in indoor systems or exhibits in which the primary source of DO is an aeration device, and water is clear, the percent saturation should be considered along with the total DO reading. The amount of oxygen that water can hold in saturation varies with water temperature, salinity, and altitude. Of these 3 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 DO if temperature, salinity, and altitude are known. If oxygen saturation is below 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 is a problem that requires correction. Most fish do well if oxygen is > 5 mg/L; however, the % saturation should be considered an indicator of the system's health.
Gas bubble disease is caused by supersaturation of water with dissolved gases. In pet fish, it may be associated with the use of well water, which may contain high levels of nitrogen or carbon dioxide. This is easily remedied by aerating the water before it comes into contact with the fish. A common cause of gas bubble disease in public aquaria is the use of cavitating pumps and sometimes excessive turbulence in cold water exhibits. 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. Supersaturation can be assessed using oxygen saturation tables as described above. Permanent correction of the problem includes identification and correction of the source of the excess gas.
Carbon dioxide (CO2) can be toxic to fish when present at concentrations >20 mg/L. Water from affected systems often is acidic (pH < 7). A quick field test for excessive CO2 involves vigorous aeration of a bucket of suspect water for 1 hr. A significant 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. Hybrid striped bass exposed to toxic levels of CO2 (~40 mg/L) were observed at the surface with their backs out of the water and reacted dramatically to salt added to the affected tank by trying to leave the water. Nephrocalcinosis and visceral granuloma were reported in salmonid culture, supposedly induced by a high level of CO2 in the water, leading to metabolic acidosis and urinary and tissue precipitation of calcium, around which extensive granulomas develop. Treatment for CO2 toxicity is increased and vigorous aeration. Stocking density should be assessed and may need to be decreased.
Nitrogenous wastes enter the aquatic system directly from excretion by fish or degradation of fish food. Fish foods are generally very high in protein, often >38%, and can add significant quantities of nitrogen to a system. Nitrogen is eliminated from fish by the passive diffusion of ammonia (NH3) from gill capillaries. Once NH3 is released into the water, it enters the nitrogen cycle, a natural process in which bacterial populations change ammonia to nitrite (NO2) and then to nitrate (NO3). Nitrate can be anaerobically converted to nitrogen gas (N2), which is volatile and quickly leaves the system. Plants or algae in the system may use nitrogen products directly.
NH3 is highly toxic and frequently limits fish production in intensive systems. It is also dynamic, and when it enters the aquatic system, an equilibrium is established between NH3 and ammonium (NH4+). Of the two, NH3 is far more toxic to fish, and its formation is favored by high pH (>7) and water temperature. When pH exceeds ~8.5, any NH3 present can be dangerous. In general, a normally functioning aquatic system should contain no measurable NH3 because as soon as it enters the system, it should be removed by aerobic bacteria in the environment. Ammonia test kits do not typically measure NH3 directly but instead measure the combination of NH3 and NH4, referred to as total ammonia nitrogen (TAN). A TAN <1 mg/L is usually not cause for concern unless the pH is > 8.5. However, if the amount of NH3 is increased, an explanation should be sought. The amount of toxic NH3 present can be calculated using the TAN, pH, and water temperature. When NH3 levels exceed 0.05 mg/L, damage to gills becomes apparent; levels of 2.0 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 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. If TAN is extremely high (ie, > 5 mg/L) and pH is acidic (ie, < 6.0), fish should be moved to a clean system (tempered for pH and temperature) to avoid a sudden shift from ammonium to ammonia as the pH rises during the water change. Feeding should be discontinued or significantly reduced until the problem has been corrected.
Two conditions encountered in pet fish medicine are characterized by high NH3 concentrations. New tank syndrome occurs when NH3 levels rise during the first 2–3 wk after a new system is set up because the biofilter has not had time to develop. Beginning aquarists are likely to overstock and overfeed new systems, resulting in significant NH3 spikes and sick or dying fish. Daily monitoring of TAN and frequent water changes to manage ammonia will be necessary until the biofilter cycles, indicated by decreasing concentrations of TAN and increasing concentrations of NO2.
Old tank syndrome is less frequently recognized. It is characterized by extremely high ammonia levels (TAN may be >20 mg/L), extremely low pH (usually <6, may be <5 in severe cases), and a complete absence of alkalinity. The condition is caused by complete exhaustion of buffering capacity within a system, usually precipitated by improper management over a period of months. As the buffering capacity (alkalinity) is exhausted, organic acids that have accumulated drop the pH and the acidic environment kills the biofilter, leading to an accumulation of NH3. When correcting such a situation it is important to eliminate as much “bad” water as possible and avoid a shift in residual NH3-H to the toxic un-ionized state (NH3) as pH rises. A simple water change under such circumstances can result in catastrophic mortality, as pH rises above 7 and ammonium shifts to un-ionized (toxic) ammonia. Over-the-counter products that chemically remove NH3 can be helpful in preventing mortality, but the system must be thoroughly cleaned and restarted. It may take several weeks for the system to recover.
The second breakdown product in the nitrogen cycle is nitrite (NO2), which is also toxic to fish. NO2 can enter the bloodstream passively across the gill epithelium. It complexes with hemoglobin to form methemoglobin, resulting in methemoglobinemia or brown blood disease. As in other species, RBC containing methemoglobin are unable to transport oxygen, resulting in a physiologic hypoxia regardless of oxygen content in the water. There are species-specific differences in fishes' susceptibility to NO2 toxicity (eg, centrar-chids [bass, bluegill, etc] are refractory). 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. Blood samples will also be an abnormal color. Methemoglobin concentrations in the blood can be determined, although this is not necessary for clinical management. A water quality test can confirm the presence of NO2. Fish affected with methemoglobinemia typically show signs of hypoxia, often manifest by piping.
The most rapid treatment for NO2 toxicity is a water change, but this may not be feasible in large ponds. Increasing chloride (Cl–) concentration in the water creates a competitive inhibition at the gill epithelium between Cl– and NO2. Many aquaria are maintained with residual chloride levels due to the addition of salt, in which case nitrite is less likely to be a problem. In freshwater outdoor ponds, the concentration of Cl– can be increased (by the addition of salt) to a ratio of 6 parts Cl– to 1 part NO2. This will dramatically decrease the percentage of Hgb converted to methemoglobin, resulting in immediate relief to the fish and stopping most further mortality within 24 hr. To determine the amount of salt required, the concentrations of NO2 and Cl– present must be measured by commercial test kits. The concentration of Cl– needed (mg/L) = (6 × NO2)−Cl– present. Once the necessary concentration of Cl– is known, the volume of water can be calculated in acre-feet or gallons (1 acre foot = 1 surface acre, 1 foot deep or 325,850 gal.), and salt can be added to increase Cl– to the desired concentration (4.5 lb of salt will add Cl– at 1 mg/L to 1 acre-foot of water; or 1 lb of salt will add 1 mg/L Cl– to 72,411 gal.). In aquariums and garden ponds, a water change and filter maintenance are recommended, although salt may still be used to halt mortality.
Although less toxic than ammonia or nitrite, chronic exposure to nitrate has been associated with development of goiter in some species of elasmobranchs. This is exacerbated by low concentrations of iodide (I–). Iodide should be maintained at concentrations of 0.10–0.15 µM and monitored biweekly. Ozonation can remove available I– by oxidizing it to iodate (IO3), which is not biologically available.
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 dissolved oxygen. As CO2 concentration changes, the pH of the water also changes. As CO2 concentration decreases during daylight hours, pH rises, reaching its peak late in the afternoon. Conversely, as CO2 concentration increases during the night, pH falls, reaching its lowest level just before daylight. A diurnal pH change from 6.5 to 9.0 is not unusual in a freshwater fish pond with a healthy algal bloom. Most freshwater fish can tolerate reasonable fluctuation in pH, and the lethal limits for many species are about 4 and 10. Marine fish are much less tolerant of pH fluctuation; the marine environment is much more stable, with a pH of 8.2–8.3. For marine tanks, pH in the range of 7.8–8.5 is usually considered normal.
Although fish kills caused by improper pH are rare, hydrated lime (CaOH) is sometimes added to freshwater ponds by mistake. CaOH will rapidly increase the pH to >10, killing all fish present. Correct liming of ponds is discussed below.
CO2 released into an aquatic system enters the carbonate cycle: H2O + CO2 ↔ 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). 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, and the compound cannot be used safely if the 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. Alkalinity will change slowly, so it should be monitored for several days, or weeks if necessary, following 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) has been confused with TA in the past. Both TH and TA are reported as mg/L of CaCO3. The difference is that the test for TA measures the CO32– fraction and the test for TH measures the calcium (Ca2+) fraction. The test for TH is also influenced by the presence of 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.
The salinity of seawater is determined by a complex array of salts. Seawater is ~3% salt, which is 30 ppt (30 g/L). For marine fish, many of the micronutrients present in sea water are essential, so it is necessary to buy or make “sea salts.” In freshwater, salinity may be increased using table or water softener salt (NaCl). Salt is often used in freshwater systems to reduce osmoregulatory stress or to eliminate certain ectoparasites. Salinity can be measured with a clinical refractometer or with a hydrometer purchased from a pet store. It is important not to confuse the chloride test, which is used in the assessment of NO2:Cl in freshwater systems with high nitrite, with salinity. The chloride test measures ppm chloride, and if any salinity at all is present in the water (ie, salt has been added) the test will not work properly because the amount of chloride present is so high. 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 ppt. Most nonpond freshwater systems should be maintained with a residual salinity of 1–3 ppt, while most saltwater systems will have a salinity of 30–33 ppt.
Last full review/revision July 2011 by Ruth Francis-Floyd, DVM, MS, DACZM