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Sudden (or almost sudden) Deaths

Chris Bourke, Principal Research Scientist (Poisonous Plants)
Orange Agricultural Institute, Forest Rd Orange NSW

Posted Flock & Herd February 2011


Outbreaks of sudden death can be very dramatic, the attending veterinarian may be confronted with large numbers of animals that are either dead or dying, in a herd or flock that was apparently normal 24 to 48 hour beforehand. Many plants have the potential to cause this problem, but most rarely do because they are either not very palatable (hence not eaten unless there is nothing else available) or alternatively not usually present in large enough amounts to cause a significant number of deaths. With some plants, toxicity only occurs in some seasons of some years because several environmental factors are required to occur at the same time to render the plant toxic.

For convenience plants with a sudden death potential can be divided into three groups: common paddock plants, less common and garden-restricted. The less common paddock plants will be much more geographically restricted, but may still be a significant cause of deaths in some districts. The homestead garden plants only become a problem when clean up trimmings are thrown over the fence for livestock to eat or when animals accidentally gain access to the garden area.

Since all the field and laboratory investigative effort under the sun will never make something what it isn’t, vets are well advised to start each investigation into an outbreak of ‘sudden death’ by spending more time in defining just exactly what their something is. For example don’t just see the scene as dead animals, sometimes affected survivors are still present and can be clinically assessed by the attending veterinarian. At other times everything affected is dead but the livestock attendant may be able to describe what clinical signs were seen prior to death. Failing this, some impressions can be gained by looking at the dead carcasses prior to autopsy, for example was the death quiet or is there evidence of paddling and frothing at the mouth or of diarrhoea, finally do some autopsies. The overall intent is to try and establish the major focus of the organ system failure, was it gastrointestinal, or nervous, or muscular, or cardiac, or respiratory, or hepatic, or renal, or particular combinations of these. Establishing this focus will greatly reduce the diagnostic possibilities.

Group A. Common ‘sudden death’ paddock plants

a) Nervous signs

    Lolium rigidum (Annual ryegrass)
    Agrostis avenaceae (Blown grass)
    Polypogon monspiliensis (Annual beard grass)
    Water damaged cereal grains

b) Muscular signs

c) Cardiac signs

d) Gastrointestinal signs

e) Hepatic - haemolytic signs

f) Respiratory signs

Group B. Less common ‘sudden death’ paddock plants

a) Nervous signs (autonomic nervous disorders)

b) Cardiac signs (cardiac glycocides cause cardiac, respiratory and GI signs)

c) Gastrointestinal signs

d) Hepatic signs

e) Respiratory signs

f) Mixed signs

Fluoroacetate plants (cardiac, respiratory and nervous signs)

Group C. Homestead restricted ‘sudden death’ garden plants

a) Nervous signs

b) Cardiac signs (cardiac glycocides cause cardiac, respiratory and GI signs)

c) Gastrointestinal signs

Sudden death syndromes to be presented in more detail

Phalaris aquatica ‘sudden death’
Nitrate poisoning
Cyanide poisoning
Kikuyu grass poisoning
Cestrum (Cestrum parqui) poisoning

Phalaris aquatica ‘sudden death’ highlights

Two types of sudden death are possible in ruminants grazing P. aquatica, one is a cardiac disorder and the other is a nervous disorder. The cardiac disorder is uncommon and affects very few animals. The presentation is one of sudden collapse following mustering the animal has a pounding heart and discolouration of the mucous membranes. There is either death, or instant recovery, within minutes of collapse.

The nervous form of sudden death is much more common and kills much larger numbers of animals. For the last decade it has been called ‘Phalaris PE-like sudden death’, because the clinical signs and brain histopathology displayed some similarities to a speculated peracute form of PE. Most affected animals are found dead, typically along a fence line, if affected survivors are still about they will display signs of convulsions or CNS depression. It has now been established that the brain changes and the nervous signs associated with this syndrome are the result of peracute ammonia toxicity. The presumption is that the plant contains a urea cycle enzyme inhibitor which can exert a clinical effect in nitrogen naive ruminants that are suddenly exposed to high plant nitrogen ingestion levels. To become nitrogen naive the ruminant need only be on a low nitrogen ration for 3 consecutive days. Likewise the toxin itself can only exert a significant negative effect on the urea cycle of a toxin naive animal for about 48 to 72 hours. After this time the liver of the animal simply compensates for the effect of the toxin by producing more of the affected enzyme.

Confirmation can be made on aqueous humour samples collected within 24 h of death and tested for ammonia within 48 hours of collection. Histopathology on brain sections, when examined by a determined pathologist, will reveal consistent changes. These include cerebral cortical oedema and the presence of swollen astrocytes. Affected survivors will have much lower ammonia levels but more obvious brain pathology than animals found dead.

Nitrate poisoning highlights

Ruminants are susceptible to nitrate-nitrite poisoning, horses and pigs are not. Nitrate-nitrite poisoning affects oxygen transport and presents as: many deaths and acute respiratory distress, in a group of animals with diarrhoea, some of which are recumbent and displaying nervous signs. When rain follows a protracted dry spell a lot of nitrate is translocated up into plants. The rumen microflora convert nitrates to nitrites to ammonia, prior exposure to rising nitrate levels allows for rumen adaptation and ultimately the safe handling of large nitrate loads. Adaptation takes about 5 to 10 days.

Consequently nitrate poisoning rarely occurs in a pasture situation. It commonly occurs when animals are locked up in small, urine and faeces rich, holding paddocks which are infested with young but stalky nitrate accumulating plants. It also commonly occurs when drought affected groups of animals are suddenly fed large amounts of nitrate rich batches of hay. The nitrate content of a plant is not concentrated in leaf material but rather it is heavily concentrated in stems and stalks. Hay frequently contains large amounts of stems and stalks. The nitrate content of a fodder crop can be reduced by about 50% when it is processed as silage. Cattle are more susceptible to nitrate poisoning than sheep. Confirmation of poisoning can be made on aqueous humour samples from animals found dead.

Cyanide poisoning highlights

Ruminants are more susceptible than horses and pigs to cyanogenic glycoside poisoning. Many plants can accumulate cyanogenic glycosides but the Sorghum, Lotus and Linseed plant families are the most common offenders. Cyanide poisoning affects cellular oxygen utilisation and presents as: many deaths and acute respiratory distress, in a group of animals some of which are recumbent and displaying nervous signs. Ruminants display a very limited amount of adaptation to the cyanogenic glycoside content of cyanide accumulating plants. Consequently they tend to display a fixed per hour rate of cyanide detoxification, if this is exceeded they will die, regardless of how many days beforehand they have been ingesting cyanide accumulating plant material for.

The best doing animals will be at the greatest risk of poisoning because they will be more inclined to exceed the safe per hour ingestion rate. The ingestion of cyanogenic plants soon after a rainfall event carries a much greater risk of poisoning. Cattle are more susceptible to cyanide poisoning than sheep. Confirmation of poisoning is difficult because cyanide is unstable but fresh liver and muscle samples can yield positive results.

The cyanide content of a fodder crop can be reduced by about 50% when it is processed as silage. Use of a sulphur feed supplement may improve the ruminal rate of cyanide detoxification. Cyanide levels are higher in leaf material than in stems and stalks consequently green chop feeding or hay or silage feeding will be safer than selective grazing. When grazing at risk sorghum fodder ensure the growth is at least half a metre tall. Always test the cyanide content of at risk plant material so that you can establish the maximum safe per day rate of ruminant ingestion.

For example the minimum lethal dose is 2.0 mg free HCN per kg body weight per day but using the as fed plant sample measured cyanide content this value becomes about 4.0 mg of measured cyanide per kg body weight. A 500 kg cow will eat about 15 kg of dry matter per day hence can tolerate plant material that contains less than 200 ppm cyanide (20mg per 100gm dry wt basis) when only 15 kg of it is ingested over 12 to 24 hours. The same plant material will kill it if 15 kg is ingested in less than 6 hours. Alternatively if the plant material contains 2000 ppm then the cow can only safely ingest 1.5 kg of it over 12 to 24 hours. Should it ingest even this small amount of dry matter in less than 6 hours, it will die.

Kikuyu grass poisoning highlights

This is a peracute gastrointestinal disorder that occurs in cattle in association with autumn rain following a protracted dry summer. It is more common on pastures that have been spelled for several weeks. Autopsy reveals a rumen full of kikuyu and fluid. Rumen pH will be normal. Histopathology on rumen, reticulum and omasum sections will demonstrate typical inflammatory changes. Death results from severe dehydration and subsequent renal failure. The cause of pasture toxicity appears to be a transient rise in an unknown substance in the grass. This substance seems to be directly toxic to the epithelial lining of the forestomach and associated with this toxic effect there is a rapid movement of fluid out of the circulation and back into the rumen. The animal thus feels thirsty but at the same time it feels full of fluid, hence it sham drinks.

This toxicity first appeared in the mid 1950's and its occurrence has become more frequent since then. It remains possible that the increasing use of nitrogenous fertilisers on kikuyu pastures may be favouring the development of this toxicity. However it does not involve either nitrate poisoning, peracute ammonia toxicity, or a form of urea poisoning. All other suggestions as to its cause have been subsequently demonstrated to be incorrect.

For example it does not involve: oxalates, army worm caterpillars, a pasture litter fungus, a soil fungus, a plant pathogenic fungus, or a macrocyclic trichothecene mycotoxin such as either roridin or verrucarin. There is one report of a fungal endophyte being isolated from a toxic pasture at Bega, but the possible contribution, if any, of this endophyte to kikuyu poisoning has not been explored.

Cestrum parqui poisoning highlights

This can present as a peracute hepatopathy hence deaths within hours of plant ingestion. Affected survivors will be developing an hepatic encephalopathy hence they are depressed but irritable, usually recumbent, and ultimately either comatose or convulsive. Some affected survivors may have diarrhoea. On autopsy there will be signs of liver damage together with haemorrhages throughout the carcass. Histopathology on liver from affected survivors will confirm the presence of centilobular hepatocellular necrosis, plus brain sections may demonstrate an hepatic encephalopathy.

Both Cestrum parqui plants and Xanthium spp seedlings (Bathurst and Noogoora burrs) produce very similar hepatotoxic glycosides, namely carboxyparquin and carboxyatractyloside respectively. Consequently they cause very similar clinical signs. Cestrum also produces small amounts of solanum glycosides and cardiac glycosides but neither of these appear to contribute to the clinical disorder that affects ruminants.


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