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This article was published in 1960
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INSTITUTE OF INSPECTORS OF STOCK OF N.S.W. YEAR BOOK.

Toxicity of the Newer Insecticides

A REVIEW

F. L. CLARK, B.V.Sc., Veterinary Inspector, Armidale

In recent years a large range of new insecticides has come into widespread use. Some of these compounds have been found to be of use as drenches against certain internal parasites;e.g. "Neguvon" (Bayer L 13/59). Experimental work also is being undertaken on the possibility of using some of these chemicals as systemic insecticides in domestic animals. Already some of them are being used for this purpose in plants.

The use of these organic insecticides is growing and it is obvious that cases of poisoning in livestock will occur from time to time.

Generally the newer insecticides can be divided into two groups: (a) The Chlorinated Hydrocarbons, and (b) The Organic Phosphorus Compounds.

(a) THE CHLORINATED HYDROCARBONS

Since D.D.T. first appeared on the market, a wide range of chlorinated hydrocarbon insecticides has been developed; including such insecticides as benzene hexachloride, toxaphene, chlordane, aldrin, dieldrin and endrin.

These compounds are insoluble in water, but they are soluble in fat and fat solvents. They all can penetrate intact skin when applied in the form of an oily solution or an emulsion. Dieldrin can be absorbed also from the dry powder.

Garner (1957) states that the ease of absorption of these insecticides in the powder form through the cuticle of insects, as compared with the skin and intestinal mucosa of mammals probably accounts for the much greater toxicity in insects than in mammals.

Symptoms of Chlorinated Hydrocarbon Poisoning.

These compounds act primarily on the central nervous system and the symptoms range from depression to convulsions; to death from respiratory paralysis.

Individual animals show a great variety of symptoms. The first seen usually is increased awareness of surroundings. Excitement is common and usually is seen within 24 hours of exposure. Muscular fasciculations which start at the head and gradually extend over the rest of the body are often observed. In the initial stages. champing of the jaws and increased salivation may occur. The muscular fasciculations may abate or increase to spasms; or finally convulsions. This muscular involvement may be continuous or intermittent. Very high body temperatures (118°F in cattle) have been recorded in cases where convulsive seizures occurred.

Explosive symptoms and convulsions are not uncommon. Some affected animals may exhibit depression and drowsiness; while others may show alternate periods of depression and excitement.

Jerome (1958) records symptoms encountered in a field case; where 218 Hereford steers were affected by chlorinated hydrocarbon poisoning out of 370 head sprayed with toxaphene for fly control. The toxaphene solution had been mixed in an old drum which previously had contained endrin concentrate for crop spraying. Insuffcient cleaning of the endrin residues from the drum resulted in the toxaphene solution containing 0.34% of endrin.

183 of the affected cattle died; 95% of deaths occurring within 2½ hours of spraying.

The author was able to describe three different sets of symptoms.

(a) Peracute: Cattle would appear normal whilst grazing and suddenly throw up their heads as if startled. They exhibited a twitching of the facial muscles and ears. There was rapid blinking of the eyes. Symptoms rarely lasted for more than 30 seconds before there was complete respiratory and cardiac arrest.

(b) Acute: These cases would show tetanic spasms without warning. After falling, the affected steers would make spasmodic attempts to rise. Excess salivation and respiratory embarrassment was noted, and if untreated all these cases would die within a few minutes.

(c) Sub-Acute: Nervous symptoms were milder. Spasms would last about 30 seconds; about two minutes after which grazing was resumed. Animals did not always fall to the ground whilst exhibiting tetanic spasms. In this group complete recovery occurred where cases were treated with sedation. In untreated cases recovery gradually occurred within 48 hours, or symptoms increased in severity until the acute syndrome was evident.

Garner (1957) states that as well as acute toxic symptoms, the chlorinated hydrocarbons also can give rise to chronic toxic symptoms due to the persistence of the insecticide in the body fat. The onset of chronic symptoms is slow (in the case of D.D.T., 2-5 days).

Symptoms of chronic poisoning usually first appear as tremors of the head and neck, which gradually extend over the rest of the body and give way to convulsions which become more frequent and severe. Finally, depression occurs; terminating in respiratory failure.

Young animals and emaciated animals are more susceptible to poisoning with chlorinated hydrocarbons than adult animals in good condition. The ability of the body fat to take up large amounts of chlorinated hydrocarbons apparently provides some protection to well conditioned animals. The increased susceptibility of young animals probably is largely due to lack of body fat. In all ages, however, there is a wide variability of individual susceptibility.

Radeleff and Bushland (1953), carrying out experiments after a heavy mortality, found that lactating emaciated ewes were approximately 8 times as susceptible as lactating ewes in good condition. Dips containing as low as 0.03% of gamma isomer have poisoned emaciated nursing ewes. They were found also to be increasingly susceptible to toxaphene and chlordane, but not to the extent observed with B.H.C.

Garner (1957) states that anorexia is a characteristic feature of poisoning with chlorinated hydrocarbon insecticides. This is particularly so in the case of aldrin and dieldrin. Anorexia may persist after sub-lethal doses of aldrin for 2-5 weeks.

Autopsy Findings.

These are variable and alone are not diagnostic. There is usually cyanosis and congestion of the lungs. There are often haemorrhages on the heart. Often an excess of fluid occurs in and around the brain and spinal cord.

Microscopic lesions are few except in chronic cases; when fatty changes and some degeneration are seen in the liver and kidney.

Diagnosis.

Diagnosis is made mainly from the history of exposure to chlorinated hydrocarbon insecticides and the symptoms exhibited.

The body fat can be analysed for the presence of these insecticides. However, positive findings are not always diagnostic of poisoning as these compounds can be stored in the fat from previous exposure.

Radeleff (1958) states that it is important to understand that extremely high residues of chlorinated hydrocarbon insecticides can be present in an animal's fat without appearing to affect its health or well being. He states that excessive amounts on hair or in ingesta would be more reliable indicators of excessive exposure.

Treatment.

There are no specific antidotes. Treatment is confined to controlling the symptoms of depression or convulsions, as the case may be.

Unabsorbed insecticide on the hair or in the alimentary canal should be removed by washing well and using saline purgatives.

(b) ORGANIC PHOSPHORUS COMPOUNDS

Organic phosphorus compounds were developed originally by German chemists as nerve gasses for anti-personnel use. Since World War II these substances have been subjected to intensive research and many useful insecticides evolved.

Many of these substances are extremely toxic. However, their superior insecticidal powers and the fact that insects have been progressively acquiring resistance against the chlorinated hydrocarbons has resulted in their widespread use. The greater part of the research in insecticides is at present being conducted on the organic phosphorus compounds.

Symptoms of Organic Phosphorus Insecticidal Poisoning

The symptoms are related to the interference in the activity of the enzyme that destroys cholinesterase. An exception is made in the case of Dow ET. 57 (vide infra).

Thus signs of poisoning are those that would be expected to result from the persistence of an excess of acetylcholine at nerve endings.

The characteristic signs of poisoning are excessive salivation, with thin watery saliva; respiratory distress, in which animals breath with the mouth open and show greatly exaggerated respiratory movements; stiffness of the legs; and restlessness. Abdominal symptoms may be present, such as vomiting, diarrhoea and hypermotility of the intestines, which may be evident through the abdominal walls.

In severe cases the animal may lose co-ordination and fall to the ground. Respiration may become more and more laboured, and death occur after varying periods.

Radeleff and Woodard (1957) describe the symptoms of poisoning with Dow ET. 57. They state that the predominating syndrome is similar to that of the chlorinated phenols. There is depression, pronounced muscular weakness, inco-ordination and prostration; usually accompanied by diarrhoea. Symptoms appear within 24 hours of exposure and may continue for several weeks. At high dosage, some salivation and dyspnoea may be seen 5-8 days after exposure.

Autopsy Findings

There are no definite pathological changes. Sometimes there may be congestions and oedema of the lungs.

Treatment

Atropine is a specific antidote and it may be administered subcutaneously, intravenously or intramuscularly.

Radeleff, Woodard and Bushland (1956) recommend giving approximately one fourth of the total dose intravenously and the remainder either subcutaneously or intramuscularly.

They recommend for cattle:— atropine sulphate at the rate of 45 mg. per 100 lbs. of weight. Higher doses must be given if the animal is severely poisoned.

They recommend for sheep:— an initial dose of 1 mg, for each pound of body weight.

Regardless of the initial dose, additional doses must be given in most cases to keep the animal under the influence of atropine; usually for at least 24 hours.

Radeleff (1958) states that there is a point of no return in poisonings of this type; beyond which, even though clinical signs are controlled, death will occur.

Woodard (1957) details experimental treatment of organic phosphorus insecticidal poisoning in cattle and sheep.

He found that the use of atropine alone in cattle gave disappointing results; as maintaining a poisoned animal under atropinisation caused death from exhaustion in many instances. However, if atropinisation were not maintained the symptoms of organic phosphorus insecticidal poisoning reappeared and the animal succumbed.

He found that a combination of atropine sulphate and 2-PAM (2 pyridine aldoxime methiodide) was the most effective treatment for cattle poisoned by oral doses of 100 mg./kg. of "Parathlon", or 30 mg. kg. of Diazinon.

The atropine is administered in two doses - 12.5-20 mg. and 37.5-50mg.: each dissolved in 10 ml. of distilled water. The smaller dose is administered intravenously and slowly, and the larger dose is given subcutaneously.

The 2-PAM at the rate of 50 mg./kg. suspended in 100-125 ml. of physiological saline is administered subcutaneously in the cervical region; administering not more than 50 ml. at each injection site.

If symptoms of organic phosphorus insecticide poisoning return; or if the animal does not respond satisfactorily, the treatment can be repeated; but care should be taken not to overdose.

2-PAM is reported to be a specific cholinesterase reactivator.

The author states that 2-PAM was tried exhaustively in sheep by various routes and dose levels, in combination with atropine sulphate, with disappointing results.

He recommends the use of atropine sulphate alone for the treatment of poisoned sheep at the rate of 4-6 mg./kg. in 2 or 3 doses. An initial application of 2 mg./kg., one-third given intravenously in 10 ml. distilled water and two-thirds subcutaneously in the same volume of water, has proved to be the most effective treatment. This usually controls symptoms for 4-6 hours. The remainder of the atropine should be given subcutaneously in divided doses; not more than 4 mg./kg. per treatment in 20 ml. refined peanut oil.

According to the author, sheep can tolerate 4-5 times more atropine than cattle. However, an excess of atropine is worse than not enough, because of its exhaustive powers on poisoned subjects.

References

Radeleff, R. D. & Sushland R. C. (1953)—Vet. Med. 48 : 53
Radeleff. R. D. Woodard, G. T. & Bushland, R. O. (1956)—Animal Diseases, Year Book cf Ag. (1956), U.S. Dept. Agr., pp. 131-142
Garner. T. J. (1957)—Veterinary Toxicology. pp. 209-231. Balliere, Tindall and Cox
Woodard G. T. (1957)—Vet. Med. 52: 571
Radeleff, R. D. & Woodard. G. T. (1957)—Am.Ver.Med. Assoc. 130 : 215
Radeleff, R. D. (1958)—Advances in Veterinary Science IV, pp. 265-273, Academic Press
Jerome. Q. R. (1958)—Vet. Med., 53 : 409.