COPPER

Copper is an essential trace element that

catalyses various processes in heme synthesis
and iron absorption.
It acts as a co-factor in the function of cellular
enzyme such as Tyrosinase Cytochrome
Oxidase, Dopamine-beta-hydroxylase and
preoxidases.
Copper has interrelationship with elements
such as Molybdenum and Sulphur.

Properties:

Copper occupies a position between Nickel and

Zinc in group 1B of the Periodic table.
Copper exists in three oxidisation states they
are: metallic copper (0), cuprous ion (+1,
monovalent) and cupric ion (+2, divalent).
Copper is a strong oxidising agent.

Source of Toxicity:

Acute toxicity : due to

Contamination of food and water.

Excessive use of copper in agricultural and

veterinary practices.

Chronicity toxicity:

Genetic susceptibility and continuous copper intake.

Accidental administration of excessive amounts of

soluble copper salts in mineral mixture, rations, etc.

Animals may ingest copper from sprayed foilage, copper

containing pesticides such as Bordeaux mixture.
Copper sulphate used indiscriminately for a longer time or
in excessive amount may produce toxicity.
Contamination of forages, pasture or soil in the vicinity of
mines and also occur from effluents from industries using
copper-like dye.
Soils and plants fertilised with used poultry litter or swine
manure also possible sources of poisoning.
.

Factors affecting Toxicity:

Species:
All species are susceptible.
Sheeps are commonly affected.
Horses and swine are relatively tolerant to copper.
Dogs are more susceptible to copper overload.
Poultry are more resistent to copper poisoning.

Interaction:
Low levels of dietary Molybdenum and sulphate increases
toxicity of copper.
Deficiency of Manganese, Iron, B-Vitamins can cause
copper to accumulate in the body.

Breeds:
Some breeds of dog like Bedlington Terrier breeds are
highly sensitive to copper toxicosis.

Stress:
Stress from any cause contributes to copper imbalance.

Soil:
Sandy soil with low pH possesses the greatest potential
leaching copper.

Hepatotoxic Substances precipitate copper toxicosis.

Toxicity:
Acute or chronic copper poisoning is encountered in most
parts of the world.
Minimum safe and toxic concentration of copper in diet of
different species.
Class of Animal

Dairy Cattle
Beef Cattle
Sheep
Swine
Poultry
Horse

Copper
Requirements in
Total Diet (ppm)

Toxic Level in Total

Diet (ppm)

12-16
10 (4-15)
7-11
5-6
6-8
9

40
100
25
>250
250-800
not known

Toxicokinetics:
The absorption of copper from GIT depends on:

Chemical form of copper,

Interaction with other metals.

Mechanism of Toxicity
Copper accumulation in liver may occur from any
of these three processes:
Abnormal absorption
Abnormal storage
Defective excretion

Mechanism of Toxicity
A)

Ruminants:

1. Excessive accumulation of copper occurs in hepatic mitochondria and

lysosomes.

Affects integrity of plasma membranes.

Damages lysosomal membrane,

leakage of copper and enzymes into the cytosol,

Causes cellular degeneration or necrosis and hepatocyte organelle

damage.

2. Inhibits essential metabolic enzymes.

Dihydrolipoyl dehydrogenase inhibition of pyrovate dehydrogenase

system disturbance the energy metabolism of cell.
3. Liver damage and necrosis releases large amount from the liver into the
blood.

Increase fragility of membrane leads erythrocyte lysis,

Freeing haemoglobin and causing haemolytic crisis.

Excess haemoglobin causes clogging of renal tubules leading to renal

tubular and glomerular necrosis and production of darkened (gunmetal)
kidneys and death.

Swine: copper inhibits absorption of iron from GIT

leading to iron deficiency anaemia.
Dogs: Autosomal recessive defect causes
increased copper retention in liver hepatic
damage.

abnormal binding of copper with hepatic

metallothionein sequesters copper in hepatic
lysosomes prevents normal biliary excretion
of copper.

Clinical Signs:
Acute Toxicity:
Severe gastroenteritis, salivation, reduced feed
consumption, colic, diarrhoea, melena, shock, collapse
and death.
Haemolysis and haemoglobinuria, jaundice and
necrosis of liver.
Chronic Toxicity:
Anaemia, depression, weakness and trembling,
anorexia, thirst, haemoglobinuria, jaundice, dyspnoea,
shock, cold extremities, tachycardia and death.
In laying hens decreased egg production, diarrhoea
and oral mucosal ulcers and vesicles seen.

Post-mortem Findings:
Acute copper poisoning :
Gastroenteritis with erosions and ulcerations in
abomasum.
Chronic poisoning :
Jaundice ,methaemoglobin.
The lesions include pale yellow liver, enlarged pulpy
spleen, distended gall bladder with greenish bile and
bluish-black kidneys (known as gunmetal kidneys).
Microscopic Lesions:
Hepatocyte vaculation, periportal fibrosis, renal tubular
necrosis and haemoglobin casts in renal tubules and
excessive fragmented erythrocytes in spleen .

Diagnosis:
History,
Clinical signs and lesions ,
Copper level in the body fluids, faeces and tissues.
Acute copper poisoning, there is evidence of blue-green
ingesta, elevated faecal (8,000-10,000 ppm) and kidneys (>15
ppm) copper levels.
Chronic poisoning, blood and liver copper concentration are
elevated during the haemolytic period
Changes in laboratory parameters include elevated bilirubin
levels, haemoglobinaemia and haemoglobinuria, elevated
levels of AST, LDH, SDH and arginase.
Differential Diagnosis:
Gastroenteritis and leptospirosis as well as Arsenic, Mercury
toxicosis and phenothiazine.

Treatment and Management:

A)Specific Therapy:

Chelating agents:
Penicillamine bind with copper in blood or tissue and
promote its removal through the kidney.

D-pencillamine:
Sheep: 50 mg/kg orally for six days.
Dogs: 10-15 mg/kg twice daily by oral route.

Ascorbic Acid:
Given with metals has been found to decrease
intestinal absorption of copper in dogs.
Dogs:500-1000 mg/day

Oral dose of ammonium molybdate (0.5-1

mg/kg/day) and sodium sulphate (6-20 mg/kg/day)
may be given to combat chronic copper poisoning.
Ammonium tetrathiomolybdate (1.7-3.4 mg/day)
three treatments on alternate days by I.V. or S.C.
Oral Zinc supplementation decreases intestinal
absorption of copper.
Dogs: 5-10 mg/kg, orally twice daily.

B) Supportive Therapy:

Complications from hepatic encephalopathy

and ascites should be treated as they occur.
Anti-oxidant therapy with Vitamin E (400-500
mg/kg, orally) has protective affect against
hepatic damage in dogs.
Symptomatic Therapy should be carried out to
alleviate shock and colic pains.
Alkalisation of urine helps to decrease renal
damage from haemoglobin.

Prevention:

Feed samples should be analysed routinely to monitor

the copper : molybdenum ratio in the diet.
Supplemental feeds which are known to be low in
copper should be used whenever possible.
Feeding a properly fortified trace mineralised salt is
essential to the health and production of the flock.
Steps should be taken to remove the hepatotoxic
plants from the pasture and forage.

Thank u!