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.
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