Toxicity of Rodenticides

RODENTICIDES

            Rodenticides are agents which destroy the rodent pests. Some of the commonly used rodenticides are alpha-naphthyl thiourea (ANTU), warfarin, zinc phosphide, red squill etc.

Alpha-naphthyl thiourea (ANTU)

            Source of poisoning Accidental ingestion of baits intended for target rodents.

            Mechanism of toxicity ANTU interferes with effective uptake of O₂ from pulmonary alveoli by producing extensive edema of the lungs due to increased capillary permeability and seepage of fluid into the airways. This leads to formation of froth which further blocks the air passage and virtually the animal drowns in its own body fluids.

            ANTU induces vomiting in dog if the stomach is empty as it is highly irritant to gastric mucosa.

However, ANTU will fatally poison an animal if the stomach is full.

            Clinical symptoms Signs of ANTU poisoning include vomiting, dyspnea, cyanosis, rales, tachycardia, anorexia, incoordination, prostration, cough, snort, asphyxiation, coma, clonic convulsions and death.

            Lesions Cyanosis, dark colored arterial blood, heavy and edematous lungs, presence of blood-tinged fluid and froth in the bronchi, hydrothorax, hyperemic tracheal, bronchial and GI mucosae, liver and kidneys may be noted.

            Diagnosis History of employing ANTU as baits; Clinical signs; Post mortem lesions.

            Treatment Emetics or gastric lavage; Sedatives like barbiturates; Oxygen under positive pressure. Competitive ANTU antagonist, l-ethyl-l-phenyl thiourea may reverse ANTU toxicosis in rats. Alpha adrenoceptor antagonists to dilate pulmonary vessels. Osmotic diuretics (50% glucose or mannitol).

Warfarins

            Warfarins and its analogs are anticoagulant rodenticides. Commonly used warfarin rodenticides are warfarin, pindone, chlorphacinone, naphthyllindandione etc.

            Sources of poisoning Ingestion of residues of the rodenticides or baits intended for rats and mice. Pigs, dogs and cats, if they ingest dead rats or mice which are killed by these groups of agents.

            Mechanism of toxicity Warfarins interfere with normal function of Vitamin K and cause coagulation defect characterised by decreased blood concentrations of coaugulation proteins - factor II (prothrombin), factor VII (proconvertin, autoprothrombin I), factor IX (Christmas factor, autoprothrombin II) and factor X (Stuart factor, autoprothrombin III). The decreased coagulation factors cause massive internal bleeding and the onset time is 2-5 days and death of animals is due to tissue hypoxia.

            Clinical symptoms Massive haemorrhages, blood discharge from body orifices, haematomas under skin and at joints, purpura, dyspnea, weakness, shock and death.

            Lesions Massive internal haemorrhages, blood is found in GIT, thorax, joints and pericardium, hepatic necrosis and jaundice may be seen.

            Diagnosis  History; Clinical signs; Post-mortem lesions.

            Treatment Sedatives or transquilizers; Artificial respiration; Provide clotting factors by blood transfusion at the rate of 20 ml/kg body weight. Injection of Vitamin K, 5 mg/kg, slow IV dogs and cats. Repeat for two days by IM route. In large animals, a dose of 0.5- 1.0 mg/kg by slow IV injection and oral Vitamin K should be administered daily for 4-6 days.

Zinc Phosphide

            Zinc phosphide (Zn₃P₂) is commonly used rodenticide for destroying the rats, mice, ground squirrels and dogs.

            Sources of poisoning Baits intended for target rodents may be eaten by other animals or birds. Malicious poisoning.

            Mechanism of Toxicity Zinc phosphide is directly irritant to gut. This action causes vomition, a life saving reflex in animals that can vomit. Produces severe gastroenteritis.

            Acute Zn₃P₂ toxicosis is neither due to zinc nor phosphorus. The Zn₃P₂ liberates phoshine (PH₃) in the stomach and upper intestine. Any factor which stimulates the gastric H Cl concentration, Zn3P2 toxicity. Absorbed phoshine is responsible for development of toxicosis. However, toxicity is possibly due to both Zn₃P₂ and phoshine.

            Clinical symptoms Anorexia, lethargy, increase in rate and depth of respiration, sterterous respiration, abdominal pain, bloat (in ruminants), ataxia, weakness, prostration, dyspnea, gasping, convulsions, coma and death in 4-48 hours.

            Lesions Pulmonary congestion and edema, pleural effusion, subpleural haemorrhages, congestion of liver and kidneys and gastroenteritis. Acetylene odour in stomach may be detected.

            Diagnosis History, Clinical signs and Post-mortem lesions.

            Treatment No specific treatment, however, following supportive therapies may be given. Gastric lavage with 5% sodium bicarbonate. Injection Calcium borogluconate. Treatment for shock. Anticonvulsants.

Fluoroacetate

            Fluoroacetate as such is non-toxic but becomes highly toxic after its conversion in the body to fluorocitrate (lethal synthesis).

            Mechanism of toxicity Due to structural similarities, fluoroacetate competes with acetate. In place of acetate, fluoroacetate condenses with CoA and oxalocetate to form fluorocitrate. Fluorocitrate competes with citrate for the active site of Kreb's cycle enzyme aconitase (the target receptor of fluoroacetate poisoning). This results in inbihition of aconitase leading to slowing of Kreb's cycle and decreasing cellular respiration. The brain and heart functions are most severely affected.

            Clinical signs CNS excitation, restlessness, vomiting, diarrhoea, urination, hyperirritability, hypermotility, frenzied running, barking, frothing at mouth, clonic-tonic convulsions, terminal coma, gasping and death within 2-12 hours have been observed in dogs and guinea pigs. In horse, cattle, sheep and goats, colic, unrest, trembling staggering, cardiac arrythmias, tachycardia, terminal ventricular fibrillation and death. Both CNS and cardiac signs are observed in swine, cats and hasmters.      .

            Diagnosis History of accidental ingestion of fluoroacetate bait. Clinical signs.

            Treatment No specific treatment. Barbiturates to control the convulsions. Glycerol mono acetate 0.1-0.5 mg/kg, IM. Treatment for cardiac arrythmias may be tried.

Red Squill

            Red squill is obtained from the plant-Urginea martima sea onion. Red squill contains a cardiac glycoside-scilliroside. This compound is comparatively one of the safest rodenticides as it is non-toxic to poultry, causes emesis in animals that are capable of vomiting and very unpalatable to domestic animals. Red squill is more toxic to female rats than males.

            Clinical signs Small doses of red squill cause convulsions and higher doses may produce cardiac arrest before exhibiting convulsions. In livestock, CNS stimulation symptoms such as hyperasthesia, incoordination and flank convulsions may be noted.

            Lesions Gastritis and enteritis-sometimes haemorrhagic. Pronounced congestion of mesenteric vessels; swelling and congestion of kidneys, liver, lungs and myocardium may be noticed. Histopathological examinations of these organs may reveal degenerative changes.

            Diagnosis  History; Clinical signs.

            Treatment Symptomatic and supportive therapies.