Production Diseases Flashcards
What are the maintenance requirements for calcium in a cow
25g/day maintenance
+13.9g late pregnancy
+ 30g colostrum
+73g 40l milk
Risk factors for hypocalcemia
Freshly calved high parity
Around calving with rapid calcium requirement increases
Age of cow - older reduces reserves
Symptoms of hypoglycemia
Muscle weakness
Poor heart contraction
Poor uterine involution
Thrashing limbs
Hyperaesthesia
Constipation
Ruminal bloat
Sunken eyes
Diarrhoea
Unable to weight bare (one or more legs)
Treatment for hypocalcemia
400ml 40% calcium borogluconate slow IV - monitor heart rate during
Should results in eructation, defecation and standing very quickly
Nsaids
Additional calcium - subcut/oral
Phosphorus often also low, should increase with Ca
Herd management for hypocalcemia
Decrease Ca and K in late dry period, increases PTH and makes them very slightly acidotic increasing GI calcium uptake. With increased GI uptake increase in calcium at calving can compliment
Cause of ketosis
Negative energy balance
Physiology of type 1 ketosis
Underfeeding at peak lactation
Reduced supply of proportionate (and glucose)
Incomplete oxidation of NEFAs in liver leading to ketone body production
Type 2 ketosis
Hepatic lipidosis early lactation
Excessive mobilisation of fat increased NEFAs
Incomptoxidatiob of NEFAs and excess fat accumulation in liver
Reduced gluconeogenesis and liver function
Difference in clinical signs between ketosis and hepatic lipidosis
Both
- off food
- milk drop
Ketosis
- can smell ketones
- nervous ketosis
Hepatic lipidosis
- immunosuppression
- collapse
- liver failure
Signs of nervous ketosis
Unusual
Can look blind
Can be aggressive
Furious licking - walls/bars
Ketosis diagnostic tests
Blood - ketone meter
Urine - ketone dipstick
Milk - rotheras reagent - changes colour with presence
Diagnosis of hepatic lipidosis
Blood for NEFA
Look for liver damage (AST, GGT), assess fat (biopsy/necropsy)
Treatment of ketosis
Best - propylene glycol (glucose precursor) 300g daily
Glucocorticoid - promotes glucone
Glucose orally
Pregnancy toxaemia in sheep
Pregnancy ketosis
Energy demands in late pregnancy exceed supply
Can’t distinguish from hypocalcemia
Cs- off feed, dull depressed, blindness or dead
Prevention of ketosis
Aim for BCS 2.5-3 at calving
AVOID >3
Max decrease 0.5 BCS between dry and mid lactation
Metabolic profiles of energy balance
BHB - betahydroxybuterate - ketone body, energy supply/demand measures
NEFA - transport form of fat, indicator of mobilisation
>/= 3/12 cows abnormal suggests a problem
Milk parameters
Used to suggest energy balance
Butter fat : protein ratio
Negative energy reduces protein and increases butter fat
Higher fibre diet = higher butterfat
Increased yield lowers protein and butterfat (spread through more milk)
Dry matter intake
Kg fed/cow - kg refusals/cow
X
% dry matter of ration
How to improve dry matter intake
Minimize impact of group changes
Easy food access
Maximize ration palatability
Avoid over conditioned cows
Manage environment
Diets with low DCAB
Mild metabolic acidosis
Enhanced Ca uptake from GI tract
Ca mobilisation from bone
Higher VitD activation/unit PTH
Increased tissue sensitivity to PTH
Full vs partial DCAB
Full - requires use of amniotic salts and Ca supplementation. Involved/expensive
Partial - low DCAB feeding, good in lower yielding herds
Ovine pulmonary adenocarcinoma
Caused by jaagseikte sheep retrovirus - long incubation
Transmitted by aerosol
CS - laboured breathing, I’ll thrift, sudden death
Diagnosis - PM only definitive
Control can’t treat
Identify/cull, limit age mixing, snatch lambing
Border disease
Pestivirus - respiratory and placental transmission, semen of PI rams
CS - hairy shaker lambs, poor fertility, high abortion, weak lambs
Diagnosis - antibody/antigen detection
Treatment/control - none, natural immunity (exposure if non-pregnant), optimize nutrition and parasite control
Ovine johnes disease
Infection early in life with long incubation
Faecal-oral transmission
Cs- reduced fertility, weightloss. Thin sheep, high culling rates, poor performance
Diagnosis - serology but antibodies low until disease
Treatment/control - culling, flock separation
Sheep susceptible to cattle strain
CLA - corynebacterium pseudotuberculosis
Bacterial infiltration through skin
CS - lymph node abcessation of head neck and scrotum
Diagnosis - bacteriology (have to open abscess), serology (antibodies wax and wane)
Control not treatment
ZOONOTIC
Maedi visna
Lentivirus (long incubation)
CS - chronic wasting, labour breathing
Diagnosis - serology(wax and wane) PM
Control not treatment
Regional variation (Leicestershire and Gloucestershire high)
Oronasal transmission
Cattle vs sheep johnes
Both - production losses, faecal-oral transmission
Cattle - scour, some resistance to sheep strain, individual testing feasible
Sheep - no scour, susceptible to cattle strain, vaccination and management more cost effective than testing
Difference between border disease and BVD
Both - pestivirus and can create PIs
BD - 0-60day PI development, PIs less likely to survive, no vaccine, poor ewe fertility, hairy shakers, high abortion, weak lambs. Moderate transmission through flocks
BVD - vaccine available, rapid transmission, 45-145PI development, immunosuppression, reproductive losses, congenital deformities
Disease impacts
Animal welfare
Reproductive efficiency losses
Reduced longevity
Poor lamb health
Financial effects
