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Farm (year 4) > Nutrition > Flashcards

Nutrition Flashcards

1
Q

what is the capacity of the rumen?

A

200+ litres

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2
Q

what type of fermentation occurs in the rumen?

A

anaerobic

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3
Q

what is the role of the fibre in the rumen?

A

traps food and provides a home for the rumen microbes (bugs)

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4
Q

what side of the abdomen is the rumen on?

A

left

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5
Q

what contractions occur in the primary rumen cycle?

A

first reticular contraction
second reticular contraction
dorsal rumen contraction
ventral rumen contraction

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6
Q

what is the ration of primary to secondary rumen contraction cycles?

A

2 primary : 1 secondary

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7
Q

what contracts in the secondary rumen cycle?

A

dorsal rumen

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8
Q

what does the first reticular contraction do?

A

moves coarse material into the dorsal sac

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9
Q

what does the second reticular contraction do?

A

move fine material into the cranio-dorsal blind sac and omasum

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10
Q

what does the dorsal rumen contraction in the primary cycle do?

A

move fine material from crania-dorsal blind sac to reticulum

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11
Q

what does the ventral rumen contraction do?

A

move fine material into the cranial blind sac with some exchange with the dorsal sac

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12
Q

what is the function of the secondary rumen contraction cycle?

A

eructation (push gas up oesophagus)

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13
Q

what do the rumen bugs break down food into?

A

volatile fatty acids
methane
carbon dioxide

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14
Q

what does the cow do with the VFAs produced by rumen bugs?

A

absorbs them and uses the to supply energy or fat/glucose synthesis

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15
Q

why do dietary changes need to be implemented slowly?

A

allow the rumen microbes to adapt

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16
Q

what is milk production determined by?

A

genetic merit
nutrition
health

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17
Q

what is the order of consideration, when formulating a diet?

A

dry matter intake
energy
protein
minerals
vitamins

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18
Q

how can DMI of a cow be estimated?

A

percentage of bodyweight

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19
Q

what is the estimated DMI of a dry cow?

A

2% bodyweight

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20
Q

what is the estimated DMI of a cow producing 25L a day?

A

3% bodyweight

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21
Q

what is the estimated DMI of a cow producing 50L a day?

A

4% bodyweight

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22
Q

what are some factors that influence DMI?

A

body weight/fatness (fat cows eat less)
milk yield/stage of production
type of food (digestibility…)
palatability
access/availability
social factors and stress
rumen health

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23
Q

what is metabolisable energy?

A

energy available to the cow for metabolism (maintenance, growth, lactation…)

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24
Q

what is metabolisable energy measured in?

A

MJ/Kg DM

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25
Q

what are the two groups of carbohydrates?

A

long chain (slow fermentation)
short chain (fast fermentation)

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26
Q

what are some long chain carbohydrates?

A

cellulose
hemi-cellulose

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27
Q

what are some short chain carbohydrates?

A

sugars
starch

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28
Q

what are the three VFAs?

A

acetate, butyrate, propinate

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29
Q

what does the breakdown of carbohydrates by the rumen microbes create?

A

VFAs, CO2, CH4

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30
Q

what VFA is used in glucose synthesis?

A

propionate

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31
Q

when are fats and oils used in a cows diet?

A

if DMI doesn’t meet energy requirements

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32
Q

why are cows in negative energy balance at the start of lactation?

A

depressed DMI after calving coincides with huge energy demand for milk production (don’t want them to lose more than 0.5 BCS)

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33
Q

what is the typical maintenance energy requirement for cows?

A

65-70 MJ

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34
Q

how much energy does a cow need to make a litre of milk?

A

5MJ

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35
Q

what is crude protein split into?

A

rumen degradable protein
rumen undegradable protein

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36
Q

what is rumen degradable protein?

A

protein that is broken down by rumen microbes into NH4 (ammonium) used by the bugs for protein synthesis

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37
Q

what is rumen undegradable protein?

A

protein that passes through the rumen and is digested in the abomasum/SI

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38
Q

what is SARA?

A

subacute rumen acidosis

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39
Q

what is the aim for DMI at peak yield?

A

4% bodyweight

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40
Q

what is DM of clamp grass silage?

A

20-35%

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41
Q

what is the energy of clamp grass silage?

A

10-12 MJ ME/Kg DM

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42
Q

what is the energy of maize silage?

A

11-11.5 MJ ME/Kg DM

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43
Q

what are the features of maize silage in terms of protein, starch and fibre?

A

high starch
low protein
poor fibre

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44
Q

what is the DM of maize silage?

A

30-35%

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45
Q

what is the DM of big bale silage?

A

30-35%

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46
Q

what is the energy of big bale silage?

A

8.5-10.5 MJ ME/Kg DM

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47
Q

what is the DM of hay?

A

85%

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48
Q

what is the energy of hay?

A

8-9 MJ ME/Kg DM

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49
Q

what is the DM of straw?

A

85%

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50
Q

what is the energy of straw?

A

5.5-6.5 MJ ME/Kg DM

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51
Q

what is the DM of grass?

A

20%

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52
Q

what is the energy of grass?

A

10-12.5 MJ ME/Kg DM

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53
Q

what is the energy of concentrates/cake?

A

12.5 MJ ME/Kg DM

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54
Q

what is the aim for the length of the calving index?

A

370-400 days

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55
Q

what is the aim for the length of the dry period?

A

60 days

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56
Q

what is the aim of dry cow management?

A

enables cows (and heifers) to transition from pregnancy to lactation with minimal issues whilst achieving their genetic potential of milk yield

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57
Q

what happens to the glucose at the onset of lactation?

A

almost all of it is directed to milk production

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58
Q

how long before calving to DMI begin to drop?

A

about a week

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59
Q

what is the main reserve used when a cow is in NEB?

A

body fat

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60
Q

what is released from adipose tissue to provide energy to cows in NEB?

A

non-esterified fatty acids

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61
Q

where are non-esterified fatty acids processed?

A

liver

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62
Q

what happens if excess NEFAs are released when a cow is in NEB?

A

they are converted back to triglycerides and stored as fat in the liver (this can compromise its function)

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63
Q

why don’t we want dry cows to be too fat?

A

their DMI will be lower so they will mobilise more adipose tissue which will end up being stored in the liver

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64
Q

how does fat accumulation effect liver function?

A

increased NEFAs
reduced response to insulin
increased inflammatory response

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65
Q

how can the chronic disturbance of the metabolic system of dry cows lead to immune response consequences?

A

chronic disturbance leads to pro-inflammatory cytokines released from adipose tissue which activates and overstimulates an immune response

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66
Q

what is condition score a measure of?

A

subcutaneous fat (estimates visceral fat)

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67
Q

what is the traditional diet for feeding dry cows?

A

far off group (5 weeks) - low energy, high fibre, low calcium
close up group (3 weeks) - transition diet

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68
Q

what does the transition diet of the traditional dry cow diet consist of?

A

more similar to the lactation diet to allow rumen microbes to start to adapt

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69
Q

what will giving a cow in the early dry period lead to?

A

suppression of diet (lower DMI)
visceral fat deposition
metabolic disease in lactation

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70
Q

what is the energy density of a transition diet in transitional dry cow feeding?

A

9.5-10 MJ/Kg DM

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71
Q

how is a transitional diet usually formulated in traditional dry cow feeding?

A

lactating cow TMR diluted with straw/hay

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72
Q

what is the goldilocks diet?

A

diet fed for the entire period of the cow being dry

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73
Q

what is essential to the goldilocks diet?

A

chopped straw
adequate feed space (must eat a lot)

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74
Q

what is a major advantage of the goldilocks diet?

A

no social stress as the dry cows move around less (bullying…)

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75
Q

what is classed as a successful transition of the dry cow?

A

30 days of lactation without any disease with expected milk yield

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76
Q

roughly how long does it take rumen microbes to adapt to dietary change?

A

3 weeks

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77
Q

what is the issue with lactic acid be created in the rumen?

A

it is more acidic than the VFAs and cannot be metabolised

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78
Q

what two factors cause rumen acidosis?

A

excessive concentrates
insufficient fibre

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79
Q

what is normal pH of the rumen?

A

6-7

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80
Q

what does a low rumen pH encourage?

A

the growth of lactobacilli (lactic acid producing microbes)

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81
Q

if the efficiency of digestion falls due to a decrease in rumen pH, what effect does this have on the rest of the GI tract?

A

undigested particles pass through is leading to hind gut fermentation which produces acid that damages the colon wall causing osmotic diarrhoea

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82
Q

what factors effect the rumen pH?

A

how much acid (VFAs) produced
type of acid produced
rate of fermentation (fibre is slow)
rate of acid removal (absorbed by papillae)
buffering (by saliva)

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83
Q

why does SARA predispose to SARA?

A

one bout damages/destroys the rumen papillae which leads to another bout as less acid can be absorbed causing a drop in rumen pH

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84
Q

what is needed for satisfactory saliva production?

A

long fibre

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85
Q

what part of the saliva buffers the acid?

A

sodium bicarbonate (3.5kg/day)

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86
Q

what is the function of long fibre in ruminants diet?

A

encourages cudding (buffers acid)
forms a rumen mat (microbe home)

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87
Q

what are some possible risk factors for SARA?

A

insufficient long fibre
insufficient fodder provided
overtaxed TMR (chops too short)
excessive feeding of sugar/starch
poor dry cow management
concentrates in parlour
irregular/deprived feeding
poor cow comfort

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88
Q

what is the benefit of TMR on rumen pH?

A

pH is constant
whereas giving cake in parlour will drop the pH then it will go up again (fluctuates)

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89
Q

is SARA seen on an individual or herd level?

A

herd - 30% at risk

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90
Q

how do the faeces of animals with SARA present?

A

loose and soft
undigested grains
long fibre present
(tail swishing - sore bums - acidic faeces)

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91
Q

what are the three overall effects of SARA?

A

reduced DMI
reduced digestibility
immunosuppression

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92
Q

what production effects does SARA have?

A

poor yields
milk quality - low butterfat, variable protein

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93
Q

what are some health problems that can arise due to SARA?

A

displaced abomasum
digestive upsets
ketosis
lameness (ulcers, white line disease…)
mastitis
poor resistance/health

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94
Q

why are cows with SARA more predisposed to displaced abomasum?

A

VFAs enter the abomasum as they aren’t absorbed and cause atony in the abomasum

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95
Q

what are some clues that SARA may be effecting the herd?

A

fertility issues
lameness
ketosis
LDA
faeces
sick cows

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96
Q

when observing a group with SARA, what should be observed?

A

cudding
rumen fill
tail swishing
dirt score

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97
Q

what should be observed when a faecal sieve is performed on a healthy cow?

A

short fibres - less than half an inch (long suggests poor digestion)
no/little undigested grains

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98
Q

when should samples be taken to measure rumen pH?

A

2-4 hours after feeding

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99
Q

what cows are selected for sampling of rumen pH?

A

6 from cows calved 14-21 days
6 from cows calved 60-80 days

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100
Q

why are cows calved 14-21 days sampled for rumen pH?

A

to asses transition and early management as DMI isn’t maximal yet and they are still adapting to the ration

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101
Q

why are cows calved 60-80 days sampled for rumen pH?

A

assess quality of the overall diet as their intakes are maximal and they have adapted to the diet

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102
Q

what would be considered a positive herd test for SARA?

A

if 2 cows from either group tested are below the pH threshold

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103
Q

what is the threshold for rumen pH testing?

A

<5.7

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104
Q

what is the technique for sample rumen pH?

A

restrain, clip and scrub and give local to the site
site is level with stifle and 8 inches behind last rib
insert needle

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105
Q

what percentage protein is grass silage?

A

14-16%

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106
Q

does acute ruminal acidosis tend to be a problem as an individual or herd level?

A

individual

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107
Q

what is the pathophysiology of acute ruminal acidosis?

A

excessive acid production causes the pH to drop below 5 and lactic acid production dominates

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108
Q

when does acute ruminal acidosis usually occur?

A

overeating grain (barley poisoning)
sudden introduction of high levels of grain

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109
Q

what are the clinical signs of acute ruminal acidosis?

A

distended rumen (bloat)
ataxia
diarrhoea (profuse and smelly)
depression, recumbency, shock

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110
Q

how is mild acute ruminal acidosis treated?

A

give hay and observe

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111
Q

how is subacute acute ruminal acidosis treated?

A

oral antacids and hay

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112
Q

how is peracute acute ruminal acidosis treated?

A

rumenotomy (empty rumen content)
IV sodium bicarbonate and fluids

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113
Q

why do acute ruminal acidosis cases need antibiotics?

A

damage to rumen mucosa leading to bacteria getting into the bloodstream

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114
Q

what are the four diets on a farm?

A

diet cows require
diet formulated by nutritionist
diet mixed by farmer
diet eaten by cows
(all should be the same)

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115
Q

what are the advantages of a TMR?

A

encourages maximal DMI
consistent rumen pH

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Perfectly
116
Q

what are the advantages of hybrid feeding?

A

accurate rationing
resources focused on peak yielding cows
very high yielding get adequate energy
don’t overfeed low yielders

117
Q

what is hybrid feeding?

A

feeding both in and out of the parlour

118
Q

what are the cons of hybrid feeding?

A

eat less at barrier (less long fibre??) which may cause less rumination and buffering

119
Q

what is the main type of grass used for grazing?

A

rye (often monoculture)

120
Q

when is the ideal time to graze rye grass?

A

just as the fourth leaf is emerging before another leaf dies

121
Q

what ways can nutritional status of cattle be monitored?

A

BCS and observation
production (yield)
milk quality - milk recording
biochemistry - metabolic profiles

122
Q

what observations of the cows can be made to monitor nutritional status of cattle?

A

BCS change
DMI
cudding
rumen fill
faeces
cleanliness
lying time

123
Q

what data can be analysed to assess neutron on farm?

A

bulk milk tank composition
NMR/CIS individual cow reprots
milk fatty acids
costings

124
Q

what is the minimum feed barrier space required for a holstein milking cow?

A

60cm

125
Q

what is the minimum feed barrier space required for a dry cow?

A

80cm

126
Q

what is the minimum feed barrier space required for a dry cow close to calving?

A

90cm

127
Q

what is the requirement for drinking trough space for a cow?

A

9cm

128
Q

what is milk fever?

A

hypocalcaemia (plus hypophosphataemia)

129
Q

when does milk fever occur in dairy cows?

A

at/after calving

130
Q

what are the homeostatic mechanisms that control calcium?

A

parathyroid hormone - mobilises calcium from bones and increases absorption from guts
calcitonin - reduces calcium absorption and availability
vitamin D - increases absorption from gut

131
Q

what are the forms calcium is found in blood?

A

bound (to albumin)
ionised (active)
(this depends on the pH of blood)

132
Q

what effects the amount of ionised calcium in blood?

A

blood pH (reduced binding with reduced pH

133
Q

what are some roles of calcium?

A

muscle function, nerve impulses, immune response…

134
Q

what are the clinical signs of milk fever?

A

initial tremors
recumbency
guts stop - no faeces/urination, dry nose, bloat, slow pulse/HR
cold extremities (low temp.)

135
Q

what are some possible differential diagnoses for milk fever?

A

acute coliform mastitis - high temp. and HR
botulism
acute disease
injury at calving - nerve or femoral head damage
(can be coupled with milk fever)

136
Q

what is done to treat hypocalcaemia?

A

IV calcium (slow infusion)
subcutaneous calcium
place in sternal recumbency (avoid bloat)
(phosphorous as well if needed - no harm)

137
Q

what product is used to treat hypophosphataemia?

A

vigophos - phosphorous and B12

138
Q

what are the options for preventing hypocalcaemia?

A

reduce calcium to less than 0.7% or increase to greater than 1.7% in the dry period

139
Q

what is the aim of feeding a low calcium diet in the dry period?

A

tone up the parathyroid hormone system prior to calving (high magnesium fed in diet)

140
Q

what does DCAD dry cow ration stand for?

A

dietary anion/cation difference

141
Q

what is the aim of a DCAD dry cow ration?

A

create a negative balance of anions and cations to reduce the blood pH

142
Q

how does DCAD effect the urine?

A

makes it acidic (below 6)

143
Q

why is DCAD difficult in grass based systems?

A

grass diets are high in potassium which is a positive ion

144
Q

what is the issue with using calcium binders to reduce calcium levels in dry cows?

A

binders also bind phosphorous

145
Q

what is partial DCAD dry cow ration?

A

control calcium for a minimum of 14 days pre calving

146
Q

how is partial DCAD done?

A

low potassium forage
magnesium chloride flakes
some maize as forage

147
Q

what is hypomagnesaemia also known as?

A

grass staggers

148
Q

does the body store magnesium?

A

no

149
Q

what are the clinical signs of hypomagnesaemia?

A

twitchy/hypersensitive
recumbent and convulsive

150
Q

what are risk factors for hypomagnesaemia?

A

lush pasture
high milk output
stress - weather, movement, handling

151
Q

what is done to treat hypomagnesaemia?

A

quiet!! - don’t set off convulsions
control convulsions - xylazine IV
calcium IV
very slow magnesium IV (mix with calcium then give the rest under the skin)

152
Q

what is glucose produced from in cattle?

A

propionate via gluconeogenesis

153
Q

what are ketone bodies used for?

A

energy source for muscles (not milk or brain)
feedback regulator of lipolysis

154
Q

what does the liver do the non-esterified fatty acids (NEFA)?

A

metabolises them to ketones
resynthesises them to fat

155
Q

if acetyl CoA formed from fat mobilisation can’t enter the Krebs cycle, what happens?

A

ketone bodies are formed

156
Q

what ate the clinical signs of ketosis?

A

(initial lack of energy)
reduced milk yield
selective appetite (refuse concentrate)
ketone bodies in blood - sweet smell breath
firm/shiny faeces

157
Q

what is done to treat ketosis?

A

propylene glycol
corticosteroids - dexamethasone
glucose IV
vitamin B12
keystone - monensin bolus

158
Q

what does a kexxtone bolus contain?

A

monesin

159
Q

what is a kexxtone bolus used for?

A

inhibit growth of gram-positive bacteria which produce lactate
this increases propionate and glucose production

160
Q

why must care be taken on farm when giving kexxtone boluses (monensin)?

A

monensin is toxic to dogs

161
Q

what conditions do kexxtone boluses reduce the risk of?

A

ketosis
displaced abomasum

162
Q

what are the clinical signs of nervous ketosis?

A

hyperexcited, twitchy, licking, salivation

163
Q

how is subclinical ketosis diagnosed?

A

beta-hydroxybutyrate in blood

164
Q

why is lying time important in observing nutritional health?

A

cows ruminate when they lie down so is an indicator of this

165
Q

what is the target BCS in the dry period?

A

2.5 (3.0)

166
Q

t is the target BCS in early lactation?

A

2.0-2.5

167
Q

what can be measured to monitor metabolic status?

A

BHB - beta-hydroxybutyrate
NEFA
glucose
fat
protein
urea (milk)

168
Q

what does a beta-hydroxybutyrate test tell you?

A

information about ketosis and suggestive of NEB

169
Q

what is the cut off for a beta-hydroxybutyrate test?

A

> 1.2 mmol/L

170
Q

what is a NEFA test used to provide evidence for?

A

whether there is evidence of fat mobilisation

171
Q

what is the cut off for testing NEFA?

A

> 0.4 mmol/L

172
Q

what is measured in a metabolic profile?

A

energy - beta-hydroxybutyrate, NEFA, glucose
protein - urea, TP, albumin, globulin
minerals - magnesium, phosphorous, copper, selenium

173
Q

what cows should be selected for metabolic profiling?

A

random cows (not problem cows) from dry, early lactation, mid lactation and late lactation (6 from each group)

174
Q

what is measured in milk quality tests?

A

milk protein
urea
butterfat
fat/protein ratio

175
Q

what does a low/high butterfat suggest about the diet?

A

low - lack of fibre
high - high fibre

176
Q

what is crude protein a measure of?

A

feed nitrogen content

177
Q

what is ERDP?

A

effective rumen degradable protein (able to be broken down by microbes)

178
Q

what can be used to examine rumen function?

A

faecal sieving - mucus, fibre length, grain processing
rumen pH - rumencentesis

179
Q

how many trace elements are found in the body?

A

73

180
Q

what are the three classifications of trace elements?

A

deficiency elements
toxic elements
elements in excessive

181
Q

what are some deficiency trace elements?

A

selenium, iodine, manganese, cobalt, zinc, copper

182
Q

what are some toxic trace elements?

A

copper, selenium, cobalt, iodine, cadmium, lead

183
Q

where are the majority of 2+ ions absorbed?

A

via the same transporter in the small intestines (competition)

184
Q

what syndromes can be caused from copper deficiency?

A

swayback, coat colour, falling disease…

185
Q

what syndromes can be caused by selenium deficiency?

A

white muscle disease, cardiomyopathies

186
Q

what syndromes can be caused by cobalt deficiency?

A

reduced growth, wool changes

187
Q

what syndromes can be caused by iodine deficiency?

A

weak neonates

188
Q

what are some sources of trace elements?

A

grass, forage, blends
free access minerals and blocks
boluses
drenches
water (bore hole)

189
Q

how is feeding concentrates beneficial to trace elements?

A

increases the absorption of trace elements from the SI

190
Q

what is measured in blood for selenium?

A

GSHPx - enzyme containing selenium

191
Q

what is measured in blood to test for cobalt?

A

vitamin B12

192
Q

what is measured in blood to test for iodine?

A

PII (can use thyroid weight for this)

193
Q

what DM is used to work out maximum permitted levels of trace elements?

A

88%

194
Q

do additives with a maximum permitted level have to be declared?

A

yes - have to declare maximum permitted level on the feed label

195
Q

where is copper stored?

A

liver

196
Q

what does copper toxicity cause?

A

haemolytic crisis (jaundice and death)

197
Q

are texels sensitive to copper toxicity or deficiency?

A

toxicity but not deficiency

198
Q

are north ronaldseys sensitive to copper toxicity or deficiency?

A

toxicity

199
Q

are scottish black faces sensitive to copper toxicity or deficiency?

A

deficiency but not toxicity

200
Q

how do the different silages vary in copper availability?

A

maize has the most and grass the least

201
Q

what elements can cause copper deficiency?

A

molybdenum and iron in the rumen

202
Q

what should always be done before supplementing copper?

A

check liver copper (by biopsy)

203
Q

what drenches contain trace elements?

A

anthelmintics

204
Q

what effect does zinc deficiency have?

A

reduced appetite and intake
immune effects - endometritis, mastitis…
teratogenic effects - congenital abnormalities
loss of hoof, horn, hair integrity

205
Q

what does selenium toxicity cause?

A

acute - blind staggers
chronic - alkali disease (dullness, rough coat, hairless, lameness, death

206
Q

what does iodine have a vital role in?

A

thyroid function

207
Q

what is the human health issue associated with johnes?

A

possible link to crohnes disease

208
Q

what are the main clinical signs of johnes?

A

older animals (>3 years)
profuse bubbly diarrhoea
weight loss

209
Q

when are most animals infected with johnes?

A

at newborns (first 4 weeks)

210
Q

what are some infection routes of johnes?

A

in utero
dirty environment
dam faeces - teats, environment…
colostrum and waste milk

211
Q

how is the early stages of johnes disease progression halted?

A

cell mediated immunity

212
Q

what immune response causes an animal to become a shedder and infectious?

A

antibody response suppresses cell mediated immunity

213
Q

what are the ways of diagnosing johnes?

A

faecal culture and PCR
ELISA antibody
actiphage - breaks open MAP to release DNA
gamma interferon

214
Q

what are the issues with using faecal culture to diagnose johnes?

A

expensive and time consuming (MAP is hard to grow - fastidious)

215
Q

what is the first diagnostic tool used to detect johnes in a herd?

A

30 cow screen - milk/blood antibody of animals most like to be positive (lame, thin, mastitis, older…)

216
Q

what is the gold standard test for johnes?

A

faecal culture

217
Q

how long does it take faecal culture to develop for you to be able to say the result is negative?

A

3 months

218
Q

what does the sensitivity of johnes ELISA depend on?

A

age distribution - older animals more likely to be positive as they are mopre likely top be shedding
stage of disease - needs to e shedding

219
Q

what are the six control strategies of the national johnes management plan?

A

biosecurity protect and monitor
improved farm management
improved farm management and strategic testing
improved farm management test and cull
breed to terminal sire
firebreak vaccination

220
Q

what test can MAP interfere with?

A

can give false negatives due to the avian strain

221
Q

how can transmission of johnes to youngstock be reduced?

A

reducing risk factors
cull animals likely to be shedding

222
Q

what ways can risk factors of johnes be reduced?

A

avoid faeces
snatch calving
clean pens/hutches
only feed dams colostrum
no waste milk feeding

223
Q

what is the MAP vaccine used for?

A

reduce incidence of clinical disease (doest prevent infection)

224
Q

what nematodes are found in the abomasum of cattle?

A

Haemonchus
Ostertagia ostertagi
Trichostrongylus axei

225
Q

what nematodes are found in the small intestines of cattle?

A

Trichostrongylus spp
Nematodirus spp.
Cooperia spp.

226
Q

what nematodes are found in the large intestine of cattle?

A

Oeophagostomum radiatum
Bunostomum phlebotomum
Chabertia ovina
Trichuris spp.

227
Q

what are the main nematodes causing parasitic gastroenteritis in cattle?

A

Ostertagia ostertagi
Cooperia spp.

228
Q

what is the prepatent period of Ostertagia ostertagi and Cooperia spp.?

A

3 weeks

229
Q

what is the pathology of ostertagiosis?

A

abomasal wall damage due to larval development leading to raised pH causing poorer digestion and bacterial overgrowth

230
Q

what is the pathology of Cooperia spp.?

A

damage intestinal mucosa causing impaired absorption of nutrients and water

231
Q

what are the clinical signs of PGE?

A

diarrhoea, poor appetite, weight loss

232
Q

what is type 2 ostertagiosis?

A

animals pick up infection at the end of the season leading to L4 becoming arrested in the walls of the abomasum and then emerging on mass to causes acute disease

233
Q

what cows are at risk of PGE?

A

first season dairy heifers
autumn born suckler calves
spring born suckler calves

234
Q

what cows are at risk of PGE?

A

first season dairy heifers
autumn born suckler calves
spring born suckler calves

235
Q

can cattle develop immunity to PGE?

A

yes

236
Q

when do cattle develop immunity to PGE?

A

over first 1-2 grazing seasons

237
Q

how strong is the immunity developed to PGE?

A

incomplete meaning subclinical infections are common in adults

238
Q

how is PGE diagnosed in cattle?

A

grazing history/signalment
clinical signs
FEC
(plasam pepsinogen - ostertagiosis)
post mortem
antibody ELISA - exposure rather than infection

239
Q

what is the issue with using FEC for type 2 ostertagiosis?

A

only detects patent infection that are producing eggs, this isn’t the case for overwintering larvae

240
Q

how will a mild winter effect the levels of PGE nematodes on the pasture at turnout?

A

lower levels of infection at turnout due to the larvae being more active over winter so will use up their energy reserve quicker

241
Q

how will a dry summer followed by rain effect the risk period of PGE?

A

will be slightly later risk period as the larvae haven’t been dispersed over summer

242
Q

what is lungworm of cattle called?

A

Dictyocaulus vivparus

243
Q

what is the rough lifecycle of Dictyocaulus viviparus?

A

adults reside in lungs, they lay eggs which develop to L1 and are coughed up and swallowed, the L1 is then passed in faeces where it develops to L3, this is then ingested and migrates to the lungs

244
Q

what stage of lungworm is passed in faeces?

A

L1

245
Q

how are lung worm L1 dispersed from larvae?

A

Pilobolus fungi and rainfall

246
Q

how long does lungworm remain on pasture?

A

6 weeks (aren’t necessarily present at turnout)

247
Q

what is the main source of lungworm infection from year to year?

A

carrier animals

248
Q

what time of year is lungworm most prevalent?

A

September (late summer)

249
Q

what is the prepatent phase of lungworm?

A

L4 larvae in the alveoli migrate towards the bronchi causing alveolitis, bronchiolitis and bronchitis

250
Q

what is the patent phase of lungworm?

A

adult worms in the larger airways lay eggs which develop to L1 causing obstructive bronchitis and aspiration pneumonia (possibly secondary bacterial infection)

251
Q

what are the mild clinical signs of lungworm?

A

intermittent cough when exercised

252
Q

what are the moderate clinical signs of moderate lungworm infection?

A

frequent cough at rest
laboured breathing
squeaks/crackles on auscultaion

253
Q

what are the clinical signs of severe lungworm infection?

A

sever tachypnoea
dyspnoea
air hunger position
mouth breathing
(death)

254
Q

how is lungworm diagnosed?

A

signalment and clinical signs
post mortem
baerman test (L1 in faeces)
antibody ELISA - bulk milk, serum

255
Q

what is liver fluke called?

A

Fasciola hepatica

256
Q

what is the rough lifecycle of liver fluke?

A

eggs passed in faeces that hatch miracidium, these burrow into the mud snail and develop to cercaria, these are shed and develop to metacercariae and ingested by the cow/sheep

257
Q

what is the main risk period for liver fluke?

A

autumn

258
Q

do cattle develop immunity to liver fluke?

A

no - most animals considered to be at risk

259
Q

what causes acute disease of liver fluke?

A

juvenile fluke migrating through the liver parenchyma causing tissue damage and haemorrhage (2-6 weeks post-infection)

260
Q

what causes chronic disease of liver fluke?

A

adult flukes that reside in the bile ducts cause chronic anaemia and hypoalbuminaemia (bottle jaw) - seen from 10-12 weeks post infection

261
Q

how is liver fluke diagnosed?

A

signalment and clinical signs
serum biochemistry
fluke egg sedimentation
copra-antigen ELISA
antibody ELISA - serum/milk

262
Q

what is the risk period for type 2 ostertagiosis?

A

late winter/early spring

263
Q

what endoparasite of cattle has a vaccine available?

A

liungworm

264
Q

what are the four ways of using anthelmintics?

A

strategic - keep pasture contamination low
therapeutic - in response to disease
housing
quarantine

265
Q

what are the classes of anthelmintic available for PGE/lungworm in cattle?

A

1 - benzimidazoles
2 - levamisole
3 - macrocylic lactone

266
Q

what are the colours of the three anthelmintic drenches used for PGE in cattle?

A

1BZ - white
2LV - yellow
3ML - clear

267
Q

what anthelmintic groups used for PGE in cattle have residual activity?

A

3ML - varying residual activity

268
Q

what is the residual activity of ivermectin?

A

14 days

269
Q

what is the dosing regime for ivermectin when turning out animals to protect against PGE?

A

3, 8 and 13 weeks after turnout

270
Q

what is the residual activity of doramectin?

A

5 weeks

271
Q

what farms is lungworm vaccine recommended for?

A

only for farms with disease history (live vaccine)

272
Q

what is the vaccination protocol for lungworm?

A

calves >8 weeks old
2 doses 4 weeks apart
2nd dose at least 2 weeks before turnout
(oral drench)

273
Q

what consideration should be taken into account when treating round worm and fluke with albendazole?

A

fluke requires a higher dose so may not be treating it if using the roundworm dose

274
Q

what drug is effective against all stages of fluke?

A

triclabendazole (high resistance)

275
Q

what is the 5Rs regarding anthelmintic treatment?

A

right product
right animal
right time
right dose
right administration

276
Q

how can you test for anthelminitc resistance on farm?

A

take egg count on day 0 (when drug administered
take another egg count 2 weeks later (for BZ and ML)
should see a 95% reduction

277
Q

what age animal is effected by cryptosporidium?

A

young calves (14-21 days)

278
Q

what is the main clinial sign of cryptosporidium?

A

diarrhoea

279
Q

how can cryptosporidium be diagnosed?

A

history/clinical signs
faecal smears (look for oocyst)
pen-side antigen test

280
Q

why is cryptosporidium often difficult to get rid of on farms?

A

oocysts are resistant and build up in the environment

281
Q

how can cryptosporidium be controlled/treated?

A

good hygiene
reduce stocking density
halofuginone
supportive treatment

282
Q

what aged animals are effected by coccidiosis?

A

young calves (variable) - often 3-4 weeks post weaning

283
Q

what are the main clinical signs of coccidiosis?

A

bloody dysentery
tenesmus
chronic wasting/poo appetite

284
Q

how can coccidiosis be controlled/treated?

A

reduce environmental contamination
prophylaxis/treatment - toltrazuril and diclazuril

285
Q

what is used to treat coccidiosis?

A

toltrazuril and diclazuril

286
Q

what is the definitive host of Neospora?

A

dogs

287
Q

what spreads summer mastitis?

A

Hydrate irritans

288
Q

what is the treatment for redwater?

A

imidocarb

Farm (year 4) (17 decks)

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