Diseases caused by inorganic and farm chemical

Diseases caused by inorganic and farm chemical - medicine Al-Khafaji Nazar

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Diseases caused by inorganic and farm chemicals

Toxicology: Is the study of the harmful effects of chemical compounds on biological systems, including their properties, actions and effects?

Toxic agents: Is referred to a toxicant or poison.

Toxin: Refers to poisons produced by a biological source (e.g. venoms, plant toxins).Toxicosis, poisoning and intoxication are synonymous terms for the disease produced by a toxicant.

Toxicity (sometimes in correctly used instead of poisoning) refers to the amount of a toxicant necessary to produce a determined effect.

Synergism: Is the implication of the combined actions of two or more agents having the same biological effects?

Antagonism: Is the inhibition or elimination of the effect of one agent by another, it may be chemical or functional.

Toxicant accumulation and biomagnifications occurs when absorption exceeds the capacity of the body to destroy or excrete a xenobiotic (foreign) compound.

Tolerance: Is the ability of an organism to show less response to a specific dose of a chemical than it demonstrated on prior occasion? It refers to acquired, not innate resistance.

Metabolism of poisons:

Absorption occurs by way of the alimentary tract, skin, lungs, or via the eyes, mammary gland, or uterus, as well as from sites of injection.

Toxic effects may be local, but the poison must be dissolved and absorbed to some extent to affect the cell .the primary factor affecting absorption is solubility.

Insoluble salts and ionize compounds are poorly absorbed , while lipid soluble substances are generally readily absorbed , even through intact skin , for example barium is toxic , but barium sulfate can be used for intestinal contrast radiography because of low absorption.

Distribution or translocation of the toxicant follows via the blood stream to reactive sires, including storage depots.

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The liver receives the portal circulation and is the organ most commonly involved with intoxication (and detoxification).

The selective deposit of foreign chemicals in various tissues depends on receptor sites.

The ease of chemical distribution depends largely on its water solubility.

Polar or aqueous soluble agents tend to be excreted by the kidneys. Lipid soluble chemicals are more likely to be excreted via the bile and accumulate in fat depots,

There are two phases of metabolism:

Phase I: includes oxidation, reduction, and hydrolysis mechanisms. These reactions, catalyzed by hepatic enzymes, generally converted foreign compounds to derivatives for phase II reactions.

Phase II principally involves conjugation, or synthesis reactions.

Commonly (common conjugates) include glucuronides, acetylation products, and combination with glycine.

Metabolism of xenobiotic agents seldom follows a single pathway. Usually, a fraction is excreted unchanged and the rest is excreted or stored as metabolites.

Excretion of most toxicants and their metabolites is by way of the kidneys

.many polar and high molecular weight compound are excreted by way of the bile.

An entertohepatic cycle occurs when these products are excreted from the liver via bile, reabsorbed from the intestine and returned to liver.

Milk is also an excretion pathway for some toxicants.

Suspicion of poisoning is aroused when illness occurs in a number of:

Previously healthy animals.

All affected at the same time.

And showing the same signs and necropsy findings.

To the same degree of severity.

These conditions, of course, may also apply to some infections, metabolic and nutritional deficiency disease.

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Poisonous plants often show geographical limitation in distribution; particular industrial enterprises may create poison hazards in local areas.

Certain agricultural practices, including the spraying of orchards, the dipping or spraying of cattle for ectoparasites and the use of prepared concentrated feed for pigs and cattle, may also lead to poisoning in groups of animals.

The appearance of clinical illness soon after feeding, after a change of ration, after medication or spraying, or after change to new pasture is a common history in many outbreaks of disease caused by chemical agents.

Diagnosis:

Diagnosis is based on:

History, clinical signs, lesions, laboratory examinations, and in all cases, bioassay procedures.

The report which accompanies material for toxicological analysis should include a full record of history, clinical signs and necropsy findings and particularly the results of a search of the environment for access to a poison.

If the animal has been treated, the drugs that were used and the dates of administration should be given as they may create difficulties for the analyst.

The poison or a group of poisons suspected should be defined.

Specimens for analysis should include a sample of the suspected source material.

Next most important is a specimen of alimentary tract contents, so that ingestion of the material can be proven.

And sample of tissue, usually liver to prove that absorption of poison has occurred.

Most toxic chemicals are ingested but percuyaneous adsorption and inhalation must be considered as possible portals of enter.

Additional specimens required, other than liver and alimentartry tract and contents, vary with the poison and the following list is suggested for the common chemicals:

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Arsenic – kidney, skin, and hair.

Lead – kidney, bones and blood.

Phosphorus – kidney and muscle.

Mercury – kidney.

Copper – kidney and blood.

Sodium chloride – alimentary tract and ci=ontent only.

Fluorine – bones, teeth and urine.

Hydrocyanic acid – ingesta in a filled and air tight containers, blood and muscle.

Nitrate and nitrite – ingesta ( plus chloroform or formalin ) in an airtight filled container , blood

Strychnine – blood, kidney and urine.

Careful packing of specimens is necessary to avoid loss of some poisons by escape as gas or conversion by bacterial fermentation, and to prevent contamination.

No preservative should be added except in the case of suspected nitrite poisoning.

If preservative is necessary because of distance from the laboratory packing in dry ice or ethyl alcohol (1 ml / g of tissue) is advisable, in this instance a specimen of the alcohol; should also be sent.

Specimens should be packed in glass or plastic to prevent contamination by lead in soldered joints of cans.

A suitable amount of material should be submitted for analysis, 1 kg of ingestra, 1kg of liver, and proportionate amount of other viscera are suggested to cover all contingencies.

Some of the factors which affect susceptibility to plant poisoning are

Hungary, ravenous animals are more likely to be affected.

Curious , excited animals are likely to sample the plants they would not otherwise eat,

Young animals are less discerning and are less easily put off.

Plants that are different in texture, e.g. sprayed weeds, lopped foliage, often appear to be attractive.

Pica due to other cause.

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Poisoning is in most instances accidental.

Principles of treatment in cases of poisoning:

There are certain principles which apply to all cases of poisoning.

Treatment for poisoning includes three basic principles.

The two main principles are:

Removal of the residual poison from the alimentary tract or skin.

Provision of chemical and physiological antidotes to the poison that has been absorbed

1.

Prevention of further absorption.

2.

Supportive / symptomatic treatment.

3.

Specific antidotes/

Prevention of further absorption:

Topically applied toxicants usually can be removed by thorough washing with soap and water, clipping the hair or wool may be necessary. However, emesis is of value in dogs, cats and pigs if done within a few hours of ingestion

In farm animals gastric ravage and emetics are of little or no practical value and the removal of residual poison from the alimentary tract dependents largely upon the use if adsorbents and purgative. The only effective adsorbent is activated charcoal. The dose rate is 1-3 g /kg B.Wt. repeated as necessary. It adsorbs chlorinated hydrocarbon, organophosphoryus compounds, and myxcotixins and plant alkaloids.

Emesis is contraindicated when the swallowing reflex is absent, the animal is convulsing, corrosive agents, volatile hydrocarbons, or petroleum distillates are involved, or a risk of aspiration pneumonia is imminent.

Oral emetics include syrup of ipecac (10-20 ml) PO in dogs and hydrogen peroxide (2 ml /kg PO). kg.

Apomorphine can be used in dogs parenterally at a dose of 0.05- 0.1 mg /

Gastric lavge using an endotracheal tube and the largest bore stomach tube possible, is done on the unconscious or anaestrhized animal. The head is lowered to a 30 angle and 10 ml of lavage fluid (water or saline per kg body

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Purgative is necessary to remove the combined adsorbent and poison. It can be administered simultaneously with the adsorbent.

The use of irritant purgative is not advisable when the poison is an irritant and has already caused gastroenteritis, and oily purgatives are preferable in these cases saline purgatives are of value in the treatment of non – irritant poisons such as cyanogebnetc glycosides.

Cathartics and laxatives may be indicated in some instances for more rapid elimination of the toxicant from gastrointestinal tract.

When the poison can not physically remove, certain agents administered orally can adsorb it and prevent its absorption from the alimentary tract.

Activated charcoal (1-2 g/kg) is effective in adsorbing a wide variety pof compounds and usually is the adsorpant and detoxicant of choice when poisoning suspected.

Neutralization of residual poison in the alimentary tract can be effect in some cases. for example oxidizing agents por tannic acid preparations are effective in precipitating alkaloids , proteins , including milk and eggs , are effective chemical antidotes for poisons that coagulate proteins , lead is precipitated by the addition of sulfated to the alimentary tract contents .

Poison that has already been absorbed can in some instances be inactivated or its excretion facilitated by the provision of chemical antidotes .for instances.

Sodium nitrite and sodium thiosulfate are effective systemic antidotes to hydrocyanic acid, and calcium versenate is an effective antidote against lead.

Treatment of the effects of a poison includes:

Provision of physiological antidote e.g. the injection of calcium salt in cases of overdosing with magnesium salts.

Ancillary treatment /Supportive therapy:

The type of supportive therapy depends on the animal's clinical condition and may include control of convulsive seizures, maintenance of respiration, treatment of shock, correction of electrolytes and fluid loss, control of cardiac dysfunction, and alleviation of pain.

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Provision of fluid in dehydration, due to diarrhea, demulcents in gastroenteritis, sedatives in excitements, stimulants in case of central nervous system depression.

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Arsenic poisoning

Arsenic poisoning in animals is caused by several different types of inorganic and organic arsenical compounds.

Toxicity varies with a state of arsenic, solubility, species of animal involved, and duration of exposure,

Inorganic arsenicals

These include arsenic trioxide, arsenic pent oxide, sodium and potassium arsenate, sodium and potassium, arsenite and lead or calcium arsenate.

The lethal dose of sodium arsenite (orally) in most species is from 1-25 mg/kg. Cats may be more sensitive.

Arsenates (pentavalents) are 5- 10 times less toxic than arsenates.

Arsenite are used to some extent as dips for tick control. Lead arsenate is sometimes used as ataeniacide in sheep.

Toxic kinetics and mechanism of action:

Soluble forms of arsenic compounds are well absorbed orally. Following absorption, most of the arsenic is bound to RBC, it distributes to several tissues, with the highest levels found in the liver, kidneys and heart and lungs.

In sub cutaneous or chronic exposure, arsenic accumulates in skin, nails, hooves, sweat glands and hair. The majority of the absorbed arsenic is excreted in the urine as inorganic arsenic or in methylated form.

The mechanism of action of arsenic toxicants, tissues that are rich in oxidative enzymes such as the GIT, liver, kidneys, lungs, endothelium and epidermis are considered more vulnerable to arsenic damage.

Trivalent inorganic, and aliphatic organic arsenic compounds exert their toxicity by interacting with sulphhydryl enzymes, resulting in disruption of cellular metabolites.

Clinical findings

Poisoning is usually acute with major effects on the GIT and cardiovascular system.

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Arsenic has a direct effect on the capillaries, causing damage to micro vascular integrity, transudation of plasma, loss of blood, and hypovolemic shock. Profuse watery diarrhea, sometimes tinged with blood, is characteristic as are severe colic, dehydration, weakness, depression, weak pulse, and cardiovascular collapse.

The onset is rapid, and a signs are usually seen within a few hours (or up to

24 hr).

The course may run from hours to several weeks depending on the quantity ingested.

In per acute poisoning, animals may simply found dead.

Lesions

In per acute toxicosis, no significant lesions may be seen. Inflammation and reddening of GIT mucosa (local or diffuse) may be seen followed by edema, rupture of blood vessels, and necrosis of epithelial and sub epithelial tissue.

Necrosis may progress to perforation of the gastric or intestinal wall.

GI contents are often fluid, foul swelling and blood tinged. They may contain shreds of epithelial tissues.

There is diffuse inflammation of the liver, kidneys, and other visceral organs. The liver may have fatty degeneration and necrosis, and the kidneys have tubular damage .in cases of cutaneous exposure, the skin may exhibit necrosis and be dry or leathery.

Diagnosis

Chemical determination of arsenic in tissues (liver or kidney) or stomach contents (provides confirmation, liver and kidneys of normal animals rarely contain > 1 ppm arsenic (wt.wt). toxicity associated with as concentration > 3 ppm.

The determination of arsenic in stomach contents is of value usually within the first 24- 48 hr after ingestion.

Treatment

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In animal with recent exposure and no clinical signs emesis should be induced (in capable species). Followed by activated charcoal with a cathartic and then oral administration of protectants (small animals 1-2 hr after charcoal) such as kaolin- pectin, and fluid therapy as needed.

In animals already showing clinical signs , aggressive fluid therapy , blood transfusion if needed .and administration of dimercaprol 4-7 mg /kg I.M. TID for 2-3 days or until recovery .

In large animals, thioctic acid may be used alone (50 mg / kg IM. TID as a

20% solution). Or in combination with dimercaprol 3 mg /kg IM every 4 hr for the first 2 days, QID for the third day and BID for the next 10 days or until recovery.

Organic arsenicals

Organic arsenicals are less toxic than inorganic compounds.

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Cyanide poisoning

Cyanide inhibits cytochrome oxidase and cause death from histotoxic anoxia.

Etiology

Cyanides are found in plants, fumigants, soil sterilizers, fertilizers, and rodenticided (e.g. calcium cyanomide).

In livestock, the most frequent cause is ingestion of plants that contain cyanogenic glycosides e.g. sorghum spp (Johnson grass, Sudan grass, common sorghum).

Eucalyptus spp, have been implicated in deaths of small animals.

The cyanogenic glytcosides in plants yield free hydrocyanic acid (HCN) , when hydrolyzed by beta – glycosidase or when other plant cell structure is disrupted or damaged e.g. by freezing , chapping , or chewing .microbial action in the rumen can further release free cyanide .

Ruminants are more susceptible than monogastric animals, and cattle slightly more so than sheep.

Clinical findings

Signs can occur within 15- 20 min to a few hours after animals consume toxic forage. Excitement can be displayed initially, accompanied by rapid respiration rate.

Dyspnea follows shortly with tachycardia. Salivation, excess lacrimation and voiding of urine and feces may occur.

Muscle fasciculation is common and progresses to generalized spasms and death. Animals stagger and struggle before collapse.

Mucous membranes are bright red but may become cyanotic terminally.

Death occurs during severe asphyxia convulsions.

The whole syndrome usually does not exceed 30 – 45 min.

Most animals that live≥ 2 hr after onset of clinical signs recover, unless continuous absorption of cyanide from the GI tract occurs.

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Lesions

In acute or per acute cyanide toxicosis, blood may be bright cherry red; initially but can be dark red if necropsy is delayed. It may clot slowly or not at all.

Mucous membranes may also be pink initially, and then become cyanotic after respiration ceases.

The rumen may be distended with gas, and the odor of bitter almonds nay be detected after opening.

Liver, serosal surfaces, tracheal mucosa, and lungs may be congested or hemorrhagic. Some froth may b e seen in respiratory passage.

Diagnosis

Appropriate history, clinical signs, post mortem findings, and demonstration of HCN in rumen (stomach) content support a diagnosis of cyanide poisoning.

Differential diagnosis

Include:

Poisoning by nitrate or nitrite , urea , organophosphate , carbamate , chlorinated hydrocarbon pesticides , and toxic gases ( carbon monoxide and hydrogen sulfide ) , as well as infectious , and noninfectious diseases that cause sudden death .

Treatment

Sodium nitrite (10 g / 100 ml of distilled water or isotonic saline) should be given IV at 20 mg /kg body weight, followed by sodium thiosulfate 20% IV at ≥

500mg /kg.

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Lead poisoning

Lead poisoning is most common in dogs and cattle.

In cattle, many cases are associated with seeding and harvesting activities when used oil and battery, disposable from machinery is handled improperly.

Other sources of lead include , paint , grease , linoleum , lead weights , lead shot , and contaminated foliage growing near smelters or along road sides .

Pathogenesis

Absorbed lead enters the blood and soft tissues and eventually redistributed to the bone.

Lead has a profound effect on sulfhydryl – containing enzymes, thiol content of erythrocytes, antioxidant defenses, and tissues rich in mitochondria.

In addition to the cerebellar hemorrhage and edema associated with capillary damage, lead is also irritating, immunosuppressive, gametotoxic, teratogenic, nephrotoxic, and toxic to the hemotopoietic system

Clinical findings

Acute lead poisoning is more common in young animals.

The prominent clinical signs are associated with the GI and nervous systems.

In cattle , the signs that appear within 24- 48 hr of exposure include ataxia , blindness , salivation , spastic twitching of eyelids , jaw champing , bruxisam , muscle tremors and convulsions.

Sub acute lead poisoning , usually seen in sheep or other cattle , is characterized by anorectic , rumen stasis , colic , dullness , and transient constipation , frequently followed by diarrhea , blindness , head pressing , bruxism , hyperesthesia and in coordination.

GI abnormalities, including anorexia, colic emesis, and diarrhea or constipation, may be seen in dogs.

Anxiety, hysterical barking, jaw champing, salivation, blindness, ataxia, muscle spasms, opisthotones, and convulsions may develop.

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CNS depression rather than CNS excitation may be evident in some dogs.

In horses, leading poisoning usually produces a chronic syndrome characterized by weight loss, depression, weakness, colic, diarrhea, laryngeal or pharyngeal paralysis (roaring) and dysphagia that frequently results in aspiration pneumonia.

Lesions

Gastroenteritis. In nervous system, edema, congestion of the cerebral cortex.

Treatment

Calcium EDTA IV or SC (110 mg / kg / day) divided into 2 treatments daily for 3 days.

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Mercury poisoning

Mercury exists in a variety of organic and inorganic forms.

Inorganic mercurials

These include the volatile elemental form of mercury (used in thermometer) and the salted forms (mercuric chloride (sublimate) and mercurous (chloride (calomel).

Ingested inorganic mercury is poorly absorbed and low in toxicity.

Large amounts of these mercurials are corrosive and may produce vomiting, diarrhea, and colic.

Renal damage also occurs, with polydipsia and anuria UN severe cases.

In rare cases of chronic inorganic mercurial poisoning, the CNS effects resemble those of organic mercury poisoning.

Mercury vapor from elemental mercury produces corrosive bronchitis and interstitial pneumonia, and if not fatal, may lead to neurologic signs as do organic forms.

Organic mercury

The organic mercurials are absorbed via all routes and bioaccumulate in the brain and to some extent in the kidneys and muscle.

Animals poisoned by organic mercury exhibit CNS stimulation and locomotors abnormalities after a lengthy latent period (weeks).

Signs may include blindness, excitation, abnormal behavior and chewing, in coordination and convulsions.

Mercury is also, mutagen, teratogen, and carcinogen and is embryocidal.

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Mycotoxicoses

Aflatoxicosis

Aflatoxins are produced by toxigenic strains of Aspergillus flavus and A. paraiticus on peanuts, soybeans, corn (maize) and other cereals other in the field or during storage when moisture content and temperatures are sufficiently high for mold growth.

The toxic response and disease in mammals and poultry varies in relation to species, sex, age, nutritional status, and the duration of intake and level of aflatoxins in the ration.

Aflatoxicosis affects growing poultry, young pigs, pregnant sows, calves, and dogs.

Adult cattle, sheep, and goats are relatively resistant to the acute form of the disease but are susceptible if toxic diets are fed over long periods.

Aflatoxins bind to macromolecules, especially nucleic acids and nucleoproteins.

Their toxic effects include mutagenesis due to alkylation of nuclear DNA, carcinogenesis, teratogenesis, reduced protein synthesis and immunosuppression.

Reduced protein synthesis results in reduced production of essential metabolic enzymes and structural proteins for growth .the liver is the principal organ affected.

High doses of aflatoxins result in severe hepatocellular necrosis, prolonged low dosages result in reduced growth rate and liver enlargement.

Clinical findings

In acute outbreaks, deaths occur after a short period of in appetence, sub acute outbreaks are more usual, and unthriftiness, weakness, anorexia and sudden deaths can occur.

Lesions

In acute cases

There are widespread hemorrhages and icterus.

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The liver is the major target organ.

In sub acute cases, the hepatic changes are not so pronounced, but the liver is somewhat enlarged and firmer than usual. There may be edema of the gall bladder.

Prolonged feeding of low concentrations of aflatoxins may result in diffuse liver fibrosis (cirrhosis) and carcinoma of the bile ducts or liver.

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Ergotism

This results from continued ingestion of sclerotia of the parasitic fungus clavuiceps purpurea, which replaces the grain or seed of rye and other small grains or forage plants, such as the bromes, bluegrasses and ryegrasses.

The hard, black, elongate sclerotia may contain varying quantities of ergot alkaloids, of which ergotamine and ergonovine (ergometrine) are pharmacologically most important.

Cattle, pigs, sheep. And poultry are involved in sporadic outbreaks and most species are susceptible.

Etiology

Ergot causes vasoconstriction by direct action on the muscle of the arterioles and repeated dosages injure the vascular endothelium.

These actions initially reduce blood flow and eventually lead to complete stasis with terminal necrosis of the extremities due to thrombosis.

A cold environment predisposes the extremities to gangrene. In addition, ergot has a potent oxytocic action and also causes stimulation of the CNS, followed by depression.

Ergot alkaloids inhibit pituitary release of prolactin in many mammalian species, with failure of both mammary developmenr in late gestation and delayed initiation of milk secretion, resulting in agalactia at parturition.

Clinical findings and lesions

Cattle may be affected by eating ergotize hay or grain or occasionally by grazing seeded pastures that are infested with ergot.

Lameness, the first sign, may appear 2- 6 wk or more after initial ingestion, depending on the concentration of alkaloids in the ergot and the quantity of ergot in the feed.

Hind limbs are affected before forelimb but the extent of involvement of a limb, and the number of limbs affected depends on the daily intake of ergot.

Body temperature and pulse and respiratory rates are increased .associated with lameness as swelling and tenderness of the fetlock joint and pastern.

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Within 1 wk, sensation is lost in the affected part, and indented line appears at the limit of normal tissue, and dry gangrene affects the distal part. Eventually, one or both claws or any part of the limbs up to the hock or knee may be sloughed.

In a similar way, the tip of the tail or ears may become necrotic and slough.

Exposed skin areas, such as teats and udder, appear unusually pale or anemic. Abortion is not seen.

The most consistent lesions at necropsy are in the skin and subcutaneous parts of the extremities.

The skin is normal to the indented line, but beyond, it is cyanotic and hardened in advanced cases .subcutaneous hemorrhage and some edema occurs proximal to the necrotic area.

Clinical signs in sheep are similar to those in cattle. Additionally, the mouth may be ulcerated, and marked intestinal inflammation may be seen art necropsy.

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Strychnine poisoning

Strychnine is an indole alkaloid obtained from the seeds of the Indian tree strychnosnux – vomica.

It is mainly used as a pesticide to control rats, moles, gophers and coyotes.

Strychnine is highly toxic to most domestic animals. Its oral LD50 in dogs, cattle, horses, and pigs is between 0.5 – 1 mg /kg, and in cats is 2mg /kg.

Accidental strychnine poisoning occurs mainly in small animals, especially dogs and occasionally cats, and rarely in livestock.

Pathogenesis

Strychnine is ionized in an acidic pH and then rapidly and completely absorbed in the small intestine .strychnine inhibits competitively and reversibly the inhibitory neurotransmitter glycine at post synaptic neuronal sits in the spinal cord and medulla .this results in unchecked reflex stimulation of motor neurons affecting all the striated muscles .

Because the extensor muscles are relatively more powerful than the flexor muscles. They predominate to produce generalized rigidity and tonic – clonic seizures. Death results from anoxia and exhaustion.

Clinical findings

The onset of strychnine poisoning is fast. After oral exposure, clinical signs may appear within 30- 60 min. presence of food in the stomach can delay onset.

Early signs, which may often be overlooked, consist of apprehension, nervousness, tenseness, and stiffness. Severe titanic seizures may appear spontaneously or may be initiated by stimuli such as touch, sound, or a sudden bright light. An extreme and overpowering extensor rigidity cause the animal to assume (a sawhorse) stance.

Hyperthermic (104- 106 oF (40- 41 oC) due to stiffness and seizures is often present in dogs.

The titanic convulsions may last from a few seconds to 1 min. respiration may stop momentarily. Intermittent periods of relaxation are seen during convulsions but become less frequent as the clinical course progresses. The mucous membranes become cyanotic, and the pupils dilated. Frequency of the

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If untreated, the entire syndrome may last only 1-2 hr. there are no characteristic necropsy lesions. Animals dying from strychnine poisoning have rapid rigor mortis.

Diagnosis

Tentative diagnosis of strychnine poisoning is usually based on history of exposure and clinical signs.

Recovery of strychnine alkaloids from the stomach contents, vomitus, liver, kidneys, or urine should be considered diagnostic.

Treatment

Strychnine poisoning is an emergency, and treatment should be instituted quickly.

Decontamination consists of removal of gastric contents by inducing emesis or gastric lavage.

Binding of remaining bait in the GI tract with activated charcoal.

Emesis should be induced with 3% H2O2 (small animals and pigs) at 1-2 ml/kg PO maximum 3 tbsp, repeated once after 30 min.

Apomorphine (dog only) at 0.03 mg /kg IV or 0.04 mg /kg IM. Or xylazine

(dogs or cats) at 0.5 – 1 mg /kg IV or IM

Gastric lavage should be performed with taped water. Animals that are already seizuring should be anesthetized first (with pentobarbital).

After emesis or gastric lavage, activated charcoal should be administered at

2-3 g/kg in small animals and 0.5 – 1 g/kg in large animals with magnesium sulfate at 250 mg PO.

Seizures should be controlled in small animals with pentobarbital IV to effect repeated as necessary. well.

Muscle relaxants such as methobarbamol at 100- 200 mg /kg IV also work

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In large animals, chloral hydrate or xylazine can be used to control seizures.

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Snake bite

Venomous snakes fall into 2 classes

1.

The elapines , which include the cobra , mamba , and coral snakes

2.

The 2 families of viperines , the true vipers ( e.g. puff adder , Russel's viper and common European adder ) and the pit vipers ( e.g. ratle snakes , cottonmouth moccasin , copper head , and fer- de- lance ).

Elapine snakes have short fangs and tend to hang on and chew venom into their victims .Their venom is neurotoxic and paralyzes the respiratory center.

Animals that survive these bites seldom have any sequelae.

Viperine snakes have long, hinged, hollow fangs, they strike, inject venom

(a voluntary action), and withdraw.

Many bites by vipers reportedly do not result in injection of substantial quantities of venom.

Viperine venom is typically hemotoxic, necrotizing and anticoagulant, although a neurotoxic component is present in the venom of some species e.g. the mosave rattle snake (crotalus scutulatus scutulatus).

Fatal snake bites are more common in dogs than in any other domestic animal.

Due to the relatively small size of some dogs in proportion to the amount of venom injected, the bite of even a small snake may be fatal .because of their size, horses and cattle seldom die as a result (a direct result) of snake bite, but death may follow bites on the muzzle, head, or neck when dyspnea results from excessive swelling.

Serious secondary damage sometimes occurs; livestock bitten near the coronary band may slough a hoof.

Snake bite, with envenomation, is a true emergency. Rapid examination and appropriate treatment are paramount.

Diagnosis

In many instances, the bite has been witnessed, and diagnosis is not a problem. However, many conditions though by the owner to be snake bites are

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When possible, owners should be instructed to bring the dead snake along with the bitten animal (the needed is to snake's head) because identification may depend on the morphology of the head.

Many bites do not result in envenomation or are made by non poisonous snakes.

Typical pit viper bites are characterized by severe local tissue damage that spread from the bite site.

The tissue becomes markedly discolored within a few minutes, and dark, bloody fluid may ooze from the fang wounds if not prevented by swelling.

Frequently, the epidermis slough when the covering hair is clipped or merely parted.

Hair may hide the typical fang marks. Sometimes only one fang mark or multiple puncture are present.

In elaphine snakebites, pain and swelling are minimal, systemic neurologic signs predominante.

Treatment

Intensive therapy should be instituted as soon as possible because irreversible effects of venom begin immediately after envenomation.

Animals bitten by an elaphine may be treated with antivenin (which may be available on an as – needed basis through larger human hospital emergency rooms). And supportive care, including anticonvulsants if necessary.

The progression of events after pit viper envenomation can be divided into

3 phases

The first 2hr .The ensuing 24 hr and a variable period (usually – 10 days after ward)

The first 2 hr is the acute stage in which untreated, severely envenomize animals usually die,

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If dearth does not occur during this period, and the untreated animal is not in shock or depressed, the prognosis usually is favorable.

The acute phase can be prolonged for several hours by use of corticosteroids and if they are administered, prognostication should be with held.

If the animal is active and alert often 24 hours, death due to the direct effects of the venom is unlikely.

The third phase is convalescent period in which infection (possibly anaerobic) may be of concern

If necrosis has been extensive, sloughing occurs and may be so severe as to involve an entre limb.

In dogs and cats, mortality is generally higher from bites to the thorax or abdomen than from bites to the head or extremities.

Sensitivity to the venom of pit vipers varies among domestic animals. In decreasing order, sensitivity is reportedly horse, sheep, goats, dog, rabbits, pig, and cat.

Treatment of pit viper envenomation should be directed toward preventing or controlling shock, neutralizing venom, preventing or controlling disseminated intravascular coagulation, minimizing necrosis and preventing secondary infection. Rapid – acting corticosteroids may help to control shock, protect against tissue damage, and minimize the likelihood of allergic reactions to antivenin.

Antivenin is highly beneficial because its action is the only direct and specific mechanism for neutralizing snake venom.

Up to 100 ml of antivenin may be necessary for small dogs bitten by large snake. 5- 10 ml may inject into the tissues around the bite, and the remainder IV.

Broad spectrum antibiotics to prevent wounds infection and other secondary infections .tetanus antitoxin. Blood transfusion.

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Copper poisoning

Sheep are affected most often although other species are also susceptible

.acute poisoning is usually seen after accidental administration of excessive amounts of soluble copper salts , which may be present in anthelmintic drenches

, mineral mixes , or improperly formulated rations .

Many factors that alter copper metabolism influence chronic copper poisoning by enhancing the absorption or retention of copper.

Low levels of molybdenum or sulfate in the diet are example.

Primary chronic poisoning is seen most commonly in sheep when excessive amounts of copper are ingested over a prolonged period.

The toxicosis remains subclinical until the copper that is stored in the liver is released in massive amounts.

Blood copper concentrations increase suddenly, causing lipid perioxidation and intravascular hemolysis.

The hemolytic crisis may be precipitated by many factors, including transportation, pregnancy, lactation, strenuous exercise, or a deteriorating plane of nutrition.

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Nitrate and nitrite poisoning

Many species are susceptible to nitrate and nitrite poisoning, but cattle are affected most frequently.

Ruminants are especially vulnerable because the ruminal flora reduced nitrate to ammonia, with nitrite (10 times more toxic than nitrate). As an intermediate product.

Nitrate reduction (and nitrite production) occurs in the cecum of equids but not to the same extent as in ruminants.

Acute intoxication is manifested primarily by methemoglobin formation

(nitrite ion in contact with RBC oxidizes ferrous iron in Hb to the ferric state, forming stable methemoglobin in capable of oxygen transport.) and resultant anoxia. Secondary effects due to vasodilatory action of the nitrite ion on vascular smooth muscle may occur.

Ingested nitrates may directly irritate the GI mucosae and produce abdominal pain and diarrhea.

Although usually acute, the effects of nitrite or nitrate toxicity may be sub acute or chronic and are reported to include retarded growth, lowered milk production, Vitamin A deficiency, minor transitory goitrogenic effects, abortion and fetotoxicity

Etiology

Nitrate and nitrite are used in pickling and curing brines for preserving neats, certain machine oils and antirust tablets, gun powder and explosive, and fertilizers. They may also serve as therapeutic agent for certain non infectious diseases e.g. cyanide poisoning. Toxicosis occurs most commonly from ingestion of plants that contain excess nitrate, especially by hungry animals engorged themselves. Nitrate toxicosis can also result from accidental ingestion of fertilizers or other chemicals

Clinical findings

Signs of nitrite poisoning usually appear suddenly due to tissue hypoxia and low blood pressure as a consequence of vasodilation. Rapids, weak heart beat with subnormal body temperature; muscular tremors, weakness and ataxia are early signs of toxicosis when methemoglobinemia reach 30-40%. Brown,

27


=========================================================================== cyanotic mucous membranes develop rapidly as methemoglobinemia exceeds

50%. Dyspnea, tachypnea, anxiety and frequent urination are common.

Some monogastric animals usually because of excess nitrate exposure from non plant sources, exhibit salivation, vomiting, diarrhea, abdominal pain, and gastric hemorrhage.

Affected animals may die suddenly without appearing ill, in terminal anoxic convulsions within 1 hr, or after a clinical course of 12-24 hr or longer.

Acute lethal toxicosis almost always is due to development of ≥ 80% methemoglobinemia.

Some animals that develop marked dyspnea recover but then develop interstitial pulmonary emphysema and continue to suffer respiratory distress; most of these recover fully within 10 – 14 days.

Abortion and stillbirths may be seen in some cattle 5- 14 days after excessive nitrate / nitrite e4xposure , but only in cows that have survived a =>

50% methemoglobinemia for 6- 12 hr or longer.

Lesions

Blood that contains methemoglobin usually has a chocolate – brown color, although dark red hues may also be seen. Then may be pinpoint or larger hemorrhage on serosal surfaces. Dark brown discoloration evident in moribund or recently dead animals is not pathognomonic, however, and other methemoglobin induces must be considered.

If necropsy is post pond too long, the brown discoloration may disappear with conversion of methemoglobin back to hemoglobin.

Diagnosis

Excess nitrate exposure can be assessed by laboratory analysis for nitrate in both pre and post mortem specimens.

High nitrate and nitrite values in post mortem specimens may be an incidental finding, indicative only of exposure and not toxicity.

Plasma is the preferred pre mortem specimens, because some plasma – protein bound nitrate could be lost in the clot if serum was collected.

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Additional post mortem specimens from either toxicosis or abortions include ocular fluid, fetal pleural or thoracic fluid, fetal stomach contents, and maternal uterine fluid.

All specimens should be frozen in clean plastic or glass containers before submission, except when whole blood is collected for methemoglobin analysis.

Field tests for nitrate

The diphenylamine blue test (1% in concentrated sulfuric acid) is more suitable to determine the presence or absence of nitrate in suspected forages.

Nitrate test strips (dipsticks) are effective in determining nitrate values in water supplies, and can be used to evaluate nitrate and nitrite content in serum, plasma ocular fluid and urine.


Include poisoning by cyanide , urea , pesticide , toxic gases ( e.g. carbon monoxide , hydrogen sulfide ) , chlorates , aniline dyes , aminophenols , or drugs ( e.g. sulfonamides , phenacetin , and acetaminophen , as well as infectious or non infectious diseases e.g. grain overload , hypocalcemia , hypomagnesemia , pulmonary adenomatosis or emphysema and any sudden un explain deaths .

Treatment

Slow IV injection of 1% methylene blue in distilled water or isotonic saline should be given at 4-22mg /kg body weight or more depending on severity of exposure.

Lower dosages may be repeated in 20-30 min if the initial response is not satisfactory. Rumen lavage, with cold water and antibiotic s may stop the continuing microbial production of nitrite.

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Ammonia toxicosis

Poisoning by ingestion of excess urea or other sources of non protein nitrogen (NPN) is usually acute, rapidly progressive, and highly fatal.

Sources of NPN have different toxicities in various species, but mature ruminants are affected most commonly.

After ingestion, NPN undergoes hydrolysis and release excess ammonia

(NH3) into the GI tract, which is absorbed and leads to hyper ammonia.

Etiology

The most common sources of NPN in feeds are urea, urea phosphate, ammonia (anhydrous), and salts such as mono ammonium and diammonium phosphate.

Natural protein sources such as rice hulls, cotton seed, meal, and straw or other low quality forages may be treated with anhydrous ammonia to increase available nitrogen in supplemented livestock diets.

Ammonia or NPN poisoning is a common sequel of abrupt change to urea or other NPN in the diet when only natural protein was previously fed. Animals have to be gradually acclimated to NPN so that rumen microflora can increase in numbers to use the NH3 produced. Also, farm animals sometimes drink liquid fertilizers or ingest dry granular fertilizers that contain ammonium salts.

Ruminants are most sensitive because urease is normally present in the functional rumen after 50 days of age.

Dietary exposure of un acclimated ruminants to 0.3- 0.5 g of urea /kg body weight may cause adverse effects.

Doses of 1-1.5 g/ kg are usually lethal.

Urease activity in the equine cecum is 25% that of the rumen.

Horses are more sensitive to urea than other mono gastric, and doses of ≥ 4 g / kg can be lethal.

Ammonium salts at 0.3- 0.5 g/ kg may be toxic in all species and ages of farm animals, doses ≥ 1.5 g / kg usually are fatal.

Clinical findings

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The period from urea ingestion to onset of clinical signs is 20-50 min in cattle, 30- 90 min in sheep, and longer in horses.

Early signs include muscle tremors (especially of face and ears), exophthalmia, abdominal pain, frothy salivation, poly uria, and bruxism.

Tremors progress to incoordination and weakness.

Pulmonary edema leads to marked salivation dyspnea and gasping.

Horses may exhibit head pressing, cattle are often agitated, hyperirritable, violent and belligerent as toxicosis progresses, and sheep usually appear depressed.

An early sign in cattle is ruminal atony , as toxicosis progresses , ruminal tympany is usually evident , and violent struggling and bellowing , a marked jugular pulse , severe twitching , titanic spasms , and convulsions may be seen.

The PCV and serum concentration of NH3, glucose, lactate, potassium, and phosphorus, AST, ALT and BUN usually are significantly increased.

As death nears, animals become cyanotic, dyspneic, anuria, and hyperthermic and blood pH decreases from 7.4- 7.0

Regurgitation may occur, especially in sheep.

Death related to excess NPN usually occurs within 2 hr in cattle, 4hr in sheep and 3-12 hr in horses.

Survivors recover in 12-24 hr with no sequalae.

Lesions

Carcass4es of animals dying of NPN poisoning appear to bloat and decompose rapidly, with no specific characteristic lesions.

Frequently, pulmonary edema, congestion and petechial hemorrhages may be seen.

Mild bronchitis and catarrhal gastroenteritis are often reported.

Regurgitated and inhaled rumen contents are commonly found in the trachea and bronchi, especially in sheep.

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A ruminal or cecal pH ≥ 7.5 from a recently dead animal is highly suggestive of NPN poisoning.

Diagnosis

Ammonia or NPN poisoning is suggested by signs, lesions, history of acute illness, and dietary exposure.

Specimens for NH3 –N analysis include ruminal – reticular fluid, serum, whole blood, and urine.


Include poisoning by , nitrate / nitrite , cyanide , organophosphate , carbamate pesticides , raw soybean overload , 4- methylimidazole , lead , chlorinated hydrocarbon pesticides , and toxic gases ( carbon monoxide , hydrogen sulfide , nitrogen dioxide ) , acute infectious and non infectious diseases such as encephalopathies , enterotoxaemia , or rumen autointoxication ,.

Protein engorgement, grain engorgement, ruminal tympany, and pulmonary adenomatosis.

Treatment

Ruminal infusion of 5% acetic acid 10.5 – 2 L in sheep and goats and 2-8 L in cattle.

32


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Halogenated Aromatic poisoning

PCB, PBB, Dioxins and others common persistent halogenated aromatics

(PHA) include polychlorinazed and polybrominated biphenyls (PCB, PBB) naphthalenes, benzens, and diphenylethers (PCDE, PBDE) as well as a number of pesticides such as DDT.

Polyhalogenated aromatics are chemically stable, lipid soluble, and bioaccumulative. They are rapidly absorbed by all routes of exposure, and accumulate in adipose tissue, from where they are gradually eliminated during fat mobilization.

Livestock feed, and pet food contamination as well as fish and fish meal were previously considered the major sources of exposure.

It is now known that airborne (vapor phased) and forage exposure are nearly universal.

Most toxic effects include

1.

Wasting (weight loss not necessarily accompanied by decreased food consumption).

2.

Skin disorders (Chloracne, edema, alopecia, and hyperkeratosis).

3.

Immune suppression

4.

Enlarged liver with fatty change and enzyme induction.

5.

Endocrine disruption ( antiestrogenicity , hypothyeroxinemia )

6.

Reproductive disorders (abnormal cycling, reduced conception, fetotoxicity and fetal resorption, tratogenesis).

7.

Carcinogenesis.

Treatment

Elimination the source of exposure. Bathing animals with detergent and coal water after dermal. Exposure.

Repeated large oral doses of activated charcoal (1-4 g/kg small animals, 1-2 g/.kg large animal).

Gastric lavage may be of benefit after oral exposure.

The charcoal will trap some PHA in the intestine preventing absorption into the body and reducing fatty tissues concentrations.

33


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It is important to minimize stress and optimize environmental conditions following severe exposures.

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Insecticides and acaricide (organic) toxicity

Each exposure, no matter how brief or small, results in some of the compound being absorbed and perhaps stored. Repeated short exposures may eventually result in intoxication.

The cholinesterase inhibiting property of organophosphates may be used to indicate degree of exposure if the activity of the blood enzyme is determined frequently.

Carbamate insecticides

Carbaryl, carbofuran, methomyl

Clinical findings

The carbamate insecticides act similarly to the organophosphates in that they inhibit cholinesterase at nerve junctions.

Sings include hypersalivation , GI hypermotility , abdominal cramping , vomiting , diarrhea , sweating , dyspnea , cyanosis , miosis , muscle fasciculating ( in extreme cases , tetany , followed by weakness and paralysis ) and convulsions.

Death usually results from hypoxia due to bronchoconstriction and pulmonary edema.

Diagnosis

1.

History of exposure to a particular carbamate

2.

Response to atropine therapy

Treatment

Treatment of carbamate poisoning is similar to that of organophosphate poisoning in that atropine sulfate injections readily reverse the effects .atropine for dog and cats 0.2 – 2 mg /kg – one – fourth of the dose given IV and the remainder given SC

Cattle and sheep 0.6 – 1 mg/kg one- fourth of the dose IV and the remainder SC.

Horse and pigs 0.1 – 0.2 mg /kg IV

Pralidoxine (2PAM).

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Chlorinated hydrocarbon compounds

Chloradene, Dieldrin, Heptachlor, Methoxychlor, Toxaphene, aldrine, BHC

Only lindane and methoxychlor are approved for use on or around livestock.

Aldrin is a portent insecticide similar to dieldrin.

Benzene hexachloride (BHC, hexachlorocyclohexane) was a useful insecticide for large animals and dogs but is highly toxic to cats in the concentrations necessary for parasite control.

Only the gamma isomer (lindane) is a useful insecticidal agent, the other isomers are stored for excessively long periods in body tissues.

Chlordane

Exposure occurs when livestock consume treated plants or when they come in direct contact through carelessness and accidents.

Clinical findings

The chlorinated hydrocarbon insecticides are general CNS stimulants .they produce a great variety of signs. Neuromascular tremors and convulsions.

Body temperature may be very high. Muscle fasciculation occurs, becoming visible in the fascial region, and extending backward until the whole body is involved. Large doses of DDT, DDD .and methoxychlore cause progressive involvement leading to trembling or shivering, followed by convulsions and death.

Convulsions may be continuous, clonic, or tonic lasting from a few seconds to several hours or intermittent and leading to the animal becoming comatose.

Behavioral changes such bas abnormal postures (head pressing, keeping the head down between the forelegs, continual chewing movements) _ may be seen.

Treatment

Thorough bathing without irritating the skin (no brushes) using detergents and copious quantities of cool water is recommended. If exposure is by ingestion, gastric lavage and saline purgative are indicated. The use of digestible oils such as corn oil is contraindicated

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Activated charcoal

When signs are excitatory, a sedative anticonvulsant such ads abarbiturate or diazepam is indicated.\

Remove or avoid any stress, noise

If animal show depression, anorexia, and dehydration therapy should be directed toward rehydration

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Organophosphates

Organophosphates (OP) have replaced the banned organochlorine compounds and are a major cause of animal poisoning.

Organophosphate insecticides with active EPA Registration as of 2002

Azinphos –methyl ( or ethyl ) chlorpyrifos , coumaphos ,Diazinobn , Dichlorvos

, Dimethoate ,Disulfoton , Fenthion , malayhion , Methyl pathion ,Oxydemeton

– methyl , Parathion ( Diethyl Parathion ) , phosmet , temephos , tetrachlorvinphos , Trichlorfon .

Organophosphate insecticides with no active EPA registration (As of 2002)

Carbophenothion, Chlorfenvinphosd, crotoyphos, Demeton, diaxathion, EPN,

Pamphur, Famphur. Mevinphos, Rounel, Rnelene, terbufos, Tetraethyl pyrophosphate (TEPP).

Clinical findings

In general, OP pesticides have a narrow margin of safety. Signs of OP poisoning are those of cholinergic over stimulation, which can be grouped under 3 categories: Muscarinic, nicotinic and central.

Muscarinic signs, which are usually, first to appear, include hypersalivation, miosis, frequ4ent urination, diarrhea, vomiting, colic and dyspnea due to increased bronchial secretions – and bronchoconstriction

Nicotin effects include muscle fasciculations and weakness

The central effects include nervousness, ataxia, apprehension, and seizures

Cattle and sheep commonly show severe depression .CNs stimulation in dogs and cats usually progresses to convulsions.

Onset of signs after exposure is usually within hours but may be delayed to > 2 days

In acuter poisoning, the primary clinical signs may be respiratory distress and collapse followed by death due to respiratory muscle paralysis.

Diagnosis

An important diagnosis aid is the cholinesterase activity in blood and bras in.

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Lesions

Animals with acute OP poisoning have no specific or no lesions. Pulmonary edema, and congestion, hemorrhages and edema of the bowel and other organs may be found.

Treatment

Three categories of drugs are used to treat Op poisoning

1.

Muscarinic blocking agents

2.

Cholineesrerase reactivators

3.

Emetics, cathartics, and adsorbants to decrease further absorption.

Atropine sulfate blocks the central and peripheral muscarinic effects of OP. in dogs and cats 0.2 – 2 mg / kg b. wt. every 3-6 hr or as often as clinical signs indicate

For horse and pigs 0.1 – 0.2 mg /kg IV repeated every 10 min as needed

Fort cattle and sheep 0.6 – 1 mg /kg one –third given IV the remainder IM or

SC.

Atropinization is adequate, when the pupils are dilated, salivation, ceases, and the animal appears more alert.

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