Pets often gain access to rodenticides by eating baits or the poisoned rodents (see Poisoning: Strychnine Poisoning). Many rodenticides are toxic to pets. Early veterinary intervention in cases of ingestion provides the best chance for successful treatment.
Anticoagulant Rodenticides (Warfarin and Related Compounds)
Anticoagulant rodenticides interfere with blood clotting. They are the most frequent cause of poisoning in pets. Pets may be poisoned directly from baits or indirectly by eating poisoned rodents. Different anticoagulants have different toxicity levels. Some require multiple feedings to result in toxicity, some require fewer feedings, and some are highly toxic after a single feeding.
Signs generally reflect blood loss from ruptured blood vessels, including anemia, semisolid masses of blood in the tissues, or bleeding into various areas of the body (the gastrointestinal tract, the eye, the nose, the lungs, or the urine). The animal can develop weakness, lack of coordination, colic, and panting or rapid breathing. Depression and loss of appetite are seen in all species even before bleeding occurs.
Anticoagulant rodenticide poisoning is usually diagnosed based on history of ingestion, blood tests, and a good response to vitamin K1 treatment. Vitamin K1 may need to continue for 2 to 4 weeks. Administration of oral vitamin K1 with a fat-containing ration, such as canned dog food, increases its effectiveness 4 to 5 times as compared with vitamin K1 given by mouth alone. Blood transfusions may be needed if bleeding is severe. Blood clotting should be monitored weekly until values remain normal for 5 to 6 days after treatment stops.
Use of ANTU has nearly been abandoned. However, dogs are occasionally poisoned. Animals with an empty stomach readily vomit after eating ANTU, but food in the stomach decreases the stimulation to vomit, and deadly quantities may be absorbed. Signs include vomiting, excessive drooling, coughing, and difficulty breathing. Animals prefer to sit. Fluid builds up in the lungs, and the skin and mucous membranes develop a bluish tinge. Other signs include weakness, lack of coordination, rapid weak pulse, and below normal temperature. Death can occur within 2 to 4 hours of ingestion, while animals that survive 12 hours may recover.
Medications that cause vomiting should be used only if the animal is not having trouble breathing. If respiratory distress is severe, the outlook is grave.
Bromethalin is a nonanticoagulant rodenticide that can cause either a short- or longterm syndrome. In dogs, sudden, severe effects include hyperexcitability, muscle tremors, seizures, heightened reflexes of the hindlimbs, central nervous system depression, and death about 10 hours after ingestion. Longterm effects are seen with lower dosages and may appear 1 to 4 days after ingestion. This syndrome is characterized by vomiting, depression, lack of coordination, tremors, and a reluctance to stand. The effects may be reversible if exposure to bromethalin is discontinued. Bromethalin toxicosis should be considered when swelling of the brain or paralysis of the hind end is present.
Medical treatment is directed at blocking absorption from the gastrointestinal tract and reducing brain swelling. Using activated charcoal for several days may improve the recovery rate.
Rodenticides containing cholecalciferol are a significant health threat to dogs and cats. Cholecalciferol produces excess calcium in the blood, which results in calcification (hardening) of soft tissue throughout the body. Signs generally develop within 18 to 36 hours of ingestion and can include depression, loss of appetite, passing large amounts of urine, and excessive thirst. As blood calcium concentrations increase, signs become more severe. Vomiting blood and bloody diarrhea may develop. As excess calcium in the blood continues, mineralization of the kidneys results in progressive kidney damage.
Diagnosis is based on history of ingestion, signs, and excess calcium in the blood (see Hormonal Disorders of Dogs: Hypercalcemia).
Treatment usually includes removing the stomach contents, followed by administration of activated charcoal. Medications that increase urination are given for 2 to 4 weeks. Blood calcium levels should be monitored up to 2 weeks after stopping treatment. A low-calcium diet should be provided. Recently, pamidronate disodium has shown promise in treating dogs with cholecalciferol poisoning.
Metaldehyde is used as a snail or slug bait (see Poisoning: Metaldehyde Poisoning). Signs in dogs range from drooling and vomiting to anxiety and lack of coordination with muscle tremors, spasms, and heightened senses. Eventually, muscle spasms are continuous, leading to fever, physical weakness, and death. Diagnosis can be confirmed by finding metaldehyde bait or pellets in the vomited stomach contents.
Treatment is most effective if started early. Further absorption should be prevented by inducing vomiting, flushing the stomach, and giving activated charcoal. Tranquilizers, muscle relaxants, or even light anesthesia may be needed to control the muscle spasms. Fluid treatment promotes toxin excretion, and combats dehydration and metabolic abnormalities. Continuous supportive care is important. The outlook depends mostly on the amount of bait that was eaten.
In its white (or yellow) form, phosphorus is hazardous to all domestic animals. It is infrequently used as a rodenticide today, but dogs occasionally become exposed by eating fireworks that contain white phosphorus. Phosphorus is locally corrosive and toxic to the liver when absorbed. Signs begin suddenly, with vomiting, severe diarrhea (often bloody), abdominal pain, and a garlic-like odor to the breath. Animals can appear to recover up to 4 days after ingestion, but additional signs of severe liver damage may develop, including blood loss from ruptured vessels, continued abdominal pain, and jaundice. Toxic substances may build up in the blood and affect the brain, leading to convulsions and death.
Prognosis is grave unless treatment is started early. Vomiting is induced and the stomach is flushed, followed by giving activated charcoal and medications that cause emptying of the bowels. Because fats favor additional absorption of phosphorus, a no-fat diet should be fed for at least 3 to 4 days. Mineral oil by mouth has been recommended because it dissolves phosphorus and prevents absorption.
This rodenticide is made from the plant Urginea maritima. It is rarely used. Red squill is more toxic to rats because they cannot vomit. Large quantities are required for poisoning in farm animals. Red squill is considered relatively safe, but dogs and cats have been poisoned. Signs are vomiting, lack of coordination, and heightened senses, followed by paralysis, depression, convulsions, and heart abnormalities. The signs seldom last longer than 24 to 36 hours.
Treatment consists of supportive care, including emptying the gastrointestinal tract by flushing the stomach and using medications that cause emptying of the bowels. Medications to support heart function are also given.
Sodium Monofluoroacetate (1080)
1080 is a colorless, odorless, tasteless chemical, and its use is restricted to certain commercial applications. It is highly toxic to all animals, including people, because it overstimulates the central nervous system and causes numerous abnormalities of heart function. Central nervous system stimulation is the main effect in dogs, while the heart effects are more common in horses. Cats appear about equally affected by both.
Nervousness and restlessness begin 30 minutes or more after ingestion. Marked depression and weakness follow in all species except dogs. Animals rapidly become physically weak, and have a fast, weak pulse. Usually, dogs quickly develop muscle spasms, and many dogs show signs of severe pain. Dogs usually lose control of their bladder and bowels and can run in a frenzy. Animals die within hours after signs appear. Few animals that develop signs recover.
If signs are present, vomiting should not be induced. Flushing the stomach and giving activated charcoal and medications to control seizures are recommended. The outlook is grave if signs are severe.
The danger of secondary poisoning caused by eating rodents killed with 1080 is high. In the US, only certified, insured exterminators can purchase 1080, and a black dye must be mixed with it for identification.
Sodium Fluoroacetamide (1081)
1081 causes signs similar to those of 1080 (see Poisoning: Sodium Monofluoroacetate (1080)) and requires the same treatment.
Thallium sulfate can affect all species of animals. It has been banned for use as a rodenticide. Onset of signs may be delayed 1 to 3 days. All body systems are affected, with the gastrointestinal system, lungs, skin, and nervous system affected most commonly. Signs include inflammation of the gastrointestinal tract, abdominal pain, difficulty breathing, blindness, fever, conjunctivitis, inflammation of the gums, and tremors or seizures. After 4 to 5 days and an apparent recovery, or after repeated small doses, the skin can become inflamed, red, and thickened, and hair can be lost.
Treatment of thallium poisoning includes inducing vomiting, flushing the stomach, and administering sodium iodide. Diphenylthiocarbazone can be used as an antidote but is effective only if given within 24 hours of exposure. At the same time and for another 2 weeks, Prussian blue dissolved in water should be given. Symptomatic treatment of the diarrhea and convulsions is needed with particular attention to hydration, diet, prevention of secondary infection, and good nursing care.
Zinc phosphide has been used extensively around farms and barns as a rodent bait. Poisoning causes gastrointestinal tract irritation and cardiovascular collapse. Signs begin rapidly and include vomiting, abdominal pain, and aimless running and howling, followed by depression, difficulty breathing, and convulsions. Death is due to respiratory arrest. Diagnosis is based on history of exposure to zinc phosphide, signs, and detection of zinc phosphide in stomach contents. Zinc levels in the blood, liver, and kidneys may be increased. Treatment includes supportive care, fluids, calcium gluconate, and sodium bicarbonate to neutralize stomach acidity.
Last full review/revision July 2011 by Barry R. Blakley, DVM, PhD; Cheryl L. Waldner, DVM, PhD; Rob Bildfell, DVM, MSc, DACVP; William D. Black, MSc, DVM, PhD; Herman J. Boermans, DVM, MSc, PhD; Cecil F. Brownie, DVM, PhD, DABVT, DABT, DABFE, DABFM, FACFEI; Raymond Cahill-Morasco, MS, DVM; Keith A. Clark, DVM, PhD; Gregory F. Grauer, DVM, MS, DACVIM; Sharon M. Gwaltney-Brant, DVM, PhD, DABVT, DABT; Larry G. Hansen, PhD; Safdar A. Khan, DVM, MS, PhD, DABVT; Garrick C. M. Latch, MASc, PhD; Gavin L. Meerdink, DVM, DABVT; Lisa A. Murphy, VMD; Frederick W. Oehme, DVM, PhD; Gary D. Osweiler, DVM, MS, PhD; Mary M. Schell, DVM; David G. Schmitz, DVM, MS, DACVIM (LA); Norman R. Schneider, DVM, MSc, DABVT