Copper toxicity in sheep 🐑

DIFFERENTIAL DIAGNOSIS

PATHOPHYSIOLOGY

EPIDEMIOLOGY

CLINICAL SIGNS

DIAGNOSIS

TREATMENT

CONTROL

ACUTE

CHRONIC

CAUSED BY

COPPER TREATMENT FOR THE PREVENTION OF COPPER DEFICIENCY

THE ACCUMULATION OF COPPER IN THE LIVER

EXCESSIVE INTAKE OF COPPER FROM THE DIET

WITH LOW DIETARY INTAKE OF MOLYBDENUM AND SULFUR

REDUCED FORMATION OF COPPER MOLYBDATE OR COPPER SULFIDE COMPLEXES IN TISSUES

IMPAIRS THE EXCRETION OF COPPER IN URINE OR FECES

INGESTION OF PLANTS, TRIFOLIUM SUBTERRANEUM,

CAUSE MINERAL IMBALANCE AND RESULT IN EXCESSIVE COPPER RETENTION

ACUTE

CHRONIC


CAUSES SEVERE GASTROENTERITIS


ABDOMINAL PAIN

DIARRHEA

DEHYDRATION

ANOREXIA

SHOCK.

HEMOLYSIS AND HEMOGLOBINURIA

DEPRESSION

WEAKNESS

RECUMBENCY & RUMEN STASIS

LETHARGY

ANOREXIA, & THIRST

DYSPNEA

PALE MUCOUS MEMBRANES

HEMOGLOBINURIA & JAUNDICE

• DO NOT FEED CONCENTRATES HIGH IN COPPER LEVELS TO SHEEP

• DO NOT USE COPPER SULPHATE FOR THE CONTROL OF SNAILS IN AREAS WHERE SHEEP ARE GRAZING

• IF CASES OF COPPER POISONING OCCUR, IMMEDIATELY NOTIFY THE NAMED VETERINARY SURGEON

• ENSURE MOLYBDENUM CONCENTRATIONS ARE ADEQUATE IN FORMULATED RATIONS

• HANDLE AND MANAGE ANIMALS IN WAYS THAT MINIMISE STRESS

BLUE-GREEN INGESTA

INCREASED FECAL (8000-10000 PPM)

COPPER LEVELS (ACUTE)

BLOOD AND LIVER COPPER INCREASE DURING HAEMOLYTIC PERIOD (CHRONIC)

BLOOD CONCENTRATION RISE TO 5-20MCG/ML

MOLYBDENUM TISSUE CONCENTRATION TO DIFFERENTIATE PRIMARY AND SECONDARY INFECTION

BACTERIA (EPERYTHROZOONOSIS)

PARASITES (BABESIA)

COPPER TOXICITY

SYMPTOMATIC TREATMENT FOR SHOCK MAY BE USEFUL

OFTEN THE TREATMENT UNSUCCESSFUL

PLANT POISONING

POOR PROGNOSIS

PENICILLAMINE / CALCIUM VERSANATE FOR COPPER EXCRETION

VITAMIN C TO REDUCE OXIDATIVE DEMAGE

HAEMOLYTIC ANAEMIA

AMMONIUM TETRATHIOMOLYBDATE

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Copper toxicity in sheep usually results from the accumulation of excess Cu in the liver over a period of a few weeks to more than a year with no clinical signs, followed by a sudden release of liver Cu stores to cause toxicity (rapid breakdown of red blood cells).

In these situations, chronic Cu poisoning may result from excessive Cu intakes or from low intakes of Mo, S, zinc, calcium or following liver damage. Stresses, such as weather, environment, poor nutrition, transportation and handling, can also cause the liver cells to die and release the stored copper into the bloodstream.

Affected sheep are lethargic and anemic. They may grind their teeth incessantly and experience extreme thirst. Membranes are very pale and may appear yellow, as jaundice sets in. Urine is a bloody color. Death usually occurs 1 to 2 days after the onset of clinical symptoms.

MUHAMMAD HAZMI BIN MUSTAFFER (192126)
MUHAMMAD HAZMAN BIN MUSTAFFER (191918)
MEGAT AIMAN HISYAM BIN MEGAT AZAMUDDIN (192120)