11 Main Types of Poisoning Found in Animals

List of eleven major types of poisoning found in animals. The types are: 1. Food Poisoning—Botulism 2. Arsenic Poisoning 3. Lead Poisoning 4. Saltpeter Poisoning 5. Mercurial Poisoning 6. Salt Poisoning 7. Caustic Alkali Poisoning 8. Copper Sulphate Poisoning 9. Carbon Tetrachloride Poisoning 10. Hydrocyanic Acid Poisoning 11. Poisoning by Weeds.

Type # 1. Food Poisoning—Botulism:

This food poisoning is caused by ingestion of toxins produced by the activity of Clostridium botulinum in decomposed animal or vegetable matter. Botulism cause rapid motor paralysis. The pathological changes are unknown.

Symptoms:

The onset of symptoms is within a few hours to 4 or 5 days after ingestion of toxin and it may be as long as a week to 10 days. The animal may develop paralysis and die within 24 hours. The dominant symptoms are muscular weakness and paralysis and it is progressive re­sulting in death of animal in a few hours to 3 or 4 days. Usually several animals are attacked at about the same time. Paralysis of pharynx and tongue is not uncommon and the tongue hangs from the mouth. Pulse and temperature are normal.

Control:

No effective remedy has been found. Antitoxin is an effective prophylactic. Vac­cination with botulism toxoid confers high degree of immunity for at least one year.

Type # 2. Arsenic Poisoning:

Acute poisoning:

This is the usual form in domestic animals. It is due, as a rule, to Paris Green (Copper arsenite), white arsenic (arsenic trioxide) or Sodium arsenite. It is extensively used as an insecticide, as a parasiticide, as a poison for rodents and this may cause accidental and crimi­nal poisoning. Paris green is frequently the cause of poisoning.

Lesions:

The chief lesions are those of severe haemorrhagic gastroenteritis. The gastric mucosa is congested, swollen and haemorrhagic. Paris green may be found in stomach contents. In cattle, it may cause perforation of abomasum or the rumen.

Symptoms:

There is a history that one or two animals have died suddenly. Others may be extremely sick. The onset is sudden with marked prostration, staggering, trembling of muscles and muscular twitching. In cattle, mucous membranes congested, pupils dilated, pulse above 100, respi­rations about 30 and the temperature may be normal or little raised. Bowel evacuations may be foetid and bloody and there may be increased thirst. Marked distress is shown by rapid breath­ing, colic and groaning.

Treatment:

The treatment is hopeless when animal has taken a large quantity of poison. In most cases, severe gastroenteritis is present when the case is discovered. The most effective antidote is Sodium thiosulphate. 15 to 30 gms dissolved in 250 ml of water to be given orally, 2 to 10 gms in 10 to 15 ml of water intravenously. Atrophine may be given hypodermically to relieve intestinal cramps and pain.

Type # 3. Lead Poisoning:

It is the most common form of metallic poi­soning in animals. The reason is wide distribution of lead and use of different lead preparations in agriculture—in and the animals are very suscep­tible. The main lead preparations are lead oxide, red oxide of lead, white lead acetate and arsenate of lead. Lead is a cumulative poison.

It is quite corrosive when comes in contact with mucous membrane. It acts as an irritant to nerve centres and specially upon the psychic and motor centres of the cortex and vasomotor cen­tres. It causes atrophy of the peripheral motor nerve endings which results paralysis of striated muscles.

Among the domestic animals, cattle are very sensitive and calves may die from ingestion of very small quantity. Arsenate of lead is the chief cause of lead poisoning. Because of the general use of arsenate of lead spray on veg­etables, the feeding of refuse from garden is a source of lead poisoning. Paint is another source of lead poisoning.

Lesions:

In acute poisoning, acute gastroent­eritis is observed in abomasum and small intes­tine. This is a marked degeneration of liver. Liver and kidneys show a marked parenchymatous de­generation.

Symptoms:

In acute cases, the onset is sud­den and the course is relatively short. Prostration, staggering and inability to rise are prominent symptoms. Temperature may be normal or it may be as high as 104° F (40° C.) In acute lead poison­ing, two distinctive groups of symptoms are no­ticed—gastroenteritis and cerebral symptoms. Cattle often manifest excitation of consciousness and motor irritation and these assist in making a diagnosis.

Poisoned cattle walk in circles, rim into objects because of blindness and there is a change of voice. Other nervous symptoms are grinding of teeth, rapid chewing of the end and a “Kink” in the neck due to contraction of lateral cervical muscles. Pupils are dilated. Loss of appetite, pa­ralysis of digestive tract and a foetid diarrhoea. The faeces are thin, watery and foetid; tenesmus has been observed. The mortality in acute lead poisoning is often 100 per cent.

Treatment:

The chemical antidote is diluted Sulphuric acid or the sulphates of magnesium and sodium. These form an insoluble sulphate of lead. Camphor and strychnine are recommended for paralytic condition. Large and frequent doses of aromatic spirits are useful. Atrophine sulphate (gr 1/4) 15 milligrams is beneficial in the treat­ment of acute symptoms. Sodium citrate may be administered and it helps in increased urinary excretion of lead and a fall in blood lead concen­tration.

Type # 4. Saltpeter Poisoning (Potassium Nitrate, Sodium Nitrate):

There have been cases of accidental poison­ing due to administration of excessive amounts of Potassium nitrate when it was mistaken for salt or Sodium chloride. This chemical is used in many farms for use as a fertiliser and animals may accidentally consume enough to cause death in a few hours.

A dose of 25 gms of Potassium nitrate per 45 kg body weight may cause suffi­cient methemoglobinemia to cause death in calves. The conversion of haemoglobin to methemoglobin increases until it reaches 80% of the total blood pigment, at this time the animal dies.

Morbid Anatomy:

Mucous membrane of the abomasum and small intestine is dark red, purple, or cherry-red in colour and it may be eroded from the caustic action of the salt. Congestion and haemorrhage are sometimes found in the blad­der and kidneys.

Diagnosis:

The diagnosis can readily be made by drawing a little quantity of blood into a syringe and observing the colour, which is dark chocolate brown.

Symptoms:

It causes severe gastroenteritis and the course is rapidly fatal. Cows turned to pasture in the morning may be found dead at night. It begins suddenly with severe colic, saliva­tion, vomiting, bloating and polyuria. Depres­sion, weakness and prostration soon appear. Temperature normal. It may be mistaken as lightning strike or anthrax when the animals have been found dead without any apparent cause of death.

Treatment:

Methylene blue in doses of 2 grams per 225 kg body weight injected intrave­nously immediately counteracts the effect of the nitrate by converting the methemoglobin into haemoglobin. Stimulants should also be adminis­tered to combat prostration. Mucilaginous sub­stances to counteract the caustic action.

Type # 5. Mercurial Poisoning:

The most common cause is found in the faulty use of mercurial preparations for medicinal purposes. Cattle are very susceptible and they are the usual victims. The drug calomel is very toxic to cattle.

Morbid Anatomy:

There is haemorrhagic gastroenteritis and ulceration in the stomach. The mucosa is oedematous. Liver and kidneys are swollen and the latter may show haemorrhages under the capsule. The lungs are congested and presents areas of Broncho-pneumonia with ab­scess formation. The blood is dark red and coagu­lates slowly.

Symptoms:

Calomel and gray mercurial oint­ment are the main cause of mercurial poisoning. The general symptoms are depression, refusal to eat, increased rulse rate, respiration and tempera­ture. There may be skin lesions with itching, loss of hair and formation of thick scabs. Cough with a foetid breath and there may be pulmonary haemorrhage. The course is brief and almost fatal. There may be bleeding from all organs, especially from the mucous membranes of the nose, lungs and intestines.

Treatment:

Main emphasis is’ given on the mechanical removal from the alimentary canal before it reaches the portal circuit. Administer white of eggs, large quantity of milk to precipitate the mercury. Any mercurial preparation on the skin should be washed off. Ferrous sulphate may be given to form insoluble compound. To combat depression, administer coffee and atropine.

Type # 6. Salt Poisoning (Sodium Chloride):

It is a normal food and not a poison. But when it is consumed in large amounts, sickness may result.

Symptoms:

The main symptoms are diar­rhoea and diminished milk flow. When excessive amounts have been consumed, there may be com­plete loss of appetite, redness and dryness of the oral mucosa, colic, polyuria and blindness. The nervous symptoms are marked weakness and paralysis of hind parts or general paralysis.

Morbid Anatomy:

Gastroenteritis, the mu­cosa of abomasum is swollen and haemorrhagic. Blood may be bright red and thin.

Treatment:

Give linseed meal gruel or Bis­muth subnitrate in milk. Give camphorated oil or Ammonium carbonate of Caffeine sodium benzoate.

Type # 7. Caustic Alkali Poisoning:

These include Caustic Potash, Caustic Soda, Quick lime and Ammonia.

Morbid Anatomy:

On autopsy, one finds croupous and diphtheretic stomatitis, pharyngitis and Oesophagitis. The stomach presents gelati­nous swelling and corrosion with extensive oedema. It causes diffuse moist necrosis. The blood forms a brown, thick gelatinous mass.

Symptoms:

Its action is very corrosive. It causes swelling, salivation and difficulty swallow­ing. Burning of lips and mouth is marked. Corro­sion caused by caustic alkalis in soft and greasy (‘Colliquation’) in contrast to dry and brittle cor­rosion caused by acids (‘Solid mortification’). In­halation of ammonia fumes causes painful cough, nose bleed, irritation of the mucosa of the nose, throat and eyes, bronchitis, pneumonia. In stom­ach, it causes severe pain and gastroenteritis.

Treatment:

In the first stage, dilute acetic acid or weak vinegar are indicated. For the local effect, give oily and slimy mixtures and narcotics to control the pain. Mineral oil, linseed oil gruel, milk and Bismuth sub-nitrate mixture is beneficial. Prognosis is not good.

Type # 8. Copper Sulphate Poisoning (Blue Vitriol):

Animals have been poisoned from eating plants and grain after sprinkling with Copper sulphate solution. It causes severe and fatal gastroenteritis.

Morbid Anatomy:

Intense inflammation of the abomasum and small intestine is noticed. In addition to gastrointestinal haemorrhage, the liver is brownish yellow and swollen, spleen enlarged and kidneys are congested. The kidneys are swol­len and tubules filled with bloody casts.

Symptoms:

It is characterised by abdominal pain, vomiting and purging. After a time, there may be collapse and convulsions. Pulse and tem­perature are high and mucous membranes are congested. There may be anorexia and great thirst. Sometimes, jaundice may develop if course is prolonged.

Treatment:

The antidotes of Copper sulphate poisoning are Magnesium oxide, Sulphur, white of eggs, milk and dextrose. The mortality is high, stimulants may be prescribed for weakness.

Type # 9. Carbon Tetrachloride Poisoning:

Carbon tetrachloride is now being extensively used as a vermifuge in sheep for liver fluke dis­ease and for the expulsion of hook worms. Fol­lowing dosing with this drug, deaths may occur within 24 hours from severe pulmonary oedema or may occur 3-7 days later due to renal and hepatic insufficiency. The normal dose is 1 to 2 ml given in capsules. Inhalation of Carbon tetrachlo­ride causes acute depression of central nervous system and peripheral and circulatory collapse.

Symptoms:

The poisoning starts with stag­gering, falling, progressive narcosis, collapse, con­vulsions and death due to respiratory failure.

Postmortem Lesions:

There is severe inflam­mation of the abomasum and the intestines. There may be marked degeneration of liver and echymoses in the omentum and peritoneum. The renal lesions comprise extensive degeneration and necrosis of the tubular epithelium.

Treatment:

In inhalation poisoning, artificial respiration and respiratory centre stimulants are indicated in seriously affected animals, repeated parenteral injection of glucose and protein hydrolysate should be given.

Type # 10. Hydrocyanic Acid Poisoning (Prussic Acid, HCN):

Hydrocyanic acid is a colourless, volatile liq­uid possessing a characteristic odour described as that of peach blossoms. Animals are poisoned by eating certain plants and grass which are capable of developing hydrocyanic acid and it is formed from various glucosides. Sorghum is one of the more common sources of cyanide poisoning in animals and it is believed that glucoside is split by the enzyme emulsion into hydrocyanic acid, dextrose and benzaldehyde.

The following plants are capable of producing hydrocyanic acid:

1. Choke cherry

2. Black cherry

3. Sorghum

4. Johnson grass

5. Flax

6. Arrow grass

7. Velvet grass

8. Christmas berry and

9. Sudan grass.

Poisoning of animals may be caused by graz­ing on plants containing cyanide or by accidental or criminal use of cyanide compounds. The cyanide-containing grasses and sorghum are poison­ous when growing green in a stunted manner. Linseed cake or meal may also cause poisoning.

Action of cyanides:

The cyanides act on the protoplasm and suspend the activity of all forms of living matter. Acute cyanide intoxication causes a histotoxic anoxia and resultant tissue asphyxia. Oxygen exchange is suspended and oxygen is retained in the blood, giving it a characteristic bright red colour. If the course is prolonged, the blood may be dark red due to inhibition of respi­ration and restriction of oxygen intake. Because of the severity of anoxia, the major manifestation of cyanide poisoning is that of cerebral anoxia with tremor and convulsions and dyspnoea.

Symptoms:

Hydrocyanide acid poisoning is always acute and affected animals rarely survive more than 1-2 hours. In the most acute cases, animal becomes affected within 15 minutes of eating toxic material. There is dyspnoea, anxiety, restlessness, moaning, recumbency and terminal clonic convulsions. In less acute cases, the animal shows depression, staggering, muscle tremor and lacrimation.

The muscle tremor is evident first in head and neck and later involve rest of the body. Animal becomes weak and goes down. Pulse is faint and weak and rapid. In the terminal stages, there is dilatation of the pupils and cyanosis and accompanied by clonic convulsions and vomiting. The course may be 1-2 hours.

Diagnosis:

The suspected plant material and ruminal contents may be tested for presence of hydrocyanic acid. The shredded plant material or rumen contents is placed in a test tube will little water and a few drops of chloroform and heated very gently in the presence of sodium picrate paper. A rapid change in the colour of the reagent paper from yellow to red indicates the presence of free hydrocyanic acid. It may take 5 to 10 minutes before the colour change commences.

Postmortem Findings:

In very acute cases, the blood may be bright red in colour but, in field cases, it is dark red due to anoxaemia. The muscles are dark and congestion and haemorrhage may be noticed in the trachea and lungs. A smell of bitter almonds in the rumen is described as typi­cal of hydrocyanic acid poisoning.

Treatment:

A mixture of Sodium nitrate and Sodium thiosulphate in the proportion of 3 g of Sodium nitrate and 15 g of Sodium thiosulphate in 200 ml of water to be given intravenously for cattle; and for sheep, 1 g of Sodium nitrate and 2.5 g of Sodium thiosulphate in 50 ml. The treat­ment may have to be repeated. Sodium nitrate or Sodium thiosulphate may be given alone but the combination is more effective.

Sodium thiosul­phate should also be given orally and directly in the rumen to fix the free hydrocyanic acid in the rumen. The acid is taken up by thiosulphate to form thiocyanate which is non-toxic and readily excreted. According to latest observation, cobalt has a marked antagonistic effect against cyanide. So, when it is combined with Sodium thiosulphate or Sodium nitrite, it gives better result. ,

Control:

Cattle and sheep must not have access to toxic plants, specially Sorghum, when they are immature, wilted, frost bitten or growing rapidly after a retarded growth. Linseed meal should be given in small quantities without soak­ing and gruel containing linseed should be thor­oughly boiled to drive off any free hydrocyanic acid.

Type # 11. Poisoning by Weeds:

In India, lantana poisoning occurs in cattle, sheep, goat, horse etc.

Etiology:

Lantana contains a hepatotoxic sub­stance Lantadene A, a terpene compound.

Lantana poisoning cause hepatic insufficiency and renal tubular lesions, neither of which are specific. Iriterpenes are considered to be principal toxic agent in this plant. Of them, lantadene A is the most toxic substance and lantana toxin inhib­its the active secretion of bile acids into bile canaliculi.

Symptoms:

Disturbances in consciousness, muscle weakness and jaundice are major abnor­malities in this disease. Lantana has secondary toxic effects on kidneys causing fatal nephro-toxicosis, nephrosis and uraemia and also cause chronic constipation.

Postmortem Findings:

Destruction of liver cells and replacement by fibrous tissue is seen. There may be inflammation of abomasum with acute hepatic degeneration and petechial hae­morrhages scattered all over the subcutaneous tissue and viscera.

Diagnosis:

It is quite difficult. This disease produces a syndrome which is similar in many ways to primary disease of nervous system. It may be mistaken for Equine encephalomyelitis but fever is absent here. In cattle, it may resemble rabies, lead poisoning. In sheep, the diagnosis is difficult except photosensitization is a frequent sign.

Treatment:

It is of little value. Intake of car­bohydrate food must be increased either by forced oral or intravenous feeding to tide over the seri­ous liver dysfunction.