Introduction

Poisoning is also referred to as toxicosis or intoxication. Pets are unable to distinguish between harmful substances and are unable to know if a substance is harmless, harmful or poisonous.

All toxic effects depend on the lethal dose and the amount of the harmful substance present. Symptoms to poison develop also in close relation to the exposure. Absorption of a poison is necessary for systemic poisoning.

1.1 Corrosive substances

In contradiction to poison, chemical substances described as corrosive substances, will destroy tissue but might not absorb through the skin. Common corrosives are either strong acids, strong bases, or concentrated solutions of acids or bases. They can exist as any form such as liquids, solids, gases, mists or vapours.

1.2 Chemical substances

In warfare, chemical substances are constructed to act as deadly nerve agents. A well-known chemical substance is the “VX nerve agent.” Nerve agents are the most toxic and fast-acting substance known in chemical warfare, according to the US Centres for Disease Control and Prevention (CDC).

1.3 Difference between humans and animals

Humans and animals differ insofar their ability to be in danger when exposed to different products and household substances, due to the notable metabolic differences between animals and humans.

Metabolism or metabolic actions are the set of life-sustaining chemical transformations within the cells of living organisms.

1.4 Metabolic actions within the body has three main purposes;

the conversion of food or fuel to energy to run cellular processes

the conversion of food or fuel to building blocks for proteins, lipids, nucleic acids, and some carbohydrates

the elimination of nitrogenous wastes.

1.5 Dosages

Many food and other substances are fine with humans, but lethal to pets. It can cause organ failure and or shock. A small dose of poison may be undetectable and have no harmful effects. Large dose of poison can be fatal.

https://www.youtube.com/watch?v=2z35_1e1MtI

 

2. How do animals get poisoned?

Pets are often poisoned by eating toxic baits (for rodents)

By eating poisonous seeds and plants.

By drinking toxic fluids such as antifreeze and other harmful household substances.

By the sting of a bee, insects, scorpions and spiders.

By the saliva of parasites such as ticks, fleas and various fly species.

Spit and bites from a range of venomous snakes and,  

By their owners, by administering human drugs, sugar, certain foods, alcohol and even corrosive substances for treatment extremely toxic to pets.

 

2.1 Poison, toxins and venom

In biology, poisons can be labelled as elements that cause disorders in and to living organisms. In veterinary medicine and zoology, poisons are categorised as poisons, toxins and venom. Their activity is usually on a molecular scale. The mode of action with poison is usually via chemical reaction in the bloodstream of the victim, affecting vital organs such as the heart, lungs, kidneys in the organism’s body.

2.2 Delivery method

The difference between venom and other poisons are the delivery method.

Poisons are manmade and constructed to disturb or eliminate plants or living organisms such as parasites, rats, cockroaches, fleas flies etc. Mostly ending up in the bodies of their victims, in animals such as vultures, in soil then into plants, in air as in breathing, in fish as in water resources.

Toxins are poisons broadly produced by plants, as in flowers, fungi and bacteria.

Venoms are toxins injected by a bite or sting from an animal

2.4 Pesticides

Are poisonous substances constructed to control specific living organisms such as pests on crop such as cotton and maize, weed control in crops, flies in dairy’s and laughter houses, rats in the home, cockroaches, ticks and fleas etc.

 

 

Dogs, with their enormous ability to smell, explore what they smell and the places they do smell these things that tickle their curiosity. of interest. Their curiosity might lead them to explore harmful substances or dangerous places such as bushes, wood piles, storage areas, dump sites or holes. Their smelling ability and curiosity leads them to insects excreting pheromones, or to smelly material with bacteria and organisms hiding in bait, dead animals or toxin plants.

It is very possible that the exact cause of poisoning will never be known.

4.1 Malicious poisoning

In South Africa, intentional and malicious poisoning of especially dogs and cats is a factor to reckon with and is perhaps more famous than unintentional poisoning. Malicious poisoning usually is with rat poisons or a plant poison known here as Temik.

4.2 General treatment of poison

It is in all cases important to determine what substance the animal is poisoned with. If the substance is unknown, it is important to induce vomiting soonest possible.

4.3 Do not induce vomiting if;

The animal has already vomited

The animal is in shock, having breathing difficulties

The animal is unconscious or convulsing

The dog has swallowed a sharp object that could stuck in the oesophagus, or perforate the stomach

The animal has swallowed acid, alkali, any harmful cleaning solution, household chemicals and or petroleum products

The animal is in stupor or non-responsive

Shows any sign of neurologic involvement

The label on the product says, “Do not induce vomiting.”

There are two groups of chemicals where vomiting should never be induced. The products, when ingested injures the mouth, cause blister like wounds to the oesophagus and stomach. Severe cases cause perforations of the stomach and muscle tissue of the oesophagus.

4.5.1 Corrosive and caustic chemicals

This group are the acids and alkalis which are found in general household cleaners. They are toilet bowl cleaners, dishwashing liquids, washing detergents, anti-rust mixtures, fat removers, alkaline batteries, drain cleaners and many other commercial solvents.

4.5.2 Petroleum Products

This group can be categorised as petrol, diesel, kerosene and turpentine. They cause pneumonia when inhaled. They also gastrointestinal upset. Petroleum products are very irritating to the skin and must be washed of as quickly as possible with luke warm water and soap. Wash the mouth with water to remove petroleum deposits.

5. Steps to Induce Vomiting

Vomiting has one important goal in mind. That is to prevent poison absorption. Vomiting focus on poison that was swallowed.

5.1 Step 1:

Option 1: Induce vomiting is by administrating with a sterile syringe, a 3% hydrogen peroxide solution per kg weight as follow;

1 teaspoon or 5 ml peroxide per every 4.5 kg body weight

Repeat every 15 to 20 minutes, up to three times, until the dog vomits.

Walking the dog after giving each dose may help to stimulate vomiting.

 

Option 2

Administer with a syringe a solution of 1 tablespoon of washing power, diluted in one 250 ml cup of luke-warm water.

Administer the soapy solution slowly and prevent the solution from entering the lungs

Administer the solutions from the side of the mouth, whilst holding the head a little up. It is important to find a natural but forced position that force the animal to swallow the solutions by itself.

Repeat until the dog is vomiting.

Stop when the dog has vomit.

5.2 Step 2

Step 2 has also two options. Activated charcoal and egg white solution

5.2.1 Activated Charcoal

Once the dog has vomited and the poison has been cleared from the dog’s stomach, administer activated charcoal to bind any remaining poison and prevent further absorption.

Activated charcoal must be administered orally.

The best product is a compressed tablet. It is measured and easily administered

Activated charcoal also comes in a power, in granules, a liquid and in 5 gram tablets.

The recommended dose per 4.5 kg of body weight, is one 5-gram tablet activated charcoal.

 

5. 2.2 Egg white solution

If activated charcoal is not available, coat the intestines with milk and egg whites

Collect a ¼ cup, which is approximately 60 ml of egg whites, and blend with a ¼ cup of full creamed milk.

This would suit a dog of 4.5 kg of body weight.

A dog of 9 kg would need 120 ml off egg white and ½ a cup of full creamed milk

Administer the egg white and milk solution into the dog’s cheek using a plastic syringe.

6.  Hypoxia

Poison intake can cause seizures and seizures can cause lengthy periods of hypoxia.

6.1 Seizures and epilepsy

Seizures caused by poisons that stimulate responses from the central nervous system, such as alkaloids, i.e. strychnine, may cause confusion and the result may be a judgement mistakenly for epilepsy.

Atropine is used to reduce saliva and fluid in the respiratory tract that could cause hypoxia.  

There is a true difference between epileptic seizures and seizures causes by poison. Seizures caused by poison return usually as a norm within minutes. It distinguishes itself from epilepsy by exhibit tremors, lack of coordination, weakness, abdominal pain, and diarrhoea.

In the case of epilepsy, seizures are brief, seldom last more than two minutes and is followed by a quiet period in which the dog appears disorientated, but otherwise normal.

7. Contact Poisons

In situations where animals are exposed to poisonous substances;

Always use rubber gloves

Hose the animal down with water in an area, such as a tub, that will not harm the immediate environment and or other living creatures

Wash the animal in a tub of luke warm water with a mild soap, to prevent any intake by licking

Flush the immediate contaminated area with large amounts of water, or with products as suggested on the label of the product.

Have a conservative attitude towards contact poisons. Wash and remove and prevent.

 

8. Drug poisons

8.1 Human drugs

Many people administer “over the counter” human drugs and medicines, even prescription drugs to their pets to treat a variety of symptoms.

This is a very dangerous practise. Human drugs are in general extremely toxic to pets because they do not have the same metabolic enzymes to detoxify and break down these drugs within the liver, bloodstream or kidneys.

It may seem to be harmless after it is being administered, but it is far from the truth. It leads to an accumulation of dangerous substances that hides somewhere in the storage places of the body, as the body nor the immune system recognise these foreign particles or know how to deal with them.

Severe and sudden organ damage can happen because of this. Symptoms develop quickly, after the body’s ability to sustain these chemicals are over extended. Symptoms include abdominal pain, salivation, vomiting, and weakness.

Human drugs that produce a variety of toxic effects are birth control pills, hormone prescriptions, antihistamines, sleeping pills, diet pills, heart pill, blood pressure pills and vitamins.

Treatment: If you suspect your pet has swallowed any drug, induce vomiting immediately.  

8.2 Veterinary drugs

Many drug poisoning occur with veterinary prescription drugs. Veterinary products are also often filled with attractive flavourings to encourage the intake of the drug. There is no such thing as safe medicine of a safe drug.

Prevention: Accidental poisoning can be prevented Store all drugs in a secure place to prevent inadvertent consumption by pets and children. Never assume that a human drug is safe for pets!

9. Rat and rodent poisons

Rat and rodent poisons consists of

anticoagulants and

hypercalcaemic agents.

 

9.1 Anticoagulants:

Anticoagulants are referred to in general as blood thinners. It consists of substances that prevent the coagulation of blood and or prolongs the time of blood clotting. In Nature, anticoagulants occurs in blood-sucking animals such as ticks, leeches and mosquitoes. Anticoagulants keeps the blood thin and unclotted for as long as the blood sucking parasite needs in his blood meal to suck blood.

In human medicine, anticoagulants are used in therapy for thrombotic disorders. Disprin tablets are used in many instances.

In rodent poisons, the function of anticoagulants in this poison is to block the synthesis of vitamin K, which is an essential vitamin in normal blood clotting.

9.2 Vitamin K deficiency

Vitamin K deficiency, caused by anticoagulants in rat poison, will result in various spontaneous bleedings in the poisoned animal. Dogs will become weak and pale from blood loss and the physical signs would be;

nose bleeds

vomiting blood

rectal bleeding

haemorrhages beneath the gums

hematomas - local collection of blood outside the blood vessels

bruises- (A discoloration of the skin, commonly known as a bruise, is a type of hematoma of tissue in which capillaries are damaged by a bump or traumatic incident, allowing blood to seep into the surrounding interstitial tissues.)

Vitamin Kl is therefore with anticoagulants a specific antidote. It is given by subcutaneous injection and repeated subcutaneously or orally as necessary until clotting time returns to normal.

With first-generation anticoagulants, bleeding often occurs within a week. With long-acting anticoagulants, treatment takes up to a month because of the length of time the poison remains in the dog’s system.

9.3 Different anticoagulants generations

Literature refer to three generations of anticoagulants. The second group are closely related to group three.

Anticoagulants with a cumulative mode 

Anticoagulants with immediate effect

Anticoagulants from the “Indanedione” class

9.3.1 The first group or generation is known as cumulative poisons. The rodent needs to feed a few times from the bait before it will kill the rodent. These poisons contain the anticoagulants warfarin and hydroxycoumadin.

Anticoagulants are not only to be found in rodent poisons. It is also available in many household products. Anticoagulants are:

Warfarin

Hydroxycoumadin

Brodifacoum

Bromadiolone

Pindone

Diphacinone

Diphenadione

Chlorophacinone

9.3.2 The second generation of anticoagulants kills the animal after one single feeding. They contain bromadiolone and brodifacoum. These poisons are 50 to 200 times more toxic than warfarin and hydroxycoumadin.

These products are extremely dangerous to pets. It will therefore be able to kill a small dog, if it eats the dead rodent, with the left over residual poison in its stomach. Closely related to the second-generation of anticoagulants, are the extremely toxic long acting anticoagulants of the “Indanedione” class.

They are

Pindone

Diphacinone

Diphenadione and

Chlorophacinone.

 

9.3.2 Treatment of anticoagulants

Induce vomiting as described above, with activated charcoal or egg white

Administering Vitamin K tablets orally

Seek immediate veterinary help, especially with second generation anticoagulants 

Always try to get hold of the product container to identify the poison.

Treatment will depend on whether the poison was a first- or second generation anticoagulant.

Spontaneous bleeding caused by all anticoagulants, may involve intravenous administering of fresh whole blood or frozen plasma, determined by the rate and volume of blood loss.

9.2 Hypercalcaemic agents.

Hypercalcemic agent poisoning is a highly poisonous substance consisting of toxic levels of calcium, containing Vitamin D3 (cholecalciferol). This substance is a popular substance in rat poison. It could also be found many other environmental and home-use substances. Hypercalcaemic agents are a very popular agent because rodents do not develop resistance to them.

Occasionally, with exception of smaller dogs, dogs who eat poisoned rats will not develop any sign of illness or any toxicity. In almost all cases, the dog must eat the poison itself to become poisoned and ill.

 

9.3 Toxicity

Hypercalcemic poisons are toxic to all the dog’s tissues. The nervous and cardiovascular systems are targeted, with the greatest harm done to the kidneys. Vitamin D3 is used in human supplements as a dietary additive. Vitamin D act as the hypercalcemic agent in rodent poison. It raises the calcium content in the blood serum to toxic levels which can lead to cardiac arrhythmias and death.

Hypercalcaemic agents are developed to release extreme high levels of calcium in the blood. These substances contain vitamin D, developed to raise the calcium content in the blood to extreme levels of toxicity. Elevated levels of serum calcium may persist for weeks.

9.4 Signs of ingestion

When ingested by dogs, signs of hypercalcemia appear between 18 to 36 hours after ingesting. It includes;

Hypertension, - Abnormal high arterial blood pressure

Renal or kidney failure, and

Cardiac failure-  A condition where the dog’s heart do not pump adequate or enough blood to meet the body’s needs) as well as other life-threatening conditions.

Thirst

Frequent urination

Vomiting

Lethargic

Generalized weakness

Muscle twitching

Seizures and

Death.

Treatment:

It is important to correct the fluid levels and electrolyte imbalances in dogs and lowering calcium levels using diuretics, prednisone, oral phosphorus binders, and a low-calcium prescription diet. Calcitonin is a specific antidote, but it is difficult to obtain and has only short-term effects.

10. Antifreeze

There are two generations of antifreeze.

Glycol ethylene, the older generation of antifreeze

Polyethylene glycol, which is a food grade product and regarded as safer.

10.1 Glycol ethylene

10.3 Effects

Glycol ethylene primarily affects the brain and the kidneys.

10.4 Polyethylene glycol

A newer generation of antifreeze contains propylene glycol and not ethylene glycol, which is regarded “generally safe.” Ingesting propylene glycol antifreeze can cause lack of coordination and might result in seizures, but is unlikely to be fatal.

Signs of toxicity

Antifreeze toxicity is dose- related. Signs of been intoxicated within 30 minutes to 12 hours after ingestion.

Various volumes will poison dogs of different weight and size.

Depression

Vomiting

clumsy “drunken” walks

seizures

Coma and death can occur in a matter of hours.

Dogs who recover from acute intoxication frequently develop kidney failure within one to three days and

Death is common.

Treatment: If treatment from a veterinarian is not immediately available;

Induce vomiting even with a small amount of antifreeze

Administer activated charcoal to prevent further absorption of ethylene glycol.

A specific antidote (4-methylpyrazole) needs to be administered treat ethylene glycol poisoning.

Best results are when given shortly after ingestion

Intensive care earliest possible stage may prevent kidney failure.

Prevention:

Keep all antifreeze containers tightly closed and properly stored

prevent spills

Dispose used antifreeze safely

11. Poison baits

Worldwide, well known poison baits are baits that contain strychnine, sodium fluoroacetate, phosphorus, zinc phosphide, and metaldehyde. These baits are highly palatable and therefore affect scavenging dogs as well.

Many of these substances are or was used in the South African environment for bait to kill jackal and or other predators in farming communities. Having a huge detrimental effect on birds such as vultures and such like scavenger birds.

These poisons are known to be extremely toxic. Will kill an animal in a matter of minutes. Fortunately, it seems that they are better controlled these days and less frequently use. Occasionally, it is being misused. These poisons also have a detrimental persistence in the environment, and has the potential to poison innocent people, pets and children.

11. 1 In all cases, prevent exposure to these products. If ever confronted with these poisons

Implement safety measures such as surgical gloves and a mask

Prevent exposure

Enforce vomiting

Administer activated charcoal per weight

Seek veterinarian assistance

Pyrethroid is an organic compound comparable to natural pyrethrins. Pyrethroids, for many safety reasons are a popular product in many commercial household pesticides.

12.1 Pyrethrin

Synergists

Synergists or adjuvants are pharmacological and or immunological agents (in vaccines) that modifies, and enhance the pesticidal outcome or effect of the molecules/agents, such as pyrethrin, they are combined with.

Piperonyl butoxide is such a synergist or an adjuvant. On its own, piperonyl butoxide has no pesticidal activity. Acting as a synergist, it enhances the potency of molecule it is combined or associated with.

Pyrethrin’s are more popular than organophosphates and organochlorides. The latter compounds have shown significant persistent toxic residue and effects to humans.

Pyrethrins is classed as “biodegradable compounds.” It is also preferred above pyrethroids, which is the name of a group of artificial equivalents of pyrethrin that accumulates in the environment.

12.2 Pyrethroids

Pyrethroids have effective insect repellent properties. It is regarded as harmless to mammals and birds in low doses. It can though be harmful to sensitive individuals and are known to be toxic to aquatic organisms.

Pyrethroids are extremely sensitive to sunlight and ultraviolet rays. Its efficacy is eliminated with exposure to the sun within a day or two. When allied though with any suitable environmental residue such as water, it can persevere for some time and contribute to toxicity of the immediate environments.

12.3 Toxicity

Some dogs may be adversely affected by that level of pyrethrins.

Signs of toxicity;

Drooling

Depression

muscle tremors

staggering

vomiting

rapid heavy breathing.

Toxicity occurs primarily in small dogs. Death is rare. Simultaneous exposure to organophosphates increases the toxicity of pyrethroids.

12.4 Treatment:

Induce vomiting

Do not induce vomiting if the product contains a petroleum distillate.

With topical exposure, remove residual insecticide by bathing the dog in lukewarm and a safe canine shampoo to dilute the chemical effect.

Do not use any flea shampoo

Rinse thoroughly

Use ordinary luke warm tap water. Hot or cold water may increase the rate of absorption or cause hypothermia, which might increase toxicity.

After bathing keep the dog calm and warm.

Take it for proper veterinary care and examination

12.5 Prevention

History indicates that most cases of poisoning occur because of improper application of tick and flea-control products.

Never use more product as per instruction on the label.

Do not ever combine a product with other tick and flea control product.

Follow all rules and safety instructions carefully.

13. Arsenic poisoning

Arsenic is known as a “heavy metal”. Heavy metals are found naturally in the earth. They become concentrated because of human activities and enter the body through inhalation, diets, animal consumption and manual handling.

Arsenic is used in herbicides, insecticides, and wood preservatives. Sodium and potassium arsenate are used in ant poisons. Arsenic has a very rapid action and death can occur quickly, even before symptoms are observed. It is used though less these days.

13. 1 Signs of poisoning;

Thirst

Drooling

Vomiting

Staggering

Abdominal pain

Cramps

Diarrhoea

Paralysis and death.

The breath of the dog has a strong garlic odour.

13. 2 Treatment:

Dimercaprol, also called British anti-Lewisite (BAL), is a medication used to treat acute poisoning by arsenic, mercury, gold, and lead. May also be used for antimony, thallium or bismuth poisoning. it is given by injection into a muscle.

Transport the animal to the nearest emergency veterinary facility.

14. Garbage and foodborne poisons

Foodborne illness is also known or referred to as food poisoning. Dogs who scavenge will find garbage, decomposing food as well bacteria infested dead animals.

Any illness that results from the contaminated food, pathogenic bacteria, viruses or parasites that infect food, can be described to as foodborne poisoning.

Natural toxins in plants such as mushrooms, species of beans not well cooked present toxins.

Mould on household foods in the fridge given to the dog

Wheat gluten or melamine in kibble and canned foods

Substance in foods such as dye, colourants, gluten, enhancers and or preservatives

Decaying fish or scombroid food poisoning

Contaminated water

The incubation period from ingested infected food ranges from hours to days, depending on the infected type of food and on how much was consumed. The incubation period is very misleading as the time since ingestion does not always relate the cause or the symptoms.

14.1 Symptoms

Signs appear within a few hours.

Bloody vomiting

Fever

Aches

Gastroenteritis or diarrhoea

Bad breath

Shock and death in severe cases.

Treatment:

Induce vomiting immediately

Administer liquid anti acid medication every 12 hours for two days.

Administer by plastic syringe in liquid form

Administer tablets if anti - acid is not available as a liquid

Keep the dog rehydrated with electrolytes

15. Chocolate

Most dogs will eat chocolate, but it can be dangerous. Chocolate is being made from the fermented seeds of the cocoa tree.   Cocoa solids are a source of flavonoids and alkaloids, such as theobromine, phenethylamine and caffeine. Chocolate also contains anandamide.

15.1 Theobromine

The alkaloid theobromine contains methylxanthines, which is an indirect sympathomimetic drug that is known to constricts blood vessels. Restricted blood vessels mean inadequate oxygen flow to the heart, lungs and reproductive organs.

Theobromine also causes bronchodilation, inhibits peristalsis in the intestines and has diuretic effects, which mean an increase in the production of urine and the excretion thereof. Methylxanthines are not toxic to people in the concentrations found in chocolates and or baked goods. But when ingested by dogs, the effects can be lethal.

There are dogs that tolerate chocolate better than others.

As a rule, dangerous levels of chocolate consumption in dogs would be the following. A dog of;

2.3 to 4.5 kg could die after eating +- 113 g of baking chocolate

9 to 18 kg dog could die from 450 grams of chocolate

15.2 Signs of chocolate toxicity

Chocolate poisoning will occur within hours after the dog ingests the chocolate. They include;

Hyperexcitability

Vomiting

frequent urination

diarrhoea

rapid breathing

weakness

seizures

comas

Death by cardiac arrest.

15.3 Treatment:

Induce vomiting soonest

15.4 Prevention:

As a rule, prevent dogs from eating any chocolate or sugar related sweets

Baking chocolates are extremely toxic to dogs

Explain the dangers of chocolates to children and family members.

16. Fruit and vegetable poisons.

16.1 Raisins and grapes

Possible acute and fatal kidney failure. Dogs will vomit the raisins or grapes within hours, but the damage may already be done. Blood calcium levels will go up and kidney failure will follows

Grape poisoning will cause dogs to stop;

 Eating

develop diarrhoea and

signs of abdominal pain will be eminent

16.1.1 Treatment

Induce vomiting

Fluid therapy to flush out the toxins, which can be oral fluid therapy or intravenous fluid therapy from a veterinarian.

16.2 Macadamia nuts

Dogs eating these nuts will show mild to severe weakness in the rear legs

16.2. 1 Treatment.

Dogs will recover over time, but treatment with activated charcoal accelerates recovery.

16.3 Onions

Onions have sulphur complexes that can lead to a special type of haemolytic anaemia.

Haemolytic anaemia is a condition or status where red blood cells are ruined or destroyed from the bloodstream. Elimination from the blood stream have many reasons. It could be poisons, blood related illnesses, chemical compounds and or harmful organisms.

Sulphur complexes in onions can cause haemolytic anaemia in a dog. It will then will destroy the blood cells in the blood stream before their functional lifespan is over. Bone marrow will react to the situation. It will reproduce more blood cells when there is a shortage of blood cells in the body.

With haemolytic anaemia, the bone marrow can't reproduce and or replace the needed blood cells fast enough to meet the required or adequate amount the body needs. Haemolytic anaemia leads to many other health issues. Fatigue, physical tiredness, tissue pain, irregular heartbeats, (arrhythmias), enlarged heart, heart failure, poor immune system and susceptibility to various viruses, fungi and bacteria are all consequences of haemolytic anaemia. .

16.3 .1 Treatment

If a dog has swallowed onions, induce vomiting and follow with activated charcoal.

16.4 Yeast

Active yeast in raw bread dough produce ethanol as the bread rises. Ethanol poisoning may follow in dogs who ingest the dough.

Unsteady walk and behaviour will be the first signals.

16.4.1 Treatment

Induce vomiting

Activated charcoal to follow

Fluid therapy might be necessary as well as the antidote yohimbine to deal with ethanol alcohol poisoning.

16.5 Xylitol

 

16.5.1 Treatment

Induce vomiting soonest, even with just in sugar-free gum

Administer activated charcoal.

17. Poisonous and hazardous household products

Many household cleaners are corrosive and caustic chemicals (acids and alkalis). These poisons are found in;

toilet bowl cleaners

dishwasher liquids

general detergents

anti-rust compounds

degreasers

alkaline batteries

drain cleaners

commercial solvents such as paraffin, benzine and turpentine.

17.1 Damage

When ingested;

cause burns of the mouth

burns to the stomach.

Perforations of the stomach

Damage to the strictures of the oesophagus or throat

Tissue damage.

17.2 Treatment:

The goal with treatment is to dilute the acid or alkali in the stomach. Therefore;

Do not induce vomiting.

Vomiting can burn the stomach wall and the throat

Rinse the dog’s mouth immediately after contact

Administer immediately water or milk (35 ml per 3kg of body weight) by plastic syringe

With topical exposure, wash or hose the area with mild soap and water for 30 minutes.

18. Petroleum Products.

Petroleum products such as petrol, kerosene, and turpentine can cause pneumonia if aspirated or inhaled.

Ingesting petroleum products will cause gastrointestinal upset.

18.1 Signs of toxicity

Vomiting

Swift laboured breathing

Body tremors

Convulsions and coma.

Death is by respiratory failure.

18.2 Treatment:

Do not induce vomiting

Vomiting can rapture o burn the stomach or throat

Flush the mouth with water to remove petroleum residue.

Petroleum products have a nuisance and irritating reaction on the skin and must be removed from the skin with luke warm soapy water.

Tar on the coat can be removed with butter or margarine

 

19. Heavy metal or toxic metal poisoning

Toxic heavy metal poisoning is any metalloid, known for its potential to harm man and animal and the environment, that is harmful for man and animals. An example would be contaminated water in an in environmental contexts.

The toxic effects of arsenic, mercury, and lead have a long history in Literature.

19.1 Treatment

Metal poisoning is an important matter and is listed in the World Health Organisation’s (WHO) list of chemicals.

Heavy metal poisoning is generally treated by the administration of chelating agents. Some of these heavy metal elements regarded as toxic, are contradiction to its poisonous character, essential in small quantities for human and animal health.

19.2 Metals listed as important in public as well as health interest are;

Manganese

Chromium

Cobalt

Nickel

Copper

Zinc

Selenium

Silver

Antimony

Thallium

Arsenic

Mercury

Lead

Repeatedly flush the dog’s mouth using a garden hose and lots of water and induce vomiting

 

20. Aldicarb, Temik or “Two Step” poisoning

20.1 Introduction

The illegal use of aldicarb (a carbamate) as a method is one of the most despicable ways to get rid of companion animals. It is important to note that aldicarb poisoning is a serious killing agent and needs immediate and knowledgeable emergency care to ensure a reasonable outcome.

Knowledge and the correct diagnosis of aldicarb poisoning is critical. Treatment depends on

Vomiting the whole consumption

administering activated doses of charcoal or the white of 60 grams of egg

the timely use of an anti-muscarinic drug, such as Scopolamine or Atropine.

20.2 A muscarinic drug is a substance that blocks the activity of the poison through a complex set of activities in the blood, tissue and nervous systems in the animal.

20.3 Aldicarb or Temik® is an insecticide and nematicide, registered for agricultural use in South Africa under the Fertilizers, Farm Feeds, Agricultural and Stock Remedies Act (Act 36 of 1947). Only certified farmers are legally able to purchase the product and strict control is enforced regarding the use and storage of the product on farms (Act 36 of 1947)  

In South Africa Temik® is sold illegally by informal street traders as a rodenticide called 'Two Step'56 and it is often the cause of accidental poisoning in children and intentional poisoning in adults.

It is estimated that at least 60 % of the aldicarb-containing pesticides used in South Africa for the poisoning of dogs, are illegally smuggled across the border into South Africa from neighbouring countries such as Mozambique and Zimbabwe, where there is a complete lack of agricultural product control. (G H Verdoorn, Griffon Poison Information Centre)

 

 

Criminals planning to gain access properties where dogs are present insert aldicarb granules into cheap meat baits, such as sausages, viennas, chicken or polony to kill the dog. Dogs do not have the taste receptors on their tongue, the same as humans do, and that makes dogs vulnerable to aldicarb poisoning in meat.

20.4 Classification

Aldicarb is according to the World Health Organization classification of pesticides, an extremely toxic substance and is classified as an “extremely hazardous pesticide” (class 1a).  The canine oral lethal dose is about approximately 6.5 mg per kg. (Griffin Poisoning Centre, Dr Gerhard Verdoorn) 

Mode of action of aldicarb in dogs

Both carbamate and organophosphate pesticides are classified as cholinesterase inhibitors. (A cholinesterase inhibitor is a chemical compound that prevents the enzyme to break down acetylcholine and choline esters that function as neurotransmitters)

20.5 Clinical signs

The clinical appearances of carbamate and organophosphate poisonings are vague from each other.

If a dog therefor shows clinical signs, indicating possible organophosphate or carbamate toxicity, the person dealing with the dog should conservatively assume carbamate poisoning, due to the very high prevalence of malicious misuse of aldicarb in South Africa.

Clinical signs described in Literature include

muscle tremors- involuntary muscle contraction and relaxation

hypersalivation- excessive production of saliva

vomiting or emesis- throwing up

miosis- constriction of the pupil

bradycardia- slowness of the heartbeat

seizures - abnormal neuronal activity in the brain.

Dyspnoea- shortness of breath

Excessive urination- releasing of urine through the urethra

paresis - muscular weakness

paralysis- loss of muscular function

 

20.6 Causes of death

20.6.1 Bronchospasm

Death is caused by respiratory failure due to bronchospasm. Bronchospasm is constriction of the muscles in the walls of the bronchioles. It is caused by the release of substances from mast cells or basophils. It causes difficulty in breathing which can be very mild to severe. Inflamed airways and bronchoconstriction narrows the airways because of wheezing. Bronchospasms is associated with asthma, chronic bronchitis and anaphylaxis, as an effect of the use or intake of drugs, food, medicines, allergic responses to insects.

20.6.2 Paralysis of the diaphragm and Respiratory Centre

Paralysis is loss of muscle function in the diaphragm. The same effect as a person getting his wind knocked out of in contact sports, where diaphragm spasm occurs when sudden force is applied to the abdomen, which puts pressure on the solar plexus, (a complex of nerves located in the abdomen) and intercostal muscles, causing a depression of the respiratory centre, which are a part of the brain stem.

The Respiratory Centre receive governing signals from neural, chemical and hormonal nature.  These signals control the;

respiratory rate

the depth of respiratory movements of the diaphragm and

respiratory muscles such as the intercostal muscles. 

Intercostal muscles are those group of muscles that runs between the ribs. The assist in the movement of the chest wall are mainly involved in the mechanical aspect of breathing. Injury to these centres due poisoning, may lead to central respiratory failure and death.

21. Diagnosis

There is with aldicarb poisoning not really time to confirm a definite diagnosis of aldicarb poisoning. Dogs vomit unfamiliar food in which the aldicarb granules were concealed. Or food stuffs were found black granules.

21.1 Emergency procedures

Emergency procedures should commence immediately, as in 5 where steps to induce vomiting is being discussed as well as the administrating of activated charcoal.

21.2 Veterinary care

It is essential for a veterinarian to administer atropine as soon as possible. The mortality of clinical cases is high even after speedy treatment. The veterinarian would direct his treatment towards reversing or preventing over-stimulation of the muscarinic receptors that slows the heart rate, increase glandular secretory activity and the stimulation of muscle contractions.

Muscarinic receptor antagonists compete with acetylcholine, (ACh) an organic chemical that functions in the brain and body of many types of animals as a neurotransmitter. ACh is a chemical released by nerve cells, sending indifferent signals to other cells by binding on the muscarinic receptors, changing the normal message to muscarinic receptors.

21.2.1 Muscarinic receptor opponents

The administration of an anti-muscarinic drug such as atropine, is critically important in all cases. Aldicarb over-stimulate the muscarinic receptors and that results in fatal consequences. The acetylcholine muscarinic receptors, changing the normal message to muscarinic receptors cause then bradycardia, (slowing of the heart rate) and bronchospasm, sudden constriction of the muscles in the walls of the bronchioles in the dog’s lungs. It is often life-threatening and need to be treated immediately.

 

 

21.2.2 Atropine

Atropine is well absorbed from all routes of administration, reaching peak effects 3-4 min post intravenous or IV administration

Atropine administration reverses the severe bronchospasm, bronchorrhea, bradycardia and circulatory depression associated with over-stimulation of the muscarinic receptors.

Atropine will not counteract the muscle tremors, weakness and paralysis associated with aldicarb toxicity

Atropine may lower the cerebral glucose and reduce the likelihood of brain damage during seizures.

The dose of atropine required to counteract the effects of aldicarb toxicity is extremely high.  A dose of up to 0.5 mg/kg appears to be adequate in most cases.

21.2.3 Atropine side effects.

The high doses necessary to treat aldicarb poisoning effectively in dogs may result in neurological complications such as drowsiness, lack of muscle movements, seizures and respiratory depression. Gastro-intestinal side effects include a dry mouth, difficulty in swallowing, constipation and vomiting.

Problem with eyesight may be blurred vision, the dilation or size of the pupil, paralysis of some eye muscles, and photo-phobia, the intolerance of visual perception of light.

Cardiovascular signs, (veins and blood vessels) include rapid heart rates, high blood pressure, irregular heartbeat and rhythms and cardiovascular failure, the inability of the heart to pump and adequate supply of blood.

21.2.4 Potential complications to the dog due to aldicarb poisoning  

There could be difficulties with animals saved from aldicarb poisoning.

Dysfunctional pancreas

Acute painful abdomen

 

REFERENCES

1. Aaron C K 2001 Organophosphate and carbamates. In Ford M D, Delaney K A (eds) Clinical toxicology (1st edn). W B Saunders, Philadelphia: 819-828        [ Links ]

2. Anastasio J D, Sharp C R 2011 Acute aldicarb toxicity in dogs: 15 cases (2001- 2009). Journal of Veterinary Emergency and Critical Care 21:253-260        [ Links ]

3. Arendse R, Irusen W 2009 An atropine and glycopyrrolate combination reduces mortality in organophosphate poisonings. Human and Experimental Toxicology 28:715-720        [ Links ]

4. Aslan S, Cakir Z, Emet M, Serinken M, Karcioglu O, Kandis H, Uzkeser M 2010 Acute abdomen associated with organophosphate poisoning. Journal of Emergency Medicine (in press) DOI: 10.1016/j.jemermed. 2010.05.072        [ Links ]

5. Aygun D, Doganay Z, Altinop L, Guven H, Onar M, Deniz T, Sunter T 2002 Serum acetylcholinerase and prognosis of acute organophosphate poisoning. Journal of Toxicology - Clinical Toxicology 40:903-910        [ Links ]

6. Bardin P G, Van Eeden S F 1990 Organophosphate poisoning: grading the severity and comparing treatment options between atropine and glycopyrrolate. Critical Care Medicine 18:956-960        [ Links ]

7. Baron R L 1994 A carbamate insecticide: a case study of aldicarb. Environmental Health Perspective 102:23-27        [ Links ]

8. Campbell A, Chapman M 2000 Carbamate insecticides. In Handbook of poisonings in dogs and cats. Blackwell Science, Oxford: 102-105        [ Links ]

9. Centers for Disease Control and Prevention (CDC) 1997 Poisonings associated with illegal use of aldicarb as a rodenticide - New York City 1994-1997. Morbidity and Mortality Weekly Report 46:961-963        [ Links ]

10. Clemmons R M, Meyers D J, Sundlof S F, Rappaport J J, Fossler M E, Hubbell J, Borsey-Lee M R 1984 Correction of organophosphate-induced neuromuscular block by diphenhydramine. American Journal of Veterinary Research 45:2167-2169        [ Links ]

11. De Bleecker J L 2006 Intermediate syndrome in organophosphate poisoning. In Gupta R C (ed.) Toxicology of organophosphate and carbamate compounds. Elsevier Academic Press, Amsterdam: 371-380        [ Links ]

12. DeSilva H J, Wijewickerema R, Senanayeke N 1992 Does pralidoxime affect the outcome of management in acute organophosphate poisoning? Lancet 339:1136-1138        [ Links ]

13. Dressel T D, Goodale R L, Hunninghake D B, Borner J W 1979 Sensitivity of the canine pancreatic intraductal pressure to subclinical reduction in cholinesterase activity. Annals of Surgery190:6-12        [ Links ]

14. Eddelston M, Buckley N A, Eyer P, Dawson A H 2008 Management of acute organophosphorus pesticide poisoning. Lancet 371:597-607        [ Links ]

15. Erdman A R 2004 Insecticides. In Dart R C (ed.) Medical toxicology (3rd edn). Lippincot Williams & Wilkins, Philadelphia: 1475- 1496        [ Links ]

16. Fikes F D 1990 Organophosphorous and carbamate insecticides. Veterinary Clinics of North America: Small Animal Practice 20:353-367        [ Links ]

17. Fikes F D 1990 Organophosphorus and carbamate insecticides. Veterinary Clinics of North America: Small Animal Practice 20:353- 367        [ Links ]

18. Firth A 2000 Treatments used in small animal toxicoses. In Kirk RW (ed.) Kirk's current veterinary therapy: XIII Small animal practice. W B Saunders, Philadelphia: 207-211        [ Links ]

19. Frank M E, Bouverat B P, MacKinnon B I, Hettinger T P 2004 The distinctiveness of ionic and nonionic bitter stimuli. Physiology and Behavior 80:421-431        [ Links ]

20. Frazier K, Hullinger G, Hines M, Liggett A, Sangster L 1999 Clinical reports: 162 cases of aldicarb intoxication in Georgia domestic animals from 1988-1998. Veterinary and Human Toxicology 41:233-235        [ Links ]

21. Garcia S J, Aschner M, Syversen T 2006 Inter-species variation in toxicity of cholinesterase inhibitors. In Gupta R C (ed.) Toxicology of organophosphate and carbamate compounds. Elsevier Academic Press, Amsterdam: 145- 158        [ Links ]

22. Goswamy R, Chaudhuri A, Mahashur A A 1994 Study of respiratory failure in organophosphate and carbamate poisoning. Heart and Lung 23:466-472        [ Links ]

23. Grauer G F, Hjelle J J 1988 Toxicology: Introduction. In Morgan R V (ed.) Handbook of small animal practice. Churchill Livingston, New York: 1083-1086        [ Links ]

24. Gupta R C 2006 Classification and uses of organophosphates and carbamates. In Gupta R C (ed.) Toxicology of organophosphate and carbamate compounds. Elsevier Academic Press, Amsterdam: 5-24        [ Links ]

25. Haddad L M 1983 The organophosphate insecticides. In Haddad L M, Winchester J F (eds) Clinical management of poisoning and drug overdose. W B Saunders, Philadelphia: 704-710        [ Links ]

26. Haddad L M 1983 The carbamate, organochloride and botanical insecticides; insect repellents. In Haddad L M, Winchester (eds) Clinical management of poisoning and drug overdose. W B Saunders, Philadelphia: 711-712        [ Links ]

27. Hoffman R S, Manini A F, Russell-Haders A L, Felberbaum M, Mercurio-Zappala M 2009 Use of pralidoxime without atropine in rivastigmine (carbamate) toxicity. Human and Experimental Toxicology 28:599-602        [ Links ]

28. Jenkins W C 1989 Drugs affecting gastrointestinal function. In Booth N M, McDonald L E (eds) Veterinary pharmacology and therapeutics (6th edn). Iowa State University Press, Ames: 657-671        [ Links ]

29. Johnson M K, Vale J A, Marrs T C, Meredith T J 1992 Pralidoxime for organophosphate poisoning. Lancet 340: 64        [ Links ]

30. Jokanovi? M, Maksimovic M 1997 Abnormal cholinesterase activity: understanding and interpretation. European Journal of Clinical Chemistry and Clinical Biochemistry 35:11-16        [ Links ]

31. Jokanovi? M 2009 Medical treatment of acute poisoning with organophosphorus and carbamate pesticides. Toxicology Letters 190:107-115        [ Links ]

32. Lee H S 1989 Acute pancreatitis and organophosphate poisoning - a case report and review. Singapore Medical Journal 30:599- 601        [ Links ]

33. Leibson T, Lifshitz M 2008 Organophosphate and carbamate poisoning: review of the current literature and summary of clinical and laboratory experience in southern Israel. Israel Medical Association Journal 10:767-770        [ Links ]

34. Li H, Schopfer L M, Nachon F 2007 Aging pathways for organophosphate-inhibited human butyrylcholinesterase, including novel pathways for isomalation, resolved by mass spectrometry. Toxicological Sciences 100:136-145        [ Links ]

35. Lima J S, Reis C A 1995 Poisoning due to illegal use of carbamates as a rodenticide in Rio de Janeiro. Journal of Toxicology - Clinical Toxicology 33:687-690        [ Links ]

36. Lotti M, Moretto A 2005 Organophosphate-induced delayed polyneuropathy. Toxicology Reviews 24:37-49        [ Links ]

37. Lotti M, Moretto A 2006 Do carbamates cause polyneuropathy? Muscle Nerve 34:499-502        [ Links ]

38. Makridges C, Koukouvas M, Achillews G, Tsikkos S, Vounou E, Symeonides M 2005 Methomyl-induced severe acute pancreatitis: possible etiological association. Journal of the Pancreas 6:166-171        [ Links ]

39. Marrs T C, Vale J A 2006 Management of organophosphorus pesticide poisoning. In Gupta R C (ed.) Toxicology of organophosphate and carbamate compounds. Elsevier Academic Press, Amsterdam: 715-733        [ Links ]

40. McDonough J H, McLeod C G, Nipwoda M D 1987 Direct micro-injection of soman or VX into amygdale produces repetitive limbic convulsions and neuropathology. Brain Research 435:123-137        [ Links ]

41. McEntee K, Poncelet L, Clercx C, Henroteaux M 1994 Acute polymyopathy after carbamate poisoning in a dog. Veterinary Record 135:88-90        [ Links ]

42. Moritz F, Droy J M, Melki J, Bonmarchand G, Leroy J 1994 Acute pancreatitis after carbamate insecticide intoxication. Intensive Care Medicine 20:49-50        [ Links ]

43. Motas-Guzman M, Maria-Mojica P, Romero D, Martinez-Lopez E, Garcia-Fernandez A J 2003 Intentional poisoning of animals in southeastern Spain. A review of veterinary toxicology service from Murcia, Spain. Veterinary and Human Toxicology 45:47-50        [ Links ]

44. Mount M E 1989. Toxicology. In Ettinger S J (ed.) Textbook of veterinary internal medicine. W B Saunders, Philadelphia: 456-483        [ Links ]

45. Nelson L S, Perrone J, DeRoos F, Stork C, Hoffman R S 2001 Aldicarb poisoning by an illicit rodenticide imported into the United States: Tres Pasitos. Journal of Toxicology - Clinical Toxicology 39:447-452        [ Links ]

46. Olson M E, Vizzutti D, Morck D W, Cox A K 1993 The parasympatholytic effects of atropine sulfate and glycopyrrolate in rats and rabbits. Canadian Journal of Veterinary Research 57: 254-258        [ Links ]

47. Paul N, Mannathukkaran T J 2005 Intermediate syndrome following carbamate poisoning. Clinical Toxicology 43:867-868        [ Links ]

48. Pazdernik T L, Nelson S R, Cross R, Churchill L, Giesler M, Samson F E 1986 Effects of antidotes on soman-induced brain damage. Archives of Toxicology 9:333-336        [ Links ]

49. Platt S R, McDonnell J J 2000 Status epilepticus: managing refractory cases and treating out-of-hospital patients. Compendium on Continuing Education for the Practicing Veterinarian 22:732-741        [ Links ]

50. Plumb D C 2008 Plumb's veterinary drug handbook (6th edn). Blackwell Publishing, Iowa        [ Links ]

51. Ragoucy-Sengler C, Tracqui A, Chavonnet A, Daijardin J B, Simonetti M, Kintz P, Pileire B 2000 Aldicarb poisoning. Human and Experimental Toxicology 2000 19:657-662        [ Links ]

52. Risher J F, Mink F L, Stara J F 1987 The toxicological effects of the carbamate insecticide aldicarb in mammals: a review. Environmental Health Perspectives 72:267-281        [ Links ]

53. Riviere J E 1985 Clinical management of toxicoses and adverse drug reactions. In Davis LE (ed.) Handbook of small animal therapeutics. Churchill Livingstone, New York: 657-683        [ Links ]

54. Roberts M D, Aaron C K 2007 Managing acute organophosphorus poisoning. British Medical Journal 334:629-635        [ Links ]

55. Rosman Y, Makarovsky I, Bentur Y, Shrot S, Dushnistky T, Krivoy A 2009 Carbamate poisoning: treatment recommendations in the settling of a mass casualty event. American Journal of Emergency Medicine 27:1117-1124        [ Links ]

56. Rother H A 2010 Falling through the regulatory crack: street selling of pesticides and poisoning among urban youth in South Africa. International Journal of Occupational and Environmental Health 16:202-213        [ Links ]

57. Satoh T 2006 Global epidemiology of organophosphate and carbamate poisonings. In Gupta RC (ed.) Toxicology of organophosphate and carbamate compounds. Elsevier Academic Press, Amsterdam: 89-100        [ Links ]

58. Singh S, Ranjit A, Parthasarathy S, Sharma N, Bambery P 2005 Organo-phosphate induced delayed neuropathy: report of 2 cases. Neurology India 52:525-526        [ Links ]

59. Stevens J T, Brekenridge C B 2001 Crop protection chemicals. In Hayes A W. (ed.) Principles and methods of toxicology (4th edn). Taylor & Francis, Philadelphia: 583-591        [ Links ]

60. Sultatos L G 2006 Interactions of organophosphorus and carbamate compounds with cholinesterases. In Gupta RC (ed.) Toxicology of organophosphate and carbamate compounds. Elsevier Academic Press, Amsterdam: 209-218        [ Links ]

61. Sungur M, Güven M 2001 Intensive care management of organophosphate insecticide poisoning. Critical Care 5:211-215        [ Links ]

62. Tomlin C. 1994 The pesticide manual (10th edn). Crop Protection Publications, Farnham: 25        [ Links ]

63. VealeDJH,WiumCA, Müller G J 2010 A prospective study of the incidence and spectrum of acute poisonings in South Africa based on hospital admission and Poison Information Centre data. Clinical Toxicology 48:284        [ Links ]

64. Verster R S, Botha C J, Naidoo V, van Schalkwyk O L 2004 Aldicarb poisoning of dogs and cats in Gauteng during 2003. Journal of the South African Veterinary Association 75:177-181        [ Links ]

65. Verma S K, Ahmad S 2009 High dose pralidoxime in organophosphorus poisoning: a critical appraisal. API Medicine Update 19:448-452        [ Links ]

66. Waseem M, Perry C, Bomann S, Pai M, Gernsheimer J 2010 Cholinergic crisis after rodenticide poisoning. Western Journal of Emergency Medicine 11:524-527        [ Links ]

67. World Health Organization 2009 The WHO recommended classification of pesticides by hazard and guidelines to classification. Geneva        [ Links ]

Treatment rationale for dogs poisoned with aldicarb (carbamate pesticide)

Outpatients Clinic, Onderstepoort Veterinary Academic Hospital, Department of Companion Animal Clinical Studies, Faculty of Veterinary Science, University of Pretoria, Private Bag X04, Onderstepoort, 0110  South Africa

Department of Paraclinical Sciences, Faculty of Veterinary Science, University of Pretoria, Private Bag X04, Onderstepoort, 0110 South Africa

Tygerberg Poison Information Centre, Division of Pharmacology, Department of Medicine, Stellenbosch University, PO Box 19063, Tygerberg, 7505 South Africa

 

General Treatment of Poisoning         

Contact Poisons        

Drug Poisons             

Rodent Poisons         

Antifreeze   

Poison Baits

Insecticides 

Garbage and Food Poisons   

Chocolate   

Raisins, Grapes, and Other Food Poisons        

Corrosive Household Products           

Petroleum Products

Poisonous Plants      

Lead             

Zinc

Frogs and lizards

 

 

 

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