Pyrethrins and pyrethroids are used extensively for insect control particularly in small animals (dog and cat) but all species can be accidentally poisoned. These drugs are of low toxicity, and considering how widely they are used, poisoning is rare.
Environmental sources include pyrethrum flowers that are cultivated commercially in NZ and other countries (particularly E. Africa). However, the pyrethrin content of these is low.
Agricultural use of pyrethrin rarely results in poisoning because low environmental persistence limits the probability of toxic residues in plants and food.
Commercial use and home pest control can give rise to problems. Pyrethrins and pyrethroids are used for flea control in small animals. They are also used where other persistent pesticides are undesirable such as in dairies and food areas. As a result, excessive use of flea control sprays or dips may lead to dermal exposure. Also spraying in enclosed areas can lead to the inhalation of vapours and open aquariums may be contaminated and fish poisoned. In addition, concentrated pesticides may be accidentally consumed by pets and livestock.
Pyrethrins are natural insecticides produced from extracts of pyrethrin flowers of the genus Chrysanthemum (Pyrethrum). The pyrethroids are synthetic insecticides that resemble pyrethrins in structure and action. They include:
Type 2 pyrethroids (i.e. those with the alpha cyano moiety) are generally more toxic than type 1 pyrethroids . Acute oral toxicity of common pyrethrins ranges generally from 1000 - 2000 mg/kg body weight.
Drugs, chemicals and nutritional changes that alter the effectiveness of the mixed function oxidase (MFO) system can change toxicity of the pyrethrins and pyrethroids.
MFO inhibitors (e.g. piperonyl butoxide, N octyl bicycloheptene dicarboximide (MGK 264) suppress the hydrolysis of pyrethrins and pyrethroids, increasing their toxicity. Commercial pyrethrin insecticides contain synergists.
Only products labeled for use on cats should be applied as cats are sensitive to these compounds.
The potential for secondary toxicosis is limited because of the low acute toxicity and rapid detoxification of the pyrethroids.
Pyrethrins are lipophilic and readily absorbed orally, dermally or by inhalation. Because of their rapid metabolism, the pyrethrins and pyrethroids are poorly distributed throughout the body, if at all.
The ester linkages of the absorbed insecticide are rapidly hydrolysed by liver and plasma esterases. The hydrolysed insecticide is less toxic. Further ingested insecticide is rapidly metabolised in the digestive tract, hence oral toxicity is very low.
Any absorbed metabolites are conjugated with glycine, glucuronic acid, or sulphates and excreted in the urine.
The pyrethrins act on sodium channels in axonal membranes, decreasing but prolonging inward sodium conductance and suppressing potassium outflow. These insecticides are often termed as open channel blockers. They may also inhibit adenosine triphosphatases (ATPases), which may affect cation conduction at axonal membranes. The net result is decreased action potential amplitude and the generation of repetitive nerve impulses.
In addition, type 2 pyrethroids interfere with binding of GABA and glutamic acid at receptor sites. This antiinhibitory action could lead to hyperexcitability of nervous tissue and contribute to the clinical signs.
Clinical signs mainly involve the nervous system and may vary slightly depending on the type of pyrethroid. In experimental animals (e.g. rats) type 1 pyrethroids cause an increased response to stimulation, muscle tremors, excitement and paralysis, while type 2 pyrethroids induce salivation, weakness and a distinctive “writhing” or burrowing syndrome.
In dogs, cats and large animals, the clinical signs are usually similar for both types of pyrethroids.
These include:
A confirmed diagnosis may be difficult as the haematology values and clinical chemistry are normal, except for stress related responses such as a neutrophilia and hyperglycaemia.
A positive chemical analysis for pyrethrins/pyrethroids residues on the skin will confirm the exposure. Pyrethrins are difficult to detect and confirm in blood or tissue. Any lesions found at post mortem are not usually associated with clinical toxicosis.
Following dermal exposure the animal should be bathed with soap or detergent and water. If the pyrethroid has been ingested emetics or gastric lavage can be used to empty the stomach if the exposure is recent (i.e. within the previous 4 hours) and the animal is not having seizures.
Activated charcoal and a saline or sorbitol cathartic reduce oral absorption and aid elimination.
Diazepam, methocarbamol or barbiturates can be used to control seizures and hyperexcitability. For severe CNS stimulation with seizures try diazepam 0.1 - 0.5 (- 2.0)mg/kg iv to effect. If diazepam fails to control the CNS signs phenobarbitone or pentobarbitone may be required. An alternative, methocarbamol (44 mg/kg) has been advocated for the control of seizures and muscle fasciculations. Phenothiazine tranquillisers must be avoided as they may lower the seizure threshold.
In some animals excessive muscular activity may result in an elevated core body temperature. If left untreated cerebral oedema and continued convulsions may follow.
In general the prognosis is excellent unless the exposure is massive or the animal is otherwise compromised. The onset of signs in all species occurs within minutes to hours after exposure and depending on the route of exposure. The signs resolve in either death or recovery, within 24 - 72 hours.
In general the pyrethrins and pyrethroids are safe but their careless use can result in toxicity. Residues in food of animal origin are not likely because of their rapid metabolism and excretion.
Again, within the environment they are relatively safe except that their improper disposal can contaminate waterways where fish (and some birds) may be affected.
Buckley, R. (1994). Pyrethrin poisoning in a cat. Vetscript VII (7):16.
Hansen, S.R., Villar, D., Buck, W.B. and Stemme, K.A. (1994). The Compendium. 16 (6):707 710.
Osweiler, G.D. (1996). The National Veterinary Medical Series Toxicology. Williams and Wilkins.
Whittem, T. (1995). Pyrethrin and Pyrethroid Insecticide Intoxication in Cats. The Compendium. 17