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Year 4 Livestock and One Health > Nutrition and GI: Metabolic Disease in Ruminants > Flashcards

Nutrition and GI: Metabolic Disease in Ruminants Flashcards

1
Q

What are the different diseases that can affect the dairy cow post natally?
‘post natal depression’

A
  • Milk fever
  • RFM, metritis, Endometritis
  • Mastitis
  • Displaced abomasum
  • Ketosis
  • Fertility
  • Lameness
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2
Q

What risk factors of calving add to metabolic diseases?

A
  • Reduced DMI
  • Negative energy balance
  • Immunosuppression
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3
Q
  1. What is milk fever?
  2. When does it affect dairy cows?
  3. Why?
A
  1. Hypocalcaemia ± hypophosphataemia
  2. At/after calving
  3. Drain on Ca2+ due to colostrum/milk demands
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4
Q

What controls Ca in the body?

A

Parathyroid hormone
* Mobilisation of Ca from bone
* Increased absorption from gut- Mg2+ required

Calcitonin- reduced Ca2+ absorption and availability
Vit D3= increases absorption from gut

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5
Q

What is generally the role of Ca2+ in the body?

A
  • Muscle function
  • Nerve impulses
  • Immune response
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6
Q

What are the clinical signs of acute milk fever?

A

At/After calving
* Initial hyperexitation then recumbent
* Guts/glands stop
* No faeces
* No urination
* Dry noses
* Postural bloat
* Slow pulse/HR

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7
Q

What are the differential diagnosis for recumbent cow after calving?

A
  • Milk fever- no faeces, slow/normal/fast HR
  • Acute coliform mastitis- high pulse rate/HR, variable temp, endotoxaemic- mms conjested
  • Botulism
  • Acute disease- salmonella
  • Injury at calving- nerve damage, femoral head
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8
Q

How is hypocalcaemia treated?

A
  • I/V Ca Borogluconate 40% calcium- care with rapid infusion
  • Place in sternal recumbency- bloat
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9
Q

What can be used for hypophosphataemia treatment?

A

Phosphorous containing products used for ketosis now used
* Vigophos solution injection- organis phosphorus, vitamin B12 supplementation
* Calciject 40CM for treating milk fever has 5% magnesium hypophosphite

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10
Q

How is milk fever prevented?

A
  • Low Ca diet pre-calving
  • High Mg pre-calving
  • Boluses/drench/stomach tube at calving
  • Maximise DMI pre-calving
  • Aim for negative DCAD
  • Zeolite- calcium binder
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11
Q
  1. What is DCAD?
  2. How can DCAD be monitored?
A
  1. Dietary anion/cation difference
    DCAD = Na + K - C- S
  2. Aim for negative DCAD before calving- reduce blood pH, monitor by urine pH below 6

Generally does not work easily in UK- grass high K

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12
Q

What can be done for a partial DCAD?

A
  • Control diet for 14 days pre calving
  • Housing therefore easiest
  • Low potassium forages, no slurry on land used to harvest grass
  • Magnesium chloride orally- flakes/water
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13
Q

When does hypocalcaemia affect sheep?

A
  • Pre-lambing stress
  • Movement back from ‘tack’
  • Inadequate feed barrier space
  • Often many recumbent ewes

Treatment
* 20ml Ca Borogluconate IV- diagnostic
* Farmer- 80ml CaBG S/C

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14
Q
  1. What is grass staggers?
  2. What causes it?
A
  1. Hypomagnesia
  2. No storage so when Output > input

Output- milk
Input- diet
* absorbed in rumen, retiuculm, omasum
* High K+ reduced absorption- lush grass, fertilisers

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15
Q

What are the clinical signs of grass staggers?

A

Peracute- often found dead
Early- twitchy and hypersensitive
Recumbent and convulsive

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16
Q

What effects epidemiology of staggers?

A
  • Lush pastures
  • High output of milk
  • Stress- weather, movement, handling

Spring- dairy cows, twin bearing ewes
Autumn- suckler cows with large calf

17
Q

How is staggers treated?

A
  • Emergency
  • Be quiet
  • Control convulsions- xylazine, pentobarbitone
  • Give Ca 40% IV
  • Slowly give upto 200ml MgSO4 IV
18
Q

How is staggers prevented?

A
  • Move off affected pasture
  • Give additional Mg
    Dairy cows- high mag cake
    Beef- minerals, bolus, wean calves, straw
19
Q

What are ketone bodies function?

A

Energy sourve for muscle- not milk/brain
Feedback regulator for lipolysis

20
Q

What causes ketosis?

A
  • NEB
  • Excessive mobilisation of fat for energy
  • Insufficient prioprionate from rumen
  • Insufficient oxalo-acetate
  • Acetyl CoA from fat mobilisation cannot enter krebs cycle
  • Acetyl CoA metabolised to ketones
21
Q

What are the clinical signs of ketosis?

A
  • Reduced milk yield
  • Selective appetite- refuse concentrates
  • Ketone bodies in blood
  • Firm faeces- shiny
  • Nervous ketosis
22
Q

How is it treated?

A
  • Propylene glycol
  • Corticosteroids- dexameth
  • Glucose 40% IV
  • combination of above
  • Vitamin B12
  • Thiamine B1
  • Kexxtone- monensin bolus
23
Q

What is the function of a kextone bolus?

A
  • Monensin- ‘antibiotic’
  • Inhibits growth of gram +ve bacteria- produce most of the acetate, lactate and hydrohen
  • Increase proprionate and glucose production
  • 3-4 weeks prior to expected calving
  • Target use- high or low BCS, twins, lame etc
24
Q

When does sub-clinical ketosis occur?

How is it diagnosed?

How is it treated?

A

5-50 days in milk

Diagnosis
* BOHB in blood- 1.2-2.9mmol, > 3mmol- clinical
* NEFA in blood- >0.4mmol/l

Treatment- assess rations and dry cow managment

25
Q

What are the BCS targets for:
1. Dry period
2. Early lactation
3. Drying off
4. Mid lactation

A
  1. 2.5-3
  2. 2-2.5
  3. 2.5-3
  4. 2.5-3
26
Q

How can metabolic and nutritional status be monitored?

A
  • Observation- BCS, DMI, rumen fill etc
  • BHB
  • NEFA
  • Glucose
  • Fat
  • Protein
  • Urea
  • Calcium
27
Q

How can milk quality be used for nutrition?

A

Both bulk tank and individual cow
* Milk protein- low MP, energy defecit
* Butterfat- low (lack of fibre), high (high fibre diet)

Urea- blood urea/milk urea will rise with excess ERDP or insufficient ME

28
Q

How can rumen function be examined?

A

Faecal sieving
* Mucus
* Fibre length
* Grain processing

Rumen pH and protozoa

pH measuring boluses

29
Q

How is fat metabolisation syndrome/ketosis prevented?

A

Feeding in dry period
* Low energy
* Maximise DMI in dry cows- comfort, palatable diet

Monitor CS
Avoid fat cows

Year 4 Livestock and One Health (58 decks)

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