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15 Cards in this Set
- Front
- Back
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Factors influencing absorption of dietary copper
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Sulphur
Molybdenum Iron Intercurrent disease Genetics |
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Who is suceptible to copper deficiency?
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Cattle more so than sheep
Young animals (esp. after weaning: 3-12 months of age) Young of deficient dam Animals grazing outdoors with no supplementation |
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Clinical signs
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Depigmentation: greying of coat in dark cattle, esp. round eyes
Defective keratinisation: dry sparse hair coat Bone defects: widening of the epiphyses of distal limb bones -> swollen fetlocks, spontaneous fractures, joint stiffness Ill-thrift Anaemia (of chronic disease) |
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Diagnosis
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Clinical signs (non-specific except for swayback)
Dietary levels: of molybdenum, sulphur and iron ONLY (dietary levels of copper itself USELESS) Plasma/serum copper levels: suitable for dx of clinical dz but not body copper reserves Liver copper levels: by biopsy, rarely done except maybe at PM Superoxide dismutase: expensive Response to tx: cattle ONLY (risk of toxicity in sheep) Caeruloplasmin: copper ratios? |
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Therapy
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Direct
Oral: oral copper sulphate, copper oxide needles, intra-ruminal boluses Injectable: EDTA, heptonate etc. Inclusion in feed: banned in sheep although most concentrate feeds will have low levels Free access minerals: cattle only? Medication of water supply: cattle only Indirect Application of mineral fertilizer to pasture Minimising molybdenum and iron intakes (e.g. by reducing soil intakes) Genetic selection? |
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Role of selenium and vitamin E
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Protect cells against damage by lipid peroxidases and free radicals.
Failure of this protection leads to MEMBRANE DAMAGE and TISSUE NECROSIS. Tissues with highest rate of oxidative metabolism (i.e. skeletal, cardiac and respiratory muscle) most suceptible |
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Influencing factors
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Selenium status
Supply of other dietary anti-oxidants (primarily VITAMIN E) Supply of dietary oxidants (esp. polyunsaturated fatty acids - found in young rapidly growing pastures) Generation of oxidants (e.g. via exercise at turnout, infection, toxins) |
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Clinical signs - WHITE MUSCLE DISEASE
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Congenital
Stillbirths, weak calves that fail to suckle and usually die within a few hours Delayed (usually precipitated by stress of turnout) Skeletal m. - stiffness, discomfort, inability to stand, myoglobinuria Respiratory m. - dyspnoea Cardiac m. - sudden death (more common in pigs - mulberry heart disease) |
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Clinical signs - OTHER
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Ill-thrift
Immunosuppression Retained foetal membranes Reduced fertility? |
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Diagnosis
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Biochemical indicators of muscle damage (CK, AST)
Soil and pasture levels (useful UNLIKE OTHER TRACE ELEMENT DEFICIENCIES) Selenium levels in blood and liver (short-term intake) Glutathione peroxidase (GSHPx) levels in blood (long term intake) Vitamin E levels in blood |
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Therapy
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Direct
Oral compounds Injectable compounds: short and long-term Inclusion in compound feeds Free-access minerals Medication of water supply Indirect Application of selenium fertilizers to pasture |
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Causes of iodine deficiency
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Primary
Low iodine content in soil (West of UK mostly) Secondary Ingestion of goitrogen containing plants (competitvely inhibit/prevent necessary conversion) e.g. brassicas, legumes (white clover etc) Deficiencies of other trace elements (e.g. SELENIUM) Environmental factors that increase BMR (e.g. low temperatures) |
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Clinical signs
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Goitre
Stillbirths Birth of weak calves/lambs Poor production Reduced fertility? |
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Diagnosis
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Soil and pasture levels: not v. useful
Goitre Thyroid histopathology: "gold standard" Thyroid iodine levels Iodine levels in blood, urine and milk Thyroid hormone levels (care: natural variation) Controlled supplementation trials |
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Therapy
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Direct
Oral compounds Injectable compounds: long-term Painting of 5% tincture of iodine on the flank skin fold once a week (labour intensive) Inclusion in compound feeds Free-access minerals Medication of water supply Indirect Application of iodine fertilizer to pasture Minimise effects of goitrogens: thiocyanate - FEED MORE IODINE, thiouracil - AVOID FEEDING PLANTS CONTAINING IT |
