Metabolic diseases in farm animals Flashcards
Describe the aetiology of hypomagnesaemia
- Related to Mg in diet and presence of competing cations (K, Na)
- No feedback mechanism to control Mg concentration
- Main absorption in forestomachs, increases with increasing Na:K ratio (>5:1)
- Only short term mobilisation of reserve in bone
What is a potential complication of chronic hypomagnesaemia?
Increases chances of hypocalcaemia
Compare hypomagnesaemia in adult cattle to that in sheep and calves
- Sheep: similar but less common
- Calves: similar, but less common other than milk fed white veal calves (not UK)
Explain the mortality of hypomagnesaemia in beef cattle
- ~30%
- Due to short course of disease (5-10 hours from start to death)
- Beef animals looked at less than dairy
What is the effect of hypomagnesaemia on the nervous system?
Alteration in CNS and peripheral nerve function
Identify risk factors for hypomagnesaemia
- Lush pastures with large applications of fertilisers
- Bucket fed calves
- Silage from/pastures low in Mg, generally poor quality pasture
- Pasture species, season, soil type, climate, DMI
- Increased risk in lactation/late pregnancy
- Cold, wet, windy
Explain why hypomagnesaemia occurs in lactation/late pregnancy
- Hypocalcaemia 48 hours after calving, hypomagnesaemia seen later
- Combination of calcium and magnesium deficit that predisposes to hypomagnesaemia
Explain why lush pastures with high levels of fertiliser increase the risk of hypomagnesaemia
- High levels of nitrogen and potassium and ammonia
- Compete for mg absorption in rumen
Describe the clinical signs of hypomagnesaemia
- Tetanic muscle spasms
- Whole body tremor
- Bellowing, aggressive
- Blindness
- Elevated, pounding heart rate
- Hypertonicity and seizures
- Hyper alertness, hyper responsiveness, hyperaesthesia
- Convulsions
- Sudden death after excitement/therapy
- Frothing at mouth
- Retraction of eyelids
- Pricking of ears
- Nystagmus
- Opisthotonus
- Bloating
List the differential diagnoses for hypomagnesaemia
- Acute lead poisoning
- Rabies
- Nervous ketosis
- BSE
Outline the method for the diagnosis of hypomagnesaemia
- Clinical signs and history
- Serum Mg low
- Response to treatment
- May have concurrent hypocalcaemia
- Aqueous humour or CSF Mg concentration
- Non-specific necropsy findings (rule out other conditions)
Explain the value of testing the aqueous humour or CSF Mg concentrations
- Can be done up to 12 h post mortem
- Useful where several dead cows in field
- Sample from the eye for aqueous humour
Describe the treatment of hypomagnesaemia
- Safest general recommendation: 400ml Ca-Mg bottle, 50ml for sheep
- Combined with SC concentrated solution of Mg salt
- Ideally give Mg SC, calcium IV
What are the risks of administering Mg IV?
- Cardiac dysrhythmias
- Medullary depression
- Respiratory failure
Outline the preventative methods for hypomagnesaemia
- Prophylactic oral therapy (low bioavailability, give slightly more than “right” amount)
- Top dressing of pastures, daily drenching
- Dusting, spraying
- Provision in drinking water (better absorption of MgCl), magnesium buckets
- Intraruminal Mg bolus
Compare the bioavailability of Mg carbonate, Mg oxide, Mg sulfate in cows
- Mg carbonate: 44%
- Mg oxide: 51%
- Mg sulfate: 58%
Explain how chronic hypomagnesaemia increases the chances of hypocalcaemia
- Low Mg intake inhibits ca absorption in intestine
- HypoMg inhibits PTH release
Explain how the neuromuscular blockade that masks tetany in hypomagnesaemia occurs
- Only very early in disease
- HypoMg worsens neuromuscular irritability
- Decreased Ca ions at axonal membrane initially result in tetany, looks like hypoMg
- Enough loss of Ca at neuromuscular synaptic memrbanes to reduce Ach release causing degrees of paralysis
Describe the aetiology of hypoglycaemia/nervous ketosis in cattle
- After calving due to increase in milk production
- Negative energy balance is main factor
- Excess ketone body production
- prolonged course leads to evident brain lesions
- May occur in neonatal large animals due to starvation, cold exposure or other diseases
When does nervous ketosis typically occur in sheep?
Before lambing due to energy requirements of fast growing lambs
Describe the development of brain lesions with nervous ketosis
- Mainly sheep
- Cerebro-cortical neuronal necrosis
- Hypoglycaemic for a few days
Compare the prognosis of nervous ketosis in sheep and cows
- Sheep: highly fatal, possible effects (hypo-glycaemic encephalopathy) on fetuses
- Cattle respond readily to treatment
Describe the clinical signs of nervous ketosis in cattle and sheep
- Muscle weakness, tremor
- Head pressing
- Compulsive licking
- Ataxia
- Blindness
- Hyperaesthesia
- Anorexia
- Drop in milk production
- Opisthotonus
List the differentials for nervous ketosis in cattle
- Rabies
- Hypomagnesaemia
- BSE
- LEad poisoning
- Listeriosis
List the differentials for nervous ketosis in sheep
- Listeriosis
- Cerebral abscess
- Rabies
Describe the diagnosis of nervous ketosis
- Clincal signs, history
- Ketones (breath, urine, milk)
- BOH/BHB serum levels
- Non-specific necropsy findings (twin lambs in sheep, fatty liver in cows)
Describe the treatment for nervous ketosis in cattle and sheep
- Dextrose IV (400ml 50%)
- Oral propylene glycol (225g BID for 2 days)
- Glucocorticoids (reduce milk yield, 40mg dex sodium phosphate or 5mg flumethasone)
- Insulin (off label use, where economics allow, must give glucose first)
- induced parturition or caesar in ewes
Describe the aetiology of hypocupraemia in sheep
- Dietary deficiency of Cu in dam during gestation
- Copper required for myelin formation
- Bilateral symmetric loss of myelin in dorsolateral spinal cord tracts
- Low copper perinatal period causes abnormal mitochondria function and cytochrome-C oxidase activity in CNS
- Lambs and kids) may be affected clinical at birth or shows delayed onset
- Congenital only when Cu deficiency extreme
What is hypocupraemia also known as?
Swayback, enzootic ataxia
Describe the clinical signs of hypocupraemia
- Excessive joint flexion, knuckling over fetlocks, wobbling, falling
- Appetite unaffected
- Depression
- Tremors
- Wool abnormalities (loss of crip, depigmentation)
- Anaemia, scouring, unthriftiness, infertility in adults
- Incoordination starting with hindlimbs, erratic movement
- Spastic paralysis
- Blindness
List the differential diagnoses for hypocupraemia
- Congenital abnormalities of spinal cord
- Trauma
- Spinal abscess
- Ischaemic myelopathy
- Border disease
- Cerebellar hypoplasia
- Hypothermia
Outline the diagnosis of hypocupraemia
- Clinical signs, history
- Microscopic examination of nervous tissue (characteristic lesions of myelin degeneration)
- Low concentrations of liver copper
Outline the treatment of hypocupraemia
- Supplement copper (oral, injectable, bolus) but usually unsuccessful due to advanced nature of lesions
- Correct copper, molybdenum, sulphur, iron to prevent further cases
Describe the aetiology of hepatic encephalopathy in cattle
- Reduced detoxification of compounds esp, nitrogenous waste due to liver damage
- Hyperammonaemia, hypoglycaemia
- Severe acute or chronic liver disease
- Congenital acquired porto0systemic shunt
- Hepatotoxic encephalopathy due to plants
- Hyperammonaemia
Explain how hyperammonaemia may occur in cattle and lead to hepatic encephalopathy
- Exposure to ammonia containing feedstuffs or fertiliser
- Urea in total mixed ration drives protein building in rumen, but also raises ammonia in blood, liver unable to cope
- Leads to hepatic encephalopathy without liver disease
Describe the clinical signs of hepatic encephalopathy
- Blindness
- Aimless wandering (dazed)
- Compusive activity
- Aggression
- Ataxia
- Facial and ear tremors
- Seizures
- Coma (death)
- Tenesmus/urine spillage/rectal prolapse
- +/- photosensitisation
List the differentials for hepatic encephalopathy in cattle
- HypoMg
- Nervous ketosis
- BSE
Outline the diagnosis of hepatic encephalopathy in cattle
- Blood ammonia
- Liver biopsy (easy)
- Histology: astrocyte proliferation, hypertrophy with swollen pale nuclei
Outline treatment of hepatic encephalopathy in cattle
- Difficult
- Put in quiet environment and hope they recover
- Remove hepatotoxins from environment if cause
