Plant Toxicology

Introduction

The incidence of plant poisoning has decreased over the years due to improved husbandry and increased awareness of the farmer or owner.

In general, grazing animals will avoid poisonous or malodorous plants but will be forced to eat them if overstocking or lack of herbage occur. Hedging, ditching, fencing or spraying may increase the accessibility of poisonous plants, and herbicides may accelerate their growth.

In pets, boredom if left alone or confined for too long may lead to chewing of toxic plants. Puppies and kittens are very inquisitive and mouth and chew almost anything. Pets will also explore changes in environment and are more likely to chew new household and garden plants.

Toxin content varies between plant and between seasons and sites. Wet seasons may incraese mould toxicosis. Dry, hot and sunny weather leads to more photosensitisation.

Berries, pods and seeds are seasonal.

Snow can produce a relative drought, and toxic plants may be the only ones to appear, such as rhododendron and bracken.

Some plants can still be toxic when cut and dried, for example Ragwort.

Pregnant animals may be less selective and hungry and thin animals are more susceptible to poisoning.

Severity of the the poisoning will depend on the amount ingested and the presence or absence of other ingesta.

Ruminants and horses do not vomit but may attempt to or pass fluid from their nose.

The rumen can perform some detoxification.

The cause of the poisoning cannot always be adequately defined, and a common clinical approach can be used.

Plant poisons

Cyanide

Many plants contain hydrocyanic acid, either free or as a cyanogenic glycoside which becomes hydrocyanic acid on ingestion. Most toxins are in the seeds or leaves. Damaged plants may be more dangerous as the formation of hydrocyanic acid may start before ingestion. Young plants and highly fertilised plants contain more glycoside.

Plant sources of cyanide: Linseed, Flax, Vetch, Elders, Maize, Lima beans, Acacia, Prunus spp (cherries, apricots, peaches), White Clover, Hydrangea.

Species affected: any species, ruminants are most susceptible.

Mechanism: prevents ATP formation leading to cellular hypoxia. Oxygen is not removed from haemoglobin so the blood stays bright red

Clinical signs: sudden death, dyspnoea, tachypnoea, excitement tremors, salivation, muscle weakness, ataxia, collapse, convulsions.

PM findings: bright "cherry-red" blood, pink mucous membranes, petechiae in gastro-intestinal tract and cardiac muscle.

Treatment: Sodium nitrite and sodium thiophosphate to help in the detoxifying process. Vitamin B12 forms a complex with cyanide.

Prognosis: favourable after 24 hours survival.

Nitrate/Nitrite

Some plants can accumulate nitrates in their stalks. Fertilisers may contrain high levels of nitrate and have a salty taste.

Plants containing nitrates: Sweet clover, Beets, Brassica spp (Rape, Kale, Turnip), Thistle, Radish, Wheat, Barley, Oats, Poison Hemlock, Pumpkin, Carrot, Sunflowers, Lettuce.

Species affected: all species, ruminants are most affected as rumen microbes convert nitrate to nitrite, which is the toxic factor.

Mechanism: Nitrate converts haemoglobin to methaemoglobin which causes hypoxia. It is also a vasodilator and causes hypotension.

Clinical signs: GIT irritation, muscle weakness, convulsions, tachycardia, dyspnoea, cyanosis, death. Emphysema and abortion in recovered animals.

PM findings: Dark chocolate blood. Petechiae, congestion and darkening of organs.

Treatment: Slow intravenous 2-4% methylene blue. Vitamin C. Oxygen, blood transfusion, epinephrine. Broad spectrum oral antibiotics to decrease nitrate conversion.

Oxalates

In general, oxalate-containing plants are palatable and cause acute poisoning. It forms soluble and insoluble salts.

Plants containing oxalate: Beets, Docks, Sorrels, Tea and Coffee, Rhubarb, Spinach

Species affected: all species. Ruminants can become tolerant due to rumen micro-organisms adapting to metabolise oxalates.

Mechanism: some oxalate forms into insoluble calcium oxalate with dietary calcium and some is absorbed. It causes acute hypocalcaemia and shock may intervene. Chronically, there may be renal damage due to crystal formation. Also crystal formation in the brain.

Clinical signs: dullness, inappetance, salivation, gastritis, twitching, tetany, collapse, convulsions

PM findings: crystals in the kidney and urinary tract, haemorrhagic gastritis, hypocalcaemia and decreased blood clotting.

Treatment: Calcium. Gradually introduce animals to a pasture. No treatment once renal damage occurs

Glycosides

Many different types of glycosides occur:

1. Cyanogenic glycosides: see Cyanide
2. Goitrogenic: some plants contain thiocyanates and thioxazolidone which can cause goitre. This occurs with Brassica spp (Cabbage, broccoli, rape, kale)
3. Irritant oils: this occurs with Crucifera spp, Brassica spp and Buttercups.
4. Coumarins: spoilt Sweet Clover causes clotting disorders
5. Steroid glycosides: including cardiac glycosides (Digitalis from Foxglove), saponins (Agave, Yucca) which cause haemolysis, and ostrogens in Subterranean Clover.

Alkaloids

1. Atropine: Deadly nightshade and Thornapple contain hyoscine or atropine.
2. Pyrrole alkaloids: cocaine from Coca spp
3. Pyrrolizidine alkaloids: Ragwort
4. Pyridine: nicotine from tobacco
5. Other alkaloids

Polypeptides and amines

Algae, mushrooms, ergot

Resins

Cannabis resin, Water hemlock, Rhododendron

Phototoxins

Some plants contain photodynamic substances: St John's Wort, Buckwheat, Hypericin.

Others cause secondary hepatogenous photosensitisation due to phylloerythrin.

Alcohols

Water Hemlock and Cotton

Phytoxins

Cause GIT irritation and oedema. Castor oil contains ricin which is highly toxic.

Enzymes and enzyme inhibitors

Thiaminase in Bracken (Pteridium aquilinum)

Mycotoxins

Mycotoxins are fungal metabolites formed during growth and multiplication of fungi in footstuffs.

Not all moulds are toxigenic and some feeds may have toxic even though they do not appear mouldy.

Hepatotoxins

These are toxins produced by Aspergillus and Penicillin spp

Sources: occur worldwide in peanuts, cottonseed, maize, silage, wheat, barley.

Species affected: Pigs, poultry, cattle and dogs are most commonly affected. Sheep and horses are more resistant.

Mechanism: The toxins interact with liver structures and enzymes, are potent teratogens, carcinogens, and immuno-suppressors. Formation of blood clotting proteins is decreased.

Clinical signs: anorexia, depression, dyspnoea, anaemia, epistaxis, jaundice, melena, convulsions, abortion, death.

PM findings: Raised liver enzymes, lowered TP and BUN, jaundice, anaemia, widespread haemorrhages, hepatic necrosis, cirrhosis, yellow kidneys and oedematous fat, hepatic neplasms.

Treatment: Remove source, ensure adequate protein in diet. Oxytetracylcine to interfere with the cytotoxic mechanisms. Vitamin E and Selenium as antioxydants.

Nephrotoxins

These are also produced by various species of Aspergillus and Penicillin. Mainly recognised in Europe, especially Denmark. Found in wheat, barley, maize, peanuts and beans.

Species affected: Mainly poultry and pigs

Clinical signs: Poulty are listless, have a depressed growth rate, have low quality and quantity eggs and may die.

Pigs show polyuria, polydipsia, anorexia, vomiting, dehydration, weight loss and diarrhoea.

PM findings: glycosuria, casts and protein in urine, pale kidneys with cortical necrosis, tubular degeneration and fibrosis. Gastric ulcers.

Treatment: Symptomatic and supportive.

Neurotoxins

There are many toxins in this group which cause staggers syndromes.

Examples include: Ergot, Lolitrem A and B from ryegrass.

Clinical signs: Signs are neurological and renal. Tremors get worse with excitement or exercise. There is swaying, ataxia, nystagmus, lateral recumbency and death.

Treatment: Diazepam/barbiturates. Removal from grass may result in recovery with no lasting effects.

Plant Toxicology Learning Resources
Flashcards Test your knowledge using flashcard type questions	Avian Medicine Q&A 07

References

Ayliffe, T. (2008) Plant Toxicology Student Notes from St George's Veterinary School

Merck and Co (2008) Merck Veterinary Manual Merial