Be it cultivated tobacco (Nicotiana tabacum) or wild growing tree tobacco (Nicotiana glauca), consumption by a pet can have potentially lethal consequences. All parts of these plants except the seeds contain the potent alkaloids nicotine and anabasine (sometimes referred to as neonicotine). As a testament to its lethality, anabasine, which is chemically similar to nicotine and acts upon the body in a similar fashion, has historically been used as insecticide for crops. Nicotine, unbeknownst to most is a super toxin in its own right, being drop for drop more lethal than strychnine or diamondback rattlesnake venom and three times deadlier than arsenic. The lethal dose (LD50-dose at which 50% of animals will die) for nicotine in dogs is reported to be around 9.2 mg/kg, whereas it would take around 20 mg/kg of Diamondback rattlesnake venom to have the same effect.
Nicotiana glauca, the variety a pet is most likely to encounter originated in Argentina, Paraguay, and Bolivia but can now be found growing wild in elevations below 3000ft throughout the Southern United States from California, to North Carolina. Nicotiana tabacum on the other hand is only found in cultivation. The specific concentration of toxin in each plant will vary and largely depends upon external factors such as soil type, culture and environmental conditions. One thing that is consistent is that the level of toxin increases with the age of the plant. Most plants contain 2-8% nicotine; around 60% of that is in the leaves, 18% in the stem and the rest is in the root and flowers. Nicotiana glauca occasionally accumulates nicotine as a defense against herbivores, but more commonly produces anabasine, the pyridine alkaloid very toxic to herbivores and humans (Baldwin and Callahan 1993, Parker 1972). The pharmacological and toxicological effects of abasine intoxication mirror those of nicotine intoxication in nearly all respects.
An excellent description of how nicotine lethally effects the body can be found in the Journal of Veterinary Diagnostic Investigation (1994), in an article titled: Lethal Nicotine Intoxication in a Group of Mules; authored by Robin Sanecki, Ramesh C. Gupta and Wade L. Kadel:
”The pharmacological and toxicological effects of nicotine occur primarily in the central nervous system (CNS), cardiovascular system, skeletal muscles, and gastrointestinal tract. CNS signs depend upon the dose and vary from mild stimulatory effects, such as tremors, hyperexcitability, and auditory and visceral disturbances, to severe excitatory signs, such as marked incoordination and clonic and tonic convulsions. Nicotine transiently stimulates and then severely depresses the CNS. Cardiovascular signs, such as tachycardia and hypertension, are a result of stimulation of sympathetic ganglia and the adrenal medulla along with sympathomimetic activation of chemoreceptors of the aortic and carotid bodies. In skeletal muscles, nicotine initially stimulates nicotinic receptors of the motor end-plate and in large doses it blocks the receptors. Death is from respiratory paralysis of the diaphragm and chest muscles, resulting from descending paralysis and depolarization block of the neuromuscular junction.
“In the gastrointestinal tract, nicotine activates the smooth muscles and secretory glands, resulting in excessive salivation, increased gastric secretion, vomiting, and increased peristalsis and defecation. The respiratory response to nicotine overdose is tachypnea. The findings presented here and elsewhere indicate that diagnosis is possible by residue analysis of nicotine or its major metabolites in body fluids, tissues, or stomach contents.”
In the vast majority of cases involving anabasine or nicotine ingestion, there will be a a delay of between one and two hours from the time of ingestion till the onset of symptoms; probably due to the slow gastric absorption rate of anabasine and nicotine from tobacco leaves. Once clinical signs present the severity is going to depend on the amount of the plant ingested and can generally be expected to be excessive salivation (drooling), vomiting, hyperexcitability followed by depression, diaphoresis, headache, dizziness, mental confusion, marked weakness and hypertension. In more severe cases the symptoms can progress to include paralysis of the respiratory muscles, and finally collapse with cardiac arrest. In the majority of reported fatal cases of nicotine poisoning, death usually occurred within one hour of the onset of symptoms. The prognosis is generally good if prompt veterinary care is provided. It has been said that if a patient manages to survive nicotine poisoning during the first 4 hours, they will usually recover completely.
While the prognosis with prompt treatment is considered good (i.e. the animal is witnessed eating a plant of the Nicotiana genus, stopped and treated), the sad fact is that most animals that ingest a potentially lethal dose of nicotine or anabasine will go unnoticed until clinical signs develop. Due to the poor gastric absorption rate of nicotine and anabasine from tobacco leaves, there is generally a delay of between 1 and 2 hours from the time the plant is ingested until the manifestation of clinical signs. In cases where a large amount of the plant has been ingested the time between the onset of symptoms and death can be as little as an hour. In simplest form this means that many animals are destined for a fatality by the time signs present and most will die before being seen by a veterinarian to institute treatment.
In the case of dogs and cats, it is rare that a fatal amount will be ingested as tobacco has emetic properties which would generally cause the animal to start vomiting shortly after ingestion. As previously stated the absorption of nicotine and anabasine from raw tobacco leaves by the gastrointestinal tract is poor, so many dogs and cats will vomit out the plant prior to absorbing a fatal amount of the toxins. Raw or wild tobacco also has a harshly bitter taste that most pets will find unpalatable which further reduces the likelihood that a dog or cat would ingest a massive amount of the plant.
In the case of horses, they are unlikely to choose the plant as a food resource unless other sources of food are unavailable. Regardless, it should not be allowed to grow in or around pastures or other areas where grazing animals are likely to come into contact with it.
There is no definitive antidote for nicotine or anabasine poisoning. Treatment is largely symptomatic and supportive with the emphasis being on respiratory support as death is almost always due to acute respiratory failure. In cases of a witnessed ingestion, where only a small amount of the plant may have been consumed vomiting should be induced. Activated charcoal is also a valuable tool at neutralizing ingested nicotine in the stomach. The pet should be watched closely for worsening signs of neurological distress and treated accordingly. In many cases of a minor ingestion, the pet will make a full recovery in a matter of hours.
In cases of acute toxicity where a large amount of the plant may have been ingested and advanced clinical signs are starting to manifest aggressive respiratory support, and treatment of shock are important countermeasures. As with ingestion of smaller amounts vomiting should be induced; gastric lavage could also be performed. The "universal antidote" or activated medical charcoal should also be given as it is a valuable adjunct in neutralizing ingested nicotine in the stomach. After charcoal has been in the stomach 15 minutes re-induce vomiting. Tannic acid solution, however, although useful in precipitating some other alkaloids (e.g. strychnine), is of little use for this alkaloid. Alkaline solutions, which facilitate absorption, should be avoided. Diluted potassium permanganate (1:10,000) solution in the lavage fluid can also be used to dilute the nicotine. Following the permanganate rinse, the patient should be calmed and kept warm to avoid shock. Apply artificial respiration if necessary to keep patient breathing.
Symptoms of parasympathetic or sympathetic hyperactivity should be controlled with atropine and phentolamine given intravenously or intramuscularly. Cardiac arrythmias can be treated with propranolol . Patients exhibiting convulsions may require sedation (e.g. intravenous diazepam) and vasopressor drugs if hypotension fails to respond to the usual therapy.
In both nicotine and anabasine poisoning the primary cause of death is respiratory paralysis. In cases where a large amount has been ingested, it is highly likely that artificial respiration will be needed to keep the patient breathing and alive until antidotes and the body's natural detoxification mechanisms can destroy the nicotine and reduce it to non-toxic concentrations. On a positive note, nicotine is rapidly detoxified in the liver, thus if the patient can be stabilized during the initial hours after consumption and clinical presentation, the likelihood of a full recovery, although not guaranteed, is good. Prevent further ingestion of the plant and contact your veterinarian.