After reading this article you will learn about various toxicity caused by metals and non metals in animals.
1. Arsenic Poisoning:
Inorganic Arsenicals:
Arsenic trioxide, arsenic pent-oxide, sodium and potassium arsenate, sodium and potassium arsenite and calcium and lead arsenate are included as inorganic arsenicals.
Source:
Pasture near smelters, paints, strong solution of lead arsenate- for animal dipping, milk from arsenic-poisoned cattle, rodenticides, weedicides, baits and insecticides, use of lead arsenate as taenicide etc.
Toxicity:
Arsenic is a cumulative poison, stored principally in the liver, skin and hair. The oral lethal dose of sodium arsenite in most animals is 1 to 25 mg/kg. Sodium arsenite is ten times more toxic than arsenic trioxide.
Average total oral lethal dose of arsenic trioxide and sodium arsenite is as follow:
It is excreted slowly in the urine, faeces and milk. Trivalent and pentavalent arsenic compounds are similarly bound in bovine tissues. In cow, arsenic acid is absorbed and excreted rapidly in the urine. As a result, there is little storage in the tissues and these levels are rapidly depleted in a feed off period and represent ‘transit’ rather than true storage arsenic.
Factors Influencing Toxicity:
(i) Species:
(a) Herbivores are commonly poisoned.
(b) Cats are poisoned.
(c) Dogs are maliciously poisoned.
(d) Swine and fowl are rarely poisoned.
(ii) Oxidation state:
(i) Inorganic trivalent arsenic is more potent than inorganic pentavalent.
(ii) Organic arsenicals are less toxic than inorganic arsenicals.
(iii) Pentavalent arsenical is converted in-vivo to trivalent and become toxic.
(iii) Solubility:
(a) Soluble fine arsenicals are more toxic than coarse poorly soluble.
(iv) Rate of excretion:
(a) If excretion slowed toxicity is raised.
(b) More toxic to dehydrated and ill animal.
(v) Tolerance:
Constant exposure may produce tolerance.
Toxicokinetics:
(a) Arsenic is distributed in almost all biological fluid of the body.
(b) Higher concentration is found in liver, kidney and spleen.
(c) In domestic animals does not stay in the body for a longer period.
(d) Rapidly excreted in urine, faeces, bile, milk and saliva.
(e) The t1/2 is 1.5 days in animals.
(f) Does not cross B.B.B. but readily cross placental barrier.
Mechanism of Action:
Trivalent arsenic binds with the sulfhydryl groups of lipoic acid which is an essential co-factor for the enzymatic decarboxylation or keto acids, such as pyruvate, Ketoglutamate and ketobutyrate. Thus, arsenic acid inactivates lipoic acid and inhibits formation of acetyl succinyl and propionyl co-enzymes A. Other oxidative decarboxylation used by lipoic acid is also inhibited. Thus, glycolysis or citrate cycle is inhibited.
Arsenic produces local corrosive action on gut. However, GI damage is seen regardless of route of absorption. Liver, kidney and intestine is rich in oxidative enzymes and arsenic has special affinity to them. Arsenic increases capillary permeability and capillary endothelial cells of these organs are very much susceptible. The wall of blood vessels and smooth muscles are dilated.
Clinical Sign:
A. Peracute Cases:
(a) The animal is found dead showing no symptom.
(b) There may be severe colic, staggering, collapse, paralysis and death.
B. Acute Gases:
Severe colic, staggering, weakness, trembling, salivation, vomiting, thirst, projectile watery diarrhoea, blood tinged faeces, fast and weak pulse, hind limbs paralysis, normal or subnormal temperature, death in 1-3 days.
C. Sub Acute Cases:
Animal may live several days, colic, anorexia, blood mixed diarrhoea, muscle shreds in faeces. Polyuria followed by anuria, dehydration, thirst, partial paralysis of hind limbs, trembling, stupor, cold extremities, temperature sub normal, hematuria, convulsion.
D. Chronic Cases:
Are characterized by wasting, poor condition, thirst, brick red coloration of mucous membrane, normal body temperature and weak irregular pulse.
Lesions:
(i) Cattle: Reddened abomasal or duodenal mucosa and sub-mucosal oedema and haemorrhage in the abomasum and duodenum.
(ii) Perforation of the gut wall.
(iii) Intestinal contents having foul smell.
(iv) The liver soft and yellow.
(v) Lungs oedematous and congested.
Swine:
(i) Fauces inflamed and oedematous.
(ii) Larynx and trachea oedematous.
Fowl:
(i) Proventriculus and gizzard inflamed.
(ii) Gelatinous exudate beneath horny line of gizzard causes sloughing of horney lines.
Differential Diagnosis:
Arsenic poisoning is sudden in onset accompanied with severe colic, bloody diarrhoea. Haemorrhagic gastroenteritis and degenerative changes of kidney and liver are important postmortem findings.
No other metal cause this type of speedy lesions except thallium. Caustics, irritant plants, urea, chlorate, pesticides and enteric diseases produce symptoms similar to arsenic poisoning. In lead poisoning the behavioural and nervous signs are of significance, however, in arsenic poisoning these signs are not seen.
Treatment:
(i) Specific antidote: BAL (Dimercaprol):
Dose: 3 mg/kg body weight i. m. as 5% solution in a 10% solution of benzyl benzoate in pea nut oil- 4 hourly on the first 2 days, every 6 hours on day 3 and twice a day for next 10 days until cure.
(ii) Sodium thiosulfate:
Cattle and Horse 20-30 g orally mixed with 300ml water twice daily till recovery.
Sheep and goats: 5-8 g orally.
(iii) Supportive therapy:
Good nourishing care is essential. The animal should be kept warm and should be treated symptomatically e.g. antibiotic, analgesics etc.
Prognosis:
Grave, if the treatment is started late or there is extensive organ damage.
Analysis:
Stomach, intestine (faeces or vomitus) liver and kidney are the suitable organs for analytical purposes. However, blood, milk and urine may also be analysed. More than 3 ppm of arsenic concentration in these organs confirm arsenic poisoning in animals.
2. Lead Poisoning (Plumbism):
Source:
(i) Paint and paint cans.
(ii) Greases, linoleum, leaded gasoline, solid lead, solder, roofing materials and industrial effluent.
(iii) Grass near busy highway contains toxic amounts of lead from auto exhausts.
(iv) Licking of discarded storage batteries.
(v) Milk secreted from lead poisoned animals.
Toxicity:
A. Acute Toxicity:
The acute single oral lethal dose in animals is as follows:
Calves-50-600 mg/kg (lead or lead salts).
Cattle-50-100 gm. (as lead acetate).
600-800 mg/kg (lead salts).
Horses and goats- 20-40 gm. (lead acetate).
600-800 mg/kg (lead salts).
Swine-10-25 gm. (lead acetate).
Dogs-10-25 gm. (lead acetate).
Fowl-16-600 mg/kg (lead salts).
B. Chronic Toxicity:
When lead is ingested for a longer period (days, weeks or months).
The single oral chronic lethal dose in various animals is as below:
Calves: 1-3 gm./day.
Cattle: 6-7 mg/kg for 6-8 weeks (lead acetate).
Horses: 1-7 mg/kg/day.
Sheep (non pregnant): 8 mg/kg/day (lead acetate).
Sheep (pregnant): 1 mg/kg/day (lead acetate).
Goats: 0.62-0.94 gm./kg/day from 18 to 49 days.
Dogs: 0.32 mg/kg/day for 6 months.
Fowl: 320-640 mg/kg/day (lead acetate).
Swine: 64mg/kg (lead acetate) for 6 days to 13 weeks.
Cats: cases of lead toxicity in cat are very less.
Factors Influencing Lead Toxicity:
(i) Age
(ii) Species
(iii) Reproductive state
(iv) Rate of ingestion
(v) Form-soluble salts of lead are absorbed readily and is more toxic.
(vi) Route of entry
(vii) General state of health
(viii) Past exposure
(ix) Hormonal influences
Toxicokinetics:
(i) 85-90% of absorbed lead is carried out on erythrocyte membranes.
(ii) Unbound fraction of lead is distributed to various tissues which is responsible for producing toxic effects.
(iii) Lead is gradually excreted in bile.
(iv) Liver tissue contains high level of lead.
(v) Renal cortex contains higher level of lead than liver.
(vi) Faeces contain fairly good amounts of lead.
(vii) Unbound lead is excreted in higher level in milk.
(viii) Lead passes blood brain barrier and Placental membranes.
(ix) Unbound lead is trapped in bones and bone is considered to be the sink of lead. Bone contains 90-98% of total body burden of lead.
Mechanism of Action:
Lead inhibits sulfhydryl group of enzymes of cellular metabolism. It destroys the blood brain barrier and produces symptoms of encephalopathy. It also causes damage to capillary endothelial cells and produces cerebral oedema and haemorrhage.
After reaching into neurons and glia, it disturbs cellular membrane and molecular mechanism. Lead decreases the concentrations of copper, iron and zinc and interferes with these metals as prosthetic groups of enzymes in mitochondria. Therefore, lead affects cellular respiration, oxidative phosphorylation and the ATP-synthetase complex.
It causes haemoglobin deficiency and leads to deficiency of hemoproteins including mitochondrial respiratory cytochromes and microsomal cytochrome. Hence, deficiency is obviously due to the sulphydryl-containing enzymes because heme synthesis utilizes sulphydryl enzymes.
Clinical Signs:
(i) Hyper excitability, bellowing, rolling of the eyes, fear.
(ii) Pressing of head against wall, attempt to climbing over wall, sudden jumping, maniacal behaviour.
(iii) Nervous symptoms-(a) Depression specially in chronic poisoning, (b) Muscle fasciculations, twitching of ears or muzzle, excessive blinking, muscle spasms, rhythmic jerking of head and neck, champing of jaw, pharyngeal paralysis, laryngeal hemiplegia (causing roaring in horses, tongue rolling, nystagmus, blindness, opisthotonus, torticollis, clonic tonic convulsions, normal body temperature, coma followed by convulsive death.
(iv) Autonomic symptoms: Salivation, inability to swallow, lacrimation, sweating, colic, thirst, diarrhoea or constipation, rumen atony, urinary incontinence and vomiting.
(v) Locomotor disturbances: Stiff, stiled gait with ataxia, rigidity of postural muscles, swaying, circling, pacing, running.
(vi) Rapid laboured breathing, anorexia, weight loss, decreased milk production, dehydration, emaciation, fetal death, general weakness.
Toxicity Symptoms:
(a) Anorexia
(b) Dull or excited
(c) Colic
(d) Trembling or blind
(e) Pressing head against object
(f) Bellowing
(g) May be found dead due to excessive ingestion of lead.
Pathological Lesions:
A. Acute:
Calves, cattle, sheep (Gross lesions):
(i) Marked gastroenteritis
(ii) Severe kidney damage (Hyperaemic)
(iii) Presence of paint, paint flakes, black colored motor oil, or other foreign material.
Microscopic lesions:
(i) Liver show centrilobular necrosis.
(ii) Hepatocytes and renal tubular epithelium contain eosinophilic, acid-fast intra nuclear inclusions.
(iii) Necrosis of cerebral cortex.
B. Sub-Acute:
(i) Gross Lesions: pale muscles, liver and kidneys.
(ii) Fluid in the body cavities or pericardium.
(iii) Excess (CSF), lung oedema and cerebral oedema.
(iv) Congestion of kidneys, lungs, brain and abomasal and intestinal mucosa.
(v) Softening of the kidneys cortex, cerebral softening and cavitation.
Microscopic changes:
(i) Necrosis of renal tubules.
(ii) Nerve cell degeneration.
C. Chronic (gross):
(i) Emaciation.
(ii) Haemorrhagic gastroenteritis.
(iii) Meningitis.
Microscopic changes:
(i) Juvenile forms of erythrocytes.
(ii) Renal and cerebral degenerative changes similar to sub-acute but more obvious.
(iii) Increased number of inclusions in renal tubular epithelium.
Differential Diagnosis:
(i) Encephalitic disease.
(ii) Organochlorine toxicity: elevated body temperature, marked neuromuscular signs, there is no blindness.
(iii) Urea poisoning: Absence of blindness, abnormal posturing, head pressing, jumping.
(iv) Organophosphate and carbramate poisoning: Atropine may alleviate many signs of poisoning symptoms.
Treatment:
Cattle:
(i) Antidote-Ca-EDTA (calcium ethylenediamine tetra- acetate)
Dose -1-2% w/v solution in 5% glucose @ 100 mg/kg twice a day for 2 days. After 2 days again repeat the same dose for 2 more days. Treatment may be continued for 10-14 days of this interrupted therapy.
Dogs:
Ca-EDTA-1 % solution (w/v) in 5% glucose @ 25 mg/kg 4 times a day for 5 days.
(ii) Thiamine hydrochloride:-200 mg/kg intramuscularly alternate day for 14 days.
(iii) Sedation to control nervous and behavioural signs.
(iv) Gastric lavage and enema (dog).
(v) Oral administration of magnesium sulfate to precipitate lead and act as a saline purgative.
(vi) Corticosteroids and antibiotics to prevent bacterial infections.
(vii) Keep the animal quiet and comfortable.
Contraindication:
(i) Forceful feeding and administration of fluids and electrolytes.
Prognosis:
Grave in acute poisoning.
Laboratory Analysis:
A. Cattle:
(i) Ingesta, liver and kidney contains lead levels above 10 ppm.
(ii) In chronic poisoning the concentration of lead in bone may be 100 ppm or more.
B. Dog:
(i) Hair contains 88 ppm of lead.
(ii) The blood contains at least 0.35 ppm, liver-17.4 ppm and urine-lead level increases markedly after Ca-EDTA therapy.
C. Chickens:
(i) Blood and liver lead level more than 10 ppm.
(ii) Faeces 1-2910 ppm lead.
D. Horse:
(i) Liver, 0.0023-0.75, Kidney, 0.0013-1, Spleen, 0.1-0.25, muscle, 0.02-0.05 and bone, 3-12 ppm.
E. Swine:
Rarely poisoned by lead.
3. Mercury Poisoning:
Source:
Mercurous and mercuric chlorides, gold mining, fungicides, paints, mercury boilers.
Route of entry:
Ingestion, respiratory tract and skin.
Toxicity:
(a) Acute:
Pain, inflammation, necrosis of oral and pharyngeal mucosa, nausea, vomiting, abdominal pain, damage of the kidney, blood tinged stool, anorexia, anasarca, tremor, ataxia, maniacal symptoms.
(b) Chronic:
Metallic taste, salivation, loosening of teeth, diarrhoea, anaemia, hepatitis, nephritis, irritability.
Treatment: 1:
Lavage and emetics for removing mercurial compounds from stomach.
2. Antidote: Dimercaprol.
4. Copper Poisoning:
Source:
(i) Feed-Mineral supplements too high in copper and low in molybdenum and inorganic sulfates.
(ii) Antifungal sprays-Bordeaux mixture (CuSO4) 1-3% used for spray in orchards.
(iii) Soils high in copper:
(a) Naturally high in copper.
(b) Contaminated by smelters and mines.
(iv) Copper given orally as medication (CuSO4)
(a) Improper dosage.
(b) Footrot treatment.
(c) Fluke treatment.
(v) Plant poison that damages liver so that liver accumulates copper (Heliotropium europeum in Australia).
(vi) Improper balance of copper and molybdenum in feed plants (Phytogenous chronic poisoning).
Susceptibility and Occurrence:
(i) Herbivores-Primarily sheep, cattle are more resistant.
(ii) Pigs, dogs, poultry and calves are more susceptible.
(iii) May be acute form or chronic.
(a) Acute form usually related to improper dosing of copper medications or exposure to forage sprayed with copper.
(b) Chronic poisoning usually associated with imbalance of copper. Molybdenum and inorganic sulfate in herbage.
Toxicity:
A. Acute:
(a) Cattle-200-800 mg/kg body weight.
(b) Sheep-20-100 mg/kg.
B. Chronic:
(a) Daily intake of 3.3 mg/kg will produce poisoning.
(b) Pasture containing 15-20 ppm/D.M. copper will produce toxicity in sheep.
(c) Pelleted feeds containing 50 ppm and mineral mixtures, containing 1400 ppm copper have poisoned sheep.
(d) A low molybdenum intake enhances the toxicity of copper.
(e) A level of 25 ppm copper in a ration can cause storage of copper in liver to a dangerous level in 8 months in sheep.
(f) 325 ppm copper in diet of chicks can produce toxicity.
Pathogenesis:
(i) Soluble copper salts in high concentration are protein coagulants and produce gastrointestinal injury.
(ii) After intravenous administration, it produces haemolysis. If absorbed 60% RBC destroyed.
(iii) Chronic intake results in storage of copper in liver. When maximum are reached in liver, it is spilled into blood stream resulting in acute poisoning.
(iv) A condition called ‘Toximic jaundice’ or secondary copper poisoning results from liver injury by plants causing excessive retention of copper.
(v) High levels of molybdenum and sulfate facilitate the elimination of copper.
Classification of Copper Problems:
A. Copper Deficiency:
(a) Demyelination of nerves (Enzootic ataxia or sway back in lambs).
(b) Anaemia.
(c) Faded hair coat.
(d) May be due to excess molybdenum or sulfate.
B. Copper Poisoning:
(a) Primary
(i) Acute-Ingestion of large amounts of copper salts
(ii) Chronic-Continued ingestion of small amount of copper.
(b) Secondary:
(i) Phytogenous chronic poisoning-Small amounts of copper are ingested, but excessive retention occurs because of specific plants which do not cause liver damage, such as subterranean clover Trifolium subterraneutii (imbalance of Mo, SO4 and Cu).
(ii) Hepatogenous-Ciironic poisoning because of excessive retention caused by plants which cause liver dysfunction e.g. Senacio spp. and others containing pyrizolidine alkaloids.
Clinical Signs:
A. Acute syndrome appears in 24-48 hours.
(i) Greenish tinged fluid faeces.
(ii) Vomition, salivation, purgation abdominal pain.
(iii) Collapse, paralysis, convulsions.
B. Chronic poisoning-usually occurs when an animal consumes a small amount over a period of time and shows little toxic signs until a critical level is reached in the liver.
(a) Sudden onset-course 24-48 hours.
(b) Weakness, trembling (exhaustion).
(c) Arching of back (renal pain)
(d) Icterus, hemoglobinuria, hemoglobinemia.
(e) No diarrhoea.
(f) Bloody nasal discharge.
Postmortem Lesions:
A. Acute:
(i) Marked gastroenteristis (inflammation and erosions) with congested spleen, liver and kidneys.
(ii) Blood is coagulated at time of death.
B. Chronic:
(i) Icterus (generalized)
(ii) Slightly enlarged, yellow, friable liver. May be atrophic after long periods of copper storage.
(iii) Gall bladder distended with thick greenish brown bile.
(iv) Kidneys enlarged/dark colour or show haemorrhagic mottling, tissue is friable, bladder distended.
(v) Spleen enlarged, deep brown to black parenchyma (black- berry jam)
Diagnosis:
(i) Clinical signs.
(ii) Postmortem findings.
(iii) Examination of feed stuffs for level of copper, molybdenum and sulfate.
(iv) Acute poisoning-Copper levels in blood and liver may be normal (blood 0.7-1.3 ppm, liver less than 350 ppm). If course longer than 24 hrs. liver levels may be elevated and blood levels may be elevated. Blood levels may fall to normal prior to death, faeces may contain 8000-10,000 ppm of copper.
(v) Chronic poisoning:
(a) Blood levels of copper elevated.
(b) Liver levels of copper falls between 1000-2000 (above 350 ppm).
Differential Diagnosis:
(i) Leptospirosis-fever and ataxia.
(ii) Post parturient heamoglobinuria.
(iii) Bacillary hemoglobinuria-fever.
(iv) Acute pasteurellosis-fever.
(v) Acute cases of heavy metal poisoning.
(vi) Hepatitis.
(vii) Phenothiazine.
(viii) Anthrax.
Treatment:
(i) Molybdenum prevents storage of copper.
Dose (sheep)-50-500 mg ammonium molybdate/day for 3 weeks.
(ii) BAL May increase excretion of copper.
(iii) Treat acute cases as for any irritant.
(iv) Ca-EDTA and Penicillamine are also effective.
(v) 0.5% Ascorbic acid in feed, Gastrointestinal sedative and fluid therapy in acute cases may be given as non specific/ancillary treatment.
5. Phosphorus Poisoning:
Phosphorus is available in three colours-white, yellow and red. The red phosphorus is inactive and non toxic whereas rest of two are poisonous and previously were used as constituent of rat poison.
Source:
(i) Direct ingestion of rodent baits.
(ii) Contamination of herbage and soil from incendiary.
(iii) Smoke of bombs.
Toxicity:
Horse and Ox – 0.5 to 2 gm.
Pig – 0.05 to 0.3 gm.
Dog – 0.05 to 0.1 gm.
Fowl – 0.02 gm.
Clinical Symptoms:
(i) Intense abdominal pain, profuse vomiting.
(ii) Garlic like odour of vomitus.
(iii) Jaundice and nervous symptoms.
(iv) Delerium, convulsion, coma and death.
Postmortem Findings:
(i) Inflammation of stomach and intestine
(ii) Fatty degeneration of liver.
(iii) Extravasation of blood in to subcutaneous tissue. skin and muscle
(iv) After opening the stomach phosphorus like odour
Diagnosis:
(i) Clinical signs and postmortem lesions.
(ii) Chemical test (vomitus, intestinal contents).
Treatment:
(i) Not successful if delayed.
(ii) Apomorphine should be used in animals capable of vomiting (Dogs and cats).
(iii) Wash the stomach after vomition with 0.4% of copper sulphate.
(iv) Purgatives should be given to evacuate the gastrointestinal tract.
(v) Heart stimulants and intravenous glucose if needed.
(vi) Noradrenaline should be given for the relief of circulatory collapse.
6. Selenium Poisoning:
Source:
(i) Soils containing high level of selenium.
(ii) Obligate accumulators (selenium indicator plants)
These plants contain 15,000 ppm of selenium e.g:
(a) Astragalus (poison vetch)
(b) Stanleya (Prince’s plume)
(c) Oonopsis (golden weed)
(d) Xylorrhiza (Woody aster)
(iii) Facultative accumulators-These plants do not require selenium but they may take up the element from soil e.g.
(a) Aster
(b) Atriplex (salt bush)
(c) Castilleja (Plant brush)
(d) Comandra (bastard toadflax)
(e) Grayia (hopsage)
(f) Grindelia (gum weeds)
(g) Gutierrezia (Snake weed)
(h) Mchaeranthera (tansy aster)
(i) Penstemon (beard tongue)
(j) Sideranthus (iron weed)
(iv) Crop plants-Corn, wheat, oats, barley, grass and hay
Toxicity:
A. Acute:
(i) The acute oral median lethal close of selenium as selenate or selenite:
(a) Horse – 3.3 mg/kg
(b) Cow – 10 mg/kg
(c) Pig – 17 mg/kg
(d) Cat, rabbit and rat – 1.5 – 3 mg/kg
(i) The
(ii) Lethal dose
Dogs – 4 mg/kg orally (selenite or selenate)
(iii) LD50 of selenite with Vit. E Pigs -1.4 mg/kg
B. Chronic poisoning:
Swine – 7 ppm
Cattle – 5-50 ppm
Poultry – 15 ppm
Sheep – 10 ppm
Toxicokinetics:
Selenium is rapidly absorbed from the gut and is distributed to liver, kidney and spleen. If selenium is ingested for a longer period it accumulates in higher concentrations in hair and hoof. It can cross placental barrier and produce foetal deformities and embryo toxic effects. Selenium does not penetrate, intact skin but can penetrate abraded skin. Selenium is excreted in urine, faeces and bile in toxicated animals.
Mechanism of Action:
Selenium replaces sulfur of amino acids such as cysteine and methionine. As a result of this replacement, abnormal enzyme proteins are synthesized which causes hoof and hair defects in chronic selenosis. It inhibits sulfhydryl containing enzymes and causes decrease synthesis of ATP. Thus, oxygen utilization is decreased in liver, kidney and brain.
Clinical Signs:
A. Acute:
Cattle-Colic, bloat, dark watery diarrhoea, polyuria, fever (39-40°C), Mydriasis, head and ears lowered, fast and weak pulse, pale mucous membranes, dyspnea with fluid sounds in lung, blood tinged froth exuding from the nares, prostration, coma and death in 1-2 days.
Horse – do not suffer.
B. Sub acute (Blind staggers):
Cattle:
The animal may not be blind and may not stagger.
First stage-Poor appetite, wander aimlessly, circling, do not avoid obstacle, respiration and temperature normal.
Second stage-Besides the symptoms of first stage there is depression, incoordination, weakness of fore legs, complete anorexia.
Third stage-Colic, subnormal body temperature, inflammation, swollen and inflammed eyelids, clouded corneas, blindness, difficulty in swallowing, dyspnea, tachycardia, coma and death.
C. Chronic selenosis (alkali disease):
The symptoms are as follow; Partial blindness, paresis, incoordination, emaciation, lethargy, peripheral circulatory insufficiency.
Postmortem Lesions:
(i) Leaky blood vessels, organs congested.
(ii) Liver, kidney, spleen, gut, heart and brain are congested.
(iii) Haemorrhagic enteritis.
(iv) Gut contents smell of rotten garlic.
(v) Emaciated carcass.
Differential Diagnosis:
Conditions that are confused with acute and sub-acute selenosis are:
(i) Pneumonia.
(ii) Anthrax.
(iii) Infectious hepatitis.
(iv) Enterotoxaemia.
(v) Pasteurellosis.
Conditions which are confused with chronic selenosis are:
Freezing, ergotism, molybdenosis, fluorosis and laminitis.
Tips to Remember:
The odour of rotten garlic in a fresh carcass indicates acute or sub-acute selenosis. However, volatile selenides may escape quickly and in such cases during postmortem odour of rotten garlic is absent. Thus, absence of odour of rotten garlic do not rule out selenosis.
Treatment:
If lesions of selenosis have appeared treatment is difficult.
However, the following treatment may be adopted:
(i) Remove the source.
(ii) Use of saline purgative.
(iii) Oxygen therapy.
(iv) Treatment for pulmonary oedema and circulatory shock.
(v) High protein diet.
Analysis:
If the blood, liver, kidney, urine and milk of animals affected with selenosis are examined they contain the following levels.
A. Acute (Bovine):
(i) Blood – 25 ppm
(ii) Liver and kidney – 4 to 25 ppm
(iii) Urine – 0.1 to 8 ppm
(iv) Milk – 3 ppm
B. Chronic (Bovine):
(i) Blood – 1 to 4 ppm
(ii) Hoof – 5 to 20 ppm
(iii) Hair – 5 to 10 ppm
Equine:
Hoof – 11-45 ppm Hair – 11 ppm
7. Chronic Fluoride Poisoning (Fluorosis):
Fluorosis is very common in cattle and other animals near a factory where chimneys are emitting large quantity of fumes that may contain hydrofluoric acid. The leaves of plants or grasses may absorb the gas and collect some of the dust on their surfaces.
Source:
(i) Phosphate and fluorine containing mineral supplements (Buns et al 1962).
(ii) Industrial plants emitting fluorine containing gases and dust.
(iii) Fluorine production by cryolite used in the small furnaces.
(iv) Brick works.
(v) Glass, enamel and colour works.
(vi) Steel and metal works.
(vii) Potteries.
(viii) Fluorine contaminated pasture near an industrial area.
Toxicokinetics:
The fluorine ingested by an animal is mainly deposited in bones and teeth. The exact chemical form in which they are stored in bone and teeth is still not known. It is mainly excreted in urine. In fluorosis, the tissue concentration is raised by two or three times than the normal value.
The high content of fluorine in feed of an animal does not affect its level in milk. It does not pass the placental barrier and do not produce any harmful effect in foetus. It is not fully known that poultry feed containing high level of fluorine, can affect the level of fluorine in yolk of eggs.
Mechanism of Action:
Fluorine causes defect of calcium excretion in animals. It causes replacement of hydroxyl groups of hydroxyapatite and alters the crystal structure and crystal lattice dimensions of bones apatite. Fluorine causes damage to the blast cells and delays the mineralization of pre-enamel, predentine, precementum and prcskeletal matrices. It also inhibits the enzymes needed for bone and tooth formation.
Toxicity:
Toxicity depends upon solubility of inorganic fluorine, in water. Sodium fluoride and sodium fluosilicate (silicofluoride) are the most toxic. The calcium fluoride (fluorspar) is minimum toxic.
A. Cattle:
(i) 40 ppm in feed causes fluorosis.
(ii) 15 mg fluorine/kg body weight.
(iii) 100 ppm in ration causes degenerative tooth change in 3 to 5.5 years.
B. Sheep:
(i) 10 ppm in water (sodium fluoride).
Over a longer period (6-7 year) causes decrease in wool production.
C. Horses:
(i) More tolerant.
D. Chicks:
(i) Are more resistant.
(ii) 350 ppm-530 ppm is borderline of toxicity.
Clinical Symptoms:
(i) Lameness-first in one leg followed by another in fore legs and hind legs.
(ii) Fracture of bones.
(iii) Stunted growth of young animals.
(iv) Skeletal abnormalities.
(v) Enlargement of sternum and lower jaw.
(vi) Metacarpals, metatarsals and phalanges increase in diameter.
(vii) Well defined exostoses.
(viii) Callus formation on the ribs.
(ix) Dental lesions-
(a) loose their lusture and become pitted/disposition of dark pigment in defective enamel.
(b) Incisor and molars show sign of excessive and irregular wear.
Post-mortem Leisons:
(i) Bone colour is changed to chalky white, surface of bone roughened and diameter enlarged.
(ii) Periosteum thickened and hyperemic.
(iii) The bone marrow shows gelatinous degeneration.
Diagnosis:
(i) Determination of fluorine content of specific tissues.
(ii) Bone: Contains more than 5,000 ppm of fluorine.
(iii) Urine-contains more than 15 ppm.
Treatment:
(i) Aluminium sulphate or chloride-0.53% of aluminium sulphate or chloride with feed.
Nitrate and Nitrite Poisoning:
Poisoning caused by nitrates and nitrites is very common in animals due to increased use of fertilizers.
Source:
(i) Chemical fertilizers.
(ii) Water containing high level of nitrates and nitrites.
(iii) Commercial dynamite.
(iv) Preserved food.
(v) Plants grown on soils containing high amount of nitrate and nitrite.
(vi) Weeds suffering from unfavourable environmental condition.
(vii) Herbicides (2, 4-dichlorophenoxyacetic acid).
(viii) Drought conditions.
(ix) Air dried leaves sprayed with 2, 4-dichlorophenoxyacetic acid.
(x) Oats infected with virus.
Plants Containing Toxic Levels of Nitrate:
Amaranthus spp.
Ammi majus
Amsinckia spp.
Aneilema accuminatum
Apium graveolens
Astragalus hamosus
Bassia spp.
Brassica spp.
Carduus spp.
Chenopodium spp.
Cucumis sativa.
Datura spp.
Emilia sonchifolia.
Heliotropium spp.
Ipomoea spp.
Polyronum spp.
Solarium spp.
Sorghum spp.
Zygophyllum spp.
Toxicity:
Nitrates as such are not toxic. They become toxic when they are converted to nitrites either in the food stuff or in the alimentary tract.
Minimum Lethal Dose:
Cattle – 0.65 to 0.75 gm./kg (sodium nitrate)
Cattle – 1 gm./kg (Potassium nitrate)
Sheep – 1 gm./kg (Potassium nitrate)
Horses – 1 gm./kg (Potassium nitrate)
Pig – 70 to 75 mg/kg (Sodium nitrites)
Treatment:
(i) Administration of methylene blue Dose-9 mg/kg as 4% aqueous solution i.v.
Repeat same dose in severe cases after an interval of 6-8 hrs.
(ii) Ascorbic acid.
Mechanism of Action:
Nitrites convert the haemoglobin of the blood into methaevioglobin. Thus the oxygen carrying capacity of blood to different tissues is reduced. Therefore, the death of animal is due to tissue anoxia.
Clinical Symptoms:
(i) Abdominal pain, diarrhoea.
(ii) Muscular weakness, incoordination, convulsion.
(iii) Increased heart rate, difficulty in respiration, progressive cyanosis, coma and death.
(iv) Pregnant animals may abort.
Pig die without showing any symptoms.
Post-Mortem Lesions:
(i) Blood – Dark, discoloured and tarry.
Diagnosis – Estimation of serum nitrite level.
8. Common Salt Poisoning:
Source:
(a) Water deprivation may be primary cause of poisoning in ruminant, swine and poultry.
(i) Frozen water.
(ii) Crowded conditions.
(iii) Medicated water resulting in less intake.
(b) Brine or whey garbage and kitchen wastes.
(c) Sodium ion may be offending agents, e.g. Na2CO3, sodium sulfonamide.
Susceptibility:
(i) Swine and young poultry are most susceptible.
(ii) Cattle and sheep have been poisoned on high concentration of salt in feed or water. Sheep can tolerate 1% sodium chloride in drinking water but 1.5% is detrimental.
(iii) The above lethal doses in animals depend on salt- hunger and availability of water.
(iv) In swine and poultry, salt poisoning occurs in hot weather and in cold weather when there is insufficient water.
(v) Dairy cows in lactation and horses in general are susceptible.
(vi) Salt poisoning is also seen in wild animals during winter.
Toxicity:
It is difficult to assign a toxic dose a numerical value.
(i) Swine- (a) Toxicity may be produced with 0.5% sodium chloride in feed if water is withheld.
(b) With ample water 10-13% sodium chloride in ration may be non-toxic.
(ii) Drinking water should not contain more than 0.5% total salts for any livestock.
(iii) Acute toxic dose of salt for pig, horse and cattle is 2.2 mg/kg and for sheep it is 6g/kg. However, toxicity depends upon availability of drinking water.
(iv) Poullry-0.25% of sodium chloride in drinking water of young birds is maximum safe level regardless of feed level. 2% in wet mash may cause toxicity to ducklings. Salt in wet mash is more toxic than in dry mash.
(v) Dog-More resistant as compared to other animals. The lethal dose in dogs is 4 g/kg.
Pathogenesis-Not Fully Known:
(i) Associated with salt hunger and availability of water in almost all animals.
(ii) Disturbance of electrolyte balance, especially sodium ion and water balance in the body, sodium propionate and acetate produces the same symptoms of toxicity as sodium chloride.
(iii) High concentration of common salt produces gastroenteritis and dehydration.
(iv) It has been proposed that a high blood level of Na+ results in high brain levels. As the blood level of Na+ decreases, the brain level does not create an osmotic gradient resulting in edema in the brain and intracranial pressure and reduced blood supply. Na+ has been found to inhibit anaerobic glycolysis.
The combination of reduced to supply increases intracranial pressure, and inhibit anaerobic glycolysis, may cause degeneration of the cerebral cortex. This does not explain the selective attraction of eosinophils in swine cerebrum.
Clinical Signs:
A. Swine:
Thirst, pruritis, constipation. After 1-5 days blindness and deafness, oblivious to surroundings, will not eat or drink, does not respond to external stimuli, wander aimlessly, push against objects, may circle, pivoting around one front or hind foot. May recover or comatose and die or develop seizures. Seizures are frequent at regular intervals and progress from cranial to caudal. Temperature does not elevate except in hot weather during seizures. Vomiting may be seen.
B. Cattle:
Alimentary tract mainly affected. Vomiting, diarrhoea, mucous in faeces, abdominal pain, anorexia. Nervous signs; blindness, knocking of fetlocks, convulsion may be seen. Polyuria, nasal discharge. Animal usually die within 24 hrs. of the appearance of clinical signs.
C. Poultry:
Excessive thirst, respiratory distress, discharge of fluid from beak, paralysis of legs.
Post Mortem Findings:
A. Gross:
(a) Marked congestion of gastric mucosa is present in acute poisoning in cattle and swine.
(b) Fluid, dark faeces.
(c) May be oedema of skeletal muscles and hydro pericardium in acutely affected cattle.
(d) May be no gross lesions present.
B. Microscopic:
Swine:
(a) Cerebral oedema and meningoencephalitis.
(b) Eosinophilic invasion of perivascular spaces and meninges in early stages disappear if animal survives 3-4 days.
(c) Polioencephalomalacia of cerebral cortex.
Diagnosis:
(i) Histopathological changes in brain.
(ii) Clinical signs, history and postmortem lesions.
(iii) Chemical findings-Cerebrospinal fluid and serum sodium levels.
(a) Serum sodium elevated-Normal level of Na+ in serum is 135-145 mEg/L. In case of salt poisoning it reaches up to 160-190 mEg/L. CSF sodium levels may be slightly greater than serum levels in salt poisoning.
(b) Serum chloride may be high or very low depending upon stage of disease. If the animal has been given free choice of excess water, chloride level in serum may be low. Normal value of chloride level in serum for most of the animals ranges between 100-110 mEg/L.
(c) Cerebrospinal fluid levels of sodium may have more diagnostic value than serum levels; almost the relation between CSF and serum sodium levels may be significant.
Differential Diagnosis:
Differentiate salt poisoning from:
(a) Pseudo-rabies-young pigs.
(b) Viral encephalomyelitis.
(c) Polioencephalomalacia.
(d) Other encephalitic diseases.
(e) Chlorinated hydrocarbon insecticide-usually high temperature during convulsions.
(f) Mulberry heart disease-older pigs, eosinophilic meningitis.
Treatment-Non specific:
(i) Initially access to fresh water should be restricted to small amounts at frequent intervals.
(ii) Advanced cases should be given limited water frequently via stomach tube.
(iii) If there is evidence of cerebral oedema-give diuretics.
(iv) Calcium gluconate and chloral hydrate may help CNS signs.
Prognosis:
Unfavourable for those affected.