Copper poisoning may occur by leaching of copper from piping systems, particularly new systems. The toxicity of copper is effected by water hardness - i.e., copper is more toxic in soft water (see review by Olsson (1999). Acute toxicity goldfish 96-h LC50 was 1.38 mg/L at water hardness of 273 CaCO3 (a relatively hard water situation).
Affected fish may show increased coughing reflex, ventilation rate and oxygen consumption, and decreased antibody production. The latter indicates that affected fish would be more susceptible to infectious diseases. Fish may also be lethargic or uncoordinated. Particularly important to zebrafish, is that copper causes retarded sexual development, reduced egg production, and progeny show poor survival and tetratogenic effects (Dave and Xiu 1991; Olsson 1998).
Microscopic changes include gill lesions and lateral line damage (Gardner and LaRoche 1973). The liver may exhibit vacuolation of hepatocytes.
Many research facilities use flow through or partially closed systems in which dechlorinated city water is used as the water supply. This certainly is an advantage for avoiding many pathogens. However, failure of the dechlorination system often results in severe mortality due to either acute or chronic chlorine toxicity. Fish are very susceptible to chlorine. City water usually contains a minimum of 0.2mg/L total chlorine but usually ranges between 0.5 –1.0 mg/L (Noga). Chlorine is also routinely used to disinfect tanks and equipment, and inadequate rinsing or ventilation is another potential source of chlorine toxicity.
Chlorine causes severe, acute necrosis of the gills, and thus fish suffer rapid respiratory distress and asphyxiation. Fish may exhibit laboured breathing, and petechial hemorrhages around the head. Cherry-red, swollen gills are characteristics of chlorine toxicity
Microscopic examination shows severe necrosis of the gills.
Chlorine toxicity is diagnosed by detecting elevated chlorine levels in the water. “After the fact” exposure is suspect in fish showing the signs described above.
Chlorine is avoided by removal with charcoal filters (for running water). For static systems, chlorine can be removed by adding sodium thiosulfate at 7.4 ppm/chlorine ppm). Mortalities in exposed fish can be reduced by adding salt to the water and by assuring that the water is adequately aerated. In addition, fish should be immediately transferred to chlorine-free, aerated water.
Ammonia and nitrite toxicity is covered in several text books on aquaculture, aquariology, and fish health (e.g., Noga 1996). Articles that review the specific subjects include Lang et al. (1987) and Speare (1998b). Ammonia toxicity is particularly problematic in newly established recirculating systems, in shipping containers, or following medication of fish by bath treatments with certain chemicals (e.g., formalin).
Fish suffering ammonia toxicity may exhibit behavioral abnormalities, such as hyperexcitability, anorexia, reduced growth, and increased susceptibility to pathogens. Other changes include decreased ventilation. In salmonids, sublethal effects as low as 0.002 mg/L have been reported.
Chronic ammonia toxicity is often associated with hyperplasia of the gill epithelium. However, some researchers report that this histopathological change is caused by other agents (either abiotic or biological) that are often associated with husbandry conditions (e.g., excessive crowding, inappropriate water exchange) that lead to elevated ammonia levels (Lang et al. 1987).
As the clinical signs and pathological changes of ammonia toxicity are rather non-specific, identification of the problem relies on detection of elevated ammonia levels.
Improving water flow and reduction in fish densities are the immediate solutions to NH3 toxicity. Changing water or increasing water flow usually increases pH, and ammonia is more toxic at higher pH. Ammonia toxicity often occurs in new recirculation systems with biological filters as it may take several weeks to establish adequate denitrifying bacteria in the filters. Therefore, fish should be added gradually to new systems, with close monitoring of ammonia levels.
Nitrite toxicity is less common in aquaria situations than ammonia toxicity, but can occur simultaneously. It is more common in ponds – e.g., nitrite toxicity is the cause of brown blood disease in catfish, in which case methemoglobin production by chemical oxidation of heme iron results in haemoglobin incapable of combining with oxygen, thus hypoxia occurs (Speare 1998a). Levels of nitrite should be kept below < 0.10 mg/L.
Gas bubble disease (GBD) occurs when fish are exposed to local dissolved gas concentrations exceeding the stable maximum dissolved gas levels for the local temperature, salinity, and pressure conditions (supersaturated conditions). If this condition is not corrected fast enough or if it is too far out of equilibrium, the gas dissolved in the water in excess of equilibrium will be released from solution. After exposure to these conditions, the fish’s internal body fluids can also become unstably supersaturated with gases. These excess gases can then be released from solution as bubbles, resulting in tissue damage. Gas bubble disease afflicts both wild and cultured fish in variety of conditions. See reviews by Weitkamp and Katz (1980) and Speare (1998). A variety of scenarios can cause supersaturation, including air injection into water in pressurized pipes (Venturi effect), and pumping water from deep wells and exposing fish to such water without prior gas “stripping”. Supersaturation by nitrogen is generally the culprit, but oxygen alone (i.e., in systems using oxygen injection) may cause GBD. With zebrafish research systems, the cause is often a leaky pipe on the suction side of the pump, which causes air injection.
Severe, acute GBD may cause macroscopically visible bubbles in the skin, fins or gills. The eyes are also a target organ, in which visible bubbles form in the retrobulbar tissues. Fish may exhibit exophthalmia. Unfortunately, many cases of GDB do not present with specific clinical or pathological changes – i.e., fish die without visible bubbles in the tissues. Fish may exhibit exophthalmia. Fish that recover sublethal GDB may be susceptible to infectious diseases.
When present, histological sections may reveal bubbles, particularly in the retrobulbar tissues. Bubbles occur within blood vessels and cause vascular occlusions, leading to formation of thrombi and possibly hemorrhage. Gas bubbles may be visible in gill blood vessels in wet mounts.
 Click for high resolution image | Zebrafish with gas bubbles around eye due to GBD |
 Click for high resolution image | Retrobulbar tissue of the eye from opakapaka (Pristipomoides filamentosus), a deep water snapper, with GBD. H = hemorrhage\\ I = chronic inflammation\\ B = clear spherical spaces where bubbles occurred |
Gas bubble disease is detected by observing superasatuarion of O2 or N2 in the water holding fish. Gas bubbles may be observed in wet mount preparations of the skin, gills or internal organs.
Gas bubble disease is controlled by identification of the source and rectifying the problem. There are saturometers and tensiometers for spot use in measuring for supersaturated gases in the water. Unfortunately, they do not work well for continuous process-type use as an alarm system. There are possible alternatives that could provide an indirect indication of this problem with process instruments (instruments for continuous monitoring of the water conditions). Less direct monitoring can be provided by a DO (dissolved oxygen) or ORP (oxidation-reduction potential; as a general indicator of a water change) meters either downstream of the last pump before the water goes to the fish in a recirculating water system or in a flow through system in the plumbing leading directly to the tanks. Change detected by these instruments could be due to supersaturation, or other causes. It could provide a preliminary indication of a problem, but further investigations are required to verify the cause and they may not be sensitive enough to identify all problems.