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Year 4 farm > Production Diseases > Flashcards

Production Diseases Flashcards

1
Q

What are the maintenance requirements for calcium in a cow

A

25g/day maintenance
+13.9g late pregnancy
+ 30g colostrum
+73g 40l milk

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2
Q

Risk factors for hypocalcemia

A

Freshly calved high parity
Around calving with rapid calcium requirement increases
Age of cow - older reduces reserves

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3
Q

Symptoms of hypoglycemia

A

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)

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4
Q

Treatment for hypocalcemia

A

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

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5
Q

Herd management for hypocalcemia

A

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

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6
Q

Cause of ketosis

A

Negative energy balance

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7
Q

Physiology of type 1 ketosis

A

Underfeeding at peak lactation
Reduced supply of proportionate (and glucose)
Incomplete oxidation of NEFAs in liver leading to ketone body production

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8
Q

Type 2 ketosis

A

Hepatic lipidosis early lactation
Excessive mobilisation of fat increased NEFAs
Incomptoxidatiob of NEFAs and excess fat accumulation in liver
Reduced gluconeogenesis and liver function

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9
Q

Difference in clinical signs between ketosis and hepatic lipidosis

A

Both
- off food
- milk drop
Ketosis
- can smell ketones
- nervous ketosis
Hepatic lipidosis
- immunosuppression
- collapse
- liver failure

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10
Q

Signs of nervous ketosis

A

Unusual
Can look blind
Can be aggressive
Furious licking - walls/bars

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11
Q

Ketosis diagnostic tests

A

Blood - ketone meter
Urine - ketone dipstick
Milk - rotheras reagent - changes colour with presence

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12
Q

Diagnosis of hepatic lipidosis

A

Blood for NEFA
Look for liver damage (AST, GGT), assess fat (biopsy/necropsy)

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13
Q

Treatment of ketosis

A

Best - propylene glycol (glucose precursor) 300g daily
Glucocorticoid - promotes glucone
Glucose orally

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14
Q

Pregnancy toxaemia in sheep

A

Pregnancy ketosis
Energy demands in late pregnancy exceed supply
Can’t distinguish from hypocalcemia
Cs- off feed, dull depressed, blindness or dead

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15
Q

Prevention of ketosis

A

Aim for BCS 2.5-3 at calving
AVOID >3
Max decrease 0.5 BCS between dry and mid lactation

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16
Q

Metabolic profiles of energy balance

A

BHB - betahydroxybuterate - ketone body, energy supply/demand measures
NEFA - transport form of fat, indicator of mobilisation
>/= 3/12 cows abnormal suggests a problem

17
Q

Milk parameters

A

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)

18
Q

Dry matter intake

A

Kg fed/cow - kg refusals/cow
X
% dry matter of ration

19
Q

How to improve dry matter intake

A

Minimize impact of group changes
Easy food access
Maximize ration palatability
Avoid over conditioned cows
Manage environment

20
Q

Diets with low DCAB

A

Mild metabolic acidosis
Enhanced Ca uptake from GI tract
Ca mobilisation from bone
Higher VitD activation/unit PTH
Increased tissue sensitivity to PTH

21
Q

Full vs partial DCAB

A

Full - requires use of amniotic salts and Ca supplementation. Involved/expensive
Partial - low DCAB feeding, good in lower yielding herds

22
Q

Ovine pulmonary adenocarcinoma

A

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

23
Q

Border disease

A

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

24
Q

Ovine johnes disease

A

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

25
Q

CLA - corynebacterium pseudotuberculosis

A

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

26
Q

Maedi visna

A

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

27
Q

Cattle vs sheep johnes

A

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

28
Q

Difference between border disease and BVD

A

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

29
Q

Disease impacts

A

Animal welfare
Reproductive efficiency losses
Reduced longevity
Poor lamb health
Financial effects

Year 4 farm (13 decks)

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