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
REFERENCE:
1.)https://www.msdvetmanual.com/toxicology/copper-poisoning/overview-of-copper-poisoning#v3353991
2.)https://www.nadis.org.uk/disease-a-z/sheep/copper-poisoning-in-sheep/
3)https://www.sheepandgoat.com/cutox#:~:text=Copper%20toxicity%20in%20sheep%20usually,breakdown%20of%20red%20blood%20cells).
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)