COMMON OLEANDER

Scientific name: Nerium oleander Family: Apocynaceae

TOXICMECHANISMThe intact glycoside act as detergents and cause severe gastroenteritis (3). Cardiac

glycosides disrupt normal heart function by inhibiting an important enzyme called sodium potassium ATPase pump (3). Inhibition of the enzyme controlling sodium and potassium levels in cells leads to a build-up of potassium outside cells and build-up of sodium inside cells (1). This triggers a release of calcium into the cells (1). This high level of calcium in the cells of the heart can cause problems with normal conductivity of the myocardium and lead to heart failure (1). Other vascular signs include: arrhythmias, premature systole, conduction block. Signs of cardiac glycoside poisoning could include: lethargy and weakness, depression, diarrhoea, cold extremities, sweating, shortness of breath, coma, and death from heart failure (1). These glycosides have vagotonia effects, which result in bradycardia and cardiac arrest (2).

TREATMENT(IFANY)There is no specific treatment available for cardiac glycoside poisoning but it is usually

symptomatic and involves multi-dose activated charcoal and atropine (2). Interestingly, properties of some cardiac glycosides have made them useful in human medicine (2).

COMMERCIALMANAGEMENTOFTOXINNot suitable for plantation in and/or around pasture and paddocks areas where animals are

kept (1).

LD50Mashed fresh oleander has an LD50 of 30-50mg/kg b.w. in horses, donkeys and calves;

330mg/kg b.w. in goats ad 110mg/kg b.w. in sheep (2).

GRADEOFTOXICITYExtremely toxic but poisoning relatively rare because the plants are generally unpalatable.

It is native to the Mediterranean region and it is widely grown in Australia as a garden ornamental

and street tree (1). It is cultivated in most subtropical and warm temperate regions (1).All parts of the tree are extremely toxic to all

species, including humans as it contains cardiac glycosides. Humans should be careful while

handling plant as it is very toxic and cause death by ingestion of one leaf or flower, and the sap

causes irritation (1)

Reference:1) Offord, Mellisa. 2006. Plants Poisonous To Horses. Barton, ACT: RIRCD.2) R. C. Gupta. 2007. Veterinary Toxicology: Basic And Clinical Principles. Academic Press.3) Gardner G. 2016. Veterinary toxicology lecture 4, Murdoch university

FOXGLOVE

TOXICMECHANISMIn general, the mechanism of toxicity of digitalis glycosides at the cellular level involves

interference with an important enzyme sodium potassium ATPase pump (1). Inhibition of the enzyme controlling sodium and potassium levels in cells leads to a build-up of potassium outside cells and build-up of sodium inside cells (1). This triggers a release of calcium into the cells (1). This high level of calcium in the cells of the heart can cause problems with normal conductivity of the myocardium and lead to heart failure (1). Other vascular signs include: strong cardiac contractions, prolonged diastole, pulse and cardiac rhythm abnormalities, hyperkalemia and ventricular tachycardia (1). Signs of cardiac glycoside poisoning could include: lethargy and weakness, depression, diarrhoea, cold extremities, sweating, shortness of breath, coma, and death from heart failure (1). These glycosides have vagotonia effects, which result in bradycardia and cardiac arrest (1).

TREATMENT(IFANY)There is no specific treatment available for cardiac glycoside poisoning but it is usually symptomatic and involves multi-dose activated charcoal and atropine (2). Interestingly, properties of some cardiac glycosides have made them useful in human medicine as cardiac drugs that help to increase the force of contraction of the heart muscle (2).

COMMERCIALMANAGEMENTOFTOXINShould not be grown as an ornamental plant where livestock are present (1). Individual plants

found growing as weeds can be removed by hand (1). Wear thick gloves and take care to avoid the sap of this plant (1). The use of herbicides can be an effective control measure for larger infestations (1). The plant should be sprayed while actively growing (1).

LD50:LD50 is 0.18mg/kg b.w. (cats), 60mg/kg b.w. (guinea pigs) (2).

GRADEOFTOXICITYHighly toxic.

It is a native to Europe and is widely grown in Australian gardens (1). In some areas of Australia the plant grows as a weed in pastures and it has the potential to contaminate hay and

other feedstuffs (3). The main toxic glycosides in foxglove include digitalis, digitoxin, or digoxin (3).

All parts of the tree are extremely toxic to all species, including humans as it contains cardiac glycosides (1). Humans should be careful while

handling plant as it is very toxic (death by ingestion of one leaf or flower, and the sap

causes irritation) (1).

Reference:1) Offord, Mellisa. 2006. Plants Poisonous To Horses. Barton, ACT: RIRCD.2) R. C. Gupta. 2007. Veterinary Toxicology: Basic And Clinical Principles. Academic Press.3) Gardner G. 2016. Veterinary toxicology lecture 4, Murdoch university

Scientific name: Digitalis purpurea Family: Scrophulariaceae

ALOE VERA

TOXICMECHANISMWhen ingested, these glycosides are metabolized by intestinal bacteria forming compounds

that increase mucus production and water in the colon. This can result in vomiting and diarrhoea. Severe diarrhoea can be life threatening because it can eventually cause dehydration and fluids would be needed. Other clinical signs seen with aloe vera ingestion include depression, anorexia, irritation of large intestines, changes in urine colour, and rarely, tremors. Acute toxic properties of Aloes are mainly an excessive laxative effect, nephritis and discoloration of the urine.

TREATMENT(INANY)Very beneficial if used in safe limits.

COMMERCIALMANAGEMENTOFTOXINThe toxic substance aloin should be removed before consumption by the animal.

LD50Oral LD50 was >21.5 g/kg b.w. in rats and > 31.6 g/kg b.w. in mongrel dogs. For alone an LD50 of 260 mg/kg bw, an LD100 of 440 mg/kg bw and a maximum tolerated dose of 50 mg/kg bw were observed in mice after intramuscular administration

GRADEOFTOXICITYMild-moderate toxicity.

Naturalised widely in Australia, occurring in the temperate and tropical

regions. Frequently used topically and orally for dogs, cats and horses. The aloe vera leaf

extract or sap contains anthraquinone glycosides which are purgatives

(medications that encourage bowel movements). One such anthraquinone is

aloin, which is the toxic compound found in the exudate.

Scientific name: Aloe vera, Aloe barbadensis Family: Aloaceae

JADE PLANT

TOXICMECHANISMToxic principles are poorly understood but are known to contain toxic bufadienolides with

digitalis-like effects on the cardiovascular system (1). The primary effect is to inhibit sodium potassium ATPase pump, thereby decreasing the transportation of sodium and potassium across the cell membrane which decreases the cardiac function (1). They can cause depression and a slow heart rate in addition to a hard-to-identify symptom, depression (1).

In cats, ingestion of any part of the jade plant may cause vomiting, signs of impaired movement or loss of muscle control, and heart rate may slow (1). Animal may appear depressed, which is hard to detect in cats (1). Common symptoms include lack of grooming, lethargy, changes in personality, aggression, increased periods of sleeping and hiding or seeking isolated areas for long periods of time (1).

TREATMENT(INANY)Owner should not interfere and get it to the vet to administer IV fluids to prevent dehydration from vomiting and may induce vomiting to get the plant matter out of the cats system.

COMMERCIALMANAGEMENTOFTOXINThe safest option to prevent poisoning is to remove the plant or prevent ingestion by:

A= providing the animal with adequate fibre in diet that it doesn't ingest theseB=picking up the dropped leaves ; monitor cat if outdoors

LD50Information not available.

GRADEOFTOXICITYMild toxicity

C. ovata is native to South Africa where it grows on rocky hillsides under the blazing sun (1). It is a common ornamental plant worldwide as it is well know for its bonsai capabilities as they have very

slow growth. There are many varieties of this plant. These succulent leaf plants require little water in summer and are infarct susceptible to

overwatering.

Reference:1) Knight, Anthony P. 2006. A Guide To Poisonous House And Garden Plants. Jackson, WY: Teton NewMedia.

Scientific name: Crassula ovata Family: Crassulaceae

POTHOS

TOXICMECHANISMInsoluble raphides which are needle-shaped calcium oxalate crystals in their stems and leaves (1). When the plant tissue is chewed by the animals, the crystals are extruded into the mouth and mucus membranes of the unfortunate animal (1). The raphides once embedded in the mucus membranes of the mouth cause an intense oral irritation and inflammation of the mouth lips and tongue (1). Other clinical signs include choking and painful swallowing, excessive drooling, vomiting, difficulty breathing, and stomach upset. It can lead to renal failure and/or death (1).

TREATMENT(INANY)Unless salivation and vomiting are excessive, treatment is seldom necessary (1). Anti-inflammatory therapy may be necessary in cases where stomatitis is severe (1). The plants should be removed or made inaccessible to the animal eating them (1).

COMMERCIALMANAGEMENTOFTOXINThese species are frequently grown for their striking foliage and consequently, household pets have access to the plants (1).

LD50Information not available.

GRADEOFTOXICITYMildly harmful in small quantities but can produce uncomfortable and serous effects in animals and humans

The species is a popular house plant in temperate regions, but has become naturalised in tropical and sub-tropical forests worldwide. It is a

long-growing, leafy vine that can reach great heights in tropical jungles. They are the easiest

household plants and are very common ornamental plants in households. All parts of the

plant are poisonous if ingested

Reference:1) Knight, Anthony P. 2006. A Guide To Poisonous House And Garden Plants. Jackson, WY: Teton NewMedia.

Scientific name: Epipremnum pinnatum aureum Family: Araceae

CASTOR OIL PLANT

TOXICMECHANISMThe plant, especially its seeds contain the most poisonous substance known, ricin (3). The A-chain of cytotoxic protein internalises itself into the cell cytosol and blocks protein synthesis by irreversibly inactivating the 60S ribosomal subunit (3). The B-chain binds to the terminal galactose residues on the cell surface (3). The two peptide chains are joined by a disulphide bridge (3).After ingestion and hydrolysis action in the gut, the ~1% remnants of the protein are enough to cause severe damage to the tissue it first comes in contact with (3). Clinical signs which predominate include nausea, vomiting, bloody diarrhoea, dehydration and death (3). Ingestion of the leaves tend to cause neuromuscular disorders (5).

TREATMENT(INANY)Not available.

COMMERCIALMANAGEMENTOFTOXIN• Deaths are rare as the plant and seeds are unpalatable.• The seeds are the commercial source of castor oil.• Grazing should to avoided on pastures infested with castor oil plant and contaminated with

its seeds.• Use of herbicides can be an effective control measure for larger infestations. (1)

LD50The LD50 of ricin depends on how it enters the body, although not clearly determined, the LD50 after injection or inhalation values are much lower than ingestion (2).LD50 was found to lie between 2-8 µg/kg b.w. by IV injection of ricin into mice and 0.03-0.06 µg/kg b.w. in dogs (4). LD50 after oral ingestion is 1.3g/kg b.w. in swine, 0.9g/kg b.w. in rabbit and 0.1g/kg b.w. in horses (4). The least toxic route is oral uptake as it is about 1000 times less toxic than parental injection or inhalation (4).

GRADEOFTOXICITYHighly toxic but deaths are rare.

Native to Asia and Africa, it is a perennial flowering shrub with seeds that are poisonous to

all animals, including humans. Naturalised throughout Australia, it is now declared as a noxious weed in NSW, NT and WA (1). It can

spread quickly, overtaking prime grazing land and making it unfit for livestock.

Reference:1) Offord, Mellisa. 2006. Plants Poisonous To Horses.

Barton, ACT: RIRCD.2) R. C. Gupta. 2007. Veterinary Toxicology: Basic And

Clinical Principles. Academic Press.3) Gardner G. 2016. Veterinary toxicology lecture 6,

Murdoch university4) Worbs, Sylvia, Kernt Köhler, Diana Pauly, Marc-André

Avondet, Martin Schaer, Martin B. Dorner, and Brigitte G. Dorner. 2011. "Ricinus Communis Intoxications In Human And Veterinary Medicine—A Summary Of Real Cases". Toxins 3 (12): 1332-1372. doi:10.3390/toxins3101332.

5) https://www.business.qld.gov.au/industry/agriculture/species/non-declared-pests/weeds/castor-oil-bush

__________

Scientific name: Ricinus communis Family: Euphorbiaceae

BALLOON COTTON (MILKWEED)

TOXICMECHANISMCotton bush contains highly cardiotoxic glycosides. All parts of the plant release a milky

sap when damaged.The intact glycoside act as detergents and cause severe gastroenteritis (3). Cardiac

glycosides disrupt normal heart function by inhibiting an important enzyme called sodium potassium ATPase pump (1). Inhibition of the enzyme controlling sodium and potassium levels in cells leads to a build-up of potassium outside cells and build-up of sodium inside cells (1). This triggers a release of calcium into the cells (1). This high level of calcium in the cells of the heart can cause problems with normal conductivity of the myocardium and lead to heart failure (1). Other vascular signs include: arrhythmias, premature systole, conduction block (1). Signs of cardiac glycoside poisoning could include: lethargy and weakness, depression, diarrhoea, cold extremities, sweating, shortness of breath, coma, and death from heart failure (1). These glycosides have vagotonia effects, which result in bradycardia and cardiac arrest (2).

TREATMENT(INANY)There is no specific treatment available for cardiac glycoside poisoning but it is usually symptomatic and involves multi-dose activated charcoal and cathartic (2).

COMMERCIALMANAGEMENTOFTOXIN• Avoid grazing on pastures infested with cotton bush.• Avoid growing them as ornamental plants in areas where animals are kept.• Check hay for contamination.• Use of herbicides for effective control measure for larger infestations (1).

LD50A dosage of 0.5% b.w. would be fatal for horses and cattle (2).

GRADEOFTOXICITYHighly toxic.

Native to southern Africa and is naturalised in most states of Australia (1). They are important

noxious weeds in WA (1). Plants are usually unpalatable but mouthfuls of young seedling may be ingested accidental due to contamination of feedstuffs or even would be ingested if other

forage is scarce (3). Cattle will indiscriminately graze on them (3).

Reference: 1) Offord, Mellisa. 2006. Plants Poisonous To Horses.

Barton, ACT: RIRCD.2) R. C. Gupta. 2007. Veterinary Toxicology: Basic And

Clinical Principles. Academic Press.3) Gardner G. 2016. Veterinary toxicology lecture 6,

Murdoch university

Scientific name: Gomphocarpus physocarpus Family: Asclepiadaceae