Potential plant poisonings in dogs and cats in southern Africa

Review article — Oorsigartikel

Potential plant poisonings in dogs and cats in southern Africa

C J Bothaa* and M-L Penrithb,c

INTRODUCTIONPlant toxicoses occur worldwide, but

southern Africa’s rich and varied floraplaces the region high on the list of areaswhere stock losses due to plant poisoningare likely. Plant poisoning in farm animalscauses serious financial losses in SouthAfrica33. In contrast, there are fewer docu-mented cases of plant poisoning in dogsand cats in this region than in the Ameri-cas, Europe and Australia. The greatestmajority of plant poisonings in dogs andcats are the result of exposure to house orgarden plants, or to substances derivedfrom plants that are used for food or otherpurposes in the home. Most of the plantsinvolved are not indigenous to southernAfrica, but are widely grown in homesand gardens throughout the region. Dogsand cats are not normally plant eaters, butmight chew plants for various reasons, inparticular boredom when confined in theowner’s absence and curiosity or teething

in puppies. Some causes of plant poison-ing in pets, like onions, grapes and raisins,may be fed to them by owners who haveno idea that they could be harmful. Dogsand cats sometimes ingest plants appar-ently to induce emesis and these reactionsshould not be confused with poisoning57,but the possibility that the animal couldselect a poisonous plant for this purposeshould be borne in mind.

This paper does not present a completelist of the potentially poisonous plants towhich dogs and cats might be exposed,but a review of the more common or inter-esting plant intoxications occurring indogs and cats. Intoxications are groupedaccording to the target organs or systemsaffected. Cyanobacterial intoxications,mycotoxicoses and mushroom poisoningsare not included, and neither is mechanicaldamage and irritation caused by sharpseeds and awns. Therapeutic modalitiesare not discussed, because in the majorityof cases there are no specific remedies andthe treatment is supportive and symptom-atic. Managing cases of poisoning usuallyinvolves removal or binding of the toxin,for example by the use of an emetic ifindicated, or by oral administration ofactivated charcoal as a general adsorbentand supportive treatment to address theclinical signs. Since poisoning often results

in an emergency, rapid intervention maybe needed without confirming the diagno-sis first. However, submission of plantsamples for botanical confirmation isuseful in order to determine ongoingtreatment protocols and prognosis and tohelp owners to make the home a saferplace for their dogs and cats.

COMMON PLANT POISONINGS INDOGS AND CATS

Plant poisoning in dogs and cats hasbeen surveyed in veterinary practices,veterinary toxicological assistance services,poison information centres and animalwelfare organisations in North America,Europe and Australia. Because the majorityof ornamental garden and house plantshave a worldwide distribution regardlessof their area of origin, the more frequentcauses of intoxication of dogs and catsoccur in all the areas surveyed, and asimilar situation might be expected insouthern Africa.

Nervous system

• Melia azedarachSyringa berry tree, Chinaberry tree,Persian lilac, seringboomNative to Asia, the Syringa is a medium

to large, deciduous tree with dark greenfoliage and sprays of sweet-scented lilacflowers. The fruits are yellow drupes(Fig. 1) with a single ribbed stone.Syringas are widespread in all but themost arid parts of the country and occurboth as invaders and as cultivated orna-mental trees in gardens79. The principaltoxins are tetranortriterpene meliatoxinsA1, A2, B1, B2

28,32 that are present through-out the plant, but the highest concentra-tions occur in the ripe berries. Toxicity isdose-related and is also apparently influ-enced by environmental factors, withsome trees not being toxic at all28. Poison-ing usually follows ingestion of the fruitsand has been documented in a wide varietyof species (pigs, sheep, cattle, goats, rabbits,rats, guinea pigs, poultry and humans)28.Poisoning in monogastric animals has ahigh case fatality rate, but affected humansusually recover. Clinical signs generallydevelop within hours of ingestion of thefruits, and may be predominantly neuro-logical or gastrointestinal. Neurologicalsigns that have been described include

0038-2809 Jl S.Afr.vet.Ass. (2009) 80(2): 63–74 63

aDepartment of Paraclinical Sciences, Faculty of Veteri-nary Science, University of Pretoria, Private Bag X04,Onderstepoort, 0110 South Africa.

bTAD Scientific, 40 Thomson Street, Colbyn, 0083 SouthAfrica.

cDepartment of Veterinary Tropical Diseases, Faculty ofVeterinary Science, University of Pretoria, Private BagX04, Onderstepoort, 0110 South Africa.

*Author for correspondence:E-mail: [email protected]

Received: January 2009. Accepted: April 2009.

ABSTRACTPlant poisoning occurs less commonly in dogs and cats than in herbivorous livestock, butnumerous cases have been documented worldwide, most of them caused by common andinternationally widely cultivated ornamental garden and house plants. Few cases ofpoisoning of cats and dogs have been reported in southern Africa, but many of the plantsthat have caused poisoning in these species elsewhere are widely available in the subregionand are briefly reviewed in terms of toxic principles, toxicity, species affected, clinical signs,and prognosis. The list includes Melia azedarach (syringa), Brunfelsia spp. (yesterday, todayand tomorrow), Datura stramonium (jimsonweed, stinkblaar), a wide variety of lilies andlily-like plants, cycads, plants that contain soluble oxalates, plants containing cardiacglycosides and other cardiotoxins and euphorbias (Euphorbia pulcherrima, E. tirucalli).Poisoning by plant products such as macadamia nuts, onions and garlic, grapes and raisins,cannabis (marijuana, dagga) or hashish and castor oil seed or seedcake is also discussed.Many of the poisonings are not usually fatal, but others frequently result in death unlessrapid action is taken by the owner and the veterinarian, underlining the importance ofawareness of the poisonous potential of a number of familiar plants.

Keywords: cats, dogs, intoxications, poisoning, poisonous plants.

Botha C J, Penrith M-L Potential plant poisonings in dogs and cats in southern Africa. Jour-nal of the South African Veterinary Association (2009) 80(2): 63–74 (En.). Department ofParaclinical Sciences, Faculty of Veterinary Science, University of Pretoria, Private Bag X04,Onderstepoort, 0110 South Africa.

excitement or depression, ataxia, paresisand convulsions and the patient maylapse into a coma, while the principalgastrointestinal signs are anorexia, vomit-ing, diarrhoea, which may be bloody,and colic, although constipation has alsobeen described28. Signs indicative ofrespiratory and cardiac distress have alsobeen reported28 and respiratory arrest islikely to be the cause of death57. There islittle information about the pathologicallesions of Melia poisoning in dogs, butexperimentally poisoned pigs showedcongestion and necrosis of the gastric andintestinal mucosa macro- and microscopi-cally, and other histopathological changesdescribed were lymphoid necrosis, necrosisof skeletal muscle and moderate degener-ative changes in the liver and kidneys46.

• Cannabis sativaCannabis, Indian hemp, marijuana,hashish, daggaThe plant is an erect annual forb that

can grow to a height of several metres,with dark green palmately branchednarrow leaves with serrated edges andhairs (Fig. 2). The leaves and flowers aredried to produce marijuana or dagga,which is smoked, or sometimes eaten inbaked products, for its euphoric effect.Hashish refers to the dried resin from theflower tops10. The active substance is THC(delta-9-tetrahydrocannabinol), for whichthere is an unique receptor in the brain(CB1), and its effects are due to modifica-tion of the function of various neurotrans-mitters including dopamine, serotonin,acetylcholine, histamine, 5-hydroxy-tryptamine, opioid peptides, prosta-glandins and noradrenalin13,30,31. Toxicityis variable because the amount of THC inplants varies. Clinical signs in dogs in-duced by inhalation or ingestion of asmall amount of the drug have beendocumented, but it has been demonstratedthat the lethal dose in dogs is more than3 g and therefore cannabis poisoning indogs is rarely fatal30,54. Few instances ofintoxication in animals other than dogshave been reported; in a veterinarypractice survey that spanned 5 years inQueensland, 62 cases of cannabis poison-ing in dogs and only 1 in a cat were re-corded44. Dogs become intoxicated owingto wilful exposure to smoke or drug-lacedcookies by their owners, by ingestion ofmarijuana cigarette butts or, in 1 docu-mented case, cut green marijuana19. Clini-cal signs develop shortly after intake,usually within 1–3 hours. The predominantclinical signs may be neurological orgastrointestinal or a combination ofboth. In a survey of 213 dogs poisoned bycannabis, 99 % exhibited neurologicalsigns, while only 30 % developed gastro-

intestinal signs31. In this survey only10 dogs had ingested cookies containingcannabis, the other 203 having eaten eitherleaves or cigarettes. The most frequentclinical signs were depression (60 %),ataxia/incoordination (59 %), vomiting(25 %), tremor (18 %) and mydriasis(10 %), all other signs described byvarious authors such as hypersalivation,urinary incontinence, weakness, headpressing, disorientation, hyper-excitability,coma, an irregular pulse and hyper-thermia occurred in less than 10 % of theaffected dogs31. Snapping at the air hasbeen reported and is suggestive of hallu-cination30. Increased heart and respira-tory rates have been reported19, as well ason rare occasions convulsions10. The signsmay be mild and non-specific, makingdiagnosis difficult if a history of ingestionof cannabis is not provided. A 4-month-old Pekinese puppy that consumed half amarijuana cigarette became ataxic 45minutes later; the ataxia persisted for

6 hours, followed by sleepiness for18 hours, after which recovery was un-eventful11. A case of allergic inhalantdermatitis (canine atopy) in a dog livingin a house where the previous ownershad cultivated Cannabis sativa in- and outof doors has been reported17. Most animalsrecover within a period of 48–72 hoursand no specific serum chemistry changesor pathological lesions have been de-scribed. In the absence of a history ofexposure to cannabis, which may be con-cealed by the owner, THC can be detectedin plasma or urine in laboratories that areequipped to perform the test30.

• Macadamia integrifolia, M. tetraphyllaMacadamia nutsMacadamia nuts (Fig. 3) are produced

by trees of the genus Macadamia, whichwere introduced into South Africa fromAustralia and are cultivated in the warmernortheastern parts of the country. Thetoxic principle is unknown. While some

64 0038-2809 Tydskr.S.Afr.vet.Ver. (2009) 80(2): 63–74

Fig. 1: The yellow drupes of Melia azedarach.

Fig. 2: Cannabis sativa leaves with serrated edges.

varieties of macadamia nuts contain toxiclevels of cyanogenic glycosides, thesehave a bitter flavour and are not used asfood. Dogs are the only species in whichtoxicity has been reported, and the reactionappears to be consistent in dogs that haveeaten macadamia kernels, suggesting thatit is not due to allergy45. The dose requiredto induce toxicity has not been deter-mined accurately, but 5–40 kernels werecapable of inducing clinical signs in arange of dogs whose cases were reported45.Clinical signs develop within 12–24 hoursafter ingestion of the nuts and are charac-terised by posterior weakness, stiffnessor paresis and muscular tremors26,45,57.Swelling and pain in the hind limbs, in-cluding the joints, have been reported45,with elevated GGT, ALT and AST inanimals where these parameters weremeasured. These effects may be secondaryto the locomotor difficulties experiencedand were not reported in an experimentalstudy in which macadamia poisoningwas induced in 4 dogs27. Some dogs arehyperthermic26,27,45. Vomiting occurs insome dogs26,27, as well as abdominal painand mucosal pallor57. Clinical pathologywas within normal limits in the experi-mental study except for a transient in-crease in serum triglycerides27. Dogsusually recover uneventfully within 48hours or less57. No pathological lesions aredescribed. While macadamia poisoning isgenerally unusual, 83 cases were reportedin Queensland, Australia, over a period of5 years44; Queensland is a major area formacadamia cultivation and farm dogsmay have access to stores. Macadamia nutpoisoning has also been reported in theUnited States of America57.

Solanaceae

• Solanum spp. Brunfelsia spp.Poison apples, nightshade,yesterday, today and tomorrowMany species of Solanum contain

solanine, a glycoalkaloid that inducesboth neurological and gastrointestinaldisturbances. Poisoning of dogs and catsdue to ingestion of annual or perennialflowering Solanum species, which bearround berry-like fruits and are mostpoisonous when green, is reported to befairly common in the USA51. Typicalgastrointestinal signs are vomiting anddiarrhoea, but in 1 case traced back toconsumption of black nightshade berries(S. nigrum), the clinical signs noted were afoul, garlic-like breath and incontinencewhen asleep12.

Poisoning due to ingestion of Brunfelsia,a genus native to South America and theCaribbean, but widely used as an orna-mental shrub in gardens, has beenreported in Australia and North America,

mainly in dogs but also in cats35,43,44,65. It isan attractive erect shrub with bright greenshiny foliage and clusters of flowers thatchange from purple through mauve towhite, giving rise to the common name(Fig. 4). The fruits are considered to be themost poisonous part of the plant, but allparts have been able to induce intoxica-tion65. Brunfelsamidine, a convulsivesubstance, has been isolated from B.grandiflora78. Onset of clinical signs is rapidand diagnosis can usually be confirmedby the presence of the plant in the gastro-intestinal tract and/or vomitus and faeces65.Clinical signs described include salivation,oro-nasal irritation, choking and gagging,vomiting, foetid to haemorrhagic diar-rhoea, frequent urination, weakness,anxiety, depression, ataxia and seizures,sometimes prolonged and only able to becontrolled with general anaesthesia4,35,43,53,65.Most dogs recover if treated early. Theplant species may influence the severityof effects. The first known intoxicationwith B. calycina var. floribunda (= B. pauci-flora) involved the death of an 11-week-old Schipperke puppy within 2 hours ofdeveloping acute onset anxiety, persis-

tent sneezing, vomiting, generalisedmuscle tremors and pyrexia of 40.7 °C thatprogressed to severe disorientation, stag-gering, ataxia, proprioceptive deficits, lossof the righting reflex and seizures, culmi-nating in death. The seeds were found inloose stools passed during this period andtoxicity was confirmed in rats and mice69.Clinical pathological changes were associ-ated with dehydration, and no specificpathological lesions were observed in lab-oratory animals in which the intoxicationwas reproduced65,69 or in a puppy thatdied35. Moderate oedema and hyperae-mia of the terminal ileum was observed in2 dogs that were poisoned experimentallyand developed severe clinical signs andmild necrosis and desquamation of thevillous epithelium was observed micro-scopically in the dog that received thehigher dose43.

• Datura stramoniumJimsonweed, thorn apple, moonflower,stinkblaar, olieboomDatura stramonium, an annual weed

with large, dentate, foul-smelling leaves,tubular white or purple flowers and spiny

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Fig. 3: Macadamia nuts.

Fig. 4: A Brunfelsia species.


fruits that contain small pitted seeds, issometimes grown as an ornamental plant.The toxic principles are parasympatholyticalkaloids, atropine, hyoscine and hyo-scyamine32. Toxicity in animals is rare, butseveral cases in horses have been describedand were due to contaminated feed52. Afatal case occurred in a 1-year-old miniaturepoodle after clinical signs that lasted for2–3 hours. These were described asagitation, aggression, ambulatory delir-ium, tachycardia, tachypnoea, mydriasis,seizures and convulsions, progressing tocoma and death. At necropsy multipleorgans were severely congested, therewas acute lung oedema, and acute cardiacdilatation with multiple pericardial pete-chiae; histopathology revealed multifocalcentrilobular hepatic necrosis, renal tubulardegeneration, and widespread conges-tion and haemorrhages, including thecentral nervous system74. The pathologi-cal changes were considered to suggestan evolution towards hypotension, heartfailure, disseminated intravascular coag-ulation and multiple organ failure74. Acase of repeated anisocoria in a dog thatwas caused by contact with damagedplant material has been described25.

Gastrointestinal tract

Bulbs and bulb-like plants

• Ornithogalum spp.Chinkerinchee, star of Bethlehem,tjienkerintjeeChinkerinchees are bulbous plants of

the family Hyacinthaceae that produceheads consisting of star-shaped whiteflowers and are frequently used as orna-mental plants in gardens or in flowerarrangements or bouquets. There are anumber of species that have been identi-fied as toxic, with O. thyrsoides (Fig. 5) andO. saundersiae particularly incriminatedin cases of livestock poisoning in SouthAfrica32. Reports of natural cases of poison-ing due to ingestion of Ornithogalumby dogs are lacking, but 0.5 g of dried,pulverised bulbs of O. saundersiae provedfatal to dogs within 4 days32 and there isalso an account of experimental poisoningof a dog by O. amoenum in North Africathat resulted in haemorrhagic enteritis anddeath within 5–6 days18. The toxic princi-ple appears to be cholestane glycosides,isolated from South African species of thegenus32. The clinical signs produced in dogshave been severe haemorrhagic enteritis18.

Phenanthridine alkaloids are present inmany popular garden lilies (Narcissusnarcissus, jonquil, daffodil; Tulipa – tulip;Amaryllis – amaryllis, crinum; Hyacinthus– hyacinth) that can cause mild to severegastrointestinal signs depending on theamount ingested57. Besides the alkaloids

the plants also contain glycosides10: thealkaloids include narcissine, narciclasine,galanthamine and lycorine, of which thelast is present at the highest concentration;glycosides include scillitoxin. Calciumoxalate crystals are also present (daffodil).Poisoning is usually due to ingestion ofbulbs but can occur after eating flowersor drinking the water in which the cutflowers have stood. Clinical signs includevomiting, diarrhoea, abdominal tender-ness, anorexia, salivation, pyrexia, lethargyand mucosal pallor10; in severe cases ataxia,collapse, hypothermia, hypotension,bradycardia, severe abdominal pain,hyperglycaemia and dehydration may bepresent, and the affected animal maynot recover. Contact with sap can causepruritis and erythema. Post mortemchanges are non-specific, consisting ofevidence of severe gastroenteritis and

plant material in the intestine. A popularSouth African lily, Clivia miniata (clivia)(Fig. 6), contains phenanthridine alkaloids(lycorine, clivonine, clivatine, miniatine,hippeastrine) in the leaves, stems andbulbs and is widely used as a garden orhouse plant, but rarely causes poisoning36.

Irises (Iris spp.) contain irritant resins(irisin, iridin and irigenin) in the rhizomesthat can cause vomiting, diarrhoea andcolic, with congestion of the gastrointesti-nal tract, and sometimes also damage tothe liver and pancreas37.

Plant lectins

• Ricinus communisCastor oil plant, kasterolieboom

• Abrus precatoriusLucky bean tree, minnie-minnieThe castor oil plant is a cosmopolitan

Fig. 5: Ornithogalum thyrsoides.

Fig. 6: Flowers of Clivia miniata.

shrub or small tree with many grey-greento reddish branches bearing large palmateleaves. The spiny 3-lobed fruits contain 3hard shiny seeds that resemble engorgedticks (Fig. 7). The toxic principle, ricin, is atoxalbumin (lectin, glycoprotein) that ispresent in all parts of the plant, but theseeds contain the highest concentrationand are usually the source of natural casesof poisoning. Pure ricin is one of the mostlethal toxins known, but the oral LD100 inmice is 25 000 times lower than when thetoxin is administered parenterally32. Thelethal dose for dogs is 1–2 g castor seed/kgbody mass, which is equivalent to 0.03–0.04 mg ricin/kg39.

Absorption of ricin from the gut is rela-tively poor, although in spite of its proteinnature it can survive the action of proteo-lytic enzymes in sufficient quantities tocause toxicity. Once absorbed into cells, itsmode of action is to interrupt protein syn-thesis32. All species investigated are highlysusceptible to ricin poisoning. Althoughthe plant is a widespread invader, is alsocultivated for oil and has even beendescribed as an ornamental plant67, it isnot generally available to companionanimals. Toxicosis in dogs is rare andinevitably associated with ingestion ofthe seeds, which must be broken bymastication or other means for the toxinto become available. Most of the reportedcases resulted from ingestion of the beansthat were available in homes for variousreasons, including in decorative handi-craft2. The castor seed cake (containing3–5 % ricin) obtained in the process ofextracting castor oil is toxic unless heattreated and poisoning of dogs due toconsumption of the cake when used asfertiliser on garden or house plants hasbeen described39,67. A survey in the USAindicated that 76 % of dogs exposed tocastor beans developed clinical signs2,suggesting that in a percentage of dogsthe beans pass through intact and toxin isnot absorbed. When toxin is absorbedfrom the gut, clinical signs usually developwithin hours; the survey cited above foundan average time of 6 hours after ingestion,with a range of 0.5–42 hours2. The mostprominent clinical sign is vomiting,followed by depression and waterydiarrhoea, which frequently containsblood. Abdominal pain, anorexia andhaematemesis are reported in feweranimals, and 5–8 % of dogs surveyedshowed weakness, ataxia, hypersalivation,recumbency or tachycardia. Fewer than10 % of the dogs died or were euthanaseddue to poor prognosis. However, thisdepends on the amount of toxin absorbedand the length of time between ingestionand treatment. All of the dogs poisonedby consumption of castor seed cake ferti-

liser died as a result of circulatory collapseor hypovolaemic shock39,67. The mode ofaction of the toxin implies that many celltypes can be affected. Two fatal cases ofricin poisoning in dogs indicated thathepatic necrosis (both cases), cardiachaemorrhage and necrosis (1 case) andelevated blood urea (1 case) occurred inaddition to gastrointestinal lesions, aswell as macro- and microscopic lesions inlymphoid tissues50,67. Elevated hepato-cellular enzymes were the most consistentblood chemistry abnormality in dogsinvestigated2. Confirmation of the diag-nosis is usually based on a history ofconsumption of castor beans and theiridentification in gastrointestinal contentor faeces, but detection of ricinine ingastric content by liquid chromatogra-phy/mass spectrometry has been de-scribed50. Ricin is antigenic and immunitycan be induced by the repeated adminis-tration of small quantities32.

The seeds of Abrus precatorius (lovebean, lucky bean, minnie-minnie) (Fig. 8)also contain a toxalbumin, abrin, that hasbeen suspected in an outbreak of poison-ing in cattle in Limpopo Province, SouthAfrica32, but poisoning in dogs or cats hasnot been documented. The seeds are

much smaller than castor beans, with avery hard shell, and therefore unlikely tobe chewed.

Araceae

• Alocasia and Colocasia spp.Elephant’s ear

• Dieffenbachia spp.Dumb cane

• Philodendron spp.

• Monstera deliciosaDelicious monster

• Zantedeschia aethiopicaArum lily, varkoor (Fig. 9)The plants belonging to this family are

ornamental garden or house plants withattractive foliage and flowers. The stemsand the large, green or varicolouredsmooth leaves contain insoluble calciumoxalate monohydrate crystals or raphidesthat have a highly irritant effect on mucousmembranes32. The crystals are containedin specialised cells called idioblasts that,when ruptured, release the sharp spiculesformed by the crystals, which becomeembedded in the mucous membranes ofthe mouth, tongue and throat. Severeirritation results from physical damage by

0038-2809 Jl S.Afr.vet.Ass. (2009) 80(2): 63–74 67

Fig. 7: The ripe fruits and seeds of Ricinus communis.

Fig. 8: Pods and seeds of Abrus precatorius.

the sharp crystals and the release of plantproteolytic enzymes that provoke therelease of inflammatory mediators in-cluding histamines24,37,41,51. Probably allspecies are susceptible, but as these plantsare most often grown indoors, poisoninghas mainly been reported in humans,dogs and sometimes cats37. Clinical signsappear immediately to up to 2 hours afterexposure. Pain is indicated by headshaking, pawing and rubbing and some-times vocalisation; increased salivation,anorexia and depression may occur and,if large amounts have been ingested,vomiting and diarrhoea, usually mild butsometimes haemorrhagic, and abdominalpain may be present37,51,57. Gastrointestinalsigns were succeeded by debilitation,twitching and trembling, and rarelyopisthotonus was reported in animalsafter ingestion of Philodendron, and therewere indications that the toxin accumu-lated24. Swelling and oedema of the oralmucous membranes are often evidentand in a severe fatal case extensivemucosal necrosis with acute respiratorydistress was reported41. Most animals re-cover uneventfully with or without sup-portive treatment. For this reason,descriptions of pathology are scant andsuperficial, referring only to mucosal in-flammation and necrosis.

• Hedera spp.English ivyIvies are perennial creeping plants used

as climbers, ground cover and houseplants. The berries in particular containpentacyclic terpenoids that cause hyper-salivation, vomiting, abdominal pain anddiarrhoea. In most cases the clinical signsare mild, but severe manifestations mayoccur57.

• Lonicera spp.HoneysuckleHoneysuckle is a popular climbing

plant that bears sweet-scented cream andpink flowers. Ingestion of fruit can causemild gastrointestinal effects within 2 hoursdue to valerianic acid and xylostein, whichhave an irritant effect. Vomiting, diarrhoea,which may be bloody, depression, lethargy,and in 1 case convulsions, have beenreported10.

• Laburnum sppLaburnum, golden rainLaburnums are ornamental shrubs that

grow to a height of several metres, withsmall green leaves and pendulous racemesof bright yellow flowers. Pods, leaves andflowers have caused poisoning in dogsthat ingested them10. The toxic principle isa quinolizidine alkaloid, cytosine, that hasa similar mode of action to nicotine on

autonomic ganglia receptors. The principalclinical signs are salivation, vomitingand diarrhoea that commence soon afteringestion and vomiting may persist for1–2 days. In severe cases, which are veryrare, neurological signs including deliriumand convulsions may occur, followed byrespiratory paralysis and death. There areno specific pathological lesions apartfrom acute gastroenteritis10.

• Erythrophleum lasianthumSwazi ordeal treeThe Swazi ordeal tree (Fig. 10) is a

medium to large tree with pinnate leaves,dense spikes of cream or yellowish flowers,and flat brown seed pods; it is describedas poisonous55. It is found on sandy soil ina small area in northeastern South Africa,Swaziland and southern Mozambique.An unpublished account of suspectedpoisoning of a puppy by ingestion ofpods of the Swazi ordeal tree exists incorrespondence with the Department ofParaclinical Sciences, Faculty of VeterinaryScience, University of Pretoria. A 2-month-

old Yorkshire terrier puppy suddenlystarted vomiting and vomited continu-ously for an hour and a half. Anorexia andlethargy followed, as well as diarrhoea,although the owner believed that thismay have been induced by de-wormingas part of the symptomatic treatmentgiven by a veterinarian. Within 24 hoursthe dog was very weak, retching andhaving occasional convulsions, as wellas diarrhoea. Recovery was gradual, butappeared to be complete. About 3–4weeks later another episode of vomitingoccurred. Pods of the Swazi ordeal treewere observed in the vomitus and thedog recovered within a few hours, possi-bly because most of the toxic material waseliminated rapidly.

Liver

Cycads

• Encephalartos spp., Cycas revoluta,Macrozamia spp., Zamia spp.Cycad palms, broodboomCycads are palm-like plants with dark


Fig. 9: Zantedeschia aethiopica flower.

Fig. 10: Pod of Erythrophleum lasianthum (Swazi ordeal tree). (Courtesy of Geoff Nichols.)

green fronds that bear male and femalefruits, the latter somewhat resembling pinecones. A strictly protected genus indige-nous to southern Africa is Encephalartos55.Twelve of 28 species have been shown tobe toxic and all should be regarded aspotentially dangerous75. Exotic cycads(Fig. 11) are also widely grown in gardensor, in the young stages, as house plants.Most of 60 cases of cycad poisoning indogs in USA3 and the only case reportedin South Africa7 involved Cycas revoluta.Macrozamia sp. has caused poisoning ofdogs in Australia48, where a 5-year surveyindicated that cycad poisoning is relativelycommon in dogs and was also reported in1 cat44. Fatal poisoning of 2 dogs by Zamiafloridana has been described64. Any part ofthe plant can be toxic but the seeds appearto be the most toxic part; however, thecase described in South Africa involvedingestion of the stem7. One of the toxins,a glycoside, cycasin, is converted byβ-glucosidase to methylazoxymethanol,which is teratogenic, mutagenic andcarcinogenic, and causes hepatic damagewith gastrointestinal signs. Two othertoxins have been reported, an amino-acidβ-methylamino-L-alanine that experi-mentally causes ataxia in rats and anunidentified compound with a highmolecular weight that may cause axonaldegeneration and hind limb paralysis incattle3,57. A variety of species may beaffected, including humans. In a survey indogs in the United States of America , theonset of clinical signs occurred from15 minutes to 3 days after ingestion andlasted for 24 hours to 9 days. Dogs usuallydevelop gastrointestinal signs, with vom-iting, sometimes with haematemesis,being the most consistent. Other signsinclude depression, diarrhoea that maybe haemorrhagic and anorexia; neurolog-ical signs that include weakness, ataxia,proprioceptive deficits, coma or seizureshave been reported57, and occurred inmore than half of the 60 dogs surveyed inthe USA3. Elevated blood levels of alanineaminotransferase, bilirubin and alkalinephosphatase appear to be consistent3,7,51,57

and indicate damage to the liver. Alter-ations in white blood cell counts andthrombocytopaenia are probably indicativeof inflammation and compromised liverfunction. Elevated levels of ammonia andblood urea nitrogen (BUN) have also beenreported3,37. Pathological lesions describedin sheep were mostly in the liver andconsist of megalocytosis, nuclear hyper-chromasia, bile stasis, fatty change andfibrosis, while renal tubular necrosisappeared also to be a fairly consistentchange34. In the American survey, 67.7 %of dogs that were treated survived thepoisoning.

Kidney

Soluble oxalate-containing plantsNumerous plants contain soluble oxa-

lates, including common garden plantsand vegetables eg. Mesembryanthemaceae(mesems, vygies), Beta vulgaris (beetroot),Spinacia oleracea (spinach), Oxalis spp.,Parthenocissus quinquefolia (Virginiacreeper) (Fig. 12), Rheum spp. (rhubarb)and Opuntia spp. (prickly pear, turksvy).Soluble oxalate poisoning has beendescribed in several species of livestock32

but is relatively rare in dogs and cats37.Poisoning occurs when the absorbedoxalates bind serum calcium, resulting insystemic hypocalcaemia. Clinical mani-festations include muscle fasciculations,tetany, convulsions, cardiac arrhythmiaand nephrosis, which is indicated bypolyuria that may progress to anuria.Animals may be weak and lethargic, andshow generalised incoordination andsigns of abdominal distress37. Blood chem-istry reveals low calcium and elevatedammonia and BUN. The most prominenthistopathological lesions are severe

nephrosis with deposition of oxalate crys-tals in the kidney tubules, dilatation andnecrosis of tubules with hyaline and cellu-lar casts, and sometimes tubular regener-ation32.

Liliaceae

• Lilium, Hemerocallis spp.Day lilies, tiger lilies, Easter liliesThe genera Lilium and Hemerocallis

(Fig. 13) contain various species that arewidely used as house and garden orna-mental plants. They have large, attractiveopen tubular flowers with prominentstamens. A study has shown that toxicityis caused by soluble compounds in theaqueous fraction of leaves and flowers,but these have not yet been identified; theconcentration appears to be higher in theflowers than in the leaves63. Cats are theonly animals to which these plants areknown to be nephrotoxic; attempts toinduce the syndrome in rabbits and ratsfailed, and dogs are reported to developonly gastrointestinal signs23. Although it isrelatively unusual for cats to eat plants,

0038-2809 Jl S.Afr.vet.Ass. (2009) 80(2): 63–74 69

Fig 11: An exotic Cycas species.

Fig. 12: Berries of Parthenocissus quinquefolia (Virginia creeper).

there have been a large number of reportsof nephrotoxicity in cats due to ingestionof Liliaceae20,22,23,40,47,57,68,70,73. Consumptionof less than 1 leaf is capable of causing thesyndrome57,80. In a survey of 52 cats thathad eaten day lilies, 77 % showed gastro-intestinal signs of vomiting and hyper-salivation, 36 % developed neurologicalsigns (ataxia, depression, tremors andseizures), and 32 % progressed to acuterenal failure, which commenced 24–48hours after ingestion and was alwaysfatal22. Vomiting, anorexia and depres-sion may be observed within 2 hours afteringestion of the plant, but signs of renalfailure appear from 24 to 72 hours.Vomiting, anorexia and lethargy persist,polyuria develops and abdominal pain isusually present due to swelling andtenderness of the kidneys20. After about12 hours, polyuria and uraemia occur,with marked elevation of BUN and serumcreatinine, and the fact that creatinine isoften extremely high in comparison toBUN has been reported to be a uniquefeature of lily nephrotoxicosis73. Later,polyuria is succeeded by oliguria pro-gressing to anuria. Mortality is high,even when cats are treated; recovery maybe uneventful or may be incomplete andthe cat may eventually succumb tochronic kidney failure20. Pathologicalchanges at necropsy are most prominentin the kidney and consist of severe necrosisof the proximal convoluted tubules withthe basement membranes remainingintact, and interstitial oedema63,68,73. Theoccasional presence of birefringent crys-tals is probably the result of decreasedexcretion of oxalates73. Cytoplasmicvacuolation of exocrine pancreatic acinarcells and hepatic lipidosis were alsoobserved in experimentally poisonedcats63. Electron microscopic examinationindicated that the toxin targets mitochon-dria63.

Grapes and raisins

• Vitis sp.Grapes and raisins have frequently

been described as a cause of toxicity indogs9,16,21,42,49,56,76. The toxic principle is asyet unknown. Investigation of availablecases appears to rule out contamination ofthe grapes with pesticides, heavy metals ormycotoxins like Ochratoxin A49; factorslike the excessively high sugar content ofgrapes and raisins leading to hypercal-caemia and the possible involvement ofvaso-active substances, as well as possibleanaphylaxis, have been discussed49,56.Grape and raisin toxicity has only beendescribed in dogs. Toxicity appears to behighly variable. The amount consumed isoften not known, particularly if grapesare eaten off the vine, but dogs have been

seriously affected by amounts varyingfrom 2.8–36.4 g/kg body mass of raisinsand a few grapes to 19.6–148.4 g/kg bodymass16. Furthermore, not all dogs appearto be equally susceptible, although nobreed or age predisposition has beenidentified. Many dogs are reported tohave eaten grapes or raisins with no illeffects16, and in 1 reported case 1 of 3 dogswas so severely ill that the owner optedfor euthanasia, while 2 other, older dogsthat also ate grapes and grape residueswere unaffected76. Clinical signs havebeen reported to develop 12–72 hoursafter ingestion16. Vomiting was reportedin all cases9,16,21,42,49,56,76. Lethargy andanorexia have been reported in more than70 % of cases, diarrhoea and decreasedurine output in around 50 %, and abdom-inal pain, ataxia and weakness in a lowerpercentage16. Animals with oliguria oranuria are considered to have a poorprognosis. Hypercalcaemia, hyperphos-phataemia and elevated serum creatinineand BUN have been reported in mostcases for which data are available and aretypical of azotaemia16. The prognosis isguarded, particularly if the dog is alreadyin acute renal failure, but it can be improvedby aggressive therapy16,56. A bull terrierthat had consumed an entire punnet ofgrapes and was immediately submittedto the veterinarian for therapy did notdevelop clinical signs15, although withthe variability in development of the syn-drome it is impossible to know whethertoxicity would have occurred had the dognot been treated. Pathological lesionshave been described consistently as acuterenal tubular degeneration and necrosis,with cast formation; basal membranesremain intact and there is evidence ofregeneration in cases of longer dura-tion16,42,49. A golden intracytoplasmic pig-ment was present in a number of casessubmitted to detailed histopathological

examination, but its nature could not bedetermined histologically49.

Skin

Euphorbiaceae

• Euphorbia pulcherrimaPoinsettia

• E. tirucalliRubber euphorbia, hedge euphorbia,kraalnaboomPoinsettias are ornamental plants with

cream, pink to bright red bracts (Fig. 14) ofwhich there are many varieties that arewidely used as garden and house plants,and whose stems contain milky latex thatis severely irritating to the skin, mucousmembranes and gastrointestinal tract.The toxic principles in the latex of euphor-bias are diterpenoid esters that causeincreased salivation, vomiting, and rarelydiarrhoea10,57. They are sometimes regardedas irritant rather than toxic51. Neverthe-less, poisoning by poinsettias was themost frequently encountered phyto-toxicosis at an Italian toxicology assis-tance centre, and most often involvedcats1. Euphorbia tirucalli is a shrub or smallto medium-sized tree without spines andwith small cylindrical leaves that rapidlyfall off the slender, cylindrical branchesthat occurs in the eastern parts of southernAfrica79. It is used as a hedge and hascaused severe skin irritation and damageto cattle32 and could therefore potentiallyharm dogs forcing their way throughhedges as well.

Cardiovascular system

Cardiac glycosidesCardiac glycoside poisoning is very im-

portant in farm animals in South Africa32,but is rarely encountered in companionanimals. It is likely that more companionanimals experience the beneficial effectsof the digitalis glycosides that are used to


Fig. 13: A Hemerocallis species.

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manage congestive heart failure than arepoisoned by ingesting plants that containthem. However, a few ornamental gar-den plants contain cardenolide cardiacglycosides and can cause acute and rap-idly fatal cardiac glycoside poisoning57.The most commonly encountered are theornamental shrubs Nerium oleander (ole-ander, selonsroos) and Thevetia peruviana(yellow oleander) (Apocynaceae). Bothare tall woody shrubs with narrow darkgreen leaves and fragrant flowers, thoseof Nerium being white, pink or red, whileThevetia has yellow flowers with the tipsof the petals twisted to the right. Digitalispurpurea and D. lanata (foxglove) arewoody flowering perennials that bearclusters of purple or white flowers thatare sometimes cultivated in gardens.Convallaria majalis (lily of the valley) isalso sometimes grown, although morecommonly in the northern hemisphere.Kalanchoe, Cotyledon and Tylecodon spp.(plakkies) contain bufadienolides. Theseare succulent plants with attractive flowersand are popular as house and gardenplants. Cardiac glycosides inhibit thesodium-potassium adenosine triphos-phatase (Na-K pump), which results indisturbances of transmembrane iso-elec-trical gradients. Cardiovascular, gastro-intestinal, neurological and respiratoryeffects may be induced. In acute cardiacglycoside poisoning death is usually dueto cardiac and/or respiratory failure32. Thephysiopathology of chronic cardiacglycoside poisoning (krimpsiekte) inducedby plakkies is less well understood, andmay involve binding of the cumulativebufadienolides to nicotinic acetylcholinereceptors at the neuromuscular junction6.Toxicity is generally high, with smallamounts of plants ingested being able toinduce severe illness. Toxicity is almostinvariably caused by ingestion of plantparts, but secondary chronic cardiacglycoside poisoning has occurred in dogs(and humans) after eating the meat ofsheep and goats that have died ofkrimpsiekte32. Here, it is interesting to notethat there are anecdotal reports of second-ary monofluoroacetate poisoning in dogsafter ingesting part of the intestinal tractand its content of ruminants that havesuccumbed as result of gifblaar poisoning(Dichapetalum cymosum).

Clinical signs ascribed to cardiac glyco-sides develop soon after ingestion of thetoxic material, and death may be almostimmediate, or occur up to 2 days afterthe onset of clinical signs57. Clinical signsinclude cardiac arrhythmias, abdominalpain, anorexia, vomiting and diarrhoeaand terminal seizures51,57. It has been re-ported that male dogs are more likely todevelop clinical signs47. Dogs suffering

from krimpsiekte exhibit a stiff or high-stepping gait, with the head bent down-ward so that the muzzle points at thechest, slackness of the jaw with salivation,and, like other affected animals, tire easilyand become recumbent32. Serum chemis-try changes include hypoxaemia, hyper-carbia, hyperkalaemia and acidosis32.Death as a result of acute cardiac glycosidepoisoning is often too rapid for significantpathological lesions to develop, but ani-mals that survive for a day or 2 may showscattered foci of myocardial necrosis61.

• Rhododendron spp.Rhododendrons, azaleasSeveral genera of shrubs belonging to

the family Ericaceae are used as ornamen-tal plants or hedges. They are native to thenorthern hemisphere, but azaleas inparticular are widely used as ornamentalplants in southern Africa. They are flow-ering shrubs (Fig. 15) that grow well inacidic soils. Various plants of the family in-cluding azaleas contain diterpene resinsknown as grayanotoxins, which bind toreceptors of cell membrane sodiumchannels, blocking them and causing cellmembranes to remain in a state of depola-risation10,37,47. As may occur with cardiacglycosides, the poisoned animal willusually exhibit gastrointestinal, nervous,cardiac and respiratory signs. Death isusually due to the cardiovascular effects47.Vomiting is the most consistent clinicalsign57. Death of a cat within hours of pre-sumed ingestion of azalea plant materialhas been described62. Clinical pathologyand post mortem findings are non-specific10,57.

• Persea americanaAvocadoPoisoning by the Hass and Fuerte vari-

eties of avocado has been documented ina wide variety of animals, but only a single

suspected case has been reported indogs32. The toxic principle appears to bepersin, which has experimentally inducedcardiomyopathy in goats at higher dosesand mastitis at lower doses32. Two dogswith a reported fondness for Fuerteavocadoes, to which they had had freeaccess for less than a year, were presentedto the University Veterinary TeachingHospital in Nairobi, Kenya, with a historyof poor appetite, exercise intolerance,constipation, abdominal enlargementand dyspnoea8. One of the dogs was deadwhen presented, and the other wasemaciated, with signs of congestive heartfailure that included orthopnoea, ascites,pitting oedema of the hind limbs, a jugularpulse, muffled heart sounds and rales andgross cardiomegaly revealed by thoracicradiography. Serum levels of alanineaminotransferase, lactate dehydrogenaseand alkaline phosphatase were moderatelyelevated. Necropsy revealed anasarca ofthe hind limbs, ascites, lung oedema andfluid in the pericardial and pleural cavities.Microscopic changes consisted of multi-focal degeneration of myocardial fibreswith infiltration of mononuclear leuco-cytes.

• Taxus spp.YewYew is an evergreen shrub or tree com-

monly planted in gardens and church-yards and often used to form hedges inthe northern hemisphere, but is notcommonly encountered in southernAfrica. It contains cardiotoxic alkaloids,taxines, that depress conduction throughthe heart. Animals frequently die withoutdeveloping clinical signs, but these maybe delayed for up to 2 days and consist oftrembling, incoordination, diarrhoea andcollapse, with death due to acute cardiacarrest10,51.

Fig. 14: The bright red bracts of a poinsettia.


Haematopoietic system

• Allium cepa, A. sativumOnions, garlicOnions and garlic are common vegeta-

bles widely used in human food andtherefore available to household pets thatare fed table scraps or, more rarely, are fedmeals prepared for them at home insteadof commercial pet food. Garlic is evensometimes intentionally given to dogs asit is perceived to be a health supplement.There are many reported cases of haemo-lytic anaemia in dogs after eating eitherraw or cooked onions, and the toxicosishas been reproduced experimentally inboth dogs and cats38,60,72. Sodium n-pro-pylthiosulphate isolated from boiledonions has been demonstrated to causehaemolysis, which is apparently aggra-vated by the presence of 2 other com-pounds, sodium trans-1-propenylthio-sulphate and sodium cis-1-propenylthio-sulphate81. Further studies have indicatedthat sodium n-propylthiosulphate in-creases methaemoglobin concentrationand Heinz body count and decreases theconcentration of reduced glutathione inerythrocytes, while another compoundpresent in onions, n-propyl disulphide,causes a marked decrease in glucose-6-phosphate dehydrogenase (G6PD) ac-tivity72. Most of the cases reported in-volved ingestion of large amounts ofonions either as a single dose or over time.Toxicosis was experimentally induced insmall dogs at 30 g/kg body mass72.Haemolytic anaemia due to consumptionof onions or garlic has been reported inhorses, cattle, sheep, dogs and cats38,60.Haemoglobinuria developed within12 hours of ingestion in dogs experimen-tally fed pure onions72; other signs ob-served in experimental and field caseswere anorexia, lethargy, depression,weakness, pale mucous membranes,

abdominal pain, vomiting, diarrhoea orsoft faeces, tachycardia, tachypnoea, sei-zures, and splenic enlargement14,29,66,72,77.Changes in blood parameters indicativeof anaemia were evident within 24 hoursand included a decrease in haematocrit,increased reticulocyte count, increase inHeinz bodies (with a peak at day 3),anisocytosis, leptocytosis, poikilocytosis,displacement of methaemoglobin to oneside in erythrocytes and intravascularhaemolysis14,29,38,60,66,72. Serum chemistrywas generally normal apart from highlevels of serum bilirubin (both direct andtotal)72. Neutrophilia with left shift wasalso reported29. Most of the changespeaked at around Day 3 and then returnedto normal over a varying period of time.Recovery is usual and pathology has notbeen described.

• Cotoneaster spp., Pyracantha spp.Cotoneaster, firethornCotoneaster and firethorn are shrubs

that are used as ornamental bushes orhedges. They bear small dark greenleaves and bright orange or red berries.They are mildly poisonous, containingthe cyanogenic glycosides prunasin(which occurs in the bark, leaves, flowersand fruits) and amygdalin (in the fruits).Cyanide prevents cellular respiration bybinding to cytochrome oxidase; oxygen isnot released from haemoglobin and astate of acute cellular hypoxia results32.Additional clinical signs such as saliva-tion, vomiting, and diarrhoea, sometimesbloody and, in 1 case, hypothermia, havebeen reported after ingestion of cotoneasterand firethorn10, but the quantity wasapparently insufficient to cause mortality.The kernels of various stone fruits, mainlypeach and apricot, also contain cyanogenicglycosides in sufficient quantities to causefatal poisoning57, but poisoning is unusual,as the stones usually pass through the

gastrointestinal tract unbroken so that theseed is inaccessible.

DISCUSSIONSurveys from various countries show

that, in comparison with other poisons,plant poisoning of dogs and cats is un-common. In 2 surveys in North America,involving 2199 calls to poison controlcentres in 1978 and 41 854 calls in1990, plant poisoning in dogs and catsaccounted for 11.6 % and 12.1 % of thecalls respectively51. In a survey in WesternAustralia, 7.6 % of poisonings in 158 dogsand 2.8 % of 36 cats presented to anacademic veterinary hospital over a periodof 12 years were due to plants59. During aprospective survey of 138 veterinarypractices in Western Australia over an18-month period, 231 cases of poisoningof dogs and 32 of cats were reported, butthe incidence of plant poisonings wasextremely low; none of the cats was poi-soned by plants, and only 1.3 % of dogsamong rural practices and 0.9 % at urbanpractices58. Among 965 cases of poisoningin dogs and cats reported in Melbourne,in eastern Australia, over a 12-year period(1971–1983), none were attributed toplants71. Finally, a survey by a poisonreporting centre at the University ofTurin, Italy, which receives calls fromall over Italy, reported that of 4297 callsrelating to poisoning in dogs and cats inthe first 7 years of operation, 5 % involvedplant poisoning in dogs and 11 % in cats,plant poisonings in the 2 species being thesubject of 6.1 % of the calls; a further 0.6 %of calls related to hashish and cannabispoisoning in dogs1. In all the surveyschemical poisoning with pesticides anddrugs accounted for by far the greatestnumber of cases, so that these substancespose a far higher risk than plants, espe-cially to dogs, which are more likely to bepoisoned owing to their more omnivoroushabits. In all the surveys where a distinc-tion was made between the 2 species, themajority of cases were reported in dogs.The overwhelming majority of plantpoisonings in dogs and cats are caused byingestion of plants24, with only occasionalreports of contact poisoning.

Plants containing calcium oxalateraphides emerge as the most frequentcause of poisoning of dogs and cats in theAmerican surveys that give an indicationof frequency24,51, followed by plants withcardiac effects and nightshades (Sola-naceae)51. In contrast, Araceae accountedfor only a small percentage of plantpoisonings in Western Australia44, wherepoisoning by macadamia nuts headedthe list, followed by cannabis, Brunfelsia,onion, and cycad seeds. In the Italiansurvey house plants were the main causes

Fig. 15: An azalea (Rhododendron species).

0038-2809 Jl S.Afr.vet.Ass. (2009) 80(2): 63–74 73

of phytotoxicity, with Euphorbia pulcherrimaand Ficus spp. predominating. In an over-view of serious plant toxicoses reportedto a control centre in the USA, the mostfrequently reported involved Liliaceae,azaleas, plants containing cardiac glyco-sides (Nerium oleander and Kalanchoe),cycads, castor beans and autumn crocus(Colchicum autumnale)47. The autumncrocus is cardiotoxic, but is not commonlyencountered in southern Africa and istherefore not included in the review.

The majority of plant poisonings indogs and cats do not have a high mortalityrate, particularly if treatment is initiatedearly. Exceptions are nephrotoxicity incats caused by members of the Liliaceae,toxicity caused by Melia azedarach, phyto-toxicoses that affect cardiac function, andtoxicity caused by high intake of ricin (forexample as seed cake), cycad seeds andBrunfelsia. Poisoning with onions andgrapes and raisins is also potentially lethal44.Some of the rarer toxicoses, like ingestionof Datura, also appear to be highly fatal74.On the other hand, poisoning with maca-damia nuts, cannabis and insoluble calciumoxalates usually results in spontaneousrecovery and these toxicoses are listed asnon-life-threatening by McKenzie44. Theprognosis always depends upon earlydetection of illness by the owners, includ-ing a history of ingestion of potentiallypoisonous plants or their derivatives, andaggressive treatment. Owner awarenessis important, and it is useful for cliniciansto make the necessary information avail-able to their clients.

Not all of the plants are invariably poi-sonous. Toxicity is often dependent onthe variety, part, growth stage or condi-tion of the plant; for example, Melia azeda-rach may not be toxic when growingunder marginal conditions28. This seemslikely, as a dog belonging to 1 of theauthors (MLP) frequently ate syringaberries (as well as avocadoes and grapes)with impunity in a garden in Windhoek,Namibia, which must be close to the limitof the tree’s tolerance for aridity. There isalso apparent variability in individualsusceptibility. This has been noted in thecase of grapes and raisins, as well asonions16,29. Both species are susceptible topoisoning by most of the plants listed,although lilies apparently cause nephro-toxicity only in cats. A number of the poi-sonings have only been reported in dogs,probably owing to the level of exposureand the more fastidious eating habits ofcats. Poisoning by syringa berries, maca-damia nuts, grapes and raisins, ricin andcycad seeds has apparently not beendocumented in cats.

It has been suggested that plant poison-ing can often be prevented, for example

by removal of poisonous parts such ascycad seeds and Brunfelsia fruits, and thatcreating awareness by providing informa-tion in veterinary practices and nurserieswould help owners to protect their petsfrom plant poisoning44.

One plant, catnip (Nepeta cataria), iseagerly eaten by cats and appears to havea beneficial effect, since genetically pre-disposed cats are reported to become ‘ec-static’ after intake, without any ill effectsfollowing the ‘trip’5. Since 70 % of plantpoisonings in cats in Italy were caused byhouse plants, it might be advisable to pro-vide catnip as an acceptable alternative ifcats are to be left alone in an environmentthat includes potentially toxic plants.

CONCLUSIONSAlthough plant poisoning of cats and

dogs is not as common as intoxication ofherbivorous livestock, many cases ofpoisoning, some with a fatal outcome,have been reported, and it is importantfor both veterinarians and pet owners tobe aware of potentially dangerous plantsand their derivatives. Lives are saved bythe prompt action of owners and veteri-narians when a cat or dog has ingested apoisonous plant. Clinical signs are oftennon-specific and the exposure may nothave been observed, but chewed plantsand/or remnants of plants in vomitus orstools can be an indicator that a plantpoisoning is involved.

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Potential plant poisonings in dogs and cats in southern Africa