Insecticides Derived from Plants (Toxicity)
Most insecticides derived from plants (eg, rotenone from Derris and pyrethrins from Chrysanthemum or Pyrethrum) have traditionally been considered safe for use on animals. Nicotine in the form of nicotine sulfate is an exception. Unless it is carefully used, poisoning may result. Pets are exposed to tobacco by ingesting commercial tobacco products (eg, cigarettes or chewing tobacco), whereas livestock may consume discarded tobacco stalks or hay contaminated with tobacco plant drippings in the barn. The minimum lethal dose of nicotine is 1 g in cattle, 0.2–0.3 g in horses, 0.1–0.2 g in sheep, and 0.02–0.1 g in dogs and cats. Affected animals show tremors, incoordination, nausea, disturbed respiration, muscle paralysis, and finally coma and death. Nicotine and related alkaloids from tobacco can cross the placenta and produce teratogenic effects. Recovery from sublethal doses is usually complete within 3 hr. Death occurs within a matter of hours from paralysis of thoracic respiratory muscles and cardiac arrest. Necropsy may reveal parts of tobacco leaves or stalks in the rumen contents. Lesions include pale mucous membranes, dark blood, hemorrhages on the heart and in the lungs, and congestion of the brain. Treatment consists of removing the material by washing or by gastric lavage with tannic acid, administering activated charcoal, providing artificial respiration, and treating for cardiac arrest and shock.
Pyrethrins are insecticides obtained from the flowers of C cinerariaefolium and have been used as insecticides for many years. Pyrethrins and pyrethroids produce toxicity affecting primarily the sodium channel, but also chloride and calcium channels of nerve cells. These insecticides also interact with nicotinic acetylcholine receptors. Synergists, such as piperonyl butoxide, sesamex, piperonyl cyclonene, etc, are added to increase stability and effectiveness. This is accomplished by inhibiting mixed function oxidases, enzymes that detoxify pyrethrins and pyrethroids; unfortunately, this also potentiates mammalian toxicity.
Pyrethroids are synthetic derivatives of natural pyrethrins. There are two types of pyrethroids. Type I compounds that lack an α-cyano substituent include pyrethrin I, allethrin, tetramethrin, kadethrin, resmethrin, phenothrin, and permethrin. Type II compounds that contain a stabilizing α-cyano-3-phenoxybenzyl component include cyfluthrin, cypermethrin, fenpropanthrin, deltamethrin, cyphenothrin, fenvalerate, and fluvalinate. Type I pyrethroids produce a neurologic syndrome through their effects on both the central and peripheral nervous systems, with signs including tremors, incoordination, prostration, seizures, and death. Type II pyrethroids work primarily by CNS mechanisms to exert the choreoathetosis/salivation syndrome, characterized by hyperactivity, hunched back, salivation, tremors, and incoordination progressing to sinuous writhing movements.
Diagnosis of pyrethrin/pyrethroid poisoning is based on clinical signs, history of exposure, and determination of insecticide residue in body tissues and fluids. These insecticides do not produce characteristic pathologic lesions.
Generally, symptomatic and supportive treatment is required after ingestion of a dilute pyrethrin or pyrethroid preparation. Toxicity may also be due to the solvent. Induction of emesis may be contraindicated. A slurry of activated charcoal at 2–8 g/kg may be administered, followed by a saline cathartic (magnesium or sodium sulfate [10% solution] at 0.5 mg/kg). Vegetable oils and fats, which promote the intestinal absorption of pyrethrum, should be avoided. If dermal exposure occurs, the animal should be bathed with a mild detergent and cool water. The area should be washed very gently so as not to stimulate the circulation and enhance skin absorption. Initial assessment of the animal’s respiratory and cardiovascular integrity is important. Further treatment involves continuing symptomatic and supportive care. Seizures should be controlled with either diazepam (administered to effect at 0.2–2 mg/kg, IV) or methocarbamol (55–220 mg/kg, IV, not exceeding 200 mg/min). Phenobarbital or pentobarbital (IV), to effect, can be used if diazepam or methocarbamol are too short-acting.
d-Limonene is the major component of the oil extracted from citrus rind. It is used for the control of fleas on cats and for other insect pests. Adult fleas and eggs appear to be most sensitive to d-limonene, which is more effective if combined with the synergist piperonyl butoxide. At recommended dosages, the solution containing d-limonene appears to be safe, but increasing the concentration 5–10 fold in sprays or dips increases the severity of toxic signs, which include hypersalivation, muscle tremors, ataxia, and mild to severe hypothermia. The inclusion of piperonyl butoxide in the formulation potentiates the toxicity in cats. Allergies have also been reported in people in contact with d-limonene, and it appears to increase dermal absorption of some chemicals. When orally administered to dogs, d-limonene causes vomiting (median effective dose 1.6 mL/kg). No antidote is available.