Page 656 - Veterinary Toxicology, Basic and Clinical Principles, 3rd Edition

Non-Anticoagulant Rodenticides Chapter | 47 621

VetBooks.ir chlorinated hydrocarbons, and plant alkaloids. 1-naphthyl-thiourea, N(1-naphthyl)-2 thiourea, Alrato,
Differential diagnosis should include lead, strychnine,
Anturat, Bantu, Dirax, Krysid, Rat-tu, and Rattrack.

Treatment Toxicokinetics and Mechanism of Action

There is no specific antidote for compound 1080 poison- Following ingestion, ANTU is rapidly absorbed from the
ing. Use of glyceryl monoacetate has shown some posi- GI tract. The exact mechanism of action of ANTU is not
tive results because it provides acetate ions to allow known. ANTU stimulates the sympathetic nervous sys-
continuation of the cellular respiration process, which is tem, and causes a major increase in the permeability of
interrupted by compound 1080. Other symptomatic and the lung capillaries; consequently, extensive pleural effu-
supportive measures following decontamination proce- sion and pulmonary edema develop. This results in respi-
dures (to prevent further absorption by activated charcoal) ratory failure.
include use of anticonvulsants, muscle relaxants, and
mechanical ventilation. Induction of emesis is contraindi-
cated because of potential arrhythmias and convulsions. Toxicity
Special attention should be paid to stabilize cardiac and
All animal species are susceptible to ANTU, but lethal
CNS functions.
doses differ widely. Lethal doses of ANTU (in mg/kg) in
Acetate and ethanol have been found to be potentially
various species are as follows: rats (3), dogs (10), pigs
effective in mice, guinea pigs, and rabbits, but not in
(25), horses (30), cows (50), cats (75), and fowl (2500).
dogs. A combination of calcium gluconate and sodium
Clinical signs of poisoning due to ANTU include
succinate has proven effective in mice (Omara and
vomiting, abdominal pain, dyspnea, shortness of breath,
Sisodia, 1990). Calcium chloride has antidotal effects in
seizures, bluish discoloration, coarse pulmonary rales,
cats (Roy et al., 1980).
pulmonary edema, and liver damage. In a time-course
study, ANTU at a dose rate of 5 mg/kg induced lung
Conclusion edema in adult albino rats (Vivet et al., 1983). After 6 h,
pulmonary extravascular water increased by 50% in
Fluoroacetate converts to fluorocitrate, which is an
ANTU-treated rats, and the volume of the pulmonary
extremely toxic metabolite. Symptoms vary markedly
effusion reached 3.4 6 0.1 mL. The most characteristic
between species. For example, carnivores exhibit more
feature is the absence of hypoxemia in ANTU-intoxicated
signs related to the CNS, herbivores exhibit signs related rats. The absence of hypoxemia is common with normo-
to cardiac effects, and omnivores show signs of both CNS baric oxygen. ANTU can produce hyperglycemia of three
and cardiac effects. Treatment relies on symptomatic and times normal in 3 h.
supportive measures. Chronic sublethal exposure to ANTU may cause
enlarged thyroid gland (goiter) and interfere with normal
thyroid function. Repeated sublethal doses in rats lead to
ALPHA-NAPHTHYL THIOUREA
the development of tolerance so that resistance to several
Introduction lethal doses develops (Peoples, 1970).
Alpha-naphthyl thiourea (ANTU) is a colorless, odorless,
crystalline powder that is exclusively used as rodenticide. Diagnosis
The technical product is gray powder. Its chemical formula
is C 11 H 10 N 2 S, and it has a molecular weight of 220.28. Its Diagnosis of ANTU poisoning is based on evidence of
structural formula is shown in Fig. 47.6. ANTU has several rodenticide exposure, clinical signs, lung and liver dam-
other names, including alpha-naphthyl thiocarbamide, age, and chemical confirmation. ANTU can be quantified
using HPLC.

Treatment
There is no specific antidote; therefore, treatment relies
on symptomatic and supportive measures. Induce vomi-
tion if the patient is not showing convulsions and seizures.
The decontamination procedure includes administration of
FIGURE 47.6 Structural formula of alpha-naphthyl thiourea. activated charcoal.