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= plant poisonings in dogs and cats = Plant toxicoses occur worldwide, but southern Africa’s rich and varied flora places the region high on the list of areas where stock losses due to plant poisoning are likely. Plant poisoning in farm animals causes serious financial losses in South Africa33. In contrast, there are fewer documented cases of plant poisoning in dogs and cats in this region than in the Americas, Europe and Australia. The greatest majority of plant poisonings in dogs and cats are the result of exposure to house or garden plants, or to substances derived from plants that are used for food or other purposes in the home. Most of the plants involved are not indigenous to southern Africa, but are widely grown in homes and gardens throughout the region. Dogs and cats are not normally plant eaters, but might chew plants for various reasons, in particular boredom when confined in the owner’s absence and curiosity or teething in puppies. Some causes of plant poisoning in pets, like onions, grapes and raisins, may be fed to them by owners who have no idea that they could be harmful. Dogs and cats sometimes ingest plants apparently to induce emesis and these reactions should not be confused with poisoning57, but the possibility that the animal could select a poisonous plant for this purpose should be borne in mind. This paper does not present a complete list of the potentially poisonous plants to which dogs and cats might be exposed, but a review of the more common or interesting plant intoxications occurring in dogs and cats. Intoxications are grouped according to the target organs or systems affected. Cyanobacterial intoxications, mycotoxicoses and mushroom poisonings are not included, and neither is mechanical damage and irritation caused by sharp seeds and awns. Therapeutic modalities are not discussed, because in the majority of cases there are no specific remedies and the treatment is supportive and symptomatic. Managing cases of poisoning usually involves removal or binding of the toxin, for example by the use of an emetic if indicated, or by oral administration of activated charcoal as a general adsorbent and supportive treatment to address the clinical signs. Since poisoning often results in an emergency, rapid intervention may be needed without confirming the diagnosis first. However, submission of plant samples for botanical confirmation is useful in order to determine ongoing treatment protocols and prognosis and to help owners to make the home a safer place for their dogs and cats.

• common plant poisonings in dogs and cats
occur in all the areas surveyed, and a similar situation might be expected in southern Africa.

Nervous system • Melia azedarach Syringa berry tree, Chinaberry tree, Persian lilac, seringboom Native to Asia, the Syringa is a medium to a large, deciduous tree with dark green foliage and sprays of sweet-scented lilac flowers. The fruits are yellow drupes (Fig. 1) with a single ribbed stone. Syringas is widespread in all but the aridest parts of the country and occur both as invaders and as cultivated ornamental trees in gardens79. The principal toxins are tetranortriterpenoid meliatoxins A1, A2, B1, B2 28,32 that are present throughout the plant, but the highest concentrations occur in the ripe berries. Toxicity is dose-related and is also apparently influenced by environmental factors, with some trees not being toxic at all28. Poisoning usually follows ingestion of the fruits and has been documented in a wide variety of species (pigs, sheep, cattle, goats, rabbits, rats, guinea pigs, poultry and humans)28.

. Clinical signs generally develop within hours of ingestion of the fruits and may be predominantly neurological or gastrointestinal. Neurological signs that have been described include excitement or depression, ataxia, paresis and convulsions, and the patient may lapse into a coma, while the principal gastrointestinal signs are anorexia, vomiting, diarrhea, which may be bloody, and colic, although constipation has also been described28. Signs indicative of respiratory and cardiac distress have also been reported28 and respiratory arrest is likely to be the cause of death57. and other histopathological changes described were lymphoid necrosis, necrosis of skeletal muscle and moderate degenerative changes in the liver and kidneys46.

• Cannabis sativa Cannabis, Indian hemp
marijuana, hashish, dagga The plant is an erect annual forb that can grow to a height of several meters, with dark green palmately branched narrow leaves with serrated edges and hairs (Fig. 2). The leaves and flowers are dried to produce marijuana or dagga, which is smoked, or sometimes eaten in baked products, for its euphoric effect. The active substance is THC (delta-9-tetrahydrocannabinol), for which there is a unique receptor in the brain (CB1), and its effects are due to modification of the function of various neurotransmitters including dopamine, serotonin, acetylcholine, histamine, 5-hydroxytryptamine, opioid peptides, prostaglandins, and noradrenalin13,30,31. Toxicity is variable because the amount of THC in plants varies.

Clinical signs in dogs induced by inhalation or ingestion of a small amount of the drug have been documented, but it has been demonstrated that the lethal dose in dogs is more than 3 g and therefore cannabis poisoning in dogs is rarely fatal30,54. Few instances of intoxication in animals other than dogs have been reported; in a veterinary practice survey that spanned 5 years in Queensland, 62 cases of cannabis poisoning in dogs and only 1 in a cat were recorded44. Dogs become intoxicated owing to wilful exposure to smoke or drug-laced cookies by their owners, by ingestion of marijuana cigarette butts or, in 1 documented case, cut green marijuana19. Clinical signs develop shortly after intake, usually within 1–3 hours. The predominant clinical signs may be neurological or gastrointestinal or a combination of both. In a survey of 213 dogs poisoned by cannabis, 99 % exhibited neurological signs, while only 30 % developed gastrointestinal signs31. In this survey only 10 dogs had ingested cookies containing cannabis, the other 203 having eaten either leaves or cigarettes. The most frequent clinical signs were depression (60 %), ataxia/incoordination (59 %), vomiting (25 %), tremor (18 %) and mydriasis (10 %), all other signs described by various authors such as hypersalivation, urinary incontinence, weakness, head pressing, disorientation, hyper-excitability, coma, an irregular pulse and hyperthermia occurred in less than 10 % of the affected dogs31. Snapping at the air has been reported and is suggestive of hallucination30. Increased heart and respiratory rates have been reported19, as well as on rare occasions convulsions10. The signs may be mild and non-specific, making diagnosis difficult if a history of ingestion of cannabis is not provided. A 4-month old Pekinese puppy that consumed half a marijuana cigarette became ataxic 45 minutes later; the ataxia persisted for 6 hours, followed by sleepiness for 18 hours, after which recovery was uneventful11. A case of allergic inhalant dermatitis (canine atopy) in a dog living in a house where the previous owners had cultivated Cannabis sativa in- and out of doors has been reported17. In the absence of a history of exposure to cannabis, which may be concealed by the owner, THC can be detected in plasma or urine in laboratories that are equipped to perform the test30.

• Macadamia integrifolia, M. tetraphylla
Macadamia nuts Macadamia nuts (Fig. 3) are produced by trees of the genus Macadamia, which were introduced into South Africa from Australia and are cultivated in the warmer northeastern parts of the country. The toxic principle is unknown. dogs are the only species in which toxicity has been reported, and the reaction appears to be consistent in dogs that have eaten macadamia kernels, suggesting that it is not due to allergy45. The dose required to induce toxicity has not been determined accurately, but 5–40 kernels were capable of inducing clinical signs in a range of dogs whose cases were reported45. Clinical signs develop within 12–24 hours after ingestion of the nuts and are characterised by posterior weakness, stiffness or paresis and muscular tremors26,45,57. Swelling and pain in the hind limbs, including the joints, have been reported45, with elevated GGT, ALT and AST in animals where these parameters were measured. These effects may be secondary to the locomotor difficulties experienced and were not reported in an experimental study in which macadamia poisoning was induced in 4 dogs27. Some dogs are hyperthermic26,27,45. Vomiting occurs in some dogs26,27, as well as abdominal pain and mucosal pallor57. Clinical pathology was within normal limits in the experimental study except for a transient increase in serum triglycerides27. Dogs usually recover uneventfully within 48 hours or less57. No pathological lesions are described. While macadamia poisoning is generally unusual, 83 cases were reported in Queensland, Australia, over a period of 5 years44; Queensland is a major area for macadamia cultivation and farm dogs may have access to stores. Macadamia nut poisoning has also been reported in the United States of America57.

• Solanaceae - Solanum spp. Brunfelsia spp.
Poison apples, nightshade, yesterday, today and tomorrow Many species of Solanum contain solanine, a glycoalkaloid that induces both neurological and gastrointestinal disturbances. Poisoning of dogs and cats due to ingestion of annual or perennial flowering Solanum species, which bear round berry-like fruits and are most poisonous when green, is reported to be fairly common in the USA51. Typical gastrointestinal signs are vomiting and diarrhoea, but in 1 case traced back to consumption of black nightshade berries (S. nigrum), the clinical signs noted were a foul, garlic-like breath and incontinence when asleep12. Poisoning due to ingestion of Brunfelsia, a genus native to South America and the Caribbean, but widely used as an ornamental shrub in gardens, has been reported in Australia and North America, mainly in dogs but also in cats35,43,44,65.

The fruits are considered to be the most poisonous part of the plant, but all parts have been able to induce intoxication65. Brunfelsamidine, a convulsive substance, has been isolated from B. grandiflora78. Onset of clinical signs is rapid and diagnosis can usually be confirmed by the presence of the plant in the gastrointestinal tract and/or vomitus and faeces65. Clinical signs described include salivation, oro-nasal irritation, choking and gagging, vomiting, foetid to haemorrhagic diarrhoea, frequent urination, weakness, anxiety, depression, ataxia and seizures, sometimes prolonged and only able to be controlled with general anaesthesia4,35,43,53,65. Most dogs recover if treated early. The first known intoxication with B. calycina var. floribunda (= B. pauciflora) involved the death of an 11-weekold Schipperke puppy within 2 hours of developing acute onset anxiety, persistent sneezing, vomiting, generalised muscle tremors and pyrexia of 40.7 °C that progressed to severe disorientation, staggering, ataxia, proprioceptive deficits, loss of the righting reflex and seizures, culminating in death. The seeds were found in loose stools passed during this period and toxicity was confirmed in rats and mice69. Clinical pathological changes were associated with dehydration, and no specific pathological lesions were observed in laboratory animals in which the intoxication was reproduced65,69 or in a puppy that died35. Moderate oedema and hyperaemia of the terminal ileum was observed in 2 dogs that were poisoned experimentally and developed severe clinical signs and mild necrosis and desquamation of the villous epithelium was observed microscopically in the dog that received the higher dose43.

• Datura stramonium Jimsonweed
thorn apple, moonflower, stinkbait, olieboom  Datura stramonium, an annual weed with large, dentate, foul-smelling leaves, tubular white or purple flowers and spiny fruits that contain small pitted seeds, is sometimes grown as an ornamental plant. The toxic principles are parasympatholytic alkaloids, atropine, hyoscine, and hyoscyamine32.

These were described as agitation, aggression, ambulatory delirium, tachycardia, tachypnoea, mydriasis, seizures, and convulsions, progressing to coma and death. At necropsy multiple organs were severely congested, there was acute lung edema, and acute cardiac dilatation with multiple pericardial petechiae; histopathology revealed multifocal centrilobular hepatic necrosis, renal tubular degeneration, and widespread congestion and hemorrhages, including the central nervous system74. The pathological changes were considered to suggest an evolution towards hypotension, heart failure, disseminated intravascular coagulation, and multiple organ failure74. A case of repeated anisocoria in a dog that was caused by contact with damaged plant material has been described25.

Bulbs and bulblike plants • Ornithogalum spp.
Chinkerinchee, star of Bethlehem, tjienkerintjee Chinkerinchees are bulbous plants of the family Hyacinthaceae that produce heads consisting of star-shaped white flowers and are frequently used as ornamental plants in gardens or in flower arrangements or bouquets. There are a number of species that have been identified as toxic, with O. thyrsoides (Fig. 5) and O. saundersiae particularly incriminated in cases of livestock poisoning in South Africa32. Reports of natural cases of poisoning due to ingestion of Ornithogalum by dogs are lacking, but 0.5 g of dried, pulverized bulbs of O. ammonium in North Africa that resulted in hemorrhagic enteritis and death within 5–6 days18. The clinical signs produced in dogs have been severe hemorrhagic enteritis18. Phenanthridine alkaloids are present in many popular garden lilies (Narcissus narcissus, jonquil, daffodil; Tulipa – tulip; Amaryllis – amaryllis, crinum; Hyacinthus – hyacinth) that can cause mild to severe gastrointestinal signs depending on the amount ingested57. Besides the alkaloids, the plants also contain glycosides10: the alkaloids include narcissine, narciclasine, galanthamine, and lycorine, of which the last is present at the highest concentration; glycosides include scaritoxin. Calcium oxalate crystals are also present (daffodil). Poisoning is usually due to ingestion of bulbs but can occur after eating flowers or drinking the water in which the cut flowers have stood. Clinical signs include vomiting, diarrhea, abdominal tenderness, anorexia, salivation, pyrexia, lethargy, and mucosal pallor10; in severe cases, ataxia, collapse, hypothermia, hypotension, bradycardia, severe abdominal pain, hyperglycemia, and dehydration may. Post mortem changes are non-specific, consisting of evidence of severe gastroenteritis and plant material in the intestine. contains phenanthridine alkaloids (lycorine, cloning, climate, miniature, Hippeastrum) in the leaves, stems, and bulbs and is widely used as a garden or house plant, but rarely causes poisoning36. Irises (Iris spp.) contain irritant resins (irisin, iridin, and irigenin) in the rhizomes that can cause vomiting, diarrhea, and colic, with congestion of the gastrointestinal tract, and sometimes also damage to the liver and pancreas37.

• Abrus precatorius Lucky bean tree, Minnie
The castor oil plant is a cosmopolitan shrub or small tree with many grey-green to reddish branches bearing large palmate leaves. (Fig. 7). Pure ricin is one of the most lethal toxins known, but the oral LD100 in mice is 25 000 times lower than when the toxin is administered parenterally32. The lethal dose for dogs is 1–2 g castor seed/kg body mass, which is equivalent to 0.03– 0.04 mg ricin/kg39. Absorption of ricin from the gut is relatively poor, although in spite of its protein nature it can survive the action of proteolytic enzymes in sufficient quantities to cause toxicity. Once absorbed into cells, its mode of action is to interrupt protein synthesis32.

Toxicosis in dogs is rare and inevitably associated with ingestion of the seeds, which must be broken by mastication or other means for the toxin to become available. Most of the reported cases resulted from ingestion of the beans that were available in homes for various reasons, including in decorative handicraft2. the cake when used as fertilizer on garden or house plants has been described39,67. A survey in the USA indicated that 76 % of dogs exposed to castor beans developed clinical signs2, suggesting that in a percentage of dogs the beans pass through intact and the toxin is not absorbed. When the toxin is absorbed from the gut, clinical signs usually develop within hours; the survey cited above found an average time of 6 hours after ingestion, with a range of 0.5–42 hours2. The most prominent clinical sign is vomiting, followed by depression and watery diarrhea, which frequently contains blood. Fewer than 10 % of the dogs died or were euthanized due to poor prognosis. However, this depends on the amount of toxin absorbed and the length of time between ingestion and treatment. All of the dogs poisoned by consumption of castor seed cake fertilizer died as a result of the circulatory collapse or hypovolaemic shock39,67. The mode of action of the toxin implies that many cell types can be affected. Two fatal cases of ricin poisoning in dogs indicated that hepatic necrosis (both cases), cardiac hemorrhage and necrosis (1 case) and elevated blood urea (1 case) occurred in addition to gastrointestinal lesions, as well as macro- and microscopic lesions in lymphoid tissues50,67. Elevated hepatocellular enzymes were the most consistent blood chemistry abnormality in dogs investigated2. Confirmation of the diagnosis is usually based on a history of consumption of castor beans and their identification in gastrointestinal content or feces, but detection of ricinine in gastric content by liquid chromatography/mass spectrometry has been described50. Ricin is antigenic and immunity can be induced by the repeated administration of small quantities32. The seeds are much smaller than castor beans, with a very hard shell, and therefore unlikely to be chewed.