Metabolic diseases Flashcards
What causes fat mobilisation syndrome and ketosis?
Negative energy balance
Causes XS mobilisation of fat (not all cows in NEB develop ketosis/FMS)
What are the clinical signs of fat mobilisation syndrome and ketosis?
Reduced milk yield
Selective appetite (refusing concentrates)
Ketone bodies in blood (sweet smelling breath)
Nervous ketosis (licking)
Firm/shiny faeces
How is ketosis/FMS diagnosed?
BOHB and NEFA in lood
How is ketosis/FMS treated?
Propylene glycol PO
Glucose IV
Dexamethasone
Vitamin B12, thiamine B1
How is ketosis prevented?
Monensin bolus 3-4 weeks pre-calving - use in high risk cows (inhibits growth of gram +ve bacteria)
Low energy, high DMI feed in dry period
Monitor BCS - avoid fat cows
What is Grass Staggers?
Hypomagnesaemia
Does the body have a store of magnesium?
No - requires dietary intake
What are risk factors for Grass Staggers/hypomagesaemia?
Lush pastures
High milk output
Stress
What is the treatment for Grass Staggers?
Xylazine or small dose pentobarbitone for convulsions, quiet
Calcium borogluconate IV
Then slow magnesium sulphate IV
Move off affected pasture and feed high Mg cake
Hypophosphataemia causes red urine. Why?
Low phosphate causes peri/post-parturient haemoglobinuria
How is hypophosphataemia treated?
Give phosphorus supplements
What is milk fever?
Hypocalcaemia +/- hypophosphataema
When is milk fever most likely to occur?
Around calving time
When is milk fever more likely to occur - for Heifers or older cows?
Cows from 3rd birth onwards
What are the symptoms of milk fever in cattle?
Hyperexcitation Tremor Recumbency - S shaped No faeces/urine output Dry nose Postural bloat Slow heart rate
What is the treatment for milk fever?
Calcium borogluconate IV
Phosphate supplements
Place in sternal recumbency for bloat
Subclinical hypocalcaemia reduces immune function, predisposing cattle to which conditions?
Mastitis and endometritis
‘Post-partum depression’
How is milk fever prevented?
Maximised DMI pre-calving
Feed low Ca, high Mg diet
Zeolite (calcium binding)
In sheep, is milk fever associated with lambing?
No - associated with DMI fall
What causes ruminal acidosis?
Excess D-lactic acid (encourages growth of Lactobacilli bacteria)
Due to XS concentrates or insufficient fibre
Why does digestion efficiency drop with ruminal acidosis?
Low pH destroys papillae
Causes ruminitis
Ruminal acidosis can lead to ruminitis, and sometimes even colon acidosis. What would be found in faeces that suggests damage to the colon wall?
Fibrin casts
What is the normal rumen pH?
6.5
What in saliva buffers acid when cudding long fibre?
Sodium bicarbonate
What is the difference between subacute and acute ruminal acidosis?
Subacute = pH <5.5 Acute = pH <5.0
Subacute ruminal acidosis (SARA) is the most common nutritional disorder in cattle. What are the clinical signs?
Swishing tail (sore bum due to faeces with mucus casts and long fibres)
Weight loss
Poor health/immunosuppression - predisposed to LDAs, ketosis, mastitis, infections
How is SARA diagnosed?
Rumenocentesis
Assess 2-4 hours after feeding
Which stage of cattle should have rumenocentesis to diagnose SARA?
Cows 14-21 days post-calving (still adapting to ration, DMI not maximal)
Cows 60-80 days post calving (adapted to ration, maximal DMI)
What acid predominates in acute ruminal acidosis?
Lactic acid
What feeds cause excess lactic acid production, leading to acute ruminal acidosis?
Grain - ‘barley poisoning’
Over-eating or sudden introduction
Acute ruminal acidosis is often an individual problem, where as SARA is a herd problem. What are the clinical signs of acute acidosis?
Mild ataxia to recumbency/shock Bloat Ataxia Profuse, smelly D+ Depression
Acute ruminal acidosis and hypocalcaemia/milk fever both cause bloat and recumbency. How do they differ in terms of clinical signs related to faecal production?
Acute luminal acidosis - profuse smelly diarrhoea
Hypocalcaemia - no faecal output
How is acute ruminal acidosis prevented?
No access to food store
Care with introducing grain
Good fibre source
Mild cases of acute ruminal acidosis seem almost normal clinically. What should be the treatment?
Give hay
Observe
Subacute cases of acute ruminal acidosis are fairly bright, eating and with no ataxia. How should they be treated?
Give hay and oral antacids
Acute and pareacute cases of ruminal acidosis have severe ataxia, recumbency, blindness and severe dehydration. How should they be treated?
Rumenotomy - empty stomach contents Sodium bicarbonate IV Calcium borogluconate Balanced fluids - restrict water intake for 12-24 hours \+/- NSAIDs/Abs
