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Narcissus Is Poisonous To Pets

Plant Name: 


Scientific Name: 

Narcissus spp




Lycorine, galantamine, glucoside scillaine (scillitoxin), narciclasine, calcium oxalate crystals

Poisoning Symptoms: 

Severe gastrointestinal upset (vomiting, diarrhea, abdominal pain), lethargy, sedation, inappetance, convulsions, shivering, abnormally low blood pressure, kidney damage, muscular tremors, and cardiac arrhythmias

Additional Information: 

Grown from a bulb, Narcissus often called Daffodil and less often Jonquil or Paper White is a genus of hardy common spring-flowering perennials in the Amaryllis family, subfamily Amaryllidoideae. Originating from the Western Mediterranean, their native range includes Europe (Spain and Portugal), North Africa and West Asia, although many species (e.g. Narcissus poeticus) have become widely naturalized in North America. Depending upon how they are classified, the number of distinct species varies widely due to similarity between species and hybridization between species and can be as low as 26 or as high as 60 or more. Due its brilliantly colored trumpet-shaped flowers, which come in all shades and tones of yellow, white, orange, pink, red and green, Narcissus and its hybrids are widely used to beautify and accent gardens and landscapes.

Daffodil poses a danger to pets as it contains various phenanthridine alkaloids, the most common of which is lycorine. Other toxins include galantamine, the glucoside scillaine (scillitoxin) and the antimitotic narciclasine; the last of which poisons with a colchicines-like effect. In laboratory studies with mice, narciclasine has a subcutaneous LD50 (lethal dose at which 50% of subjects will die) of 5mg/kg; although toxic effects can be seen with as little as 0.5 to 0.9mg/kg. Although the outer layers of the bulb contain the highest concentration of toxins, the flowers and stems also contain a notable level of toxin. Thus there is some risk of a pet being poisoned by ingesting the foliage as well as in the bulbs.

Daffodils also have idioblasts which contain raphides of calcium oxalate crystals; the highest concentration being in the stems and the sap. Found in a number of plant species both poisonous and non-poisonous, idioblasts differ from neighboring cells in that they contain non-living substances like oil, latex, gum, resin, tannin, pigments or minerals. One of these substances is raphides or bundles of needlelike crystals of calcium oxalate that tend to be blunt at one end and sharp at the other. The crystals are packed in a gelatinous substance that contains free oxalic acid.

When animals chew on the leaves, flowers or stems of the plant, the tip of the idioblast is broken allowing saliva from the animal or sap from the plant to enter the cell. This in turn causes the gelatinous material to swell forcing the raphides (needle like calcium oxalate crystals) to violently shoot out from the cells into the surrounding area. The calcium oxalate crystals then penetrate and embed themselves into the tissues of the mouth, tongue, throat and stomach causing (in most cases) immediate discomfort and aggravation as would be expected when millions of microscopic needles are lodged in ones throat and mouth. The idioblasts may continue to expel raphides for a considerable amount of time after ingestion allowing the crystals to also embed themselves into lining of the stomach and intestine causing additional gastrointestinal upset.

Daffodil ingestion by companion-animals is rare and serious daffodil intoxication is rarer yet; there are but a few documented cases most of which involve dogs. The National Animal Poison Control Center (NAPCC), located in Illinois, USA, reported it only receives a few inquires annually regarding daffodil ingestion. The Veterinary Poisons Information Service (VPIS), located in London, England reported that it had received four cases of severe poisoning; of these one animal died, another was euthanized and the other two recovered. In most reported cases, bulbs were ingested, but poisoning has also occurred after ingestion of the flowers or leaves.

Symptoms of daffodil ingestion can present in as little as 15 minutes or be delayed as long as 24 hours; in most cases the onset of clinical signs is rapid. The severity will vary based upon size and species as well as the amount ingested. The most common clinical signs of daffodil ingestion include gastrointestinal upset (vomiting and diarrhea), lethargy, sedation, inappetance, abdominal pain and dehydration related to extensive diarrhea and vomiting. In more severe cases pets can experience hypothermia (decrease in body temperature), hypotension (low blood pressure), bradycardia (irregular heart rhythm), hepatic degeneration (kidney damage), collapse, seizures and possibly death. The duration of symptoms will vary depending upon size, species and amount ingested and can be as short as 24 hours or as long as a week or more in severe cases.

First Aid: 

Treatment for daffodil ingestion is symptomatic and supportive; there is no specific treatment or antidote. If the ingestion was recent remove any existing plant matter from the mouth and flush the mouth thoroughly with water. Unless it is recognized very early on that a pet ingested a plant containing lycorine or the amounts involved are large, vomiting the patient is probably not recommended, as the emetic effects of the toxin will inevitably cause the patient to vomit spontaneously. When significant amounts are involved, and there is danger of prolonged vomiting or nongastrointestinal effects, lavage may be indicated. Although activated medical charcoal may be very useful in adsorbing these alkaloids, its use may be limited since symptoms of vomiting and diarrhea can take an hour or more to manifest from the time of ingestion. If the vomiting and diarrhea are extensive, patients should be monitored for fluid and electrolyte loss. In cases where animals have ingested a large amount, hypotension, seizures and hepatic damage has been reported; patients should have blood pressure and liver function monitored.

In the March 2004 issue of the Canadian Veterinary Journal, a successful treatment regimen was provided in an article titled, Daffodil toxicosis in an adult cat, by Dr. Sharon Saxon-Buri:

“A domestic longhair cat with a 3-day history of lethargy and vomiting after ingesting dried daffodil stems (Narcissus spp.) was severely hypothermic (33.0°C), with bradycardia (78 beats/min) and hypotension. Treatment with atropine, dexamethasone, fluid therapy, and supportive care resulted in a complete recovery by 6 days after exposure. “A 2-year old, neutered, male domestic longhair was presented with a history of lethargy and vomiting of 3 d duration. Four days earlier (day 1), the cat had expelled a hairball, but this was not considered unusual. Subsequently, on day 2, the cat had vomited food and yellow fluid several times and had displayed a marked decrease in appetite, with polydipsia and polyuria. No vomiting occurred on day 3, but the cat was lethargic and anorexic. The owners attributed these changes to hairballs and treated the cat with a teaspoon of a hairball remedy on the morning of day 4. On further questioning, the owner reported seeing the cat chewing on dried daffodil stalks, which had been removed from the flower garden for disposal on the morning of day 2, and recalled seeing plant material in the vomitus that day. “When examined, the cat was sternally recumbent, quiet, in thin body condition, and conscious, but only weakly responsive. The extremities were cool to the touch and the rectal temperature averaged 33.5°C for 3 readings. Pale oral mucous membranes were noted, and auscultation of the heart revealed bradycardia (84 beats/min (bpm); reference range, 120 to 140 bpm). Respiratory rate was normal (22 breaths/min). Dehydration was estimated at 10%, and peripheral pulses were weak. The severity of the cat’s condition was discussed with the owner, who agreed to emergency therapy for possible daffodil toxicosis.

“The cat was wrapped in warm towels and catheterization of the left cephalic vein was attempted but was not possible, probably because of hypotension. Accordingly, 180 mL of lactated Ringer’s solution (Baxter; Toronto, Ontario) was administered SC. During this procedure, the rectal temperature of the cat dropped to 33.0°C. Accordingly, the cat was immersed in a water bath at 40°C for approximately 15 min, removed, and immediately dried with warm towels and a hair dryer. Subsequently, the cat was rewrapped in dry towels with warm oat bags and placed under a heat lamp. After 15 min, the body temperature had risen to 36.0°C, and it was possible to catheterize the right cephalic vein. A 2-mL blood sample was drawn for a complete blood cell (CBC) count (QBC VetAutoread Hematology Anayzer; Idexx Laboratories, Toronto, Ontario) and serum biochemical profile (VetTest Chemistry Analyzer; Idexx Laboratories). Warmed lactated Ringer’s solution was administered, IV, at shock rate (45 mL/kg bodyweight (BW)/h). The heart rate had dropped to 78 bpm, and atropine, 0.02 mg/kg BW, IM, and dexamethasone (Vétoquinol, Lavaltrie, Quebec), 2 mg/kg BW, IV, were also administered. Detoxification procedures, such as induction of emesis, administration of activated charcoal, or gastric lavage, were not elected because more than 48 h had elapsed since the time of exposure to the daffodil stalks. The cat was monitored continuously and the rectal temperature was taken 4 times/h. Thirty minutes after warming and atropine administration, the heart rate had increased to 120 bpm and the rectal temperature had increased to 37.5°C; however, 30 min later, rectal temperature had dropped to 35.1°C. The described warming protocol was repeated with similar results. Oral mucous membranes remained a normal pink color.

“The CBC counts were within normal range; however, the biochemical profile results revealed elevated urea (42.62 mmol/L; reference range, 5.71 to 12.85 mmol/L), hyperglycemia (glucose 25.14 mmol/L; reference range, 4.22 to 8.06 mmol/L), hyponatremia (sodium 137.2 mmol/L; reference, range, 150.0 to 165.0 mmol/L), hypokalemia (potassium 2.35 mmol/L; reference range, 3.5 to 5.8 mmol/L), and hypochloremia (chloride 75.5 mmol/L; reference range, 112.0 to 129.0 mmol/L). The urinary bladder was not palpable, so it was not possible to collect urine either by cystocentesis or digital compression. Because of the difficulty in maintaining normothermia for more than 30 min and to ensure metabolic stability overnight, the cat was transferred to an emergency clinic for continuous observation and warming.

“The cat was returned from the emergency clinic to the admitting clinic on the morning of day 5. With the use of warm towels, oat bags, and warm IV fluids, average rectal temperature had reached 38.0°C. The average heart rate (measured hourly) was 120 bpm and oral mucous membranes remained pink. A serum biochemical profile revealed a return to normal ranges for urea (11.45 mmol/L), sodium (153 mmol/L), and potassium (3.8 mmol/L). Chloride remained slightly low (110 mmol/L); glucose had decreased (10.08 mmol/L) but remained above the reference range. A free-flow clear yellow urine sample (specific gravity 1.015; pH 8.5) contained trace blood and protein.

“On day 6, the cat began sitting up and walking periodically. Crackles were noted in the ventral lung fields bilaterally. The IV fluid rate was decreased to maintenance rate and furosemide (Apo-Furosemide; Apotex, Toronto), 2 mg/kg BW, IM, was administered. The cat remained quiet, alert, and responsive, urine output increased during the 3 h following diuretic administration, and lung sounds returned to normal 4 h after diuretic administration. During the next 8 h, in the absence of exogenous heat sources, rectal temperature, taken hourly, averaged 38.4°C, and the cat consumed 30 mL of Prescription Diet Canine/Feline a/d (Hill’s Pet Nutrition Canada, Mississauga, Ontario).

“On day 7, with a body temperature of 38.9°C, normal hydration, and a normal CBC count and serum biochemical profile, the cat remained quiet. Fluid therapy was discontinued and the cat remained stable. On day 8, the cat was bright and energetic, with a normal appetite. A complete physical examination was unremarkable and the cat was discharged.”-(Can Vet J. 2004 March; 45(3): 248–250. PMCID: PMC548613)

Species Affected: 
Toxic To Cats
Toxic To Dogs
Toxic To Horses
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