Environmental aspects of acid sulphate soils - ROOT of content

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suggested similar water quality changes may be involved in its pathogenesis.In this paper we briefly review the findings of these studies and discuss possiblemechanisms responsible for death or ulceration in fish exposed to water derived fromareas of acid sulphate soil.Seasonally recurrent fish mortalitiesA fish kill may be defined as any unusual increase in mortality and morbidity, dueto infectious or non-infectious causes, in a fish population.There have been several reports of seasonally recurrent fish kills in the Magela Creeksystem, part of the East Alligator River system in northern Australia. These fish killstypically occur during the transition from the dry to wet season, when ‘first-flush’water enters lagoons and other permanent water bodies. Brown et al. (1983) describeda major fish kill in a freshwater lagoon on Magela Creek which they attributed tohigh levels of toxic aluminum (up to 0.5 mg 1-I), a consequence of natural acidic waterrunoff. Hart et al. (1987) studied water quality in the Magela Creek system duringa dry-to-wet season transition and found that ‘first-flush’ water flowing across thefloodplain was acidic (pH about 4-5) with high conductivity (about 750 pS cm-’) andhigh sulphate concentrations (about 200 mg 1-I). They concluded that the source ofthe acidity, dissolved salts and sulphate, as well as high concentrations of metals, particularlyaluminum, was groundwater brought to the surface by rising watertablesin acid sulphate soil areas of the floodplain.Massive fish kills following major rain events have also been associated with acidicwater and high concentrations of aluminum in major sections of the Tweed Riverin northern New South Wales. The acidic water is derived from runoff or drainagefrom the extensive areas of potential acid sulphate soil in the floodplain. In 1987,a fish kill on the Tweed River was associated with pH values as low as 3.6 and dissolvedaluminum concentrations of 2.5 mg 1-’ in major sections of the main stream (Fraser,unpublished).Low pH, below 3-4, is directly lethal to móst fish species, causing disturbances towater and ion regulation, as well as to oxygen transport mechanisms (WendelaarBonga and Dederen 1986). However, elevated concentrations of inorganic, cationicaluminum species (less than 0.1-5 mg 1-I) are thought to be primarily responsible forinjury and death of fish in naturally acidified waters. These increased aluminum concentrationsresult, under acid conditions, from mobilisation of aluminum from watershedminerals (Driscoll et al 1980, Langdon 1988). In acidic water, inorganic aluminumaccumulates in, and injures, fish gills, causing reductions in enzyme activity and lethalosmoregulatory disturbances (Staurnes et al 1984, Witters et al 1990). Other waterquality attributes modify the toxicity of inorganic aluminum to fish; there is evidencethat high calcium and silicon concentrations protect fish against aluminum toxicity(Brown 1983, Ingersoll et al 1990a, Birchall et al 1989). Humic substances (the endproducts of biological degradation of organic material) are also protective, bindingaluminum in a non-toxic, organic form (Witters et al 1990).In response to toxic acid/aluminum exposure, some fish species are able to acclimatize,via physiological changes, or undergo longer-term adaptation, via genetic selection(Mount et al 1990). These workers showed, however, that exposure to a 6-day ‘pulse’404
of acid water with high inorganic, monomeric aluminum and low calcium concentrations,caused significant mortalities in brown trout fry not previously acclimatizedto these conditions. It is likely that fish exposed to acid ‘first-flush’ water in Australianrivers are similarly unprepared, and that similar toxic mechanisms operate.Epizootic ulcerative syndromeEpizootic ulcerative syndrome (EUS), known colloquially in Australia as ‘red spotdisease’, is an ulcerative skin disease affecting estuarine and freshwater fish. EUS wasfirst reported in Australia from the Burnett River on the central Queensland coastin 1972 (McKenzie and Hall 1976). Since then, seasonally recurrent outbreaks havebeen recorded in many rivers on the East coast, from northern Queensland (Rodgersand Burke 1981) to southern New South Wales (Callinan, unpublished). Outbreakshave occured in southwest Western Australia since 1983 (Pass, unpublished) and inthe Northern Territory since 1986 (Pearce 1990). Serious outbreaks of the disease havealso occurred in Southeast and South Asia during the past decade (Anon 199 I).Losses due to EUS, primarily in cultured freshwater fish, were estimated at A$2.5million in Indonesia in 1980, A$ 10.9 million in Thailand in 1982 and A$4.2 millionin Bangladesh in 1988-89. EUS costs commercial estuarine fisheries on Australia’sEast coast approximately A$ 1 .million in discarded fish annually.Studies in North America have examined the possible long-term effect of ‘ulcerativemycosis’, a disease of estuarine species similar to EUS, on fishery sustainability (Merrinerand Vaughan 1987). Results suggested that an incremental decline of 0.5 percent per year in survival of young fish over a 30-year period would result in a reductionof 60 per cent of the normal expected biomass. Loss caused by EUS in Australianestuaries have not been accurately quantified but; assumming that up to IO per centof young fish of susceptible species die as a result of EUS outbreaks occuring onceevery 3 years, a similar long-term decline in biomass may result.The sudden appearance and pattern of spread of EUS in Australia and Asia is consistentwith the involvement of an exotic infectious agent. Studies examining possibleprimary causative roles for viruses, bacteria and metazoan parasites have, to date,produced negative results. However, in a study of the pathology of EUS, Callinanet al (1989) showed that massive invasion of the skin by oomycete fungi plays a centralrole in the induction of ulcers. Recently, Fraser et al (1992) recovered the oomycetefungus Aphanomyces sp. in apparantly pure culture from 27 of 28 early ulcers on 3estuarine fish species from 3 widely separated river systems in Australia. Histologicallyindistinguishable fungi are also consistently present in lesions of fish affected withEUS in Asia (Roberts et al 1989).These findings indicate that an Aphanomyces sp. is the causative infectious agentof EUS. However, attempts to induce typical lesions by exposing fish experimentallyto fungal spores were successful only when skin was abraded prior to exposure (Callinanand Fraser, unpublished). This finding suggests that factors other than simpleexposure to the fungus are necessary for EUS outbreaks to occur in wild fish populations.EUS outbreaks in eastern Australia typically begin about 2 weeks after periodsof prolonged heavy rainfall in lower river catchments. There is a growing body of405
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