plants Flashcards
what is this?
TRUE LILLIES
* Lilium spp., Hemerocallis spp
-only toxic to CATS
-parts of the plant: ENTIRE PLANT TOXIC
-cats become exposed via chewing leaves, petals, drinking vase water or rubbing agaisnt pollen
true lillies mech/ target organ
- Toxin + mechanism: unknown
- Toxicity: any ingestion or exposure is clinically significant to cats
- Target organ: kidneys*
true lillies clinical features
- Onset: within a few hours post-exposure
- Earliest clinical sign: vomiting, hypersalivation, anorexia
- Vomiting subsides → cat may appear depressed or anorexic
- May appear to recover
- 24-72 hours post-exposure: rapid deterioration → development of oliguric to anuric renal failure
- PU/PD → oliguria and anuria, uremia
- Anorexia, depression, vomiting resumes
- Abdominal palpation: enlarged, painful kidneys
- Death or euthanasia within 3-6 day
true lillies clinical path signs / PM/ histo
- Clinical pathology: indicative of acute kidney injury
- Within 12 hours: azotemia, ↑ Ca and P
- Within 24 hours: tubular casts, proteinuria, glucosuria, isosthenuria
- PM: swollen and congested kidneys, peri-renal
hemorrhage and edema - Histo: proximal tubular degeneration and necrosis
true lillies management
- Decontamination: emesis, A/C if not contraindicated
- Check vomitus for lily parts
- IVFT ASAP → 48 hours
- Urinary catheter – monitor urine output
- Dermal decontamination: Remove pollen from fur/muzzle
- Frequent monitoring of chem panel, UA, and urinary output
- If anuria develops: dialysis or euthanasia
true littie toxicity diagnosis/ DDX/ prognosis
- Diagnosis: lilies present in same house as a cat,
presence of pollen on muzzle, evidence of chewing on plant, plant parts in vomitus, compatible clinical signs - DDx: ethylene glycol poisoning, vitamin D, NSAIDs, aminoglycosides
- Prognosis:
- Fluids before anuric renal failure: good
- Delayed treatment and/or anuric renal failure: poor
- 50-100% fatality rates reported
- No treatment: grave
what plants?
1 milkweed
2 lily of the valley
3 (top R) foxglove
4 bottom R OLANDER
C A R D I A C G L Y C O S I D E S navle Q
- Foxglove (Digitalis purpurea)
- Lily of the Valley (Convallaria majalis)
- Oleander (Nerium oleander, incl.yellow oleader – Thevetia peruviana)
- Milkweed (Asclepias spp.)
- Kalanchoe spp
- Most common in animals: oleander***
- All species susceptible***
- Exposure scenarios: clippings, fallen leaves, hay contamination, access to garden
cardiac glycosides mechanism + toxicity
- Cardenolide group of cardiotoxins**
- Mechanism of action: inhibition of NaKATPase → ↑ Ca2+ availability
- ↑ Ca2+: dysrhythmias
- Increased vagal tone → bradycardia
- Toxicity: a few leaves or seeds can be fatal
- Horses + oleander: 10-20 leaves
- Dried plants remain toxic
cardiac glycosides clinical features
- Onset: within 30 minutes to hours of ingestion
- Lethargic, dull, signs of discomfort (bruxism, grunting)
- Gastrointestinal: nausea, vomiting, abdominal pain, diarrhea (± blood)
- Ruminant: atony, bloat
- Horse: colic
CV: bradycardia, AV fibrilation
cold extremities, sweating, dyspena
CNS: tremors, ataxia, mydrasis
sudden death with exertion
PM: cardiomyopathy and necrosis
cardiac glycoside management
- Decontamination if not contraindicated
- Antidote: anti-digoxin Fab antibody fragment**
- Supportive care: IVFT, anti-arrhythmic drugs
- Atropine (bradycardia), lidocaine (tachyarrhythmias)
- Hyperkalemia: insulin/dextrose
- Close monitoring of ECG/BP, oxygenation, bloodwork
- Diagnosis: cardiotoxic plants accessible to pets/livestock, presence of plants in vomitus/stomach
contents/rumen contents - Detection of cardiotoxins in tissues/serum – example: oleandrin
what plant?
YEW
* All parts toxic, except fruit (“aril”)
* Fresh or dried, on plant or clippings
* Toxic year-round
* Most poisonings are in livestock
YEW mechanism _ toxicity
- Toxins: taxine alkaloids (taxine A + B)
- Target: heart**
- Mechanism of action: inhibit sodium and calcium exchange in the myocardium
- Decreased electrical conduction → acute heart failure
- Toxicity: 1-10 grams of leaves per kg BW
- Approx. 1-100 mg taxines/kg B
yew clinical features
- Onset: within minutes to a few hours following ingestion
- Acute: most often found dead**
- Subacute:
- GI irritation
- CV: lethargy, dyspnea, bradycardia, weak pulses, jugular distension
- ECG: widened QRS complex, depressed or absent P wave, bradycardia
- Cause of death: diastolic standstill
- CNS signs possible: tremors, ataxia, convulsions, collapse
- Death within 24-48 hours of ingestion
PM: yellow plants in stomach/rumen contents
yew management and diagnosis
Often unrewarding in livestock
* If the animals are alive:
* Low stress handling
* No true antidote
* Supportive care: atropine, fluids, other anti-arrhythmics
* Diagnosis: history of access to yew (plant clippings disposed
of in pasture), presence of yew in stomach/rumen contents
prognosis: grave to poor
sago palm
Often houseplants, but found in tropical and subtropical regions as native plants
* Mostly dogs
* Limited reports in other species
* All parts of plant toxic, esp. seed
- Toxicity: a few seeds, chewing one palm
- Target organ: liver, CNS, kidneys**
- Mechanism: methylation of DNA + RNA → inhibition of protein synthesis → acute hepatic
necrosis
sago palm clinical features
- Onset: within 15 minutes to several hours post-ingestion
- GI: vomiting (± blood), anorexia, diarrhea, hypersalivation
- Within 2-3 days: development of acute hepatic necrosis
Hepatic encephalopathy: ataxia, tremors, seizures, coma - Clin path: ↑ liver enzymes, indicators of liver failure
- PM: gastrointestinal hemorrhage and necrosis, severe centrilobular hepatic necrosis with hydropic degeneration
sago palm management and diagnosis
- No antidote
- GI decontamination: emesis induction if not contraindicated, activated charcoal
- Symptomatic and supportive care:
- Liver: hepatoprotectants, vitamin K, plasma, IVFT
- Diagnosis: history of ingestion of a palm or palm seed, plant parts/seed in vomitus
- No confirmatory test available
- Poor prognostic indicators: thrombocytopenia, prognosis varies
insoluble oxalates
many plants Examples: peace lily, philodendron, monstera,
dumbcane
* Mechanism: physical damage
* Mucosal irritation*
* Raphides in specialized cells called idioblasts
- GI irritants: oropharyngeal irritation due to mechanical damage by some plants, with mostly self-limiting cases of gastroenteritis
- Pain management
insoluable oxalates clinical features, management, prognosis
- In general, insoluble oxalates do not cause systemic clinical signs
- Clinical features
- Onset: within minutes of chewing
- Salivation, head shaking, pawing at mouth, vocalization
- Pain and swelling of tongue, oral mucosa, pharynx
- ± vomiting, diarrhea
- Management
- Oropharynx only: rinsing mouth with milk or water, pain management, anti-inflammatories for swelling
- Laryngeal swelling: anti-inflammatories, may need to intubate if severe
- GI irritation: gastroprotectants, analgesics, anti-inflammatories, IVFT
- Prognosis: excellent
T U L I P S & H Y A C I N T H S
- Exposure: access to bag of bulbs for planting, digging up newly planted bulbs
- Clinical features
- Oral and esophageal irritation
- Vomiting, diarrhea
- Large ingestions: vomiting, diarrhea, tachycardia
- Management
- Oral irritation: similar to insoluble calcium oxalates
- Vomiting, diarrhea: IVFT, gastroprotectant
holiday plants management and diagnosis
-gastrointestinal irritants, usually self limiting.
- Supportive care: IVFT or SC fluids, gastroprotectants
- Rinse mouth with water or milk
- Monitor hydration and electrolyte status
- Most cases do not require hospitalization
Home care: client withholds food and water for a few hours, then gradually re-introduces water, bland food - Diagnosis: history of ingestion, plant parts in vomitus
- Prognosis: excellent
what plant is this?
castor plant/ caster bean
* Part of plant: all, esp. the seeds are toxic.
* Pods release seeds in autumn
- Exposure: ingestion of seeds, feed contaminated with castor bean or castor cake, fertilizer
- Toxin: ricin**
- Mechanism of action: inactivates ribosomes →
inhibition of protein synthesis → cell death - Cardiotoxicity: Ca2+ dysregulation → myocardial necrosis
- Toxicity: 1-3 seeds can be lethal**
- Only toxic when chewed
caster plant clinical features?
- Onset: latency period of several hours up to multiple days**
- GI: abdominal pain, profuse vomiting, profuse severe diarrhea (watery, hemorrhagic)
- Dehydration, electrolyte derangements
- CV: hypotension, hypovolemia, arrhythmias
- CNS: depression, incoordination, terminal seizures and coma
- Liver and kidney damage
caster plant clin path and PM lesions
-PM: multi-organ hyperemia,
ulcerations, hemorrhages
* GI, heart, liver, kidney, spleen
- Histo: myocardial hemorrhage,
degeneration, and necrosis, renal
hemorrhage and tubular necrosis
caster plant management
- No specific antidote
- GI decontamination if not contraindicated: emesis induction, A/C
- Aggressive supportive care:
- GI: gastroprotectants, IVFT
- CV: ECG/BP monitoring, antiarrhythmics, pressure support
- Liver: hepatoprotectants
- Kidney: IVFT
- Seizures: diazepam
- Monitoring of CBC/chemistry/UA for liver, kidney, electrolyte parameters
caster plant diagnosis/ prognosis
- Diagnosis: detection of ricinine in urine, blood
- Biomarker of ricin exposure
- Excreted in urine
- DDx: severe gastroenteritis → zinc phosphide, inorganic As and Hg, DON, death cap mushroom
- Prognosis: good with aggressive supportive care
- No treatment: grave
autum crocus tox, and mech
part of plant toxic: all plant esp. tubers and seeds.
toxic principle: colchicine**
* Human medicine: gout, immune mediated diseases, cancer
* Veterinary medicine: off-label use for glaucom
- Mechanism of action: microtubule inhibitor
- Anti-mitotic agent
- PGP substrate
- Undergoes EHC
autum crocus clinical features
- GI: diarrhea (± blood), abdominal pain, vomiting, drooling
- CNS: depression, weakness, ataxia, hypothermia
- Cardiorespiratory: bradycardia, pale MM, hypotension, tachypnea
- Recumbency, seizures, collapse
- Death due to shock, respiratory failure, cardiovascular failure, or multi-organ failure
- PM: GI hemorrhage and congestion
- Histo: crypt necrosis and hemorrhages, cerebral congestion and hemorrhage
autum cross management
- No antidote
- Decontamination: emesis and A/C, IVLE
- Supportive care***
- IVFT, anti-emetics, seizure control, atropine for bradycardia,
gastroprotectants, hepatoprotectants - Mannitol for cerebral edema
- Antibiotics for bacterial translocation
- If the animal survives: continue to monitor CBC for a few weeks →
myelosuppression - Erythropoietin, filgastrim
autumn crocus diagnosis, ddx, prognosis
- Diagnosis: history of ingestion, plant identification from vomitus
- Detection of colchicine in blood and urine – limited availability
- DDx: bone marrow suppression → chemotherapeutics, immunosuppressive drugs (azathioprine),
estrogen, radiation, neoplasia, FeLV/FIV, Ehrlichiosis, many drugs - Multi-system failure: ricin, sepsis
- Prognosis: poor
true lillies key points
-cats common poisoning
* Nephrotoxic
* Toxin unknown
* Supportive care before onset of AKI, especially fluids (IVFT)
cardiotoxic plants key points
- Cardenolides: oleander, foxglove, lily of the valley, kalanchoe → confirmatory test for some plants available
- Taxine alkaloids: yew → confirmatory: plant in stomach/rumen contents, taxine alkaloids
- Disposal of clippings in pasture, access to plants
- Livestock often found dead
range plants causing acute respiratory distress
Fog fever
Nitrate
Cyanide
fog fever toxin, species, target organ, mech
Acute Bovine Pulmonary Emphysema and Edema (ABPEE) aka Atypical Interstitial Pneumonia (AIP)
aka 3-methylindole poisoning
* Associated with movement of cattle from dry to lush pastures
* Abrupt feed transition
Most at risk: cattle > 2 years old in good body condition
- Target organ: lungs
- Mechanism: excess L-tryptophan is converted to 3-methylindole by rumen microbes
- Damage to type I pneumocytes and Clara cells → acute respiratory distress
fog fever clinical features
- Onset: within 12 hours of consuming lush forage
- Follows 5-10 days after movement to new pasture
- Most animals: mild-moderate dyspnea and coughing
- Self-limiting
- Severely affected:
- Expiratory grunt
- Severe dyspnea, rapid breathing, reluctance to move can lead to recumbancy and death
fog fever clin path, management
Necropsy findings
PM: lungs fail to collapse, edema and emphysema in intralobular
spaces
* Management: no effective treatment
* Often unrewarding – NSAIDs, diuretics, bronchodilators
* Diagnosis: history of movement to green pasture, clinical signs,
gross lesions
* No confirmatory tissue test
fog fever diagnosis, DDX, prognosis/ prevention
- Diagnosis: history of recent pasture change, clinical signs, necropsy findings
- DDx: acute dyspnea/respiratory distress → nitrate, cyanide, urea
Prognosis: dependent on the severity of disease
* Mild cases can resolve without treatment
* Severely affected animals: poor prognosis
- Prevention:
- Limit use of lush pasture
- Feed hay before pasture turnout
- Monensin supplementation
nitrate poisoning
- Nitrate poisoning is typically forage related**
- Consumption of forage with high nitrate accumulation
- Less common: ingestion of nitrate fertilizers/agricultural, water
- Nitrate accumulating plants
- Crops: wheat, sorghum, corn, oats
factors affecting nitrate accumulation
- Most accumulation in lower stalks and stems
- Highest risk: hay cut during a nitrate accumulation period, younger plants
- Green feed oats, oat hay
- Stubble fields – canola, corn
Conditions of decreased photosynthesis cause nitrate accumulation:
* Drought
* Freeze/thaw
nitrate poisoning mechanism + toxicity/ target organ
Target organ: RBCs
- Mechanism of action: oxidation of hemoglobin → methemoglobin (MetHb)**
- Inability to carry oxygen → asphyxiation
-ruminants are more sensitive
nitrate poisoning clinical features
- Sudden death: multiple cattle found dead after introduction of new feed or after grazing stressed forages
- Sublethal poisoning in pregnant animals: abortion
- Acute toxicosis (>50% MetHb): respiratory distress 2° to
asphyxiation - Onset: within hours of ingestion
- Discoloured MM: brown/muddy, cyanosis
- Chocolate brown blood
- Convulsions, collapse, death
nitrate poisoning diagnosis, DDX. prognosis
-test feed, water
- DDx: acute respiratory distress and sudden death → cyanide, AIP, urea, cardiotoxic plants, ionophores
- Sulfur toxicosis (polioencephalomalacia)
- Prognosis: poor for livestock with acute respiratory distress
- Mildly affected animals may recover with minimal handling
- Encourage producers to test feed
cyanide toxicity factors affecting cyanide accumulation
-forage related
* In general: any damage to the plant that releases the cyanogenic
glycosides from the plant vacuoles
* Regrowth following impaired growth and/or poor growth
conditions:
* Drought
* Freezing
* Cutting
-young, hail damage
cyanide mech and toxicity/ species/ target
- Target: heme groups**
- Hemoglobin (Hgb) + heme-containing enzymes (cytochrome enzymes)
- Mechanism: inhibition of cytochrome oxidase in the electron transport chain + inactivation of Hgb
- Arrest of aerobic respiration
- Systemic oxygen and ATP deprivation → asphyxiation**
- All species susceptible
- Lethal dose ~ 2 mg/kg BW for most species
- Ruminants very susceptible: higher pH, rumen microbes lead to hydrolysis**
cyanide clinical features
- Sudden death or found dead after grazing stressed forages**
- Acute toxicosis
- Onset: within 15 minutes to a few hours post-ingestion
- Respiratory distress: dyspnea, hyperventilation
- Tachycardia
- Hypersalivation/frothing at mouth
- Tremors, staggering
- Terminal seizures, collapse, death
- Bright red blood**
- PM: nonspecific serosal hemorrhages
cyanide management
Medical emergency**
* On-farm: treatment may not be feasible
* Companion animals in hospital – intensive care cases
* Stabilization – mechanical ventilation, fluid resuscitation
* Frequent monitoring of blood gas, blood pressure, SpO2
* Antidotes*
* Animals often die before treatment can be give
cyanide antidotes
- Sodium nitrite ± sodium thiosulfate
-binds to MetHb
Hydroxocobalamin
* Vitamin B12 precursor
* Cyanide preferentially bind to cobalamin → cyanocobalamin
cyanide diagnosis
- Collect and freeze rumen contents in airtight containers
- HCN is volatile
- Antemortem or immediately postmortem: cherry red blood**
-no specifec PM lesions do in well ventilated area
-test forage and rumen contents
neurotoxic range plants
-water hemlock
-poison hemlock
-larkspur
-lupine
-death camas
-locoweed
water hemlock
All parts of the plant are poisonous, one of the most acutly poisoness plants
* Most toxin in the root**
water hemlock toxicity + mechanism
- Toxicity: single root is lethal to adult livestock
- Target organ: CNS
- Mechanism of action: noncompetitive GABA antagonist
- Acute neuroexcitation / stimulatio
water hemlock clinical features
- Animals usually found dead with signs of a violent struggle
- Onset: within 15 minutes of ingestion
- Initial: salivation, apprehension, facial twitching, colic
- Terminal stages: Head and neck jerking, running fits, violent intermittent tonic-clonic seizures
-death from resp failure in hours
-high anion gap metabolic acidosis, high CK
-PM: myocardial degen
water hemlock management and diagnosis
- Management: intoxication is peracute → often too late to intervene
- Seizure control, other supportive care measures
- Diagnosis: found dead where water hemlock is present, plant in rumen/stomach
- ID of plant in rumen/stomach contents
-prognosis: poor to grave
poison hemlock mech + tox
- in spring, all parts of plant toxic
- Toxins: coniine, y-coniceine
- Target organs: CNS (acute), fetus (chronic)
- Mechanism: nAChR agonists, CNS stimulation then depression
poison hemlock clinical features
- Sublethal: weakness, recumbency, CNS depression
- Recovery over 6-10 hours
- High dose: initial CNS stimulation followed by depression and paralysis
- Rapid onset (within 15 minutes)
- CNS/neuromuscular: tremors, nervousness, hypersalivation, muscular weakness, ataxia,
recumbency, and coma - Cardiorespiratory: bradycardia, cyanotic MM, dyspnea
-death from resp failure
poison hemlock management and diagnosis
- Management
- No specific antidote
- Remove herd to different area
- Seizure/tremor control
- Low stress handling
- Diagnosis: plant in rumen/stomach contents, pasture with poison hemlock presence
- Detection of piperidine alkaloids in rumen/stomach contents
- Prognosis: poor with high dose, acute poisoning
larkspur species and mech
- Species affected: cattle
- Toxins: norditerpenoid alkaloid
Mechanism of action: nAChR antagonists
→ neuromuscular blockade and
subsequent paralysis anticholinergic toxidrome.
larkspur clinical features
- Animals found dead on pasture
- Onset: within a few hours of ingestion
- Restlessness, agitation
- Frequent urination, defecation
- Weakness, stiff staggering gait, falling over
- Dyspnea, tachypnea, tachycardia
- Eventually: unable to rise\
-death due to resp failure or bloat
larkspur management + diagnosis, DDx, prevention and prognosis
- Management:
- Antidote: neostigmine (0.02 mg/kg BW) or physostigmine
- Positioning to alleviate bloat
- Diagnosis: evidence of larkspur consumption on pasture, ID of plant in
rumen/stomach contents - DDx: toxic hemlocks, nicotine, acute selenium toxicity, cardiotoxic plants
- Prognosis: poor to grave – depends on how quick cattle can be attended to +
response to therapy - Prevention: avoid larkspur containing pastures during toxic window
- Sheep can be used to graze larkspur containing pasture
