Copper Deficiency (Hypocuprosis)

Copper Deficiency (Hypocuprosis) is called Falling disease or Peat scours in cattle, Yellow calf or Unthriftiness (pine) in calves and Swayback or Enzootic ataxia in sheep.

Etiology

1. Primary Copper Deficiency

Inadequate copper in diet by fodder/ forage grown on copper deficient soil cause copper deficiency.

2. Secondary Copper Deficiency (Molybdenum toxicity)

The amount of copper in the diet is adequate, but unable to utilize copper by the body due to certain dietary conditioning factors like molybdenum, sulfur, iron, lead, calcium carbonate rich diet inhibits copper utilization.

• High level of molybdenum inhibits copper utilization even after high or required copper in the diet.
• Molybdenum reacts with sulphur in the rumen to form thiomolybdates, which irreversibly bind copper and prevent its absorption.
• ZnSO₄ application for facial eczema may depress the plasma copper level.

Risk Factors

Animal Factors

• Age: young animals more susceptible than adult especially for primary copper deficiency. Those calf/lamb fed with only milk more susceptible, because milk is poor source of copper.
• Breed: There are marked genetic differences in the copper metabolism between the breeds of sheep. For example, Welsh mountain ewe can absorb copper 50% more efficiently than the Scottish back face. Texel cross black face absorbs copper 145% more efficiently than pure black face lamb.
• Species: Significant difference in the copper requirement and tolerance between sheep and goat. Dietary copper requirement in goat is higher than sheep. Dietary level of copper could cause copper toxicity in sheep, but not in goat.
• Colostrum/ Milk: Colostrum is rich in copper, which absorbed in intestine and stored in liver. While changing colostrums to milk the copper level will decline rapidly. copper absorption efficiency (up to 80%) is high in young ones, but the absorption efficacy declines (only 2-10%) when the rumen become functional.
• Fetal liver copper: During the gestation period the level of the copper concentration is increases progressively in ovine and bovine fetal liver and decrease copper level in maternal liver.

Dietary Factors

The absorption and availability of copper is influenced by:

• Type of diet
• Presences of other substance in diet like molybdenum, sulfur and iron.
• Interaction between the diet and their chemical composition
• Genetic constitution of the animal.

copper is well absorbed from diet low in fiber like cereals, but poorly absorbed from fresh forage. Hay and silage fodder improved the availability of copper. Only slight increases in molybdenum and sulfur concentration of grass will cause major reduction in the availability of copper. That is the reason copper deficiency is more common in grazing animals than stall fed animals.

• Pasture containing < 3mg/kg dry matter of copper: Copper deficiency
• Pasture containing > 10mg/kg dry matter of molybdenum: Copper deficiency
• Pasture containing < 3mg/kg dry matter of molybdenum: safe Grass grown on
• Strongly acidic, molybdenum rich soil: low level of molybdenum (< 3mg/kg dry matter)
• Alkaline, molybdenum poor soil: high molybdenum ( >17 mg/kg dry matter), cause copper deficiency

Pathogenesis

• Tissue oxidation: Copper may protect tissues against oxidative stress from free radicals, including those generated during respiration and interact with other nutrients with antioxidant properties as it does so. copper deficiency affects tissue oxidation by inhibition of copper/zinc superoxide dismutase (copper/Zinc SOD) and Ceruloplasmin.
• Chromosomal abnormalities: Increases the frequency of chromosomal abnormalities and DNA migration.
• Skin/ wool: Copper deficiency causes inadequate keratinization by imperfect oxidation of the free thiol groups leads straightness and stringiness of the wool (steely wool).
• Reduction in body weight: Impaired tissue oxidation causes interference with metabolism.
• Diarrhea: Copper deficiency causing diarrhea due to functional disturbances, as there isno histopathological changes in gut mucosa. Diarrhea is usually only a major clinical finding in secondary copper deficiency associated with molybdenosis.
• Anemia: Copper deficiency result in anemia because copper is necessary for reutilizationof iron liberated from normal breakdown of hemoglobin for resynthesis of hemoglobin by end of life span. Anemia mainly observed in primary copper deficiency especially during later stage.
• Bone: Copper deficiency causes Osteoporosis: It is due to depression of osteoblast activity by primary copper deficiency in cattle. Over grown of epiphyseal cartilage at costo-chondral junction and metatarsal bone, which cause bending of ribs and enlargement of long bones.
• Connective tissues: Copper deficiency affects enzyme lysyl oxidease which is necessary for the formation of elastin. Due to the impairment of elastin component, disintegrity of tissues especially capillary bed, ligaments and tendon.
• Osteochondrosis: Causes severe degenerative diseases of cartilage in foal leads breakingof articular and growth plate cartilage
• Heart: Copper deficiency leads to myocardial degeneration (falling disease) which maybe attributed to either interference with tissue oxidation or terminal manifestation of anemic anoxia.
• Blood vessels: Rupture of heart and grater vessels in pigs
• Nervous tissue: copper is necessary for myelin sheath formation. copper deficiency inhibits formation of myelin and cause demyelization in lambs (Swayback).
• Immune system: Impair CMI and HI. Inhibition of phagocytic activity of neutrophil and macrophage which leads impaired immune function, decrease bactericidal activity and machining the animal more susceptible to infection.
• Infertility: copper deficiency in adult cattle cause delayed onset of puberty, anoestrum, andanovulation and decreases conception rate.

Clinical Signs in Cattle

Primary copper deficiency

• Unthirftiness, low milk yield
• Anemia is common especially at later stage of diseases
• Coat colour changes– red and black colour cattle changing to blanched
• Increased tendency to bone fracture especially on limbs and scapula
• Ataxia, hind limb weakness
• In calf– stiffness and enlargement of joints, contraction of flexor tendon (affected animal stand on their toes).

Secondary copper deficiency

• Diarrhea is common
• Falling diseases in cattle:
  • Cattle apparently healthy and suddenly die
  • Some time animal may fall down and struggle and die
• Peat scours (teart) in cattle:
  • Persistent diarrhea with watery yellow to black faeces and inoffensive odour.
  • The hair coat is rough and depigmented
  • Grayness or discoloration or of hairs around the eyes
• Unthriftiness (Pine) in calf:
  • Stiffness gait
  • Emaciation and death
  • Grayness of hair especially around the eyes (like wearing glass).

Clinical Signs in Sheep

• Abnormalities of wool is the first sign
• Fine wool become limp, glossy and loses crimp, straight and steely wool
• Anemia, scoring, unthirftiness and infertility
• Osteoporosis
• Swayback diseases:
  • Congenital form/ neonatal/ cerebral swayback: It occurs at the time of lambing. Affected lamb born dead or ataxia at birth, followed by death. Due to primary anoxic lesions in the brain stem and demyelination of the cerebral cortex. If born live lamb become weal and unable to stand and suck, incoordination and erratic gait. Blindness, softening and cavitations of the cerebral white matter.
  • Progressive/delayed sway back: It occurs few weeks after birth and clinical signs appear 3-6weeks. Uncoordinated hind-limb movements, stiff and staggering gait, swaying hind quarters, often triggered by flock disturbances.
  • Atypical/ Postnatal acute fatal sway back: It occurs in older lambs. Stands transfix, head shaking blindness and die within 1-2 days. Death usually due to cerebral edema.
• Enzootic ataxia: Affects only weaned lambs with 1-2 month age groups. Atrophy of the hind quarters and incoordination of hind limbs. Excessive flexion of joints and knuckling of fetlocks, Wobbling gait of hind quarter and falling, Death within 3-4 days etc.

Diagnosis

• History
• Clinical signs
• Laboratory examination

Estimation of plasma and liver Copper

• Plasma copper level below 20 ug/dl represent hypocuprosis (Normal level 20 – 60 ug/dl).
• Liver copper value below 30 mg/ kg dry matter in cattle and below 80 in sheep considered low (Normal level above 100/kg DM in cattle and above 800/kg DM in sheep).
• Estimation of copper content of hair is now acceptable as a diagnostic aid (Normal level 6.6-10.4 mg/kg).

Estimation of copper containing enzymes: ESOD

• ESOD value ranges from 2-6 IU/mg hemoglobin in hypocuprosis.

Estimation of copper : Protein complex (Ceruloplasmin)

Ceruloplasmin contains greater than 95% of the courting copper in normal animals. There a highly significant correlation between plasma copper level and plasma Ceruloplasmin. Normal plasma Ceruloplasmin in cattle 120-200 mg/dl and in sheep is 40-100 mg/dl.

Hematology

• Decreased Hb and RBCs level
• Heinz body anemia
• In lambs: hypo chromic and microcytic anemia
• In cattle: hypo chromic and macrocytic anemia

Treatment

• Copper sulfate (oral dosing): Calves 2-6 months of age need to give 4g and Adult cattle need 8 to 10 g at weekly interval for 3-5 weeks.
• Copper glycinate at 400 mg/cattle at single administration by IM or SC with continue for 2-3 months.
• Supplementation of the diet for the affected animals with copper sulfate added to the mineral salt mixture at level of 3-5 % of the total mixture or combination of minerals mixture of 50% calcium-phosphorus, 45% cobalt ionized salt and 3-5% CuSO4.

Prevention and Control

Supplementation of the diet with minimum requirement of copper (10 mg Copper/kg dry matter for cattle) by any of several different ways:

• Oral dosing or dietary supplementation of copper sulfate: 4 gm for cattle and 1.5 gm for sheep weekly.
• Mineral mixtures of salt licks: Containing 2 % copper sulfate for cattle.
• Parenteral injection of copper salts like copper glycinate, copper methionate, and copper calcium edebate 400 mg for cattle.
• Copper oxide needles: Fragments of oxidized copper wire up 8 mm in length and ½ mm. Diameter for oral dosing considered one of the most effective and safest methods for control of copper deficiency in ruminants. The needles retained in fore stomachs and abomasum for 100 days or more and copper slowly released, absorbed and stored in liver.