Toxic Plants and Livestock Poisoning

• Poisonous plants affect grazing livestock, costing the industry over $200 million USD annually in the USA.
• Fluoroacetate toxicity alone costs the Australian livestock industry around AUD $45 million annually.
• Pimelea poisoning costs the Australian livestock industry about AUD $50 million annually.
• Direct losses from poisonous plants include deaths, weight loss, abortions, and decreased efficiency in animals.
• Indirect losses include fencing, supplemental feeding, and management alterations to prevent poisoning.
• Plant toxins can contaminate prepared feeds, causing animal and human poisonings.
• Livestock poisoning is usually due to management and pasture/range conditions, not just the presence of poisonous plants.
• Many pastures have potentially toxic plants that livestock can tolerate in small amounts, but poisoning can occur if consumed in excess.
• Some plants are toxic even in small amounts, and others have cumulative toxins like pyrrolizidine alkaloids that damage internal organs over time.
• Plant toxicity varies by season and growth stage, with stock often ignoring toxic plants until feed is scarce.
• Poisonings can occur when animals are moved into weed-infested stockyards or are newly introduced and naïve to toxic plants.
• No common characteristics distinguish poisonous from non-poisonous plants.
• Whether a plant causes poisoning depends on toxin type/amount, the animal eating it, body weight (BW), time taken to eat it, and animal health.
• Multiple factors often contribute to livestock deaths, making plant poisoning diagnosis difficult.

Factors that Contribute to Livestock and Pet Poisoning

Plant Factors

• Palatability varies significantly among poisonous plants; fluoroacetate-containing plants like Gastrolobium spp. are highly palatable.
• Herbicides can increase the palatability of some poisonous plants, like variegated thistle (Silybum marianum), due to released sugars.
• Alkaloid-containing plants (Heliotrope spp.) are generally bitter and non-palatable.
• Cardiac glycoside-containing plants (oleander, Nerium oleander) are unpalatable.
• Low palatability plants are eaten when feed is scarce or mixed with palatable feed/hay.
• Toxin concentration and distribution varies with the stage of plant growth, with nitrates in the stem, cyanogenic glycosides, and soluble oxalates in young leaves.
• Only the seeds and first seedling leaves of Bathurst burr (Xanthium spinosum) are toxic, while only seeds of Leiocarpa brevicompta are poisonous.
• In Sorghum species, only young leaves are poisonous.

Animal Factors

• Differences exist between animal species in their susceptibility to plant poisoning because metabolism differs between ruminants, monogastric mammals, and birds.
• Rumen microbes may detoxify or potentiate toxins, with soluble oxalates largely destroyed in the rumen, and nitrate converted to deadly nitrite.
• Pet poisonings are mainly due to accidental exposure, and the nature/extent of toxicity varies between dogs and cats.
• Factors such as age, breed, pregnancy, lactation, disease status, toxicant properties, and environment can influence toxicity.
• Acute poisoning is more common than chronic poisoning
• Susceptibility varies between native and introduced species.
• Kangaroos are susceptible to several introduced species, while native animals may have regional variations in susceptibility.
• Young animals are more susceptible due to less effective detoxification, curiosity, and lack of guidance from their dams.
• Some toxins cross the placenta, inducing congenital malformations.
• Teratogenic toxic plants include Veratrum spp., Lupinus spp., and Conium maculatum (hemlock).
• Hungry animals are more likely to consume poisonous plants, so poisoning is common during feed deficits, after transport/yarding, however healthy animals are better able to cope with the effects of poisonous plants.
• Chronic toxicities take time to emerge, like pyrrolizidine alkaloids in Paterson's curse (Echium plantagineum).
• Tolerance can develop with exposure to lesser toxin doses over time via rumen microflora or liver detoxification.
• Ruminants exposed to small amounts of soluble oxalates can withstand larger doses.
• The steroidal glycoalkaloids toxins in Solanum sturtianum do not release until after the animal has drunk water.
• Most pastures contain some potentially poisonous plants, a few scattered plants are not a risk, and preferentially grazed plants should always be controlled in pastures.

Environmental Factors

• Season dictates the presence/absence of annual plants, their growth stage, and physiological status.
• Rainfall influences poisoning likelihood, with drought, flooding, and fire affecting plant growth and toxin concentrations.
• Dry conditions produce wilting that can increase concentrations of toxins like steroidal saponins.
• Soil type affects plant poisoning; selenium-accumulating plants are toxic on Se-rich soils.
• High N soils predispose plants to high nitrate and soluble oxalate concentrations; heavily fertilized stockyard soils promote these compounds.
• Fertilizers can cause a flush of potentially poisonous plants and increase toxin concentrations.
• Many weeds and garden plants are toxic to pets and livestock.

Diagnosis

• Diagnosing plant poisoning in animals can be challenging, particularly with access to several potentially toxic plants.
• Five main factors to consider:
• The poisonous plant must be present in the environment, accessible to the animal, and show evidence of consumption.
• The toxin must be present in the plant material.
• Plant material, toxins, or toxin metabolites should be present in the ingesta and biological samples of the intoxicated animal.
• The observed clinical signs of poisoning must be associated with the specific plant.
• Other less specific biomarkers, such as hematology, serum biochemistry, or tissue lesions, are consistent with the suspected poisonous plant.
• Often a dead animal will be found in a decomposed state which precludes supportive clinical data.
• Non-specific clinical signs often confound the diagnosis
• Sub-clinical concentrations of plant toxins do not always mean toxicity.
• Accurate, rapid diagnosis of intoxication is challenging, as no single test detects all possible toxicants.
• Information needed include age, sex, reproductive status, morbidity/mortality, progression of clinical signs, recent changes in feed/water, animal movements, medications/supplements, and weather.
• Samples for toxicology testing include gastrointestinal contents, urine, whole blood, serum, and milk.
• Mixed feed, unusual pasture plants, feed ingredients, supplements, tags, and labels should also be collected.

Cardiac Glycosides

• The two major groups of cardiac glycosides are cardenolides and bufadienolides; cardenolides have a butyrolactone ring with five carbons, while bufadienolides have a pyrone ring with six carbons.
• Cardiac glycosides occur mainly as cardenolides in plants.
• Animal sources for bufadienolides include Buffo (toads), Photinus (fireflies) and Rhabdophis (snakes).
• Cardiac-glycosides were used as arrow poisons by Indigenous peoples of Africa, Asia and South America.
• Cardiac glycosides consist of a steroid backbone, a lactone ring, and a carbohydrate/sugar moiety.
• The inherent activity resides in the aglycone, but the sugars increase the power of fixation of the glycosides to the heart muscle.
• All animal species are susceptible to acute poisoning.
• Cardiac glycoside-containing plants are usually not palatable, they may be eaten when scarce.
• Palatability of oleander leaves increases after trimming or shedding, and spraying with herbicide increases palatability and cardiac glycoside concentration.
• Biotransformation of cardiac glycosides is primarily hepatic
• Cardiac glycosides induce direct cardiotoxicity and indirect vagal nerve modulation by inhibiting the Na+/K+ ATPase pump.
• Na+ efflux is inhibited, intracellular Na+ is retained causes increases in intracellular Ca2+ and augments contractility,
• This causes cardiac muscle fatigue, heart failure and permanent damage
• Examples of potentially hazardous plants include: Adonis microcarpa (pheasant's eye) Bryophyllum delagoense (mother of millions) Convallaria majalis (lily of the valley) Cryptostegia grandiflora (rubber vine) Digitalis purpurea (foxglove) Gomphocarpus fruiticosus, G. physicaroys (cotton bush) Nerium oleander (oleander)
• The most obvious clinical sign of poisoning is diarrhoea, usually with blood in the faeces.
• A variety of cardiac arrhythmias and heart block may also be encountered
• Affected animals may die suddenly if exercised. Ruminal stasis will also be evident.
• Cattle consuming oleander are frequently found dead because of the effects of the toxin on the heart.
• Classic clinical signs of oleander intoxication are primarily heart and digestive disturbances and altered mental status.
• Horses often have colic.
• Diagnosis involves identification of the plant and evidence of its consumption through a history of access, clinical signs, ECG changes, clinicopathological changes and necropsy findings.
• A variety of electrocardiograph alterations have been reported with cardiac glycoside toxicity, including changes in ECG complex durations, bradyarrhythmias and ventricular tachyarrhythmias.
• The clinicopathological derangements seen in acute cardiac glycoside toxicity include hypoxaemia, acidosis, haemoconcentration, hyperkalaemia, hypochloraemia, hyperglycaemia, elevations in serum urea and creatinine and elevations in creatinine phosphokinase (CPK).
• Treatment usually involves drenching with activated charcoal and electrolyte-replacement solution, and administering anti-arrhythmic drugs.
• Diversity of cardiac glycosides and their aglycones hampers laboratory diagnosis of cardiac glycoside poisoning in livestock
• Earlier treatment yields a successful outcome.

Corynetoxins

• Corynetoxicity occurs most commonly in Australia, is caused by tunicaminyluracils
• Glycolipids are poor immunogens mean there is no natural immunity to corynetoxins and have cumulative effect.
• Corynetoxins are generated by gram-positive bacteria (Rathayibacter toxicus) infected with bacteriophages.
• R. toxicus uses the nematode (Anguina spp.) to carry it up to the seed head of the host plant.
• Multiplying bacteria produce a yellow slime on the seed heads of infected pasture grasses.
• Toxic doses are 3-5 mg/kg BW, inhibit production of glycoproteins and thus interfere with small blood vessels, decreasing oxygen delivery to tissues, and the brain is the most affected organ.
• Corynetoxins inhibit lipid-linked N-glycosylation of glycoproteins; their inhibition impedes cellular functions and the potential effects of their toxicity.
• Corynetoxin poisoning is a severe, and frequently fatal, neurologic disorder of domestic livestock.
• Most poisoning cases occur when livestock graze mature seed heads on standing pasture.
• Annual ryegrass toxicosis (ARGT) – occurs with pastures containing Lolium rigidum
• Floodplain staggers · occurs with pastures containing Lachnagrostis filiformis (blow-away grass)
• Stewart's Range syndrome – occurs with pastures containing Polypogon monspeliensis
• There is a delay between the time galls colonised and become toxic to livestock.
• Clinical signs occur at 4-6 d and all ages are affected; morbidity and mortality rates are frequently high.
• Driving an affected flock, some sheep collapse in sternal or lateral recumbency.
• Clinical signs are also exacerbated by high environmental temperatures.
• In sheep, Co deficiency increases their susceptibility to corynetoxins poisoning .
• Clinical signs in livestock appear abruptly, usually following some external stimulation.
• Early clinical signs include unsteady, high-stepping gait or 'rocking-horse' gait, muscle twitching and nodding or swaying of the head.
• Affected animals collapse with rolling of the eyes (nystagmus), spasms of limbs and neck, and paddling motions of limbs.
• Left undisturbed, affected animals regain their feet after several minutes, and stagger away with stiff-legged, jumping or swaying gait.
• Removal of stock from toxic pastures usually results in cessation of signs and mortality after about a week.
• In sheep, the liver is yellowish and friable, and the carcase is sometimes mildly icteric; haemorrhages are in gallbladder, rumen, small intestine, kidney and cervical musculature; suprascapular lymph nodes are often enlarged and contain petechial

Cyanogenic Glycosides

• Cyanogenic glucosides (cyanogens) are relatively concentrated in grasses, pulses, root crops, and fruit kernels, often contributing to their bitter taste.
• Non-toxic, these compounds can become toxic upon hydrolysis in the rumen.
• Factors such as pH and microflora, rapid ingestion and maturity, and the presence of glucosidase and the application of nitrogen fertilisers and herbicides can increase cyanogenic toxicity.
• There is considerable chemical diversity in cyanogenic glycosides, with structures varying depending on the amino acid from which they were derived .
• The toxicity of HCN is due to its affinity for the ferric heme form of cytochrome c oxidase, the final enzyme in the respiratory chain
• Examples of potentially hazardous plants include: Brachyachne convergens (native couch) Chloris truncata (windmill grass) Cotoneaster spp. (cotoneaster) Cynodon dactylon (couch grass) Dysphania spp. (crumbweeds) Eremophila maculata (Poverty bush, spotted emu bush, native fuschia) Eucalyptus calevi (Caley's ironbark) Eucalyptus cladocalyx (sugar gum) Linum usilatissimum (flax – seed in particular) Lotus corniculatus (red flowered trefoil) Paspalum dilatatum (paspalum) Sorghum halepense (Johnson grass)
• All sorghums can accumulate cyanogenic glycosides and the potential to poison stock
• Lower growing plants are stressed by wilting, crushing, droughts, frosts, trampling, hail damage and insect damage
• Clinical signs of cyanide poisoning in animals include laboured breathing, tachycardia, frothing at the mouth, bright red mucous membranes, muscle weakness or twitching, staggering, convulsing, unconsciousness and death
• Sudden death and bright red venous blood
• Treatment: Sodium thiosulphate (Na2S2O3 'hypo')