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CVSOH 4 > Bovine Clinical Nutrition > Flashcards

Bovine Clinical Nutrition Flashcards

1
Q

What are the main aims of feeding cows?

A

Efficient production, good rumen health and good cow health

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2
Q

Name some forages and their role in bovine diet.

A

Grass, silage, straw. Fibrous part and biggest volume so its quality is important, as this will have a big impact on the total nutrient intake of the animal

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3
Q

Name some supplementary feeds and their role in bovine diet.

A

Wheat, soya, maize grain/gluten. To balance out nutrients in the forage

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4
Q

What are NDFs?

A

Neutral detergent fibre content, forages around 50%, supplementary feeds less so – cell wall content, including cellulose, hemicellulose and lignin

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5
Q

Distinguish the characteristics of straw and wheat.

A

Straw will cause rumination, rumen fill, salivation, energy density is low, fermentation of straw in the rumen will cause acetate production, and straw is relatively cheap.

Wheat contains lots of starch, doesn’t stimulate rumination, rumen full or salivation, higher energy density and decreased acetate (which will increase milk fat), and is more expensive.

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6
Q

What are 2 ways of conserving forages?

A

Ensiling (fermentation using the sugars in the grass) – grass, maize silage

Drying, wilting – hay, straw

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7
Q

What does the amount and quality of grass in the diet depend on?

A
  • Soil type and rainfall
  • Variety with/without clover
  • Fertilizers
  • Sward quality
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8
Q

What happens to grass ages through the year?

A

It becomes more fibrous, less nutrient and so less fibrous

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9
Q

What are the objectives of grazing strategies?

A

Maximising DMI and minimising damage to pasture. Cattle can withstand temperatures, we house cattle to protect the fields and crops more than the cattle.

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10
Q

Name the possible grazing strategies.

A

Continuous
Rotational (“paddock”)
Strip
Zero
Extended

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11
Q

Why is grass conserved?

A
  • Increased maturity, increased dry matter, increased NDF
  • Decreased energy and decreased protein
  • Decreased moisture
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12
Q

What are the characteristics of maize silage?

A
  • Increased energy and decreased protein
  • Increased yield and milk quality
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13
Q

What is primary fermentation of stored silage?

A
  • Anaerobic
  • Lactobacilli produce lactic Acid
  • pH < 4.5
  • Rapid pH drop produces a stable silage
  • Increased water soluble carbohydrate minimum 30g/kg fwt – early season/May, wilting, afternoon cropping
  • Increased dry matter – dry, windy weather, wilting, appropriate maturity
  • Remains a stable product as longas you exclude oxygen, so are wrapped in plastic
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14
Q

What is secondary fermentation of stored silage and why do we not want this to take place?

A
  • Butyric acid/protein degradation
  • Decreased palatability and so decreased dry matter intake
  • Decreased nutritional content
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15
Q

What are the possible silage additives and their effects?

A
  • Acids or acid salts – decreased pH
  • Sugars – increased soluble CHO and increased palatability
  • Inoculants – which contains other bacteria to start and speed up fermentation or viruses to kill the bacteria you don’t want
  • Enzymes – release CHO
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16
Q

What is the first limiting step to feeding cows?

A

Voluntary feed intake – they can only get energy and protein from the food they eat/based on her appetite

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17
Q

What are the cow factors affecting voluntary feed intake?

A
  • Size – increased size increases VFI
  • Yield – increased yield increases VFI
  • BCS – increased BCS decreased VFI
  • Stage of pregnancy – pre-calving = foetal size, post-calving = rumen size, adjust to new diet
  • Presence of other animals
  • Familiarity – on a gut microbe level, them being adapted to digest this
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18
Q

What are the feed factors of voluntary feed intake?

A
  • Quality – increased NDF = increased time to digest = increased rumen fill = decreased VFI
  • Moisture content – VFI can decrease is too wet or too dry
  • Taste – select for sweet, avoid sour or bitter
  • Chop length – VFI increases if short chop length
  • Complete diet/mixed forages – increase VFI. Improved rumen function, taste and balanced nutrient intake
  • Little and often – stimulus to eat and variety
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19
Q

What are the external factors affecting voluntary feed intake?

A
  • Access - truly ad lib, bullying, space (min 70cm trough per animal)
  • Light
  • Water – constant free access
  • Ambient temperature
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20
Q

How can voluntary feed intake be calculated from DMI?

A

VFI is measured on a dry matter basis – convert wet weight intake in Kg into dry matter by multiplying by dry matter content.

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21
Q

What is the rule of thumb for predicting DMI?

A

2.5% body weight + 10% of yield. 3% body weight at BCS 2.5, mid lactation and not in calf

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22
Q

After VFI, what is the next limiting step in feeding cows?

A

Energy

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23
Q

Define FME.

A

Fermentable metabolisable energy (FME) – available for use by rumen flora as energy sources

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24
Q

How do we feed the rumen?

A
  • Some are used by the microbes and some are absorbed by the cow and then some rumen microbes feed the cow
  • Rumenal microbes require energy to make protein and nucleic acid
  • Unable to use fats and fermentation acids
  • Fermentable metabolisable energy
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25
Q

What does slow fermentation produce?

A
  • Volatile Fatty Acids (VFAs) > absorbed into the blood stream
  • Acetic acid (2C)
  • Propionic acid (3C) > oxaloacetate (glucogenic – ruminants produce glucose by proprionate, glucose often used by the microbes)
  • Butyric acid (4C)
  • Carbon dioxide and methane
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26
Q

Describe fats in the bovine diet.

A
  • Coat fibre affecting digestion
  • Most decreased milk butterfat
  • Restrict to <6% of total diet
  • Protected fats – won’t degrade in the rumen, pass through, but may pass through to the abomasum to be digested there
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27
Q

Describe the metabilisable energy system.

A
  • Gross energy = energy trapped in food if burnt
  • Goes through digested tract, some is not digested, so faecal energy is removed to get digestible energy
  • Some of this is lost as methane, in urine = metabolizable energy is the energy the animal can utilise
  • Utilised for lactation, maintenance, pregnancy and growth
  • At each step, heat is liberated and so it is metabolisable energy for each function minus the heat produced
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28
Q

What are the ME requirements of cattle?

A

Beef 65MJ metabolisable energy/day

Dairy 5MJ metabolisable energy/L

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29
Q

What is the conversion efficiency, k, and what is it dependent on?

A
  • The efficiency with which ME is converted to net energy
  • Dependent on – use of energy, quality of feed, animal production level
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30
Q

How does quality of diet affect conversion efficiency?

A

Fibrous feeds are more difficult to digest – more energy is used to make the energy available

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31
Q

How is APL calculated? What happens in APL is increased?

A

Animal production level/APL = total energy requirement / energy for maintenance

Increased APL = increased DMI = decreased gut transit time = decreased k

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32
Q

How does weight affect ME?

A

Weight loss/gain during lactation is more efficient than during the dry period

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33
Q

How is the protein content in crude protein calculated?

A
  • Nitrogen x 6.25 = Protein content
  • Does not tell you what type of protein it is, very crude measure
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34
Q

How is protein metabolised in cattle?

A
  • RDP is degraded in the protein
  • UDP travels through rumen and is digested in the small intestine
  • Proportion of proteins that degrade is determined by time in protein which is determined by DMI
  • Degrade into peptides and amino acids.
  • Ammonia and proteins are built back up.
  • Rumen microbes will utilise FME and amino acids and proteins to produce microbial proteins, which passes out of the rumen and is absorbed by the cow.
  • Nitrogenous waste is recycled in the rumen, excreted in saliva and excreted by the kidneys.
  • Excess ammonia is converted to urea in the liver and excreted by the kidney in the rumen.
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35
Q

What is rumen outflow rate?

A
  • Slow outflow = increased digestion = increased RDP
  • Outflow ~ VFI ~ APL
  • Therefore increased APL = increased UDP
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36
Q

What may elevated urea be due to in cattle?

A
  • Dehydration/hypovolaemia
  • Renal disease
  • Excessive CP in the diet
  • Lack of FME in the diet
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37
Q

What is ERDP?

A

ERDP/effective rumen degradable protein – the amount of RDP actually available to rumen microbes

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38
Q

How are FME and ERDP linked?

A
  • The ratio of FME:ERDP is critical in achieving efficient protein metabolism
  • Can’t utilise ERDP if they don’t have an energy source
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39
Q

What does every 1MJ of FME produce?

A

10-11g of MCP/microbial crude protein, as long as there is enough FME to utilise this ERDP. Exact amount depends on the APL.

1kg of organic matter yields – 200g of MCP

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40
Q

What are the problems with the MP system?

A
  • Underestimates requirements – 10%
  • Individual AAs not considered, such as lysine and methionine
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41
Q

How are calves fed from birth to weaning?

A
  • Consistent preparation of milk replacer
  • Consistent timing
  • Consistent presentation - cleanliness, concentration, consistency
  • Ad lib, clean fresh water
  • Roughage - stimulates rumen development
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42
Q

How is compound feed fed to calves?

A
  • Crude protein - for growth and rumen development, which cannot be done on just straw as rumen may impact with straw and won’t be enough microbes
  • Constant free access
  • Aim for 1Kg/day by weaning
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43
Q

When are beef and dairy cattle weaned?

A

Weaned from 6-10 months in beef and in dairy weaned 6-8 weeks

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44
Q

Why might beef cattle be fed cereal/barley?

A

Just grain, will produce a lot of acid and without reasonable fibre will get ruminal acidosis. Need to supplement with proteins. Diet allows calves to be finished at a young age but is not the most efficient

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45
Q

What are the characteristics of cereal beef systems?

A

Cereal has highest DWG, feeds the most concentrates and finishes earliest

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46
Q

How does nutrition affect profitable management?

A
  • Tight calving pattern – calve and feed as a batch
  • Minimising feed costs (max production from grass)
  • Body condition score management – low in spring, higher in winter
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47
Q

What are the target condition scores throughout the year of suckler cows?

A

Spring = 2
Summer = 2.5
Autumn = 3
Winter = 2.5

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48
Q

How does the BCS of dairy and beef cattle differ?

A

Unlike dairy cows, who are kept at constant BCS to eliminate risk of metabolic disease, beef herds have their ability to change BCS is utilised to minimise the cost of food.

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49
Q

If winter forage is given with silage alone, what happens to calves?

A

Silage alone with cause chondroplastic dwarfism in calves

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50
Q

What are the advantages of total/complete mixed rations?

A
  • Increased DMI = increased yield
  • Improved rumen function and decreases acidosis
  • Cheaper – straights not concentrates
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51
Q

What are the disadvantages of total/complete mixed rations?

A
  • Capital investment, storage and time
  • Fat cows
  • Slow entry to parlour
  • Cash flow
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52
Q

What are the advantages of multiple rations in a group?

A
  • Increased precision
  • Avoids thin and fat cows
  • Decreased standing times helps with lameness
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53
Q

What are the disadvantages of multiple rations in a group?

A
  • Increased bullying
  • Increased complexity - multiple groups, diets
  • Increased time
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54
Q

What does feeding to yield mean in dairy cattle?

A

As milk yield increases and decreases, alter rations to follow the same curve

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55
Q

What is flat rate feeding?

A

Everything gets the same, so is easy, but can end up overfeeding and underfeeding certain cows

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56
Q

What are the advantages of feeding to yield?

A
  • Simple
  • Avoids overfeeding and underfeeding
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57
Q

What are the disadvantages of feeding to yield?

A
  • Increased acidosis
  • Increased metabolic stress
  • Streep decline after after
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58
Q

What are the advantages of flat rate feeding?

A
  • Simple
  • Decreased metabolic stress
  • Decreased acidosis
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59
Q

What are the disadvantages of flat rate feeding?

A
  • Risk of underfeeding and overfeeding
  • Increased BCS loss around peak
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60
Q

What is stepped feeding?

A

Compromise between feeding to yield and flat rate

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61
Q

How much dry matter intake should dry cows get?

A

2% bodyweight or less
10-15kg/day

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62
Q

What are the physiological factors that decrease dry matter intake?

A

Increase calf size
Increased BCS as this causes decreased appetite

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63
Q

What are the management factors that decrease dry matter intake?

A

Decreased feed access and palatability

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64
Q

What is the BCS aim at drying off and calving?

A

2.5-3

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65
Q

What is the effect of BCS being above 3 at calving?

A
  • Increased calving difficulties
  • Decreased DMI and decreased yield and so increased risk of negative energy balance
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66
Q

What does BCS loss in the dry period cause?

A

Causes decreased fertility as follicles develop through the dry period, takes 60 days, so is being influenced by cow’s nutrition way before oestrous or service

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67
Q

What is energy requirements of dairy cows at drying off and near calving?

A

At drying off ~(65 + 15) = 80MJ/day

Near calving ~(65 + 45) = 110MJ/day

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68
Q

What are the protein requirements of dairy cattle at drying off and near calving?

A

At drying off (300 + 100) = 400g metabolisable protein/day

Near calving ~(300 + 190) = 490g MP/day

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69
Q

What does digested undegraded protein in the dry period cause?

A
  • Foetal growth
  • Increased milk yield + quality (due to increased protein content)
  • Increased fertility
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70
Q

What does excessive rumen digestible protein/crude protein cause?

A

Increased down cows

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71
Q

What are the aims of drying off?

A
  • Recovery from lactation
  • Maintain condition
  • Restrict energy density
  • Rumen recovery
  • Stabilise mineral/vitamin status
  • Calf growth
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72
Q

What are the aims at transition?

A
  • Fitness for lactation
  • Maximising DMI
  • Metabolic health
  • Prevention of hypocalcaemia
  • Rumen acclimatisation
  • Maintain condition
  • Calf growth
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73
Q

What are single ration diets and what is the problem with these?

A

Very high in fibre with/without shorter dry periods to offset cost, not very good at acclimatising the rumen

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74
Q

What are the advantages of single rations?

A
  • Avoids sudden change in diet during early dry period
  • Maintain DMI better
  • Allow improved energy balance
  • Reduced risk of LDAs
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75
Q

What is the effect of DMI on calcium requirements?

A

Increased DMI cause increased Ca requirement as some is lost and not absorbed with increased gut movement with eating more

10kg DMI = 15g/day
25Kg DMI = 30g/day

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76
Q

What is the maintenance calcium requirement in lactation?

A

2g per litre of milk

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77
Q

Explain how calcium deficiency causes calving complications and LDAs.

A
  • Most of the calcium in a cow is in the bones so cows are not calcium deficient in the same way you would you copper deficient.
  • There is a sudden demand surge that must be resorbed from bone.
  • If this cannot be done, you get relaxation of smooth and skeletal muscle – effects of gut, uterus, skeletal muscle.
  • If uterine tone is affected, there is calving complications, more likely to be infected.
  • Increased incidence of LDAs and cows won’t be able to eat as much so DMI decreases which exacerbates the problem.
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78
Q

How is milk fever prevented in dairy cattle?

A
  • Calcium restriction to kickstart normal calcium homeostatic mechanisms, so this why we do not feed lots of grass in the dry period as it contains a lot of calcium.
  • Magnesium supplementation
  • DCAD/DCAB manipulation
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79
Q

What are the feeding strategies used to restrict calcium to prevent milk fever?

A
  • Grass/grass silage high in calcium concentration
  • Dilute calcium concentration by increasing straw in ration
  • Tightly stock transition cows if at grass
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80
Q

How does magnesium affect calcium in dairy cattle?

A

Mg is a cofactor in mobilising calcium from bone, so cows low in Mg will be less able to mobilise calcium

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81
Q

What are the feeding strategies to supplement magnesium to prevent milk fever?

A
  • MgCl2 in TMR or drinking water
  • Can affect ration palatability
  • Will influence DCAD
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82
Q

What is the consequence of diets with low DACD/

A

Diets with low DCAD include mild metabolic acidosis due to difference in charge (not amount of each)

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83
Q

What are the consequences of metabolic acidosis?

A
  • Increased vitamin D3 is activated per unit PTH
  • Target tissues (especially bone) are more sensitive to PTH and 1,25(OH)2D3
  • More rapid mobilisation Ca from body reserves around calving
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84
Q

What are the disadvantages of fill DCAD diets?

A
  • Expensive
  • Unpalatable
  • Very soluble - wash out in rain
  • Relative pH instability in the face of variable DMI
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85
Q

What are partial DCAD diets?

A

Reduce Ca but feeding things trying to reduce DCAD. Manipulate available feeds to decrease ration DCAD

86
Q

How does glucose demand change in dairy cattle?

A
  • Increases suddenly at calving (milk)
  • If dietary propionate does not match demand for glucose, levels of OAA fall
87
Q

When are ketones produced?

A

OAA used up to produce lots of glucose, can’t uptake propionate other fats get metabolised and produce ketones

88
Q

What can over-fat cows cause?

A

Insulin resistance/type II ketosis which is analogous to type 2 diabetes, which affects their ability to maintain and moderate glucose

89
Q

What does negative energy balance in cattle cause?

A

Causes mobilisation of body fat

90
Q

How does increased BCS cause peripheral insulin resistance?

A
  • Lower DMI causing increased negative energy balance
  • Increased fat mobilisation (quantity and quickness)
  • Peripheral insulin resistance
91
Q

What is fat deposition in the liver due to?

A
  • Lack of Acetyl CoA = free fatty acid unable to enter the TCA cycle
  • Depletion of lipoproteins = liver unable to export fat
92
Q

What is the overall effect of fat deposition in the liver?

A

Impaired liver function

93
Q

Distinguish type I and type II ketosis.

A

Type I - energy intake less than output, peak lactation

Type II - insulin resistance, fat infiltration of liver, around calving

94
Q

How is ketosis prevented?

A
  • Minimise peripheral insulin resistance by careful management of BCS and avoiding excess FME in early DP
  • Maximise DMI
95
Q

How is rumen pH mostly buffered?

A

Buffering of pH largely from saliva trying to prevent falling pH

96
Q

What is the consequence of increased CHO diets?

A
  1. Increased CHO diets causes increased acid and decreased saliva, and so a decreased pH
  2. Lactic acid producing bacteria causes a very decreased pH
  3. Acute rumenal acidosis
97
Q

What is rumenal acidosis?

A

Grain overload, high quantity of CHO in a short timeframe. Can kill animal but killing off components of the microflora

98
Q

What is subacute rumenal acidosis/SARA?

A
  • Chronic exposure to high starch levels
  • Lack of physically effective NDF – stuff that is so long that it won’t easily leave the rumen so have to ruminate and so produce saliva.
  • Herd level problem
99
Q

How does frequency and amount of feed per day affect rumenal pH?

A
  • Can feed concentrate twice a day and mild day meal as long as you do not feed too much, as this will cause acidosis
  • Out of parlour feeding allows smaller increments of concentrate intake so has shallower fluctuations in pH
  • Total mixed ration in correct quantity better than partial MR which also has concentrates.
  • How starch and fibre are mixed is important – how much are cows having to chew, are they spitting cud balls out because they are acidotic?
  • Low pH cause slow cellulose digestion so will get clumps of undigested material in the faeces.
100
Q

What are the on farm observations used to diagnose subacute rumenal acidosis?

A
  • Increased or decreased faecal consistency and incomplete digestion
  • Poor cow cleanliness
  • Tail swishing
  • Decreased DMI and increased sorting
  • Decreased rumination and increased dropped cuds
  • Ration assessment
101
Q

Why does subacute rumenal acidosis cause decreased herd performance?

A
  • Decreased yields and bulk milk butterfat levels
  • Poor reproductive performance
  • Increased lameness
  • Increased environmental mastitis
102
Q

What are the main 4 metabolic conditions in cattle?

A

Hypocalcaemia
Hypomagnesaemia
Ketosis
Fatty Liver Disease

103
Q

What are the consequences of hypocalcaemia in cattle?

A
  • Ruminal stasis causing bloat and uterine inertia
  • Flaccid paralysis of skeletal muscles
  • Small muscles in the nose that produce secretions stop contracting so rhinarium looks dry
  • Heart keeps going as it responds to its own electrical impulses not externally, but respiratory muscles are affected
  • Pressure is put on the caudal vena cava
104
Q

How does hypocalcaemia in cattle cause infertility?

A
  • Dystocia (uterine inertia)
  • Prolapsed uterus – if cannot contact may turn itself inside out
  • RFM
  • Endometritis
  • Ketosis
105
Q

What is the aetiology of hypocalcaemia?

A
  • Around calving the cow is unable to mobilise calcium from bone and increase absorption from the gut quickly enough to meet the increased demands of colostrum production
  • When calcium levels in the blood fall, parathyroid hormone acts on the bones releasing calcium and phosphorus.
  • Parathyroid hormone also stimulates production of hydroxylase enzyme in the kidney, which is responsible for the second of the two hydroxylation steps which convert vitamin D to its active hormonal form, stimulates the absorption of calcium from the gut and the mobilisation of calcium from the bone
106
Q

What are the risk factors for milk fever?

A
  • Third lactation
  • Previous history of MF
  • Jersey and Holstein
  • Complete milking after calving
  • High calcium diet in the dry period
  • Low magnesium diet in the dry period
  • Leaving dry cows at grass in the autumn without supplementary feeding
  • Over fat cows
  • Fatty liver syndrome
  • Oestrogens at calving or at oestrus depress food intake
  • Stress at calving
  • No shelter from inclement weather
  • Transport – in part due to stopping DMI while they are being moved
107
Q

What causes increased milk fever cases?

A
  • Excess calcium in the diet pre-calving
  • Chronic sub-clinical hypomagnesaemia
  • Hypomagnesaemic animals have a reduced rate of Ca mobilisation
108
Q

What is the effect of a diet with high cations?

A

Resulting in a state of mild metabolic alkalosis which results in the kidney being less responsive to PTH

109
Q

What are the short term factors predisposing hypocalcaemia?

A
  • Excess feeding of Ca prior to calving
  • Oestrogen
  • Complete milking out after calving
110
Q

Why is it important to establish if and when a cow has calved with milk fever?

A

90% cases occur 24 hours before to 48 hours after calving

111
Q

What are the clinical signs of stage 1 milk fever?

A

Cow still standing
Refuses concentrates in parlour
Apprehension
Tremors
Paddling legs
Straight-hocked
Swaying
Rumen static
May grind teeth
Sometimes excitement, staggering

112
Q

What are the clinical signs of stage 2 milk fever?

A
  • Sternal recumbency
  • Eventually becomes recumbent
  • Attempts to rise
  • Dilated pupils, dry muzzle
  • Rectum distended with firm faeces and bulging backwards
  • Udder full
  • Temperature normal/subnormal
113
Q

What are the clinical signs of stage 3 milk fever?

A
  • Lateral recumbency
  • Comatose
  • Bloat
  • Temp subnormal
  • Respiration rate decreased to approximately 10/min
114
Q

What must be done for a cow in stage 3 milk fever?

A
  • Die if untreated from respiratory failure, bloat and regurgitation and inhalation of rumen contents
  • Get cow’s head as high as possible to prevent her drowning in her own rumen contents
115
Q

What is the prognosis of milk fever?

A
  • Treat as an emergency
  • Aim to restore cow to her feet
  • Very fat cows and/or have been down for more than 6 hours respond less well to treatment
  • Tends to recur at next calving
116
Q

What are differential diagnoses of milk fever?

A
  • Ataxia with MF – adductor tears fractures
  • If treated too late may develop ischaemia of hind quarter muscles
  • The consequences of dystocia resulting in obturator paralysis
117
Q

How is milk fever most rapidly confirmed?

A

The most practical and rapid confirmation of diagnosis is response to treatment

118
Q

What might be the clinical presentation of milk fever cases?

A
  • Are depressed
  • Have a full udder
  • A pulse rate < 100
  • Rectum full of firm faeces
  • Injuries – fractures, dislocations, obstetrical paralysis
  • Mastitis, metritis and enteritis
  • Peritonitis from uterine/cervical rupture
  • Udder not full, often scouring
  • Ruminal acidosis
  • Starvation/malnutrition – end stage, wasting thin cows
  • Hydroallantois – end stage, huge cow, getting bigger before recumbent
  • End stage of toxaemia
  • BSE
119
Q

How are milk fever cases treated?

A
  • If cow is flat out it is a real emergency
  • Prop the cow up
  • Good idea to take bloods before treatment
  • Ca supplementation
  • Straight Cbg or mixed prep
120
Q

How is calcium administered?

A

SC problematic as it is not absorbed well as this suppresses calcium homeostatic mechanisms and amount given CS is not enough – delay response to treatment or cause hypocalcaemia

121
Q

How is straight cbg/mixed prep be administered?

A

Prefer Ca 40 IV and monitor heart for arrhythmia and tachycardia as you administer. Put bottle lower and it will run in slower if you hear arrythmia

122
Q

What are the signs of recovery from milk fever?

A
  • Heart rate falls and becomes louder
  • Eructates
  • Defecates
  • Urinates
  • Shivers
  • Looks brighter
  • Bead of dew appear on muzzle
  • Tries to stand
123
Q

What is the presentation of subclinical milk fever pre-calving?

A
  • Tight udder
  • Soft sacro-sciatic ligaments
  • Not getting on with calving
  • Reduced appetite
  • Cervix 50-75% dilated
  • Membranes intact
  • Weak or no uterine contractions
  • Absence of straining
  • Second stage labour does not occur or if it does the calf is born dead
124
Q

How is subclinical milk fever pre-calving treated?

A

Give Ca IV and cow goes into labour

125
Q

How is subclinical milk fever post-calving treated?

A

Usually resolves rapidly after a bottle of 40% Ca borogluconate IV, often do not need phosphate given but does no harm

126
Q

Why is the cow reassessed after 4 hours of treatment for milk fever?

A
  • If still down can repeat Ca IV
  • Prevent ischaemia of muscles by moving to deep bedded yard/field. Turn frequently (minimum 4 x daily)
127
Q

How are milk fever relapses prevented?

A
  • Don’t milk fully for 24 hours minimum
  • Leave one calf on cow
  • Encourage cow to eat
128
Q

What are the possible complications of milk fever?

A
  • Inhalational pneumonia
  • Muscle ischaemia and necrosis of hamstring group
  • Superficial necrosis of skin over bony prominences
  • Fractures/dislocations/muscle tears
  • Peroneal paralysis
129
Q

How is milk fever prevented?

A
  • Avoid heavy “steaming up”. But if do, use rolled barley without added minerals or with special dry cow mineral
  • Aim for low Ca diet pre-calving
  • Cow condition score - 2.5-3
  • High concentration Ca bolus
  • Magnesium supplementation
  • SC Ca at calving) – may affect normal homeostasis
  • Manipulation of DCAD
  • Vitamin D3 pre-calving injection
130
Q

How is rhubarb poisoning treated?

A

Giving calcium

131
Q

What is the effect of hypomagnesaemia?

A
  • Magnesium has a controlling, inhibitory effect on nerve and muscle activity
  • In acute magnesium deficiency this inhibition is removed
  • Sudden in onset and unless treated proceeds rapidly to death
132
Q

Distinguish the 3 forms of hypomagnesaemia in cattle.

A

Acute – spring and Autumn affecting both dairy and beef suckler cows

Chronic – end of Winter usually in suckler cows wintered on poor diets

Subclinical – late dry period especially in pregnant dairy cows at grass

133
Q

Why is continual daily intake of magnesium important in cattle?

A
  • Very small available pool in ECF
  • Many cows live on a magnesium knife edge
  • No homeostatic mechanisms to buffer sudden dietary deficiencies
134
Q

What are the magnesium requirements in cattle?

A
  • 3g Mg to support milk yield
  • 2.5g Mg urinary loss
  • 5.5g Mg in the bloodstream (available reserve)
  • 5g from feed every day
135
Q

What may hypomagnesaemia interfere with?

A
  • Release of PTH
  • Hydroxylation of vitamin D in the liver
  • Mobilisation of calcium from bones
  • Absorption of calcium from the gut
136
Q

What are the predisposing factors?

A

Adverse weather
Stress
Weaning
Transport
TB test
Oestrous/excitement
Lush grass
Grass species
Soil type
Fertiliser usage affects grass uptake of Mg
High protein level in young grass
Less use of concentrates
Suckler cows out wintered on a low plane of nutrition with a big calf suckling it

137
Q

What are the risk periods for hypomagnesaemia?

A
  • Lactating dairy or suckler cows for 6-8 weeks after spring turn-out
  • Summer-Autumn calving dairy cows on lush Autumn aftermath
  • Outwintered suckler cows calving Sept-March
  • 2-3 days after the stress of weaning in suckler cows
138
Q

What are the subclinical signs of hypomagnesaemia in cattle?

A
  • Depression of appetite, which increases ketosis
  • Losing weight
  • Drop in milk yield and protein
  • Increased incidence of MF
  • Decreased fertility
139
Q

What are the clinical signs of hypomagnesaemia in cattle?

A

Drop in milk yield
Change in temperament
Nervous, excitable, tremors
Hyperaesthesia
Pronounced palpebral reflex (snap shut)
Frothing at the mouth
Tachycardia (very loud)
Staggering gait
Ataxia
Incoordination proceeding to recumbency
Convulsions
Nystagmus
Opisthotonus
Coma
Death/sudden death/found dead

140
Q

What are the differential diagnoses for the acute signs of hypomagnesaemia in cattle?

A

Milk fever
Nervous ketosis (acetonaemia)
Acute listeriosis
BSE
Acute lead poisoning
Stray voltage – electrocution

141
Q

What are the differential diagnoses for cattle found dead from hypomagnesaemia?

A

Anthrax
Bloat
Milk fever
Fog fever
Poisoning
Acute haemorrhage
Lightning strike/electrocution
Traumatic pericarditis
Acute salmonellosis
Acute pasteurella pneumonia
Paracute E.coli mastitis
Peracute metritis
Blackleg
Black disease
Bacillary haemoglobinuria
Botulism
Asphyxia
Choke
Inhalation pneumonia

142
Q

Why must hypomagnesaemia cows be approached very carefully?

A
  • Assume these cows as being very dangerous and chance of lashing out
  • Approaching a cow in lateral recumbency not between front and back legs or too close
143
Q

How is hypomagnesaemia treated?

A
  • If convulsing = 4ml 2% xylazine IM
  • Give 400ml of 20% calcium BG with magnesium hypophosphite slowly IV followed by 400ml 25% Magnesium sulphate SC – do not give IV, get this in SC and get out of the way, these things need to be kept alone and quite or they will thrash around and cause brain damage
  • Monitor heart
144
Q

What must you never do in treating hypomagnesaemia?

A

Never give straight magnesium IV = will kill the animal

145
Q

What are the control measures for hypomagnesaemia in cattle?

A
  • Responsible fertiliser usage
  • Magnesium supplementation 30g of Mg/cow/day, especially spring and autumn
  • Calcined magnesite can be incorporated in rolled barley and fed to sucklers during critical periods
  • Medicated drinking water
  • Roller ball mag mixed with molasses is the best prevention in low input suckler systems where bolus use is not undertaken
  • Application of calcined magnesite to pasture
  • Sprinkling calcined magnesite on silage
  • Buffer feeding - hay, straw or big bale silage each day before turn-out onto lush grazing
  • Adequate shelter to reduce stress from adverse weather
146
Q

How can blood sampling be used to control hypomagnesaemia?

A

1 clinical case of staggers means there are others at high risk. Blood sampling before and after turn-out can give advance warning of depressed Mg status, which can turn into cases within hours

147
Q

What is ketosis/acetonaemia?

A
  • Disease caused by incomplete metabolism of VFAs
  • Consequence of deficiency of oxaloacetate precursors
  • Characterised by low plasma glucose and high plasma ketones
  • Non-fatal disease, self-limiting
148
Q

Which ketone body is measured?

A

Acetone is what you can smell/pear drops (some can’t) but beta hydroxyacteone is the most stable so is the one that is measured

149
Q

Which cows are more likely to become ketotic and why?

A

Fat cows eat less, more profound NEBAL, mobilise more fat and so more likely to become ketotic/diseased condition – all cows will have slightly elevated ketones in lactation but fat cows will have this become a clinical problem.

150
Q

What is the epidemiology of ketosis in cattle?

A
  • Winter housing period
  • Secondary disease – LDA, metritis
  • Overweight at calving
  • Association of clinical ketosis with other diseases of early lactation, particularly in DAs
151
Q

What are the clinical signs of ketosis in cattle?

A
  • Inappetance/anorexia
  • Often roughage only will be eaten
  • Milk drop
  • Rapid weight loss
  • Faeces with/without firm and dry
  • Depression
  • Reduced rumen contraction frequency and strength
152
Q

What are the nervous signs of ketosis in cattle?

A

Sudden onset
Delirium
Circling
Leaning and crossing legs
Licking and chewing manias
Blindness

153
Q

How is ketosis diagnosed from blood biochemistry?

A

Hyperketonaemia
Hypoglycaemia
Ketonuria
Ketones in milk – Rothera’s reagent turns blue
Hypocalcaemia

154
Q

What are the clinical signs of fat cow syndrome (same mechanism as ketosis)?

A
  • Increased incidence of metabolic disease – less responsive
  • Increased incidence of LDA, metritis, mastitis, profound and non-responsive ketosis
  • Recumbence
  • Death
155
Q

How is fat cow syndrome diagnosed from blood biochemistry?

A

Increased beta-HB/ketotic, NEFA, GLDH, AST, GGT

156
Q

Which cows are affected by pregnancy toxaemia?

A

Affecting cows in late gestation (more common in beef herds) and cows carrying twins in late gestation

157
Q

What are the treatment options available for ketosis and fat cow syndrome in cattle?

A
  • Intravenous glucose/dextrose
  • Glucose/proprionate precursors – get Kreb’s working again, not to get rid of all the ketones but to get some glucose produced again
  • Glucocorticoids – can increase glucose levels but do not up-regulate glucose production. At certain stages of pregnancy, this will cause cows to abort
158
Q

How are ketosis and fat cow syndrome prevented?

A
  • Monensin (kexxtone) bolus in cows with a high BCS – promotes proportionate production in the rumen
  • Metabolic profiles/clinical biochemistry to monitor nutrition
159
Q

How is sampling for metabolic profiles done?

A

2 weeks or more after major management change. Representative samples of herd 6-12 animals of different stages in cycle

160
Q

When are metabolic profiles useful?

A

Useful when high incidence of postpartum problems:

  • RFM
  • Milk fever
  • LDA
  • Ketosis
  • Poor production, yield and constituents
  • Poor fertility
161
Q

Name the mineral, vitamin and trace elements that we feed to prevent disorders of.

A

Macrominerals – calcium, magnesium, phosphate

Trace elements – copper/molybdenum, cobalt, selenium, iodine

Vitamins – vitamin E and A

162
Q

What is the role of copper?

A

Oxygen metabolism/transport, enzyme systems

163
Q

Distinguish primary and secondary copper deficiencies.

A

Primary – rare in UK, poor fertility, eating enough copper but bound in the rumen in a way that they cannot utilise it so it gets lost in the faeces

Secondary – interference with uptake

164
Q

What are the clinical signs of copper deficiency?

A
  • Ill thrift
  • Poor coat condition
  • Chronic scour
  • Poor fertility (pregnancy rates)
165
Q

How is copper deficiency diagnosed?

A
  • Blood copper levels
  • Abnormal metabolites in blood
  • Liver biopsies/samples from slaughter
  • Feed/soil analyses
  • Response to treatment
166
Q

What is copper deficiency managed?

A
  • Feed inclusion
  • Boluses
167
Q

What is the role of selenium and vitamin E?

A

Powerful antioxidant with vitamin E, immune function

168
Q

What are the clinical signs of selenium and vitamin E deficiency?

A

RFM
Increased risk of mastitis and metritis
White muscle disease/sudden death in young

169
Q

How is selenium and vitamin E deficiency managed?

A

Inclusion in feed/boluses/injection – care as toxic/therapeutic levels of Se close

170
Q

What is the role of iodine?

A

Thyroid hormones thyroxine and triiodothyronine (T3), control of basal metabolic rate

171
Q

What are the clinical signs of iodine deficiency in pregnant cattle?

A

Still birth, sick and weakly calves that do not thrive

Usually not an issue in dairy cattle as there is a lot of iodine used in the parlour but heifers that haven’t been in the parlour before can react

172
Q

How is iodine deficiency diagnosed?

A

Plasma inorganic I2 (PII) or T4, PME of still born calves - weight of thyroid

173
Q

How is iodine deficiency managed?

A

Feed inclusion/pour on

174
Q

What is assessed when investigating ketosis in a dairy herd?

A
  • Body condition scores
  • Cow comfort
  • Feed space/presentation
  • DMI/rumen fill – should feel doughy
  • Silage clamps
  • Transition management
  • Silage analyses
  • Metabolic disease
  • Milk yield/constituents – urea in blood to reflect circulating levels of free nitrogen in RDP and FME
  • Metabolic profiling
  • Is the area under the sub lumbar fossa concave or convex, is this full and doughy?
175
Q

What does stiff faecal consistency indicate about bovine nutrition?

A
  • Good rumen health
  • Decreased DMI and yield
176
Q

What does loose faecal consistency indicate about bovine nutrition?

A
  • Poor rumen health?
  • BF may be depressed
177
Q

How are milk constituents altered by bovine nutrition?

A
  • Negative energy balance cause decreased milk protein, partly due to MP production in the rumen
  • Fat mobilisation causes increases milk butterfat
  • Increased peNDF causes increased butter fat
178
Q

How are milk constituents affected by dilution effect?

A
  • Higher yields → lower protein/BF
  • Protein/BF tend to rise in late lactation (as yield decreases)
179
Q

Which metabolic profiles are used to assess energy?

A
  • ß hydroxy butyrate
  • Fat metabolism
  • NEBA
  • Lactating cows
  • Non-esterified fatty acids
  • Fat mobilisation
180
Q

Which metabolic profiles are used to assess urea?

A
  • ERDP > FME causes increased urea
  • ERDP < FME causes decreased urea
  • Urea levels are a consequence of both the kidneys and the rumen
181
Q

Which metabolic profiles are used to assess albumin?

A
  • Poor liver function
  • Chronic infection
  • Inadequate dietary AA’s
182
Q

Which metabolic profiles are used to assess globulin?

A
  • TP minus albumin
  • Inflammation
183
Q

What is downer cow syndrome?

A

A cow which has been recumbent for more than 24 hours and which does not have hypocalcaemia (if down because of direct effects of MF, very different than cow that went down with MF and now has normal Ca and won’t get up still). Physical inabilities that are primary cause of the cow being down, physical inabilities as a consequence of the cow being down, or metabolic condition or disease problem occurring around parturition causing it to be down.

184
Q

What is the aetiologies of downer cow syndrome?

A
  • Complication of some periparturient problem
  • 80% result from milk fever and/or dystocia
  • Secondary consequences of recumbency (e.g. muscle ischaemia) prevent the cow from rising
185
Q

What are the predisposing factors of downer cow syndrome?

A
  • Delayed/inadequate treatment of MF
  • Unfavourable surfaces
  • Obesity
  • Dystocia
186
Q

What are the 3 main causes of primary recumbency to be considered for downer cows?

A
  • Metabolic disease
  • Toxaemia/infection
  • Periparturient injury
187
Q

What are some examples of periparturient injuries that cause downer cow syndrome?

A
  • Nerve damage, sciatic, obturator, other
  • Fractured femoral head/pelvis, hip dislocation
  • Sacroiliac joint damage
  • Bleeding from torn vaginal arteries
  • Rupture of the limb muscles – adductors, gastrocnemius
188
Q

Name 2 other possible causes of primary recumbency of downer cows.

A

Severe lameness
BSE

189
Q

How do you get secondary causes of downer cow syndrome?

A

Once down, you can get secondary causes of being down such as muscle ischaemia and pressures damage. As they get up, scrambling on slippery surfaces, can get ruptured muscles and ligaments

190
Q

What is the pathoegenesis of compartment syndrome?

A
  1. Heavy cows, compression of underneath limb
  2. Impairment of venous return
  3. Ischaemia of semitendinosus/hamstring muscles
  4. Leakage of fluid into confined space in the muscles – muscle are confined in the muscle sheath so cannot expand
  5. Further increase in pressure
  6. Further necrosis
  7. Swelling and rigidity of limb
  8. Struggling causes further damage
  9. Compression of sciatic and peroneal nerves
191
Q

How might temperature be affected by downer cow syndrome?

A

Is she pyrexic? If so check the udder and vagina for signs of mastitis/metritis

Is she cold? This could be due to toxaemia or poor nursing out in a field

192
Q

How can auscultation help diagnose downer cow syndrome?

A

Heart rate - if high this could indicate toxaemia or pain

Lungs - evidence of inhalation pneumonia. Ping the abdomen for evidence of an LDA/RDA.

Rumen movements - an absence could indicate a persistent low calcium status

193
Q

How can vaginal examination help diagnose downer cow syndrome?

A
  • Check for a second calf, retained placenta or a foul smelling discharge which may indicate metritis
  • Check for vaginal, cervical and uterine tears
194
Q

How can rectal examination help diagnose downer cow syndrome?

A
  • Stiff and impacted indicating a possible milk fever relapse
  • Watery suggesting a toxic mastitis
  • Crepitus suggesting of a pelvic fracture
195
Q

How are downer cows treated and managed?

A
  1. Treat primary cause if known
  2. Ensure cow on deep bed – or on pasture (keep them warm)
  3. Turn her regularly at least every 5-6 hrs
  4. Hoist the cow twice daily for 20 mins
  5. Provide access to food and water
  6. Analgesia – NSAIDs
196
Q

What are 4 options for hoisting a downer cow?

A
  • Bagshaw hoist – great care needed. Some cow a bit of support helps but barbaric for some cows with hip fractures as they clamp onto the tuber coxae
  • Inflatable bag
  • Harness/Net
  • Float tank
197
Q

How is pelvic nerve damage causing downer cow syndrome treated?

A
  • Place cow in deep bedding/or at pasture
  • Regular rolling
  • Make feed and water available
  • Put hobbles on hind legs to prevent splaying
  • Give NSAID
  • If cow not up within 48 hours may be worth attempting to hoist
198
Q

When are downer cows euthanised on welfare ground?

A

The cow that keeps rolling into lateral recumbency, groans persistently, fails to eat or drink, or has a fractured limb

Good policy to check on downer cows frequently to make sure that they are being properly cared for and not suffering

199
Q

What happens if straights are combined into a pellet?

A

They will sort through it, picking out the bits they want to eat.

200
Q

Summarise the ME requirements in dairy cows.

A

Maintenance = 70 MJ/d
Lactation = 200MJ for 40L or yield x 5
Pregnancy = 20 MJ/d
Calving = 45 MJ/d

201
Q

What happens if fibre is not provided in the diet?

A

Rumenal acidosis/SARA
Butterfat depression

202
Q

How is milk composition manipulated?

A
  • Raising butterfat – increase peNDF, C16 protected fats
  • Raising protein – improve energy balance
  • Genetics
203
Q

Roughly when is first cut silage grass cut?

A

May

204
Q

Which forage has the highest energy levels?

A

Maize silage

205
Q

What is the energy requirement of a 650kg cow producing 40L milk a day?

A

(10% of BW) + (5 x 40) = 265

206
Q

What is the APL of a 650kg cow producing 40L milk daily?

A

265 / 65 = 4 (ish)

207
Q

What is the energy requirement of a 650kg early lactation cow producing 50L and losing 1kg bwt daily?

A

(5x 50) + 65 = 315. 1kg a day = 20MJ energy a day. 315 – 20 = 295MJ

208
Q

What does FME provide energy for?

A

Synthesis of MCP

209
Q

An appropriate type of cattle for barley beef would be?

A

Purebred dairy or dairy cross bulls – early and late maturing animals high energy dense ration is for late maturing cattle pure bred dairy and bulls, Hereford would get too fat too quickly.

210
Q

Which nutritional disorders might be associated with cereal beef?

A

Acidosis, CCN, hypovitaminosis A, ruminal bloat, ruminal parakeratosis, as well as spontaneous long bone fractures

CVSOH 4 (25 decks)

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