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Plant poisoning: nicotine-like toxins

ISSN 2398-2950


Introduction

  • A number of plants Poisonous Plants contain toxins with clinical effects similar to those caused by nicotine. 
  • Clinical signs include rapid onset of CNS excitement, with subsequent weakness and paralysis.
  • Pet poisonings as a result of exposure to these plants are extremely rare.

Presenting signs

  • Rapid onset.
  • Initial CNS excitement (tremors and behavioral excitement).
  • Ataxia.
  • Progression to weakness or paralysis.
  • Parasympathetic signs.
  • Convulsions Seizures (during initial excitatory phase).

Acute presentation

  • Excitement and tremors.

Geographic incidence

  • From plants, dependent on the particular plant's distribution.
  • Exposure may be due to nicotine via ingestion of tobacco products.

Age predisposition

  • Young cats may be more susceptible due to their inquisitive natures.

Breed/Species predisposition

  • No breed predisposition reported.

Public health considerations

  • Plants or tobacco products that are accessible to cats are likely to be accessible to small children.

Cost considerations

  • May require intensive therapy efforts, but clinical course is usually short.

Special risks

  • None.

Pathogenesis

Etiology

  • Nicotine is a pyridine alkaloid present in produced by Nicotiana sp and is also found in tobacco products for human use, eg cigarettes, cigars, tobacco leaf, snuff, chewing tobacco, smoking cessation or nicotine replacement products (lozenges, gums, patches, inhalators, nasal sprays, electronic cigarettes), etc.
  • Nicotine and/or related pyridine or piperidine alkaloids produced by other plants in the genus Nicotiana.
  • Coniine, a piperidine alkaloid with similar mechanism of action and clinical signs to nicotine, is produced by Coniumsp, eg poison hemlock.
  • Lobeline and/or lobelidine, pyridine alkaloids with similar mechanism of action and clinical signs to nicotine, are produced by plants of the genus Lobelia.
  • Piperidine alkaloids are also synthesized by members of the genus Lupinus. The predominant toxic alkaloids in Lupinus species are quinolizidine alkaloids, but some species also produce piperidine alkaloids.
  • Cytisine, a quinolizidine alkaloid which causes similar clinical signs to nicotine, and quinolizidine alkaloids chemically related to cytisine, are produced by plants of the genera LupinusLaburnum Laburnum anagyroides, CytisusGymnocladus and Thermopsis.
  • Nicotine is used as an insecticide on plants, and is approved for this use on organic produce. Cats may be exposed to commercial insecticides containing nicotine, particularly if they have access to the gardens or crops of advocates of organic produce.

Predisposing factors

General

  • Nicotine has low bioavailability as it subject to first pass metabolism and poorly absorbed from the stomach. Chewing tobacco products and possibly plant material is more likely to cause toxicity.
  • Tobacco and smoking cessation products, particularly electronic cigarettes, are readily available online and cats may chew material delivered through the letter or mail box.
  • Access to tobacco or smoking cessation products, or access to cultivated plants containing pyridine, piperidine or quinolizidine alkaloids causing the clinical signs characteristic of nicotine poisoning.
  • A number of plants (Lobelia, Cardinal flower, Eye-bright) of the genus Lobelia are cultivated.
  • A number of plants of the genus Lupinus (lupins, lupines) are cultivated.
  • Laburnum anagyroides Laburnum anagyroides (laburnum, golden chain) is grown as an ornamental tree, as is Gymnocladus dioicus (Kentucky coffee tree).
  • Conium sp (poison hemlock) and Cytisus (Scotch broom) are common weeds in numerous areas.

Specific

  • A tendency to chew tobacco products or growing plants.

Pathophysiology

  • Best characterized for nicotine, but the pathophysiology is similar for all these toxins.
  • Nicotine mimics acetylcholine, and therefore stimulates acetylcholine receptors at sympathetic and parasympathetic ganglia, neuromuscular junctions, and some synapses in the central nervous system.
  • Ganglia are initially stimulated, followed by a persistent ganglionic and neuromuscular blockade.
  • Positive inotropic and chronotropic effects on the myocardium lead to an increase in cardiac output and blood pressure.
  • Stimulation of the adrenal medulla results in catecholamine release.
  • Death is a result of respiratory failure from neuromuscular blockade Anesthesia: non-depolarizing neuromuscular blockade.

Timecourse

  • Generally a rapid onset and progression; death may occur within minutes or hours of ingestion of a lethal dose.

Diagnosis

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Treatment

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Prevention

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Outcomes

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Further Reading

Publications

Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Novotny T E, Hardin S N, Hovda L R et al (2011) Tobacco and cigarette butt consumption in humans and animals. Tob Control (Suppl 1), i17-20 PubMed.

Other sources of information

  • Petersen M E, Talcot P A (2012) Small Animal Toxicology. 3rd edn. St. Louis, Missouri: Saunders.
  • Poppenga R H, Gwaltney-Brant S (2011) Small Animal Toxicology Essentials. Ames, Iowa: Wiley-Blackwell.
  • Osweiler G D, Hovda L R, Brutlag A G, Lee J A (2010) Blackwell's Five-Minute Veterinary Consult Clinical Companion: Small Animal Toxicology. Ames, Iowa: Wiley-Blackwell.
  • Spoo W (2009) Nicotine toxicosis. In: Kirk's Current Veterinary Therapy XIV. Bonagura J D, Twedt D C (eds), Saunders Elsevier: St. Louis, Missouri.
  • Plumlee K H (ed) (2004) Clinical Veterinary Toxicology. Mosby.

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