Common Water Chemistry Diseases in Aquaculture Associated with Water Recirculation or Reuse
Water chemistry and quality problems in aquaculture are frequently more significant to morbidity and mortality than all infectious disorders combined.
- Fig. 12.13. Marked abdominal distension due to marked gastric dilation - 'water belly syndrome'. (Photo courtesy of Dr D. Groman, Atlantic Veterinary College.)
With the popularity of water reuse systems, aquaculturists and production consultants need to be aware of a considerable range of mechanical and biological technology and also some problems related to either their misuse or failure (Lucchetti and Gray, 1988).
Oxygen is perhaps the greatest determinant of water flow demands of a fish farm. Use of supplemental oxygen is common in situations of serial reuse of water or true recirculation. The less passive the process of re-oxygenation, the greater the inherent risk of failure and disaster. Low dissolved oxygen is a critical primary rule-out during the clinical investigation of respiratory distress syndrome. Marginal oxygen levels can also contribute to mortality rates during and after episodes of infectious gill diseases since uptake efficiency across the damaged gills can be severely affected. Additionally, unexpected mortality spikes in the aftermath of static bath chemical treatments or particularly intense feeding periods are often traced to marginal oxygen levels.
Water recirculation and reuse systems can also lead to problems with ammonia and its nitrification by-products, nitrite and nitrate. Sudden drops in water temperature, exposure to antibacterial chemotherapeutics, or reduced oxygen levels, have the potential to disrupt bacterial kinetics within biological filters. The physiological effects of ammonia and nitrite toxicity in teleosts are yet uncertain and controversial. Branchial lesions from ammonia exposure have been reported (Smith and Piper, 1975; Smart, 1976; Thurston et al., 1984) although other workers have not been able to repeat the effects (Daoust and Ferguson, 1984; Lang et al., 1987). Meade (1985) suggested that gill lesions may not be directly linked to unionized ammonia, but may represent the confounding effect of other metabolites. Knights (1989) has shown in a study on European eels under intensive culture, that high ambient ammonia concentrations caused prolonged increases in oxygen consumption, and growth suppression. Similarly, for rainbow trout, Lang et al. (1987) showed that sublethal levels of ammonia increased ventilation frequency and caused reduced feed intake. Their research also showed adaptation, a feature which suggests that variability between studies, particularly field studies, is likely to occur unless similar design protocols are used. This conclusion agrees with results of a laboratory study dealing with acute ammonia toxicity of Atlantic salmon parr (Knoph, 1992).
Nitrite toxicity, a common problem in pond-rearing of catfish (Tucker et al., 1989), can also affect salmonids (Lewis and Morris, 1986). Nitrite-induced death may stem from a number of factors. Methaemoglobin production by chemical oxidation of haem iron results in a haemoglobin incapable of combining with oxygen, thus hypoxia develops. Furthermore, although not yet shown for fish, the methaemoglobin fraction also affects the oxygen dissociation of residual haemoglobin (Smith, 1980). Nitrite, being a potent smooth muscle relaxant and vasodilator, may contribute directly to cardiovascular collapse. Other iron-containing enzymes can also be affected by nitrite. Hanson and Grizzle (1985) determined that channel catfish are predisposed to bacterial diseases during chronic high level nitrite exposure. Speare and Backman (1988) described bubble gas disease (BGD) in rainbow trout following sublethal nitrite exposure. These findings generally suggest that nitrite toxicity may be directly or indirectly immunosuppressive.
Water reuse promotes elevated carbon dioxide levels. Although rarely acutely deleterious, an increased incidence of nephrocalcinosis (renal tubular degeneration and mineralization) (Harrison and Richards, 1979) and swimbladder dilation syndrome (Fig. 12.14) are anecdotally linked to chronic exposure to high levels of carbon dioxide.
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