ARCHIVE FILE
This article was published in 1994
See the original document
Suspected Blue-Green Algal Poisoning of Cattle
J B Kemp District Veterinarian, Forbes Rural Lands Protection Board
The owner first contacted me on Sunday, 27/2/1994 and reported the death of 3 Hereford steers which had died over the previous 24 hours. These steers had died in the old House Paddock into which they had moved on 20/2/1994. The 3 steers were from a mob of 83 steers consisting of 40 Herefords, 30 Simmental cross and 13 Murray Greys aged 12 months to 2 years.
1. Post-Mortem Number 1:
One of the 3 steers was post-mortemed on the afternoon of 27/2/1994. The carcase was not fresh but this steer was the one that had died most recently. The main findings were:- the mucous membrane of the fourth stomach showed sore reddening, as did much of the small intestine. Some of the duodenum was very reddened. The contents of the large intestine were very fluid; the spleen was normal; lungs were congested; heart showed some petechial haemorrhages on the epicardium and there were haemorrhages under the skin around the head and upper neck. Blood was seen in a dung pat near the carcase.
The steers had been bought in 12 months previously and had not been vaccinated with 5-in-1. (Pulpy Kidney was considered as a possible cause.)
The steers had been grazing on sparse old lucerne and water couch. The latter was green from irrigation overflow.
The water in the dam from which the cattle were drinking was inspected. No sign of true green-algal scum was seen but the water had a greenish colouration.
The preliminary differential diagnosis was:
1. Pulpy Kidney
2. Couch grass poisoning
The Regional Veterinary Laboratory, Orange laboratory report (ON94/0596) showed that the epsilon toxin of Clostridium perfringens was detected in the intestinal contents by C.I.E.P.
Microbiology was positive to Clostridium novyi. John Seaman commented that this was probably a contaminant as it is a common soil organism (it was found in the muscle). (F.A.T.) Routine culture of liver, lung and muscle and intestine showed a mixed growth which included coliforms.
Bacteriology was not considered significant.
Toxicology showed negative for nitrate (aqueous humour and rumen contents) negative for cyanide (rumen contents and plant sample (couch)) and negative for arsenic (rumen contents).
Parasitology: The worm counts on the contents of the opened abomasum showed 500 Ostertagia and 100 Trichostrongylus axei.
Histopathology was of little value due to autolysis. The Laboratory diagnosis was: Bovine mortality - cause not determined.
The steers were moved to the adjoining paddock on the 27/2/1994, i.e. Paddock number 11 but they still watered from the same dam as in the old House Paddock, the dam being on the boundary of the two paddocks (See diagram).
On the 27/2/1994, the date of the first post-mortem, one steer appeared off colour as it had lost condition, appeared depressed and walked slowly. It was not examined as it was not near yards.
2. Post-mortem Number 2:
On Thursday, 1/3/1994, a fourth Hereford steer died. District Veterinarian was not in, so the animal was post-mortemed by practitioner Jan Slack-Smith. This animal was seen to be sick at 10:00 AM and probably died about midday (J Slack-Smith). This animal was thought to be the one that did not appear well a 27/2/1994. The animal was freshly dead on post-mortem. There were massive haemorrhages into the upper part of the large intestine - about a gallon of blood in the caecum but there was no frank haemorrhage in the small intestine. There was slight petechial bleeding in the abomasum and around the heart. The practitioner noted that it was in very good condition.
Laboratory report (ON94/0627) showed:
Haematology: Blood platelets low (21x109/L).
Microbiology: gram stain (3 smears):
Clostridium sp.
Culture - rectal and large intestinal contents - Include coliforms
Salmonella: negative
Histopathology: John Seaman commented: - 'histopathology non-specific most significant finding being the presence of coccidia parasites in the caecum, possibly associated with the haemorrhages noted on post-mortem. Unfortunately the significance of this as to the cause of the ongoing mortality is not clear. Coccidiosis is usually a disease of calves. However, crowding and stress might be involved to precipitate the mortality in this case'.
Laboratory Diagnosis: Bovine mortality - suspected Coccidiosis in the large bowel.
One other steer was treated with Terramycin L.A. by the practitioner. It appeared less lively and not in such good condition as the rest of the mob. Temperature 39.7°C (practitioner commented that it may have been due to environmental effect). No other abnormality was detected. The owner reported that there was a total of 3 Hereford steers sick - the one treated by the practitioner and 2 others which were 'wobbly'.
The paddock in which this steer died was Paddock Number 11, the same paddock into which the steers were moved on 27/2/1994. This paddock contained lucerne and grass.
3. Post-Mortem Number 3:
On Thursday, 3/3/1994, the fifth Hereford steer died, also in Paddock Number 11. The animal died in an irrigation drainage channel and it was pulled away from the channel for a post-mortem. A considerable amount of blood was coming away from the rectum in the channel which only held a small amount of water.
The post-mortem was done on 3/3/1994 and the animal was fresh. There were marked subcutaneous haemorrhages along the side of the animal. Lungs were congested. Heart had severe epicardial and endocardial haemorrhages - particularly on the outside of the atria. There were petechial haemorrhages in the thymus. Some petechiae in the trachea; spleen ok; liver - showed some breakdown and small red spots in cut surface and mottling and fine dark haemorrhages under the liver capsule. Kidney showed severe congestion of cortex and white areas in cortex. The omasum was enlarged and had very dry contents. The small intestines and large intestines were not inflamed. The rectum had dark red contents. The large intestine - caecum had dark liquid contents. Muscles were pale.
Laboratory Results:
Bacteriology results were not significant.
Toxicology:- Tests for nitrate, cyanide and arsenic were negative. The plant sample was also negative for nitrate and cyanide (couch grass).
Histopathology:
Lung showed severe diffuse congestion with focal areas of haemorrhage. Heart showed extensive haemorrhage under the epicardium and the myocardium was suggestive of a myocarditis.
Liver showed moderate autolysis but there did not appear to be any significant hepatic necrosis.
There was diffuse degeneration/autolysis of the renal tubule epithelium. Rumen, abomasum and intestine showed advanced autolysis.
The Laboratory commented that 'the myocarditis appeared significant could explain the generalised congestion/haemorrhage at the post-mortem (Oleander is usually cardiotoxic)'. However, the carcase at post-mortem appeared fresh.
Blue-green algae (from dam water in Old House Paddock) sampled 3/3/1994.
The majority was Oscillatoria with a lesser amount of Anabaena.
Laboratory Diagnosis: cause not determined but poisoning suspected.
Dairy Heifer Mob:
The Dairy Heifer Mob consisted of 180 Friesians aged 6 to 18 months. This mob was originally in the old House Paddock. These heifers were moved from the Old House paddock into Paddock 10 on 17/2/1994. (which neighbours Paddock 11. Paddock 10 is watered by Dam 2. This Dam 2 is regularly topped up from irrigation channel. Paddock 10 consisted of a mixed pasture.
4. Post-Mortem 4:
The first heifer to die was on 20/2/1994 in paddock 10 watered from Dam (not post-mortemed). The heifers were then moved out onto a bore water paddock and then moved back into Paddock 10 (with Dam number 2) on 3/3/1994.
The second heifer to die was on 4/3/1994. It was 8 to 9 months of age. Post-mortem, the carcase showed extensive haemorrhages. There were extensive subcutaneous haemorrhages around forelegs and between udder and underlying muscles. Lungs were congested and petechial haemorrhages were present in lungs, trachea and bronchi. The submandibular, retropharyngeal and mammary lymph nodes were enlarged and haemorrhagic. Only a few petechial haemorrhages were present on the epicardium. There was slight inflammation in only a small part of the small intestine. The rectum was reddened. Uterus was very haemorrhagic. Liver showed changes with pale areas on the surface. Kidneys showed changes. Skeletal muscles were pale and the spleen was normal.
Laboratory Findings:
Bacteriology: In the rectum and small intestine there was moderate to heavy is growth mainly including coliforms. There was no growth from the other tissues.
Histopathology:
In the lungs, there was severe haemorrhage and oedema flooding of spaces.
Liver:- gas bubble development through autolysis and no necrosis.
Brain:- severe meningeal and ring haemorrhages around blood vessels.
Skeletal muscle: - severe focal haemorrhages throughout.
Uterus:- focal haemorrhages and severe hyperaemia of mucosa.
Subcutaneous tissue:- massive haemorrhage.
Michael Hindmarsh (Regional Veterinary Laboratory, Orange) commented that these lesions are consisted with Anabaena poisoning.
Laboratory Diagnosis:
Mortality - widespread haemorrhages - resembles Anabaena toxicity.
A third dairy heifer died on Sunday, 6/3/1994. This animal pushed a gate into the neighbouring paddock (Number 4) which was a lucerne paddock. The heifer when found was very bloated so the owner put this death down to bloat. This animal was not post-mortemed.
Total mortalities were 5 steers and 3 heifers.
In the 2nd, 3rd and 4th post-mortems, the carcases were fresh, (2nd post-mortem done by practitioner).
In the practitioner's case histopathology showed diffuse periacinar degenerative changes of the liver, moderate congestion with a generalised increase in leucocytes throughout the sinusoids.
In the 3rd post-mortem, the liver showed moderate autolysis with disruption of hepatic cords and distortion of normal architecture. In many areas there is diffuse congestion/haemorrhage around the central veins plus some degenerative changes but changes are masked by autolysis. (But the carcase was fresh).
In the 4th post-mortem, histopathology of the liver showed gas bubble development through autolysis and no necrosis. (But the carcase was fresh).
The question is whether these liver changes in fresh carcases were caused by a hepatotoxin in blue-green algae.
Blue-Green Algal Tests:
1. Sampled 3/3/1994 - 01d House Paddock Dam - Majority Oscillatoria with lesser amounts of Anabaena.
2. Sample brought in by owner, 8/3/1994 - from Dam 2 (from which the dairy heifers were drinking). Moderate amount Oscillatoria 3,000 filaments/ml and very small amount of a straight chain of Anabaena.
3. Algal toxicity tests on water from Dam 1 - Old House Paddock Dam and Dam 2 - submitted on 16/3/94. There was insufficient Anabaena, Blue-green algae for the toxin test.
4. On 4/4/1994, sample from Dam 2 submitted. No Anabaena was present in the sample. Michael Hindmarsh commented:- The Anabaena bloom may have subsided with cooler weather.
5. Water sample submitted on 27/4/1994, from Old House Dam: - no algae were seen in the sample.
These tests for Blue-Green Algae do not rule out blue green algal toxicity as the bloom does not stay static.
Source of Water for Old House Paddock Dam (DAM 1)
This dam is filled from run-off from irrigation on paddocks 11, 18, 10 & 12 and all paddocks are flood irrigated with paddocks 11 & 18 at two weeks intervals and were last irrigated two weeks prior to the mortality.
The present owner bought the part of the farm, which has its dams filled by tailwater or direct from channels, in December 1993. The previous owner of that part of the farm (over a period of 5 years) had no problems with his dairy heifers other than bloat.
The paddocks over which the irrigation water drained into the old home paddock dam were well supered over previous years (pers. comm. - present owner).
The other part of the farm which waters its stock by troughs supplied by bore water has had no problems with mortalities (except the 3rd heifer to die - 8th death - in paddock 4 from suspected bloat).
Possible Causes of Mortality
1. Nitrate poisoning from couch in Old House Paddock. Tests of post-mortem samples and couch grass were negative. Only first three steers to die had access to this paddock (also not consistent with post-mortem findings).
2. Old plunge dip site in Old House Paddock - arsenic tests on post-mortem samples negative. Animals not scouring.
3. Salmonella - negative bacteriology.
4. Oleander - growing near Old House Paddock No 12. Only access to a couple of bushes - very little sign of being disturbed or eaten. Only the first three steers to die had access to Oleander.
5. Green Cestrum (Cestrum parqui) or Mother of Millions (Bryophyllum tubiflorum) not present in the paddocks. Rock fern (Cheilanthes sieberi) was also not present.
6. Blue-green algae - Oscillatoria and Anabaena present in Old House Paddock dam and dam 2 of which the steers and dairy heifers had access.
Blue-green algal poisoning was not considered as a diagnosis initially as there was no scum on the top of the two dams to which the steer mob and the heifer mob had access. However there was an olive green discolouration of the water.
The Regional Vet Lab, Orange, March 1993, - Monthly report by John Seaman states that 'the cause of the mortality of mixed breed cattle of Forbes was not determined. On necropsy, carcass showed extensive congestion and haemorrhages .A poisoning was suspected'.
Blue-green Algal Toxins
The toxins of freshwater cyanobacteria can be classified into 3 main groups:
1. Neurotoxins - Neurotoxins are produced by several blue-green algae including species of Anabaena and Oscillatoria2. Several Anabaena toxins exist. Signs of poisoning in animals which have ingested scums contains blue-green algal neurotoxins from the edge of a waterbody include paralysis, respiratory arrest, muscular tremor, salivation, staggering and convulsions.
Neurotoxins are the most rapidly acting of the chemical groups of cyano-bacterial toxins. They produce death by paralysis of peripheral skeletal muscles, then respiratory muscles leading to respiratory arrest within a few minutes to a few hours following exposure. Anabaena samples collected from the Darling River in late 1991 showed neurotoxicity3.
A bloom of Anabaena spiroides var contracta in 1981 killed 10 of 65 pigs that ingested it (Gorham & Carmichael 1988). Autopsy revealed generalised cyanosis, flaccid myocardium, mild emphysema and ecchymotic haemorrhages of the stomach and intestine. Death occurred within 30 mins following trembling and violent shaking3.
2. Hepatotoxins - Hepatotoxins produced by several blue-green algal species are by far the most commonly encountered and have been implicated in the majority of environmental incidents involving toxic freshwater blooms. The toxins are produced by strains of species of Microcystis, Oscillatoria and Anabaena2.
Hepatotoxicosis produces a range of symptoms which differ between different animal species. Cattle may display recumbency and weakness, reduced responsiveness, reluctance to move about, anorexia, tachypnoea/dyspnoea, trembling, pyrexia, ataxia, pale mucous membranes, weight loss, tachycardia, pallor of the extremities, poor capillary refill and sometimes mental derangement, often accompanied by watery or bloody diarrhoea (Main et al. 1977). Dehydration may occur in recumbent animals and they may experience ruminal atony, possibly resulting in mild bloat (Beasley et al. 1989). Some cases may have symptoms which resemble other clinical conditions, such as milk fever (Goley et al. 1987). Animals that survive an acute hepatotoxicosis may experience secondary photosensitisation (MCBarron & May, 1966)3.
Pathology
The most evident sign that animals have died from exposure to cyanobacterial hepatotoxins is gross hepatomegaly accompanied by intrahepatic haemorrhage (Jackson et al. 1984). The liver is usually dark - coloured but can also be pale3.
3. Lipopolysaccharides - Many Blue-green algae, in common with some bacteria, produce lipopolysaccharides (LPS) as normal components of their outer layers2. Lipopolysaccharides (endotoxins) can cause gastroenteritis, skin and eye irritations, skin rashes and allergic reactions1.
Toxicity may vary between different cyanobacterial blooms and within blooms there may also be spatial and temporal variations. The casual factors for toxin variation are not known although light and nitrogen availability appear to be involved1.
To assess the potential hazard associated with the toxins, assessment of their toxicity is made by giving doses to laboratory animals. Toxicity depends upon the route of administration, the size of the dose and period of exposure2.
The Release of Blue-green Algal Toxins into Water
Toxin release varies between species of blue-green algae, but this subject has not been extensively studied under different environmental conditions. Laboratory studies with toxic Microcystis strains collected from lakes have shown that a substantial release of toxins from the cells into the water occurs when the blooms die, because of cells breaking down. A substantial release of microcystins from healthy growing cultures of Oscillatoria has been observed. Reports of microcystins found in lake water during the course of a bloom also suggest that a significant release of the toxins occurs before the blooms age and break down2.
There is no data available on the release of neurotoxins or lipopolysaccharides into water. There is a need to study toxin release from the blooms in the field because it is essential to know whether the toxins are actively secreted into the water or passively released only when the cells die.
Blue-green Algae (Anabaena sp.) poisoning in cattle
In Canada, 16 to 30 Charolais cattle including cows, calves and yearlings were found dead in and around the edge of a four hectare dam. As well, a mature cow, a yearling heifer and calf, were found alive but obviously sick. The lips of all dead animals were stained blue-green. Necropsy revealed petechial and ecchymotic haemorrhages on the pericardium, thymus and rumen wall. Clinical signs included incoordination, listlessness, depression and recumbency. Drooling, swaying of the head and muscle tremors were noticed in the calf. Microscopic examination of the water revealed a pure, heavy growth of blue-green algae. Examination of rumen contents revealed Anabaena sp.4.
Microcystis aeruginosa5 (S L Everist 1981 - Poisonous plants in Australia)
Studies in New South Wales (McBarron) implicated water containing Microcystis aeruginosa as a cause of severe losses of sheep. Symptoms included depression, bloating and in some cases, photosensitisation prior to death within 12 to 24 hours after consumption of water containing the algae. At autopsy there was usually haemorrhage in the lining of the alimentary tract, in heart muscles and sometimes in skeletal muscles, subcutaneous tissues or liver. Most animals showed evidence of liver damage either severe and accompanied by accumulation of straw-coloured fluid in the chest and abdominal cavities, or patchy and associated with some congestion of kidneys. Histopathological changes were most marked in the liver, mainly necrosis of the hepatic cells sometimes generalised and severe, sometimes patchy and accompanied by mild megalocytosis.
Rogers (1979) reported 5 out of 40 cows in southern Queensland were affected after drinking water from a farm dam covered with this algal bloom. Affected animals were tucked up, would not eat and stood with heads lowered. They recovered when removed from the dam water.
Overseas reports indicate that in most cases of algal poisoning, symptoms appear rapidly, usually 15 to 45 minutes after consumption of a toxic dose and death commonly occurs within 24 hours.
Gastro-intestinal symptoms vary in severity and are sometimes absent. Animals that do not die rapidly often show blood in the faeces, jaundice and photosensitisation
5. REFERENCES
1. Murray-Darling Basin Commission - Land and Water Resources. - Research and Developmental Corporation; Technical Advisory Group Outcomes; Contributions to the development of the Algal Management Strategy
2. 'Toxic Blue-Green Algae' - A report by the National Rivers Authority (UK Water Quality Series No 2 - September 1990
3. University of Adelaide - South Australian Health Commission - June 1993. 'Health Effects of Toxic Cyanobacteria (Blue-green algae)'. Report to theEnvironmental Health Standing Committee of the National Health and Medical Research Council.
4. Canadian Veterinary Journal 30, Oct 1989, p 832
5. Selwyn L Everist (1981). Poisonous Plants of Australia (Angus and Robertson Publishers).
ACKNOWLEDGMENTS
1. Michael Hindmarsh - for his help and references, including 'Report on the Churchill Fellowship study tour entitled 'The Biomanipulation of Blue-Green Algae' - UK & Europe, May - August 1992, by Dr Michael Hindmarsh
2. Tim McAuliffe - Water Resources Commission, Forbes - for references
3. Regional Veterinary Laboratory, Orange, for the laboratory examinations - John Seaman and Michael Hindmarsh
4. Elizabeth Haynes & Trini Coupland for the typing
5. To the owners of the property for their co-operation.
