Blue-green algal build up in farm dams and other low-flowing wet areas is not uncommon and can cause significant losses. There are many species of cyanobacteria but Microcystis sp. and Anabaena sp. are the most well known in Australia. There are factors which will increase the likelihood of poisoning occurring but cases can be sporadic and not easy to predict. The following case study outlines some of the risk factors involved in blue-green algae poisoning, the clinical signs one might expect and the common post-mortem findings.
The poisoning occurred on a small grazing block of 400 acres nestled in the middle of some larger scale broad acre cropping enterprises on heavy black soil. The cattle, approximately 30 head, were grazing the entire area which consisted mostly of dry summer grasses with some green herbage and clover underneath. Owners of the cattle phoned to report dead and dying stock, all of which were younger yearling animals. There were 5 dead cattle on arrival at the property and none still alive. Three were beside the dam and 2 others were dead along a fence line. The surrounding area of the dam had abundant noogoora burr (Xanthium occidentale) growing which appeared to have been grazed.
At the initial inspection of the dam blue-green algae were not noticed. Cattle had access to a couple of very old silos that were rusted and had some debris exuding from their openings. The debris did not appear to have been consumed.
A yearling heifer was necropsied. Grossly the liver was enlarged more than 100% on normal size and was noticeably pale in colour with large patches of darkened areas (Figure 4). The carcase was slightly jaundiced. The thorax was largely normal with some increase in pericardial fluid. The kidneys were normal in appearance. The abomasal mucosa was red and the rumen had large amounts of pink plastic round-hay-bale netting within as well as a large piece of cloth.
The samples were negative for anthrax. Beta-hydroxybutyrate was normal.
Histopathology revealed hepatic necrosis, multifocal, periacinar, chronic, severe with biliary hyperplasia and replacement fibrosis (bridging) with haemorrhage. This finding is consistent with an acute severe toxic hepatopathy and the comments were to consider fireweed and pyrrolizidine alkaloids. Subsequent water samples were positive for Anabaena circinalis
At the time of the first visit blue-green algae was not considered. Differential diagnoses included plant poisoning, theileria, and ketosis from fatty liver syndrome. Feed conditions were deteriorating and so it was postulated that a combined effect of deteriorating feed conditions and foreign material in the rumen causing a degree of anorexia may have led to a large mobilisation of fat reserves into the liver. However, none of these animals were in a state of high energy demand (pregnant or lactating) and they were not carrying excessive fat reserves prior to illness. Theileria was ruled out at the lab with blood smears and a paddock walk revealed no sign of toxic plants.
A colleague raised the possibility of blue-green algae as a differential. A second visit was organised and revealed large algal blooms within the dam water which appeared like green paint below and on the surface of the dam.
The laboratory confirmed the presence of cyanobacteria and the liver pathology was consistent with cyanotoxicity. A diagnosis of blue-green algae poisoning was made. The dam water was treated with copper sulphate to destroy the cyanobacteria. No further deaths were reported.
There are two groups of toxins recognised in cyanobacteria that cause disease: hepatotxins, which are decidedly more common, and neurotoxins, which are less frequently identified.
Some species of cyanobacteria can produce both types of toxin and therefore different syndromes may well be present within the one outbreak.
The hepatotoxins cause acute hepatic necrosis with haemorrhage and post-mortem findings include a markedly swollen liver and there may be petechial and splash haemorrhages throughout the carcase and on the liver itself.
The neurotoxin form of disease does not leave any characteristic post-mortem findings. In some cases clinical signs become evident within 30 minutes of exposure to toxic levels in water however there is a ‘slow death factor’ syndrome recognised in which liver damage leads to jaundice and photosensitisation.
In more acute cases, clinical signs recognised include muscle tremors, staggering and prolonged recumbency. Hypersensitivity is also noted in some cases as is abdominal pain, diarrhoea and dyspnoea.
Toxicity most often occurs in summer and autumn and is more likely under drought conditions. In this case the poisoning occurred in June but drought conditions were present and the temperature had been mild. The dam level was low at the time.
Other factors mentioned that predispose to blue-green algal blooms are increased nutrient (mainly nitrogen and phosphorous) content of the water, decreased salinity of brackish water areas, reduced flow rates in river systems, wind, and irrigation with contaminated water onto pastures or crops.
Apart from drought conditions, the above case exhibited two other risk factors for bloom formation. This property was surrounded by broad acre, black soil, large scale cropping enterprises. Fertiliser use on this type of country would be common for crop production and also may involve aerial dispersion at times. Run-off from this area would contain sediment with a high nutrient content, and the dam water itself may be subject to contamination from spray drift since liquid nitrogenous fertilisers are common. Wind is the other factor common to this case. The season had been particularly windy and on the days when the property was visited the wind was such that the blooms were blown to one side of the dam in particular.
Copper sulphate is known to kill cyanobacteria. The toxins are released from the bacteria following their death from copper sulphate application and so stock should always be help off contaminated water for at least 5 days following treatment. In fact dams containing sub-lethal levels of cyanobacteria may in fact become deadly after treatment due to the release of toxins from dead cyanobacteria.
In conclusion, the most important aspects of this type of disease are that there are two distinct syndromes and that within the hepatotoxic syndrome there are acute and chronic cases also. The neurotoxic effects are not reported as frequently as the hepatotoxic effects but the lack of post-mortem findings and acute nature of the toxicity may cause the neurotoxic form to be underdiagnosed. Where the water source is from a dam or stagnant area it should be checked for the presence of cyanobacteria in cases where the underlying cause of disease is unknown.