Cattle

Question 1

What design issues do bovine lungs have?

Answer 1

Small lung volume:body size
Large dead space - limited respiratory reserve, reduced phagocytic activity, decreased bacteria clearance
No collateral ventilation of alveoli - small area of pneumonia can prevent gas exchange in lots of alveoli
Alveoli easy to damage and difficult to recover - alveolar collapse is easy, re-pneumonisation is slow
Early and substantial vasoconstriction of arteries and arterioles - meant to maintain BP but cuts off blood supply to lung
Poorly developed fibrinolytic systems - lung scarring

Question 2

Consequences of bovine respiratory disease?

Answer 2

Death
Poor growth
Drug costs
Delay in age at first calving
Reduction in subsequent milk yield
Related diseases

Question 3

Estimated UK prevalence of enzootic pneumonia of calves?

Answer 3

Dairy - 30%

Beef - 80-90%

Question 4

Infectious causes of pneumonia in cattle?

Answer 4

Viruses - RSV, PI3, IBR (BVD)
Bacteria - Pasteurella, Mannheimia, Histophilus
Mycoplasma
See 3rd year lectures

Question 5

What may cause reduced host defences, causing a calf to be more prone to pneumonia/resp disease?

Answer 5

FPT - too little, too late, poor quality
Inappropriate air quality -> URT mucociliary carpet damaged
LRT inflammatory cells immunosuppression:
- stressors (weaning, disbudding, castration, movement)
- sub-acute ruminal acidosis
- BVD

Question 6

What should the plasma and serum TP be for calves?

Answer 6

Plasma TP > 56g/l

Serum TP > 52g/l

Question 7

Why is Bovine respiratory disease most common in winter?

Answer 7

Mixed age groups/limited housing
Close proximity of age groups
UV light kills viruses - less sun
Viruses thrive in damp conditions and protected by water droplets
Viruses and bacteria decay faster in dry conditions

Question 8

What are the lower critical temperatures of a 4 week ofd calf with no draught, some draught and damp floor? What about a younger calf 0-2 weeks old?

Answer 8

No draught (0.2m/s): 0C
Some draught (2m/s): 9C
Damp floor: 15C

0-2 weeks can’t tolerate lower temperatures - need 15C

Question 9

How long can a calf gut absorb antibodies from colostrum?

Answer 9

12 hours

Question 10

How close in age should calf groups be? Why?

Answer 10

<2 weeks spread between youngest and oldest

Older calves act as pathogen multipliers

Question 11

Cattle Lungworm life cycle?

Answer 11

Adults in URT
Eggs containing L1 coughed up and swallowed
Mature to L2 as pass through GIT
L2 in faeces
L2 -> L3 - spread by rain/pilobolus/wind
L3 eaten on pasture
Mature to L4 and migrate through gut wall
Spread to lungs via bloodstream

Question 12

What is the prepatent period for cattle lungworm?

Answer 12

3 weeks

Question 13

Max humidity for cattle housing?

Answer 13

80% (65% better)

Question 14

What is Fog fever?

Answer 14

Reaction to fructans in grass
Single animal
If moved, likely to die

Question 15

Which dairy breeds have a genetic predisposition for atrophic rhinitis and enzootic nasal granuloma?

Answer 15

Channel Island

Fresian

Question 16

Which beef breed has a genetic predisposition to laryngeal chondritis? Why?

Answer 16

Belgian blue

Lung volume:body weight lowest for any breed

Question 17

Which respiratory diseases are fattening cattle most prone to?

Answer 17

Mannheimiosis/Pasteurellosis

Histophilus somni

Question 18

Which respiratory disease are first lactation heifers turned out most prone to?

Answer 18

Parasitic pneumonia: Dictyocaulus viviparus

Question 19

What bovine respiratory diseases are associated with an allergic response?

Answer 19

Bovine Farmers’ Lung - reaction to mould spores
Pre-patent lungworm
Fog Fever

Question 20

What usually causes stertorous upper respiratory noise in cattle?

Answer 20

Laryngeal pathology - commonly laryngeal chondritis

• secondary to calf diphtheria (necrotic smell from mouth)
• breed predispositions

Question 21

Treatment for laryngeal chondritis in cows?

Answer 21

May respond to penicillin/anti-inflammatories

May require tracheotomy/-ostomy

Question 22

Causes of a profuse nosebleed in cows?

Answer 22

Vena caval thrombo-embolism - hopeless

Foreign body - blackthorn prickles

Question 23

What to do for respiratory clinical exam of cattle?

Answer 23

Observe general appearance - overgrown coat = too cold
Ear position - depressed/cold
Watch their behaviour - seeking shelter? depressed?
Move around to elicit coughing
TPR
Resp noise - lung fields and trachea/URT
Respiratory depth
Posture - abducted elbows = air hungry
Deep breaths = air hungry
Shallow breaths = pain - pleurisy/peritonitis

Question 24

Which animals to sample when investigating bovine respiratory disease? What to bear in mind when interpreting results?

Answer 24

Sample acute cases - before secondary infections invade
Pasteurella and Mannheimia are normal commensals
URT Mycoplasma may be commensal
URT organisms may not reflect the pathology in the LRT
Single antibody titres may be historic
Only sample if will be useful/affect decisions/affect treatment choice

Question 25

What types of individual samples are needed to test for bovine respiratory diseases?

Answer 25

Nasopharyngeal swab: IBR (RSV, PI3) Conjunctival swabs/scrape: IBR (Mycoplasma bovis if eyes affected) Paired serology 2-3 weeks apart: All, rising titre/4 fold BAL: M bovis, IBR, RSV, PI3, BVD, Histophilus Faecal sample: D viviparus (Baermann technique)

Question 26

What group sample can be used to help investigate dairy herd respiratory disease?

Answer 26

Bulk milk antibodies Useful for trends First lactation heifers only indicates recent entry into herd

Question 27

How to assess the environment when investigating bovine respiratory disease?

Answer 27

``` At level of the animals! Urea? Warm air? Underfoot squelch test Too cold/hot? Dust in air? Does it make you cough? Temperature of the bedding Smoke tests Data loggers for temperature and humidity ```

Question 28

Short term/immediate treatment for bovine respiratory disease?

Answer 28

Antibiotics in an outbreak NSAIDs Nursing Isolation/reduce numbers

Question 29

Longterm prevention of bovine respiratory disease?

Answer 29

Improve environment Colostrum and nutrition Vaccination

Question 30

What to do if group of cattle affected by bovine respiratory diseases?

Answer 30

If only treating those affected, need to take daily temps (treat if >39.5/40) Or if >25% group affected, could treat metaphylactically - more practical

Question 31

Which broad spectrum, long acting antibiotics are most commonly used for respiratory disease in cattle?

Answer 31

Oxytetracycline Beta lactams (not for Mycoplasma) Florfenicol Macrolides (licensed for calf pneumonia) - Tilmicosin, tulathromycin, gammithromycin, tildipirosin Fluoroquinolones - only if c+s suggests only thing that would work as public health issues

Question 32

What type of vaccine are IBR vaccines? Why is this good?

Answer 32

Marker vaccine gE protein deleted from the virus in the vaccine So Abs are different to those produced against intact virus and can be differentiated on serology Can tell difference between vaccinated animal vs naturally infected

Question 33

Routes of IBR vaccine administration? How often are boosters needed?

Answer 33

Intranasal (faster but local effects, IgA) Intramuscular 6-12 monthly boosters recommended

Question 34

Difference between IBR live and dead vaccines?

Answer 34

Live - CMI to deal with recent infection locally, can use in face of infection intranasally to be followed by systemic dose Dead - provokes Ab levels Young animals receive live vaccine initially with dead boosters

Question 35

Non cardiac signs of bovine cardiac disease?

Answer 35

``` Reduced production Exercise intolerance Increased urine output Syncope Poor appetite when failing ```

Question 36

What to subjectively assess without touching animal for bovine cardiac disease?

Answer 36

Condition score Visible oedema - inter-mandibular, brisket Posture Respiratory effort

Question 37

How to interpret bovine skin tone/tenting? Other signs seen?

Answer 37

4-6% loss normal (PCV 40%) 6-8% tenting 2-4s (PCV 50%) - dry nose and mouth 8-10% tenting 6-10s (PCV 55%) - cold extremities +/- recumbent 10-12% tenting 20+s (PCV 60%+) - comatose, shock 12%+ Death

Question 38

What to assess on hands on exam for bovine cardiac disease?

Answer 38

Skin tone Regional temperature for perfusion - ears Mucous membranes - mouth, conjunctiva, vulva: CRT, dry, cold, colour

Question 39

Causes of pale mucous membranes in bovines?

Answer 39

``` Anaemia -deficiencies - iron, copper, cobalt -toxicities - kale, nitrate etc -blood/protein loss - haemonchus, fascioliasis, Johne's, sucking lice, PGE, red water, leptospirosis Poor perfusion -shock (RDA) -heart failure -thrombosis ```

Question 40

Causes of red mucous membranes in bovines?

Answer 40

``` Toxaemia Salmonellosis Pasteurellosis Malignant catarrhal fever Infectious Bovine Kerato-conjunctivitis IBR ```

Question 41

Causes of cyanosis of mucous membranes in bovines?

Answer 41

Respiratory failure Nitrate/nitrite, metaldehyde poisoning Congenital cardiac abnormality - calves

Question 42

Causes of jaundice of mucous membranes in bovines?

Answer 42

``` Hepatitis Haemolytic anaemia (Babesia-red water) Photosensitisation Ragwort, kale, lupin, copper poisoning Post-partum haemoglobinuria Leptospirosis ```

Question 43

Causes of haemorrhage mucous membranes in bovines?

Answer 43

``` Anthrax Bracken Sweet vernal grass posioning Copper toxicity (acute) Leptospirosis Mycotoxicosis ```

Question 44

Normal pulse rate in calves and cattle?

Answer 44

Calves: 100-120 Cattle: 50-80 (high yielders up to 95) - give fluids if 100+ with skin tent 120+ suggests primary cardiac disease

Question 45

What happens to the jugular and subcutaneous abdominal (milk) veins in cardiac failure?

Answer 45

Distension in right sided failure | Increased venous pressure in cardiac failure

Question 46

How to assess the jugular pulse in a bovine?

Answer 46

Normal up to 1/3 way up Occluse or empty jugular to check in abnormal All way up: -endocarditis, pericarditis, haemothorax, hydrothorax, congestive heart failure, valvular stenosis/insufficiency -sporadic bovine leukosis-thymic form -enzootic bovine leukosis-cardiac form

Question 47

Where to auscultate the heart in bovines? Base, apex, left contact, right contact, pulmonary valve, aortic valve, left AV valve, right AV valve?

Answer 47

Base: 3rd-6th rib Apex: 6th rib at articulation of rib to sternum, 2cm cranial to diaphragm Left contact: 3rd rib ro 4th intercostal space Right contact: Ventral part of 4th rib Pulmonary valve: 3rd intercostal space Aortic valve: 4th rib 12cm above sternum Left AV valve: 4th intercostal space Right AV valve: 4th rib 10cm above sternum

Question 48

Which cardiac sounds can be heard in bovines?

Answer 48

S1 (lub): ventricular contraction and AV valves shut = systolic S2 (dup): closure of aortic/pulmonary valves = diastolic Ventricular filling sound nor usually heard S4: atrial contraction may be heard

Question 49

What does it mean in bovines if S1 or S2 is loud?

Answer 49

Loud S1: increased force of contraction | Loud S2: increased pressure in vessels

Question 50

Causes of heart murmurs in bovines?

Answer 50

``` Stenosis: rough, harsh Regurgitation/incompetence: softer, purr Endocarditis Congenital heart defects Interference with blood flow or inc turbulence - anaemia, myocardial weakness, extra-cardiac e.g ruminal tympany ```

Question 51

When are valvular stenosis and incompetence murmurs heard in bovines?

Answer 51

``` If pre-systolic (before S1): left or right AV stenosis If systolic (after S1): left or right AV incompetence, pulmonary or aortic stenosis If diastolic (after S2): aortic or poss pulmonary incompetence ```

Question 52

What causes endocarditis?

Answer 52

Needs persistent bacteraemia to occur e.g. after reticulates, nephritis, metritis, mastitis T pyogenes, C chauvoei, E.coli Mycoplasma - contagious bovine pleuropneumonoa Streptococci, staph Mannheimia

Question 53

Clinical signs of endocarditis in bovines?

Answer 53

``` Persistent fever Pain on pinch test HR 100+ Shifting polyarthritis due to emboli Pulsation of mammary veins ```

Question 54

Diagnosis of bovine endocarditis?

Answer 54

Take 20ml blood for culture | Neutrophilia with left shift, increased fibrinogen

Question 55

What congenital heart defects can calves have? How do the murmurs sound?

Answer 55

Ventricular septal defects: often just ventral to aorta, systolic murmur (most common) PDA: machinery murmur by day 5 (uncommon) Patent foramen ovale (uncommon) Tetralogy of Fallot (uncommon) Aortic stenosis (uncommon)

Question 56

Clinical signs of ventricular septal defects in calves?

Answer 56

Range from no effect to stunted growth to sudden death | No cyanosis

Question 57

Clinical signs of PDA in calves?

Answer 57

Exercise intolerance and weakness | No cyanosis

Question 58

What makes up tetralogy of fallot?

Answer 58

VSD Pulmonary stenosis Dextroposed aorta Secondary ventricular hypertrophy

Question 59

Clinical sign of aortic stenosis (persistent right aortic arch) in calves?

Answer 59

Milk regurgitation

Question 60

What can cause myocardial weakness in bovines?

Answer 60

Septicaemia and infection - blackleg, foot and mouth, tetanus Nutritional deficiency - copper, selenium, vitamin E Poisoning - arsenic, mercury, phosphorous

Question 61

What is pericarditis usually associated with?

Answer 61

Traumatic reticulitis

Question 62

Clinical signs of traumatic reticulitis and pericarditis?

Answer 62

Shallow abdominal breathing | Abducted elbows

Question 63

Tests for traumatic reticulitis and pericarditis?

Answer 63

Grunt or Eric Williams test Bar (xiphisternum) test Withers pinch

Question 64

Treatment for traumatic reticulitis and pericarditis?

Answer 64

Surgery Magnets Antibiotics

Question 65

Clinical signs of dilated cardiomyopathy in bovines? Age seen?

Answer 65

``` Peripheral oedema Jugular distension Fluid accumulations in body cavities Enlargement of heart with rounded 'globose' shape Well grown 2-3yo Holsteins ```

Question 66

What is caudal vena cava thrombosis in bovines secondary to? When seen?

Answer 66

Secondary to liver abscess | 1-3yo cattle - acidosis, rumenitis

Question 67

Clinical signs of caudal vena cava thrombosis in bovines?

Answer 67

Peracute - dead in pool of blood | Acute - respiratory distress, pain, pyrexia

Question 68

Clinical signs of respiratory effects of cardiac disease in bovines?

Answer 68

Nasal discharge - oedema, white and frothy Bilateral epistaxis - in pulmonary embolism Tachypnoea, cough - no pyrexia unless secondary infection

Question 69

Clinical signs of adomen effects of cardiac disease in bovines?

Answer 69

Bilateral ventral distension due to ascites - abdominocentesis, ballotment Liver enlargement - palpate right side behind ribs

Question 70

Why is GI disease a common cause of cardiac arrhythmias?

Answer 70

Abdominal distension -> vagal stimulation Acid-base and electrolyte imbalance Pain -> increased sympathetic tone

Question 71

What cardiac degenerative changes can bovines have?

Answer 71

Fatty change - reversible Atrophy Mineralisation - organomercurial posoning Xanthosis - abnormal brown pigmentation of myocardium, esp Ayrshire cattle

Question 72

What are vitamin E and selenium important for?

Answer 72

Needed by certain enzymes as antagonists of free radicals

Question 73

What syndromes can myocardial degeneration and necrosis cause?

Answer 73

Abortion and perinatal mortality Sudden death in neonatal calves Predisposing factors = low bioavailability of Se or Vit E

Question 74

Sudden death differential diagnosis for bovines?

Answer 74

``` Haemorrhage - calving injury, abomasa ulceration from NSAIDs Plant toxicity - yew Lightening Electrocution Hypomagnesaemia Hypocalcaemia Toxaemia - mastitis, metritis Bloat Blackleg Black disease Anthrax ```

Question 75

What is the Older Cattle Disposal Scheme (OCDS)?

Answer 75

Replaced OTMS for cows born in UK before 1/8/96 Market support measure for disposal and compensation Started in 2006 and ended in 2008

Question 76

What is the Over Thirty Months Scheme (OTMS)?

Answer 76

Stopped in 2005 Market support as BSE prevented animals entering food chain Fit for human consumption other than residues, so could be treated and money received

Question 77

What is the rule for emergency slaughter?

Answer 77

An otherwise healthy animal must have suffered an accident that prevented its transport to the slaughterhouse for welfare reasons Vet must be present at time of slaughter

Question 78

Clean livestock policy?

Answer 78

Category 3 = dirty | Category 3 and obove - unable to proceed for normal slaughter

Question 79

How must fallen stock (cattle) be disposed of?

Answer 79

Not burial or open burning Collection by approved transporter for disposal or an approved treatment to a: knacker, hunt kennel, maggot farm, incinerator, renderer Must be tested for BSE if >48mo Animal by products must be transported in covered leak-proof containers/vehicles and be accompanied by a commercial document

Question 80

What is NFSCo?

Answer 80

National Fallen Stock Company Transfers wholly to industry - not for profit Horses too Free membership, £1.75 admin fee per month if service used that month Actual cost charged by approved collector minus any government contribution

Question 81

Who can register as a fallen stock collector? How may they charge?

Answer 81

All premises approved under the Animal by-products regulations Knackers, hunt kennels, maggot farms, renderers, incinerators Can charge by standard container, weight for poultry, headage

Question 82

Anthrax procedure?

Answer 82

Must be an OV authorised to do anthrax tests Farmer informs vet of sudden death Vet phones local APHA office OOH can do test then phone next working day Given reference number if DEFRA want the test Can do private investigation without telling ministry of negative finding but won't be paid APHA tell police and local authority if positive

Question 83

What is ERDP? What happens to it?

Answer 83

Effective rumen degradable protein - any N containing compound Fermented in rumen to produce NH4+ NH4+ used by microbes to produce microbial protein - digested in abomasum and SI Fermentation and protein synthesis require energy If insufficient ME or excess ERDP, NH4+ absorbed across rumen wall -> increased blood urea

Question 84

What is RUDP? What happens to it?

Answer 84

Rumen undegradable protein? Passes through rumen Digested in abomasum and small intestine e.g. Soya

Question 85

How much protein does a dairy cow require? How much protein in grass silage?

Answer 85

14% if not milking (=135-145g DCP/kg BW) 16% if yield <8000L 18% if yield >8000L? 17% if yield 30L/day (=165-175g DCP/kg BW) 18.5% if yield 50L/day (=180-190g DCP/kg BW) Grass silage = 12-18% protein

Question 86

What is metabolisable energy?

Answer 86

Energy available to animal for maintenance, growth, lactation and pregnancy Assumes a healthy rumen and microflora Megajoules per kg of dry matter

Question 87

What is the rumen capacity?

Answer 87

200L+

Question 88

What are carbohydrates fermented to in the rumen?

Answer 88

VFAs - acetate and butyrate (from cellulosic foods), propionate (from starch and sugar foods) CO2 CH4 Speed of fermentation: fibre < starches < sugars

Question 89

What happens to VFAs?

Answer 89

Absorbed across rumen wall (health of papillae important) Enter Krebbs cycle Glucose synthesis from propionate (gluconeogenesis) = 1/3 of energy production

Question 90

DMI BW % for dry/normal, lactating and pregnant cows?

Answer 90

Dry cow: 2-2.5% BW (falls gradually in first 7 weeks, then rapidly falls in last week pre-calving to 1-1.5%) Increases post calving (peaks at 4-10 weeks) - Lactating cow: 3%, or 2.5% BW + 0.1 x yield (L) - Lactating 30L/day: 3% BW - Lactating 50L/day: 4% BW (aim is 4% at peak yield) ``` Correction factors: - Complete diet (e.g. TMR): + 20-30% - Out-of-parlour feeder: + 5-10% - Mixed forages: < 5% - Breed Holstein: < + 20% - Heifers with cows: - 5-10% - Self feed silage: - 5-10% Electric fence at silage face: - 10-20% Poorly preserved silage: - 10-30% Week of lactation: < - 45%  ```

Question 91

What influences ruminant DMI?

Answer 91

Body weight and fatness (fat cows eat less) Milk yield (more milk, eats more) Stage of production cycle Type of food (digestibility/rate of passage) Palatability Access - feed barrier, electric fence etc Availability Social factors e.g. bullying of heifers Stress/pain e.g. lameness Rumen health

Question 92

How much energy does a holstein dairy cow require?

Answer 92

Maintenance: 65MJ Production: 5MJ/L milk Weight gain/loss: 30MJ/kg BW Late pregnancy: 20MJ for early dry period, 40MJ for transition period (average of 30MJ ME/day from 1 month pre calving)

Question 93

What does milk yield depend on?

Answer 93

Genetic merit Nutrition Health

Question 94

What is the generic potential for milk yield of modern holsteins? And what is the national average?

Answer 94

Potential: 13,000L Average: 8,500L

Question 95

What is M/D?

Answer 95

Energy density of food Lower = 'healthier' The more food eaten, the lower the M/D needs to be for milk yield

Question 96

When is peak milk yield reached?

Answer 96

At around 8 weeks of lactation

Question 97

Why are cows in negative energy balance postpartum? What is the target BCS loss? How much is 1 BCS point?

Answer 97

Depressed DMI in first weeks post partum coincides with massive energy demand for milk production Even best fed dairy cows lose weight in early lactation Target loss: 0.5-1 BCS points 1 BCS point = 50kg BW

Question 98

How to maximise DMI in lactating cows?

Answer 98

Maximise intakes in dry period but avoid getting fat Palatable diet - mixed forages Avoid SARA - forage:concentration ratio, change diets slowly (3 week rumen adaptation period) Environment - comfort, feed space, social aspects Health e.g. lameness

Question 99

Aims for M/D for lactating and dry cow diets? Pasture DMI?

Answer 99

Lactating cow M/D: 12 MJ/kg DM Dry cow M/D: 8-8.5 (<10) MJ/kg DM Pasture DMI: no more than 14kg/day

Question 100

DM and M/D of clamp grass silage, maize silage, big bale silage, hay, straw, grass and concentrates? Protein?

Answer 100

Clamp grass silage: DM 30%, M/D 10.5, protein 15% Maize silage: DM 35%, M/D 11.5, high energy, high starch (FME) and low protein (9%), poor fibre source so feed straw/hay with it Big bale silage: DM 30%, M/D 9 Hay: DM 85%, M/D 9 Straw: DM 85%, 6.5 Grass: DM 20% or less, M/D 11 Concentrates: very dry, M/D 12.5, high FME, high proteins, no fibre

Question 101

What different feeding systems are there for lactating cows?

Answer 101

Total mixed ration (TMR) - all food at barrier 24hr/day, complete diet Traditional - silage at barrier and cake in parlour, grazing in summer Hybrid - Buffer feeding - TMR supplement to grazing in summer

Question 102

Features of TMR for lactating cows?

Answer 102

``` All food at barrier 24h/day Complete diet - forage and concentrate is balanced Diet set for given yield e.g. M + 35L Assumes DMI M/D 11.2-12.4 If cow yields more, she can eat more Encourages maximal DMI Constant pH ```

Question 103

Features of traditional feeding systems for lactating cows?

Answer 103

``` Grass silage fed at barrier May get mid-day feed on top of silage Cake in parlour - fed to yield Grazing in summer Peaks of acidity after milking ```

Question 104

Features of a hybrid feeding system for lactating cows?

Answer 104

TMR at barrier and cake in parlour

Question 105

How to monitor a cow''s nutritional status?

Answer 105

Observation - BCS changes, DMI, cudding, rumen fill, faeces, cleanliness, long time Production? Milk quality - monthly recording, milk protein (low = energy deficit), butterfat (low = lack of fibre, high = high fibre diet, very high in early lactation as excessive fat mobilisation) Biochemistry - metabolic profiles (ideally 12 cows/group, interpret using thresholds ie how many out of 12 are over threshold value)

Question 106

What metabolic profiles can be used to assess the nutritional status of a cow? When to test? Cut offs and targets?

Answer 106

``` BHOB (a ketone body) - fresh cows (5-50 DIM) - suggestive of NEB - cut off >/= 1.4mmol/l (target is <10% of cows, 0.9mmol/l in UK) NEFA (evidence of fat mobilisation) - dry cows 2-14d before calving - cut off >/= 0.4mmol/l (target is <10% of cows) Urea - palace of protein and FME ```

Question 107

How to assess a feed?

Answer 107

Smell, consistency Evidence of sorting (need long fibre 1-4in long, will sort and select if too long) Paper analysis (M/D) Feed surface Feed barrier Should always be food in front of cow DM - rule of thumb 25% easily squeeze water out, 30% cannot squeeze water out

Question 108

What is the four diet model?

Answer 108

Should all be the same: - diet formulated by nutritionist - diet mixed by farmer - diet received by cows - diet cows require

Question 109

What factors affect the four diet model?

Answer 109

``` Dry matter content Reliability of feed analyses Farmer tinkering e.g. adding extra fodder Farmer weighing and mixing Feed barrier space DMI estimates used in calculations ```

Question 110

What should the fodder:concentrate ratio be for feeding cows? How slowly should a diet be changed? What is slug feeding?

Answer 110

concentrate/fodder maximum 60:40, 40:60 better Change diets over 3 weeks Slug feeding = max 2kg cake in one feed (avoid Dolly Parton effect)

Question 111

Average calving index? How long is the dry period? Lactation period?

Answer 111

Calving index 370-400 days 60 day dry period 305-340 day lactation period

Question 112

Why should you avoid cows getting fat in the dry period? What BCS is the aim for calving?

Answer 112

Will depress appetite | Aim to calve at BCS 2.5-3

Question 113

What happens to the cow's body during the dry period?

Answer 113

Mammary regeneration | Rumen development - large and muscular, big healthy papillae, suitable bugs for post-calving diet

Question 114

What to feed in the first 5 weeks of the dry period? Why?

Answer 114

``` Low energy, high fibre About 1.5-2% BW DMI (10-14kg/day) Energy requirement = 90-100MJ M/D 7.5-8.5 MJ/day High fibre for rumen health Excessive energy at this time will suppress production and deposition of visceral fat? (suppress appetite, predispose to metabolic disease in lactation) Options: - Grass silage and straw (4-5kg straw) - Big bale silage - Hay - Grass but will get fat if not limited intake, so supply straw (3-4kg/day) and stock densely (5 cows/acre with sward height 7cm) ```

Question 115

What to feed in the last 3 weeks of the dry period?

Answer 115

= transition diet DMI declining Energy requirements increasing: 110=140MJ/day M/D 9.5-10 MJ ME/kg DM Crude protein 13-15% Options: - Custom made - High yielder TMR diet diluted with straw/hay - Silage and straw and dry cow concentrate, dry cow mineral (high Mg, low Ca)

Question 116

What is the 'Keenan' diet?

Answer 116

New strategy for dry cow feeding? One diet for whole of dry period Low energy 'Goldilocks diet': 95-100MJ/day, in 12-13 kg DMI, M/D 8-8.5 Chopped straw essential (2''): 8-10kg/head/day Adequate feed space - cows must eat a lot Reduces social stresses - no moves

Question 117

Dry cow management? What is done? Housing?

Answer 117

Stop milking Teat sealant/dry cow tube - sterile Move to dry cow group Move to calving pen in early second stage earlier (not earlier - stress) Or calve in group pen - Johne's risk etc Loose yard housing (1.3sq metre/1000L), large luxury cubicles (sand bed) - comfort important Adequate feed barrier space (at least 90cm/cow), ideally more space and cubicles than needed High comfort, low stress, low energy

Question 118

What is Fat Mobilisation Syndrome (FMS) in early lactation? Potential cause?

Answer 118

Energy deficit (negative energy balance) -> excessive mobilisation of fat for energy 'Fatty liver' Similar to diabetes type 2 - insulin resistance Obesity: Decreased DMI in dry period and early lactation - increased weight loss in early lactation, reduced milk yield

Question 119

Fat distribution in cows?

Answer 119

``` Subcutaneous fat - more in beef cows, fresians Visceral fat (hidden) - more in holsteins, channel island ```

Question 120

Problem with overfeeding during dry period?

Answer 120

Little increase in CS but omental, mesenteric and peri-renal fat (visceral fat) increases by 55-80% Decreased immune function - endometritis, mastitis Risk factor for metabolic syndrome

Question 121

BCS interpretation?

Answer 121

<3 fit >3 obese A measure of subcutaneous fat (visceral fat greater risk for FMS)

Question 122

Problems associated with post natal depression?

Answer 122

``` Milk fever RFM/metritis/endometritis Mastitis Displaced abomasum Ketosis Fertility Lameness ```

Question 123

What bugs are in the rumen?

Answer 123

Archaea - methanogens Bacteria - mostly G+ve (and bacteriophages) Fungi Protozoa

Question 124

What is the normal pH of the rumen? What happens if it falls?

Answer 124

pH 6-7 Low pH kills normal bug population and encourages growth of lactobacilli - produces lactic acid (cannot be metabolised) Efficiency of digestion falls if pH falls Low pH destroys papillae - rumenitis Undigested particles pass through to handout and fermented Osmotic diarrhoea (loose faeces) Colonic acidosis - damage to colon wall (fibrin casts in faeces)

Question 125

Factors affecting rumen pH?

Answer 125

How much acid (VFAs) produced Type of acid produced (lactic acid is strong) Rate of fermentation (fibre is slow, concentrates fast) Rate of acid removal (absorption across rumen wall by papillae) Buffering by saliva - chewing the cud

Question 126

Amount of saliva produced by a healthy cudding cow? How many cows should be cudding at any time?

Answer 126

3.5kg/day - produced when chewing long fibre 70% Contains sodium bicarbonate

Question 127

What causes rumen acidosis?

Answer 127

Excessive concentrates - FME Insufficient fibre -> reduced saliva flow, increased acid -> rumen pH decreases D lactic acid - cannot be metabolised, builds up

Question 128

Why is long fibre good?

Answer 128

Encourages cudding - bicarbonate buffers acid | Forms a rumen mat - keeps food particles in rumen to be digested, home to bug biofilms

Question 129

When is sub-acute rumen acidosis (SARA) seen? Signs?

Answer 129

'Dolly Parton' effect of large concentrate feeds Herd problem, 30% of animals at risk, pH<5.5 Energy deficit - excess weight loss Overall poor health Loose soft faeces - variable (some cows ok, some loose) Swishing tails (sore bums) Undigested grain and long fibre present in faeces

Question 130

Effects of SARA?

Answer 130

Reduced DMI Reduced digestibility - reduce energy intake, NEB Reduced milk yield Reduced milk quality - butterfat may be low (not always), variable milk protein Reduced fertility - not seen bulling, poor conception rates Immunosuppression - disease susceptibility Health - displaced abomasum (VFAs enter abomasum and cause atony), digestive upsets, ketosis, lameness (subclinical laminitis, ulcers, white line lesions), mastitis, infections - endocarditis

Question 131

Diagnosis of SARA?

Answer 131

Clues - fertility, lameness, ketosis, LDA, faeces, odd sick cows Observe - cudding, tail swishing, dirt score, BCS (dry->peak >0.5 loss) Faeces - score 1-5, sieve faeces under running water (fibre >0.5in long, undigested grain, mucus casts) History - nutritional management Measure rumen pH (2-4h after feeding), <5.7

Question 132

Selecting cows for sampling rumen pH?

Answer 132

Cows calved 14-21 days: still adapting to ration, DMI not yet maximal, assesses transition and early management Cows calved 60-80 days: should have adapted to ration, maximal DMI, assesses overall diet quality Sample 6 cows per group Record parlour cake fed Diagnosis when 2 cows from either group are below threshold pH

Question 133

Technique for sampling cow's rumen pH?

Answer 133

``` Restrain cow - nose and tail Site = level of stifle & 6-8in behind last rib Clip and scrub Local anaesthetic 3-5in needle, 16-18G Read sample immediately ```

Question 134

What does grass silage quality depend on?

Answer 134

``` Grass type First or second cut Time of day (pm best for sugars) Moisture content Chop length Compaction in clamp Fermentation ```

Question 135

Pathophysiology of acute ruminal acidosis?

Answer 135

``` Excessive acid production pH falls below 5 Lactic acid production predominates Lactic acid eating bugs killed off Cow cannot metabolise D lactate ```

Question 136

When does acute ruminal acidosis occur?

Answer 136

Overeating grain - barley poisoning Sudden introduction of high levels of grain e.g. barley beef Can occur in sheep - pre-lambing as farmer increases concentrate feed

Question 137

Signs of acute ruminal acidosis?

Answer 137

``` Often group problem Varying severity Ataxia Distended rumen +/- bloat Diarrhoea - profuse and smelly Depression Recumbency and shock Mild: almost normal ```

Question 138

How do the clinical signs progress from sub-acute to peracute ruminal acidosis?

Answer 138

Sub-acute: fairly bright, eating, no ataxia Acute - ataxia, anorexia, dilated pupils Peracute - severe ataxia or recumbency, apparently blind, severe dehydration

Question 139

Treatment for ruminal acidosis?

Answer 139

Mild - give hay to eat and observe Subacute - oral antacids (magnesium hydroxide or carbonate), feed hay Peracute - rumenotomy (empty rumen contents), 5L 5% sodium bicarbonate IV, continue with balanced fluids for 12-24h, calcium boroglucoronate NSAIDs Antibiotics Restrict water intake for 12-24h

Question 140

Prevention of ruminal acidosis?

Answer 140

Close door on feed store Care with introduction of grain to fattening animals Good fibre source Correct mixing of diets

Question 141

Rumenotomy?

Answer 141

``` Life saving emergency surgery Recumbent animal 18in incision at least Pack towels around Open rumen and empty all contents Not a sterile operation ```

Question 142

What syndromes are caused by deficiencies of the trace elements: copper, selenium, cobalt, iodine and iodine and selenium?

Answer 142

Copper - swayback, coat colour, falling disease Selenium - white muscle disease, cardiomyopathies Cobalt - reduced growth, wool changes 'pine' Iodine - weak neonates Iodine and selenium - 'stillbirth/weak calf syndrome'

Question 143

Who is at risk of trace element deficiencies?

Answer 143

Animals at pasture and not getting concentrates (concentrates all supplemented and increase absorption from gut) - beef cows and calves - fattening cattle - New Zealand style dairy cows - Dairy heifers prior to first calving if at pasture

Question 144

What causes copper to be bound up in the rumen? Where is it stored? What does toxicity cause? Sheep breed susceptibility?

Answer 144

Bound up in rumen by Mo (thiomolybdates), Fe Stored in liver Toxicity: haemolytic crisis - jaundice and death Genetic susceptibility to deficiency and toxicity in sheep Texels - susceptible to toxicity but not deficiency Scottish Blackface - susceptible to deficiency but not toxicity

Question 145

Do dairy cows need copper supplementing?

Answer 145

No - not associated with fertility (myth causing problems!) | Can cause toxicity if over-dosing

Question 146

Diagnosis of trace element deficiencies?

Answer 146

History - at pasture with no supplements Blood samples: - Se: GSHPx tells us about 60d ago - Cu: tells us how much is being transported (not how much in liver, always check liver biopsy before supplementing dairy cows) - Co: vitamin B12 - Iodine: PII (and thyroid weight and histopathology)

Question 147

How to do a liver biopsy to check copper status in cull cows?

Answer 147

``` Very easy and safe Right flank Biopsy needle Rib space 11 20cm below lumbar process ```

Question 148

Methods of supplementing trace elements for cows?

Answer 148

``` Drenches - short duration Injections: - Cu for sheep (swayback), toxicity risk with some - Co unlicensed - Co: vit B12 - short duration Rumen boluses (Cu, Se, Iodine, Co) Copper oxide boluses (releases particles into abomasum) Flank painting iodine - 7d duration ```

Question 149

Age Johne's seen? When? Clinical signs?

Answer 149

``` Older animals >3yo (age depends on pathogen load, long incubation period) Low infective dose Often after calving (stress) Profuse diarrhoea (often with bubbles) Weight loss Remains bright and eating "Bottle jaw" Individual cases ```

Question 150

What subclinical losses of Johne's are there? What % of losses are subclinical?

Answer 150

``` >50% of total losses are subclinical Reduced milk yield: give 4000kg less milk over lifetime, milk production reduces in second lactation Mastitis and high SCC: 2x more likely Infertility Lameness: 5x more likely LDA and pneumonia etc: 1.8x more likely Increased culling rate ```

Question 151

When are cows infected with Johne's? Route of transmission?

Answer 151

Infection acquired during early life Baby calves at biggest risk (80% is new born calves 0-4 weeks) Calves <12mo at risk (10% young heifers, 5% older heifers and cows) Infection of adults possible but unlikely Oro-faecal major route of transmission: dirty environment (calving area), faeces on teats Dam colostrum, pooled colostrum and waste milk (risk most likely in high and super shedders) Calf to calf (0-8 weeks, until CMI mounted) Also via uterine infection (5% of cases)

Question 152

How many cows are infected with Johne's for each clinical case? How many will be infectious? What are the stages of Johne's infection? How many animals at each stage if 1 at stage 4?

Answer 152

15-25 infected animals (most will never develop the disease) At least 30% infectious Stage 1: silent infection - calves, youngstock (10-14 animals) Stage 2: sub-clinical disease - shedders (4-8 animals) Stage 3: early clinical disease - shedders (1-2 animals) Stage 4: advanced clinical disease (1 animal)

Question 153

Immunology of Johne's?

Answer 153

Infected as calf MAP in macrophages - forms granulomas in ileum CMI response is protective: halts disease progression If CMI (TH1) fails, get TH2 response = Abs produced, which further suppresses CMI TH2 response is not protective so MAP proliferates and disease progresses (likely infectious at this point) Anergy = end stage when complete loss of immune control Susceptible -> infected but not infectious (CMI controlling infection)-> infectious (CMI lost control, Ab positive) -> resistant So clinical disease coincides with Ab rise and CMI decline Ab response can wax and wane

Question 154

How much of a risk are super shedders of Johne's?

Answer 154

``` 1 million cfu/g faeces 50kg faeces/day 50 billion cfu/day Infective dose is 100,000 cfu So could theoretically infect 50,000 calves ```

Question 155

Diagnosis of Johne's? Pros and cons? Se? Sp?

Answer 155

Clinical signs Faecal culture: - gold standard in live animal - 50-60% se against PME - detects shedders (those infectious) - +ve result in 10 days - -ve result in 3 months - expensive Faeces PCR: high se and sp ELISA: - detects Ab - highly likely to be shedding - se depends on age distribution (older = more likely Ab +ve) and stage of disease process (85% se in clinical case) - 30-40% se in adults >2yo against faecal culture - poor for detecting infected, good for infectious Actiphage - new, not yet in use, very sensitive, potential use on blood Gamma interferon - detects CMI, sp poor, se should be good for early infection

Question 156

Control of Johne's?

Answer 156

Reduce transmission to young stock by: 1. Reducing risk factors (improved farm management (IFM)): - key time is calving - snatch calving - individual calving pens (clean and disinfect in between cows) - calf pens/hutches - keep youngstock separate from adults - only feed dam's colostrum, no pooled colostrum (frozen colostrum from heifers or test -ve cows only), pasteurise? - clean collection of colostrum (teat clean and dip) - no waste milk feeding - avoid slurry and manure on grazing - avoid watercourses - esp stagnant ponds - avoid contamination of feed 2. Culling animals likely to be shedding (test and cull) - annual ELISA of all adults >2yo, cull all positives and recent daughters - ELISA se 30-40% - likely to fail if done alone so also need IFM - duration between tests - problems = poor ELISA se, duration between tests 3. Test and manage - repeated ELISAs to assess probable risk of individuals - milk or blood ELISAs 4x/year (frequent testing increases se) - traffic light system: green is currently non infectious, red is high risk - less time between tests for infectious animals to shed - reduced sp (more false +ves) - must use IFM too

Question 157

Control of Johne's for beef suckler herds?

Answer 157

Only applicable if rear replacements Breed problems - Welsh Blacks, Limousin IFM: - outdoor calving or move outside immediately after calved - cull daughters - clip and clean teats before calving - purchase bulls from CHECS low risk herds (level 1)

Question 158

Options to avoid Johne's when purchasing stock?

Answer 158

From low risk herds: no history of disease, tested negative on at least 3 occasions, CHECS level 1 ELISA test whole herd e.g. for bull purchase ELISA test or faecal culture individual animal (culture better, false confidence?)

Question 159

Johne's vaccination? Pros and cons? When?

Answer 159

``` Killed or live Doesn't prevent infection Induces CMI and Abs Reduces incidence of clinical disease and shedding Interference with TB testing Risk of granulomas Administer between 1-28d in brisket ```

Question 160

Johne's and Crohne's? Evidence of link? Sources? Genetics?

Answer 160

PCR evidence from biopsies Similar pathology Milk and milk products - pasteurisation is not 100% Meat products Water Genetics 'immune dysregulation' - failure of recognition and inappropriate responses

Question 161

How do MAP and M.bovis affect each other?

Answer 161

Cross reaction MAP and TB test (mammalian) -> false positive?? MAP and TB test (avian) -> false negative (reason to control MAP)?? TB test and MAP ELISA -> false positive (need 60d gap) MAP vaccine and TB test

Question 162

What is milk fever? When seen? Why happens?

Answer 162

Hypocalcaemia +/- hypophosphataemia Dairy cows at/after calving (uncommon at other times) Increased risk with increasing parity (3rd onwards) Drain on Ca due to colostrum/milk demands Failure to mobilise Ca from bone

Question 163

Homeostatic control of Ca?

Answer 163

PTH: mobilisation of Ca from bone stores, increased absorption from gut (requires Mg2+ to function) Calcitonin: reduces Ca absorption and availability Vitamin D3: increased absorption from gut

Question 164

What are the two forms of Ca in the blood? Ratio?

Answer 164

Bound (mostly to albumin) Ionised Ca2+ - active pH dependent (reduced binding with reduced pH) 50:50-60:40

Question 165

Roles of Ca2+ in the body?

Answer 165

Muscle function Nerve impulses Immune response

Question 166

Clinical signs of acute milk fever?

Answer 166

At/after calving Initial hyper-excitation, tremors Muscles stop working - recumbent Guts/glands stop working - no faeces/urine, dry nose, bloat, slow pulse/HR (or fast!) Can be complicated by concurrent hypomag/hypophos

Question 167

Differential diagnoses of recumbent cow after calving (Downer cows)?

Answer 167

Milk fever - no faeces/slow, normal, fast HR, normal/low temp, should respond to Ca Milk fever and hypophosphataemia - needs Ca and Phos Acute coliform mastitis - high pulse/HR, high/normal/low temp, endotoxaemic (conjgested mucous membranes), +/- diarrhoea Botulism Other acute disease e.g. salmonella Injury at calving: - nerve damage - femoral, obturator (muscle damage within 24h, prognosis worsens with time) - femoral head - ligament trauma Could be more than one!

Question 168

How does hypophosphataemia complicate milk fever?

Answer 168

'Downer cows' | Unable to rise fully unless given P - can add Foston IV to Ca boroglucoronate

Question 169

Treatment of hypocalcaemia (milk fever) in cows?

Answer 169

Slow IV Ca boroglucoronate 40% Often complicated by hypophos so also Foston IV (organic phosphorous) - won't harm if not hypophos SC Ca - little use as slow absorption Place in sternal recumbency to prevent bloat

Question 170

Problems with subclinical hypocalcaemia?

Answer 170

Risk factor for other diseases: - immune function depressed - coliform mastitis - metritis/endometritis - post-partum depression

Question 171

Prevention of milk fever?

Answer 171

``` "tone up the parathyroids" Feed low Ca diet pre-calving Feed high Mg pre-calving Boluses at calving? Maximise DMI pre-calving DCAD diets: - aim for negative DCAD before calving - induces a compensated metabolic acidosis - but grass based diets are high K - generally does not work in UK - DCAD = Na + K - Cl - S ```

Question 172

What is hypocalcaemia associated with in sheep? Main sign?

Answer 172

Not after lambing Associated with DMI fall Pre-lambing stress- movement, bad weather, inadequate feed barrier Recumbent ewes (often many)

Question 173

Where is Mg stored in the body?

Answer 173

No body stores

Question 174

Output and inputs of Mg?

Answer 174

Output: milk Input: diet (absorbed in rumen, reticulum, omasum) High K+ reduces absorption - lush grass, fertilisers

Question 175

Clinical signs of hypomagnesaemia in cows?

Answer 175

``` = grass staggers Peracute/acute - often found dead Early - twitchy and hypersensitive Recumbent and convulsive (emergency) Signs of convulsions on grass/mud Sheep usually found dead ```

Question 176

Risk factors for hypomagnesaemia?

Answer 176

Lush pasture - especially after fertiliser application High output (milk) Stress - weather, movement, handling - spring: dairy cows and twin bearing ewes - autumn: suckler cows with large calf at foot

Question 177

Treatment for hypomagnesaemia?

Answer 177

Emergency Be quiet - risk of setting off convulsions Control convulsions - IV xylazine licences to effect, pentobarbitone unlicensed to effect Ca 40% IV then slowly give up to 200ml MgSO4 IV If not recumbent, bottle of MgSO4 SC (multiple sites)

Question 178

Prevention of hypomagnesaemia?

Answer 178

``` Move off affected pasture (but stress) Give additional Mg: - dairy cows: high Mg cake - beef cows: mineral supplements, Mg boluses, wean calves (big stress though), give straw Don't make things worse by stressing ```

Question 179

What does lipolysis of adipose tissue produce?

Answer 179

NEFA (energy source) | Glycerol

Question 180

Where are ketones produced? What for?

Answer 180

Liver (from NEFA metabolism) Energy source for muscle Feedback regulator for lipolysis

Question 181

What does insulin cause?

Answer 181

Glucose entry into cells Decreased liver gluconeogenesis Suppresses NEFA entry to mitochondria and ketogenesis Stimulates lipogenesis in adipose tissue and in liver

Question 182

How do adrenaline/noradrenaline affect fat?

Answer 182

Stress -> stimulates lipolysis and NEFA release

Question 183

How is lactose synthesised in the udder?

Answer 183

From glucose from propionate and oxalo-acetate

Question 184

What causes increased production of ketones -> ketosis?

Answer 184

Insufficient propionate from rumen -> insufficient oxaloacetate -> acetyl CoA formed from fat mobilisation and acetate/butyrate cannot enter Kreb's cycle AcCoA metabolised to ketones (acetone and B-hydroxybutyrate)

Question 185

Clinical signs of clinical ketosis?

Answer 185

Reduced milk yeild Selective appetite - refuses concentrates Ketone bodies in blood - smell, Rothera's on milk, Ketostix Firm faeces - shiny Nervous ketosis - hyper-excited, twitchy, maniacal licking (Ddx hypomag, listeriosis, BSE)

Question 186

Treatment of clinical ketosis?

Answer 186

``` Propylene glycol (oral) Corticosteroids - dexaforte Glucose 40% IV Combination of above Vitamin B12 (supportive) ```

Question 187

When is subclinical ketosis seen? Diagnosis?

Answer 187

Early lactation: 5-50DIM BOHB in blood - target is <10% of at risk cows >1.4mmol/l NEFA in blood - dry cows in last 14 days before calving, target is <10% of at risk cows with >0.4mmol/l?, indicates fat mobilisation

Question 188

Key periods to monitor BCS changes?

Answer 188

``` Dry period Early lactation (target is 0.5 CS lost from dry period to early lactation, rarely achieved) 100 days prior to dry off - allows changes to be made ```

Question 189

Ideal targets for BCS in dry period, drying off, mid lactation and early lactation?

Answer 189

Dry period: 2.5-3 Drying off/calving: 2.5-3 Mid/late lactation: 2-3 Early/peak lactation: 2-2.5

Question 190

Prevention of FMS/ketosis?

Answer 190

``` Feeding in dry period: Low energy Maximise DMI - comfort, palatable food, food at all times Monitor BCS Avoid fat cows ```

Question 191

What abomasal disorders are there? What type of cows and feed are abomasal disorders associated with? What is the primary event?

Answer 191

Dilation and displacement - LDA, RDA Abomasal ulcers Geo-sedimentum abomasi (sand) Associated with high yield and concentrate feeding Primary event is abomasal atony - excessive VFA, inflammatory cytokines inhibit motility

Question 192

Risk factors for abomasal disorders?

Answer 192

``` Usually seen in early lactation Traditionally in housing (but also seen at grass) 'Imbalance of fibre and concentrate' - SARA Associated with ketosis and FMS Hypocalcaemia Concurrent inflammatory disease Cow comfort, lameness Ie anything that reduces DMI ```

Question 193

Target incidence for LDAs? Clinical signs? How does it sound?

Answer 193

0% - may accept 1-2% per annum Most common abomasal disorder Reduced milk yield - insidious Ketosis Selective appetite - prefers fibre Usually 0-4 weeks post calving Spontaneous tinkling and gurgling (shake her up) Tap rib hard -> resonant ping (indicates gas-fluid interface) Absence of rumen sounds over displaced abomasum Fat cows - no ping

Question 194

Differential diagnoses for signs caused by LDA?

Answer 194

Vagal indgestion Peritonitis Gas in rumen (starved cattle/bloat) May get LDA + another condition

Question 195

What happens to cause an LDA?

Answer 195

Abomasum is fixed by the omasum, duodenum and omentum but the middle portion is able to travel As rumino-reticulum contracts, abomasum buoyed by gas works its way to left side

Question 196

Rolling for LDA - how? Advantages and disadvantages?

Answer 196

Cast - right lateral recumbency, then roll to dorsal, then roll to left lateral Give good quality roughage Advs - cheap, non invasive, concurrent disease Disadvs - least successful, ulcer rupture

Question 197

Toggling for LDA - how?

Answer 197

Place sutures where abomasum naturally lies Clip up - avoid major abdominal blood vessels Cast - dorsal recumbency Auscultate Caudal toggle position - 6'' behind xiphoid, 2'' to right Knee in abdomen to push abomasum forwards Push trochar firmly into abomasum, place caudal toggle and clamp Cranial toggle placed 4'' cranial to first suture, let gas escape - knee in abdomen to push abomasum forwards and expel gas Tie toggles together loosely Roll over

Question 198

Advantages and disadvantages of toggling for LDAs?

Answer 198

Advs - cheap, minimally invasive, relatively straight forward, quick Disadvs - going blind, fistula formation, risk of getting kicked

Question 199

Left to right/bilateral flank surgery for LDA - how?

Answer 199

``` One person on each side Para-vertebral Incision 5cm caudal to last rib Both slide hand down wall of abdomen and shake hands Decompress abomasum - manual/needle Push abomasum to midline Pull up to right incision Omentopexy ```

Question 200

Right side (omentopexy) surgery for LDA - how?

Answer 200

Right flank incision Put hand over rumen in backwards direction and feel top of abomasum on L side (14G needle on tubing to release most of gas) Withdraw arm Put arm in abdomen - follow right body wall down and under to left side Identify abomasum (slight gas still in it) Grasp abomasum/omentum securely Firmly pull to incision Identify the pylorus - 'sows ear' Omentopexy using omentum near pylorus Stitch the omentum by pylorus into wound closure

Question 201

Left sided omentopexy/abomasopexy (Utrecht method) surgery for LDA - how?

Answer 201

Left sided incision Grasp greater curvature of abomasum or omentum Weave suture through omentum or abomasum - leave 2 long ends (3ft) Decompress abomasum with 14G needle and tube Attach needle to first thread (cranial) Take down along body wall to right ventral midline site (assistant guides from outside with forceps) - 4'' caudal to xiphoid, slightly right, avoid milk veins and other veins Penetrate body wall with needle - unthread needle Repeat with caudal suture (4'' caudal) Replace abomasum as assistant 'takes in' sutures Tie sutures tight - make sure no guts trapped

Question 202

Ventral abdominal paramedian surgery for LDA - how?

Answer 202

``` Sedation/full GA Dorsal Line block Incise where abomasum normally lies Locate abomasum - should have returned Using catgut, 4-6 mattress suture through abomasum wall, peritoneum and abdominal wall Suture up ```

Question 203

Post-op care for LDA surgery?

Answer 203

``` Antibiotics? Pen/Strep OTC Treat underlying conditions - ketosis: propylene glycol - endometritis etc High fibre diet ```

Question 204

Which method to use for LDA?

Answer 204

Toggle - quick and cheap Both sided surgery - technically easier, needs 2 vets Utrecht - anatomically correct Right sided - technically harder Paramedian - anatomically correct but GA, can see ulcers etc

Question 205

Aetiology of RDA? Pathogenesis?

Answer 205

Not fully understood Similar to LDA Progression: dilation and distension -> displacement -> torsion Dilation and displacement: atony/distension/displacement caudally on right side, dilatation phase may last few days Increased luminal pressure causes mucosal damage Volvulus phase: clockwise torsion of abomasum (vertical plane around horizontal axis) -> ischaemic necrosis

Question 206

Metabolic sequelae of right abomasal dilatation?

Answer 206

Pooling of H+ and Cl- in abomasum (Upper intestinal obstruction) - metabolic alkalosis, hypochloraemia 35-50L in abomasum Dehydration

Question 207

Metabolic sequelae of right abomasal displacement and torsion?

Answer 207

Mucosal damage Cytokine release and endotoxaemia Metabolic acidosis Severe dehydration

Question 208

Clinical signs/exam findings of dilatation and displacement phase of RDA? Torsion?

Answer 208

``` Inappetent/depressed Reduced faeces Dehydrated Tachycardia Pale and dry mm Doughy rumen Reduced rumen turnover Ping (middle to upper 1/3rd abomasum) Tense viscus rectally Torsion phase - much sicker, severe dehydration ```

Question 209

Differential diagnoses for signs seen with RDA?

Answer 209

Abomasal impaction Caecal torsion Traumatic reticulitis Intestinal obstruction

Question 210

Treatment for RDA?

Answer 210

``` Dilatation and displacement: - medical: Ca 40%, metaclopramide, fluids - surgery: drain and replace Torsion: - slaughter - surgery ```

Question 211

Surgery for RDA - how?

Answer 211

``` 5L HTS fluids pre-op Balanced fluids during surgery Purse string suture Tube Drain Leave some fluid as indicator Rotate abomasum Watch duodenum Anchor pylorus Stitch up ```

Question 212

Post op care after RDA surgery?

Answer 212

``` Hartmanns fluids 50-100L NSAIDs Antibiotics Oral KCl (50g daily) Ca 40% Propylene glycol ```

Question 213

Prevention of LDAs/RDAs?

Answer 213

Better dry cow management!

Question 214

History for caecal dilation and volvulus?

Answer 214

``` Dairy cows 1st few months of lactation Inappetant Decreased milk yield Ping in upper right flank Rectally: distended, recognisable viscus ```

Question 215

Aetiology of caecal dilatation and volvulus? Pathogenesis?

Answer 215

Excess carbohydrates which are fermented in caecum -> increased VFA, reduced pH -> caecal atony -> accumulation of ingest and gas Pathogenesis: atony, dilatation, torsion Volvulus - blind end is rotated cranially, body is distended Torsion - can occur with volvulus, twists longitudinally

Question 216

Clinical signs of caecalo dilatation? And volvulus?

Answer 216

``` Anorexia Mild abdominal discomfort Reduced milk yield Reduced faeces Ping (rt lumbar fossa) May be incidental finding Volvulus - as above and dehydration, tachycardia and abdominal pain ```

Question 217

Rectal exam findings for caecal dilatation and volvulus?

Answer 217

Distension: long cyclindrical moveable organ, blind end points to pelvic canal Volvulus - points cranial and lateral or medial

Question 218

Treatment for caecal dilatation and volvulus?

Answer 218

Medical treatment if simple dilatation: good quality hay and TLC Surgery asap if volvulus as serious (necrosis of caecum): - Caecotomy - Determine if torsion - Purse string suture - Small incision - Milk caecal contents out - Once deflated, correct torsion and suture up

Question 219

Post-op care for caecal dilatation and volvulus? Recurrence rate?

Answer 219

``` Antibiotics Feed long fibre TLC Good prognosis 11-13% recurrence rate in first week 25% recurrence rate long term ```

Question 220

Causes of abomasal ulcer?

Answer 220

``` Early lactating dairy cows: - stress of lactation - high levels of grain - increased incidence at grass? Mature bulls and feed lot cattle: - stressful events (transport, surgery, fractures) Handfed calves - common at weaning Secondary to LDA, RDA, vagal indigestion ```

Question 221

Pathogenesis of abomasal ulcers?

Answer 221

Injury to gastric mucosa -> diffusion of H ions into tissue -> damage

Question 222

Abomasal ulcer types?

Answer 222

``` Type 1: - non perforating - minimal amounts of intra-luminal haemorrhage Type 2: - major blood vessels perforates - severe blood loss - melena Type 3: - perforating ulcer - acute, local peritonitis - peritonitis localised by greater omentum Type 4: - perforating ulcer - diffuse peritonitis ```

Question 223

Where are ulcers most likely found in the abomasum?

Answer 223

Cattle: fundic Calves: pyloric

Question 224

Clinical signs of abomasal ulcers?

Answer 224

``` Abdominal pain Melaena Pale mm Sudden onset anorexia Tachycardia Perforation - hypovolaemia, unable to stand ```

Question 225

Treatment for abomasal ulcers?

Answer 225

Generally conservative Antacids: Mag oxide Blood transfusions/fluids if Hct<12% - 20ml/kg BW, shock fluids 10ml/kg/hr Surgical excision - midline, excise or over sew, cost effective? keep away from NSAIDs or steroids

Question 226

Signs of oesophageal obstruction?

Answer 226

``` Cervical oesophagus above larynx, base or heart/cardia, Inability to swallow Regurgitation of feed and H20 Salivation Bloat Stop eating Anxiety/retlessness ```

Question 227

Aetiology of oesophageal obstruction?

Answer 227

Intra-luminal - potatoes, turnips | Extra-luminal - pressure by surrounding organs (mediastinal abscesses, tuberculous LN)

Question 228

Treatment for oesophageal obstruction?

Answer 228

``` Conservative approach, many self resolve - starve and observe - sedate - buscopan - flunixin Manual removal - gag and pass hand to back of larynx, assistant push FB up Cardia - push into rumen with probing, care of strictures/diverticula If unsuccessful: - trocharise rumen - feed via rumen - wait until obstruction passes ```

Question 229

History/signs of traumatic reticulitis? Progression?

Answer 229

``` Sudden milk drop - e.g. 20L to 5L Hunched up appearance - abducted elbows Stiff gait Inappetent Often fed a TMR Increased temp 39.5C Reduced rumen contractions Dull, depressed Tachycardic Very ill - 'toxic' Heart sounds - initially pericardial rub, later very quiet/absent, 'washing machine sounds' Heart failure develops: - distended jugular veins - visible jugular pulse - sub-mandibular oedema - hopeless prognosis ```

Question 230

Where does the reticulum lie?

Answer 230

Opposite 6-8th rib on LHS

Question 231

Rumen contraction timings? Types? How does it sound?

Answer 231

3 rumen/reticulum contractions in 2 minS Primary cycle: no sound, feel rumen contract - biphasic - mixing cycle - contraction of reticulum then contraction of rumen Secondary cycle: feel rumen contract, then hear eructation - rumen contraction - starts in caudal rumen - pushes gas to cardia - eructation Primary:secondary 2:1 (varies)

Question 232

Diagnosis of traumatic reticulitis?

Answer 232

Eric Williams Test (+ve early on, -ve later on when lesion walled off) - listen over trachea, feel rumen contractions in left flank, pain on reticular contraction can cause: - reduction in primary cycles - grunt immediately prior to primary cycle - breath holding prior to primary cycle - very subtle Withers pinch - abdominal pain Pole test - abdominal pain (localise) Faeces - stiffer with long fibre, individual cow not group (SARA) WBC count - non-specific, neutrophilic and left shift (more neutrophils than lymphocytes) Metal detector Exploratory rumenotomy

Question 233

Causes of traumatic reticulitis?

Answer 233

``` From tyres - fall into feeder wagons Perished tyres Baling sheep netting Nails fall into mixer wagons etc Old fencing wire (not fussy eaters!) ```

Question 234

Consequences of swallowing a wire?

Answer 234

``` If no penetration - no effect Penetration - local reticulo-peritonitis - ventral/lateral = better prognosis - medial = damage to vagus, abscess in medial wall, no pain receptors - pericardium - pericarditis - other organs - lungs, spleen etc - generalised peritonitis ```

Question 235

Exploratory rumenotomy for traumatic reticulitis?

Answer 235

``` Left sub-lumbar fossa Incise Palpate abdomen Exteriorise cranial portion of rumen 2 bone pins act as anchors Sterile towels as a seal around rumen Incise rumen Hand forward Locate reticulum Search for FB - often ventral (pain when manipulated?, may be more than one wire) Close rumen - Cushing or Lembert ```

Question 236

After care for exploratory rumenotomy for traumatic reticulitis?

Answer 236

``` Antibiotics NSAIDs Return to milk yield Magnets for others Stop using tyres ```

Question 237

Aetiology of vagus indigestion?

Answer 237

Complication of traumatic reticuloperitonitis - vagus nerve injury (penetration in medial wall of reticulum), reticular adhesions most important cause Other causes - actinobacillosis of rumen/reticulum, fibropapillomas of cardia, late pregnancy

Question 238

Clinical signs of vagus indigestion?

Answer 238

``` Dorsal vagus nerve injury: - achalasia of reticule-omasal orifice - = enlarged rumen +/- bloat Pyloric branch of ventral vagal nerve: - achalasia of pylorus - = abomasa impaction Hypermotility or hypomotility of rumen - depends which fibre types damaged Chronic - inappetence/loss of BCS - '10 to 4' appearance - distended abomasum in lower right quadrant - Vague - Chaotic rumen contractions Dehydration Enlarged rumen Scant faeces Undigested material Inadequate response to treatment Ping on right lower flank sometimes ```

Question 239

Pathology seen with vagus indigestion?

Answer 239

Often no gross lesion - microscopic lesions in medial wall, damage of vagal tension receptors Reticular adhesions most important cause Extensive inflammation - inhibits reticular motility, disturbs the particle separation process

Question 240

Pathogenesis of vagus indigestion?

Answer 240

Disturbance in rumen outflow Disturbance in pylorus outflow - rumen distension, pasty/frothy contents Alteration in reticulorumen motility - hypermotile or hypomotile, ratio of primary:secondary contractions upset 'chaotic'

Question 241

Differential diagnoses for signs caused by vagal indigestion?

Answer 241

Chronic traumatic reticulitis Abomasal impaction/dietary in origin Omasal impaction Abomasal ulceration

Question 242

Treatment for vagus indigestion?

Answer 242

Poor prognosis - slaughter Rumen lavage Fluid therapy and laxatives Rumenotomy/red devil

Question 243

What is bloat? types?

Answer 243

Accumulation of rumen gas sufficient to change contour of rumen (visible distension) Frothy bloat - dietary: clovers - froth forms in rumen, covers gas receptors in cardia, failure to eructate -> accumulation of froth -> death Free gas bloat - excess carbohydrates - secondary to other conditions e.g. wire - secondary to chronic pneumonia - mediastinal abscesses - secondary to lateral recumbency e.g. milk fever - pass stomach tube, trochar - chronic bloat: red devil, rumen fistula

Question 244

Diagnosis and treatment of frothy bloat?

Answer 244

History - clover grazing, lucerne/alfalfa grazing Failure to relieve bloat with stomach tube or trochar Trochar will not work! Dose with surfactant - silicone based, oils (e.g. vegetable oil), then exercise If emergency - 4''-6'' incision L sub-lumbar fossa

Question 245

When is diarrhoea normally seen in calves? When do they become pathogen multipliers?

Answer 245

Diarrhoea at 1wo when start excreting bugs (can be up to 21do) Pathogen multipliers at 2-8wo

Question 246

Sources of diarrhoeal agents for calves? Other factors affecting whether a calf gets diarrhoea?

Answer 246

Diarrheic animals Asymptomatic carriers: - Adults - low doses - Other calves - pathogen multipliers (older healthy calves or diarrheic and recovered) Environment - especially Crypto, builds up over calving period (higher risk of death later in calving period), pathogens are endemic so all calves exposed Other factors: - stress - chilling - nutrition: hygiene, temperature, composition - housing: comfort, warmth, draughts

Question 247

What host defences are involved in calf diarrhoea?

Answer 247

Passive immunity from colostrum - local IgG and IgA adhering to mucosal surface Healthy gut flora - suppresses pathogen growth (competitive inhibition)

Question 248

How to minimise calf scour?

Answer 248

``` Minimise exposure: - clean calving area/calve outside - snatch calf within 2-4h - clean calf housing - hygiene at feeding - hospitalise sick calves Maximise protection: - 3.5-4L colostrum within 6h - repeat in 12h - continue colostrum feeding for 4-10d - adequate cow nutrition (important for beef cows, feed higher protein for 3 weeks pre-calving) - vaccinate dam 30d before calving for ETEC, rotavirus and coronavirus (works via colostrum/milk) Minimise stress ```

Question 249

Should you keeping feeding milk to a calf with scour?

Answer 249

Advs: - Feeding more milk allows calf to fight disease (energy for immune response) - Maintains body condition - assists in repair of gut mucosa - ensures intake of Ca, Mg, vitamins etc Disadvs: - may worsen diarrhoea via colonic overload with partially digested foodstuffs - may worsen acidosis via colonic fermentation - may discourage farmer compliance since treatments appears not to work

Question 250

What is the Sandhills system for beef cattle|?

Answer 250

``` Move non calved cows every week to leave behind the calved cows Groups then co-mingled after youngest calf is 4wo Reduces: - contact between young and older calves - build up of pathogens - eliminates pathogen multiplier effect Not very practical in UK but if calve inside can: - turn out asap - segregate cow/calf pairs by age - 7-10d age spread of calves - can mix at 4wo - abolishes pathogen multiplier effect ```

Question 251

Which calves get coccidiosis? When? Signs? Treatment? Diagnosis?

Answer 251

``` Usually in older calves (>21do) Poor hygiene - especially near feeding troughs Dark scour ± blood Tenesmus Usually bright Treatment: Sulfonamides, Vecoxan Diagnosis - faecal oocyst count ```

Question 252

Necrotic enteritis: which calves affected? how does it present? aetiology? signs? PME?

Answer 252

Affects 2-6mo suckler calves Usually sporadic cases Usually fatal Aetiology unknown - Vit E, Se, toxins ??? Pyrexia, pale mucous membranes, leucopaenia, thrombocytopaenia Not BVD although it looks like it PME - necrotic lesions of gut and respiratory tract

Question 253

Peri-weaning scour syndrome: signs? aetiology? what to do?

Answer 253

Pasty scour, poor growth, bloat, pot belly etc No bugs yet implicated Dietary origin? Ruminal development pre-weaning: SARA Look at feeding and management pre and post weaning Type of concentrate fed: pellet, coarse-mix

Question 254

Which pathogens can cause diarrhoea in calves? When?

Answer 254

``` Young calf (0-6do): - Enterotoxogenic E coli Older calf (6d+) - Rotavirus - Coronavirus - Cryptosporidium - Salmonella dublin, typhimurium ```

Question 255

Rotavirus causing scour in calves: family of virus? structure of virus? which antigen?

Answer 255

Reoviridae Double stranded RNA virus Calves: group A surface antigen

Question 256

Coronavirus causing scour in calves: family of virus? structure of virus? which antigen? what else does it cause?

Answer 256

Coronaviridae Single stranded RNA virus Also winter dysentery in adults Respiratory disease in USA and Ireland

Question 257

Cryptosporidium causing scour in calves: which species? infective dose? features of oocysts? Life cycle?

Answer 257

C parvum Excreted oocysts immediately infectious Very small infective dose and vast numbers excreted Oocysts very resistant Not host specific - zoonotic (from environment e.g. water sources, or direct contact) Life cycle: - Oocyst ingested from contaminated water/food - oocysts 'excysts' in the small intestine - asexual reproduction in small intestine to produce oocysts - oocysts pssed in host's faeces and sporulate to become infective

Question 258

E.coli causing scour in calves: features of E.coli? How often causes calf scour? Signs?

Answer 258

Features of E.coli: - Many sub types - Only 20% of genome is core to all - mutation, horizontal gene transfer - Most are non pathogenic Minor gut pathogen in calves - implicated in 5% of cases (ETEC) Acute - rapid dehydration and death in 24-48h Adhesion via pili - bind to receptors K99 and F41 most common ETECs

Question 259

What diseases does E.coli cause in cows/calves?

Answer 259

Scour Mastitis Endometritis

Question 260

How are the E.colis affecting the intestine classified?

Answer 260

``` ETEC = enterotoxigenic, diarrhoea in calves VTEC = verocytotoxinogenic, E.coli 0157:H7 EIEC = enter-invasive EPEC = entero-pathogenic EAggEC = entero-aggregative DAEC = diffusely adherent ```

Question 261

What enterotoxins can be produced by ETECs? Why does it cause diarrhoea?

Answer 261

Heat stable enterotoxin (ST): - STA = only one in calves - STB = not found in calves - produces rise in c-GMP (inhibits absorption) Heat-labile enterotoxin (LT): - produces rise in cAMP - inhibits Na (and Cl and H2O) absorption in villous cells - stimulates Na (and Cl and H2O) secretion in crypto cells - final secretion influenced by calmodulin Diarrhoea: - outpouring of Na, Cl, H2O - profuse liquid faeces - very rapid dehydration leading to shock - high mortality

Question 262

What is the major VTEC? What are the natural hosts? How many animals shed?

Answer 262

``` 0157:H7 Natural hosts = cattle (and sheep) 20% of farms infected Does not cause disease in animals 4-8% of animals = super shedders, seasonal increase in shedding in summer ```

Question 263

Define diarrhoea

Answer 263

Failure of net intestinal uptake of water and sodium, such that the colon is overwhelmed

Question 264

Pathophysiology of diarrhoea?

Answer 264

Hypersecretion (outpouring of fluid in upper SI): - ETEC - normal absorption - excess fluid to colon (overload) Malabsorption (villous damage and atrophy): - viruses, crypto - secretion at normal rate - failure of absorption - passage of partially digested foods to colon: colon fermentation, osmotic diarrhoea - excess fluid to colon (overload) Net result = dehydration/hypovolaemia (can lead to pre-renal failure and shock) and metabolic acidosis (acid produced, bicarbonate lost) Also hyperkalaemia secondary to acidosis - intracellular uptake of H+ exchanged for K+ (fatal) Hypoglycaemia - starvation

Question 265

Treatment for calf diarrhoea?

Answer 265

JUST FLUIDS (not antibiotics) Aim to correct the hypovolaemia, metabolic acidosis, (hyperkalaemia) and hypoglycaemia IV fluids if: - calf unable to stand - severely acidotic - calves failing to improve despite ORS - very severely dehydrated calves, even if standing 7-20L isotonic fluids (can also use hypertonic) Spike with extra NaHCO3 if severely acidotic If don't know if acidotic or not: - likely will be if >6do so spike fluids - unlikely if <6do so isotonic only - if eyes sunken then severely dehydrated so needs immediate isotonic fluids, then spike if >6do - if eyes not sunken but calf recumbent then severe acidosis likely cause, so spiked fluids Oral fluids: - 1st generation: correct dehydration - 2nd generation (added BIC): also corrects acidosis - 3rd generation (high glucose): addresses nutritional demands - 4th generation (glutamine): promotes villus repair and regeneration - pick depending on fluid's rehydration ability (Na conc optimum 120-130mmol/l), ability to correct acidosis (need at least 25mmol/l BIC, optimum 80-120mmol/l) and nutritional ability (glucose conc) - start as soon as scour starts - teat and bucket best - 4-8L daily - little and often - keep feeding milk Hospitalisation for 24-48h desirable Introduce milk feeding as soon as suck reflex is present Correct acidosis slowly

Question 266

What can cause metabolic acidosis?

Answer 266

Loss of bicarbonate Addition of acid and neutralisation of bicarbonate Dilution of bicarbonate (inappropriate fluid therapy)

Question 267

How acidotic do diarrhoeaic calves get?

Answer 267

Majority are severely acidotic | >6do tend to more acidotic than younger calves

Question 268

What stimulates a calf to breathe at birth?

Answer 268

Respiratory acidosis from build up of CO2

Question 269

What problems can calves have as a result of dystocia?

Answer 269

Foetal hypoxia due to: - compression of umbilical cord - premature placental separation Metabolic acidosis due to resultant lactic acid production Severe respiratory acidosis due to poor lung function End result = academia and hypoxaemia Oedema, bruising and fractures are common Can all lead to FPT, death

Question 270

Diagnosis of hypoxaemia and acidaemia in newborn calf?

Answer 270

Blood gases not very practical Time to sternal recumbency: - should be <5 mins - if >9 mins, increased risk of death

Question 271

How to rescuscitate a calf?

Answer 271

``` Airway: - intubate (7.0-9.5 ET) - laryngoscope - sternal recumbency - pull tongue out, pass tube Breathing: - ambubag - blow down tube Circulation: - 50ml 8.4% NaHCO3 IV - 500ml Haemacell (blood loss) ``` Other techniques: - cold water down ear - rub with straw - acupuncture - Dopram drops or IV - myllophylline

Question 272

What is in colostrum?

Answer 272

High energy High protein, fats, vitamins Immunoglobulins IgA, IgG and IgM are child immunoglobulins IGF1, IGF2, insulin, prolactin, GH, steroids etc Large numbers of inflammatory cells

Question 273

Causes of inadequate colostrum intake and absorption by calves?

Answer 273

Intake: - inadequate quantity - inadequate quality: dilution effect (high genetic merit dairy cows, heifers) - poor udder/teat conformation - poor mothering ability (modern holsteins) Absorption: - time from birth to sucking (should be <6h) - method of administration: cow vs teat vs tube - post-natal acidosis from dystocia - induction of parturition

Question 274

Factors affecting quality and quantity of colostrum?

Answer 274

``` When collected (decrease in Ig quantity with time) Breed of cow Parity? Pre-partum nutrition Length of dry period Pre-milking Abortion/induction Mastitis ```

Question 275

What passive immunity do young calves have?

Answer 275

Systemic: IgG, IgM (IgM declines at 5do) Local "Teflon effect": IgA and IgG1, secreted from systemic circulation for 5 days only, local Ig ingested from colostrum for 5 days only

Question 276

What is failure of passive transfer? How many calves affected? How is it assessed?

Answer 276

``` Failure to get or absorb adequate colostral Abs = major risk factor for all calf disease 30-50% affected Measure serum Ig: - Refractometer: TP should be >55g/L - ZST: should be >20 units - SST: Ig should be >20g/L - Radial immunodiffusion - "Nasal stick test" measures IgG ```

Question 277

Definition of herd with FPT?

Answer 277

>20% of calves with TP <55g/L | Take random sample of calves <10do

Question 278

How to assess colostrum quality?

Answer 278

Brix refractometer: cut off 22% | Colostrometer

Question 279

How to prevent FPT?

Answer 279

Adequate cow nutrition pre-calving - beef cows Avoid dystocia Tube feed 3.5L colostrum ASAP (within 6h) to all dairy calves Supervise beef calves Frozen colostrum

Question 280

What is the current best dairy calf practice for colostrum?

Answer 280

``` Remove calf within 2h of birth 3-4L colostrum asap within 6h 3L colostrum again within 12h Feed 1L colostrum daily for 3-5d (ensures local gut immunity) Store colostrum at 4C ```

Question 281

Which colostrum chosen for frozen colostrum? Storage?

Answer 281

``` Collected from first milking only Only freeze good quality colostrum Freeze in milk containers Free! Protection against bugs on your farm Thaw gently Collect from cows with lowest Johne's risk - heifers or test negative cows ```

Question 282

What is navel ill in calves? Signs? Sequelae? Risk factors?

Answer 282

Infection via navel or oro-respiratory route May involve umbilical arteries, veins, urachus Key sign is hard, swollen navel (Ddx hernia - reducible) Sequelae include: - peritonitis - septicaemia - polyarthritis (joint ill) Risk factors: - pathogen load (hygiene at calving) - patent navel (use of iodine) - immune status of calf (colostrum and FPT)

Question 283

Diagnosis and treatment of navel ill in calves?

Answer 283

``` Diagnosis: - CE: swollen, hard - probe - US: peritonitis, extension up the vessels (artery to bladder, vein to liver) Treatment: - antibiotics - drainage - surgery: remove infected umbilical arteries and urachus, PTS if veins affected as poor prognosis ```

Question 284

When is joint ill seen in calves? Signs? Prognosis? Treatment?

Answer 284

``` Sequel to navel ill usually Single or multiple joints - swollen, painful Prognosis: - poor - depends on joint affected Treatment: - long course antibiotics - joint lavage - arthrotomy and flush joint - antibiotic impregnated beads after flushing or arthrotomy (amoxycillin, clindamycin) - placed in or around joint, remove in 4 weeks ```

Question 285

Define bacteraemia and septicaemia?

Answer 285

``` Bacteraemia = bacteria in blood, secondary to mucosal damage e.g. rumen acidosis, mastitis Septicaemia = bacteria multiplying in blood, concurrent endotoxaemia, fatal ```

Question 286

Aetiology of septicaemia in calves? When? Risk factors?

Answer 286

E.coli, Actinomyces, Staph Prime determinant is lack of colostral Ab Most cases 0-5do associated with FPT Few cases 5-14 days associated with decline in IgM Endotoxaemia (sepsis) = invariable fatal Risk factors: - pathogen load (calving area, calf rearing area) - immune status (colostrum intake, decline in IgM after 5d)

Question 287

Clinical signs of septicaemia in calves?

Answer 287

Non specific Collapsed Shocked (endotoxaemia) Very congested conjunctiva - petechiae, DIC CNS signs sometimes, meningitis Diarrhoea not a sign but may occur at same time Usually 1-5do

Question 288

Treatment of septicaemia in calves?

Answer 288

``` Very rarely successful Antibiotics NSAIDs - flunixin Corticosteroids Fluids - care not to over do Supportive nursing, warmth, feeding ```

Question 289

What causes calf diphtheria? Signs? Risk factor? Treatment?

Answer 289

``` Fusobacterium necrophorum Oral lesions: - sore mouth - salivation and foul smell - ulcerative lesions Dirty buckets - poor hygiene Treat with penicillin ```

Question 290

What can cause abdominal swelling in young calves? How to approach a swollen calf?

Answer 290

``` Left sided swelling: - bloat - free gas in rumen Right sided swelling "abdominal catastrophe": - e.g. volvulus, torsion - calf very sick - laparotomy indicated Atresi coli: - gradual distension over first few days - total absence of faeces - euthanasia ``` Approach: - full CE: sick? - pass stomach tube to rumen: is distension completely resolved? rumen bloat if yes, is right side still swollen if no? - listen to guts before and after passing tube - for pings and splashing

Question 291

What causes rumen bloat in calves?

Answer 291

Rumen drinkers: - milk goes to rumen - failure of closure of oesophageal groove - ferments milk -> metabolic acidosis -> mild diarrhoea and bloat - risk factors: feed hygiene, worn teats, bucket placement Poor rumen development: - often pot bellied - rumen acidosis at weaning - peri-weaning scour syndrome

Question 292

Treatment of calf bloat?

Answer 292

Relieve distension with tube/trochar If repeated - red devil trochar/fistula Correct underlying risk factors Consider frothy bloat if on lush pasture

Question 293

Targets for dairy calf rearing: mortality? weaning weight? weight at 3 months? weight at service when 13-14 months old? calving age?

Answer 293

``` Mortality <5% Weaning weight >65kg 3 months weight >120kg Service weight at 13-14 months >380kg (withers height >125cm) Calving age 24mo ```

Question 294

What constraints on calf growth are there?

Answer 294

Disease - scour, pneumonia Sub-optimal nutrition Sub-optimal environment

Question 295

Why is pre-weaning ADG important? What is key to allow this?

Answer 295

Correlation between milk yield and ADG pre-weaning Feeding in first 5 weeks is key Impact on early mammary development

Question 296

What is the traditional milk feeding regime of calves? What might it change to? Why?

Answer 296

2 x 2 x 2 2L each feed 2 feeds daily 2 month weaning ``` Now thinking should feed more milk for longer E.g. 10-12 week weaning Acidifed milk ad lib? Machine feeding? FCE: - 3:1 on milk - 10:1 on solids ```

Question 297

What does a newborn 50kg calf require for maintenance energy and for growth?

Answer 297

``` Maintenenace ME = 8MJ/day Growth (1kg/day) = 14MJ/day Total ME = 22MJ/day But 4L milk replacer/day is only 9MJ/day So 50% of dairy calves lose BW in first 7 days of life ```

Question 298

Options for housing of dairy calves? Advs? Disadvs?

Answer 298

``` Hutches: - allows calf to pick own environment - calf is isolated so reduces spread of infection - ventilation and drainage Individual pens: - ventilation, drainage, hygiene Group housing: - need high standards of management - better growth rates possible - less labour - welfare: social interactions - increased disease risk ```

Question 299

Rules for group housing of calves?

Answer 299

8 calves maximum | 14 days maximum age range

Question 300

How much extra energy do neonatal calves need above maintenance if it's cold?

Answer 300

15C + 15% 10C + 27% 5C + 40% 0C + 50%

Question 301

When are calves weaned?

Answer 301

When eating at least 1.5kg daily? When at least 8wo Weighing at least 65kg? Poss better growth if delay weaning?

Question 302

What is the maintenance energy requirement of calves at weaning and puberty?

Answer 302

``` Weaning = 11MJ/kg Puberty = 9MJ/kg (falls as consumes more forage) ```

Question 303

What is fed to cows between weaning and service? ME? CP? Aim for DWG?

Answer 303

``` ME: 9-10.5MJ/kg DM 15% CP DWG: 0.91kg/day Avoid fat (CS 2.5-3.0) Options: - straw and cake - silage and cake - TMR - grass in summer ```

Question 304

How can we feed more milk replacer to calves?

Answer 304

Increase MR concentration Increase volume fed e.e. 3.5L per feed Feed 3x daily Computerised feeders (but shared teat is risk factor for pneumonia) Ad lib feeding - acidified cold milk, computerised

Question 305

Aetiology of Johne's? Features of agent? Survival in environment? Strains?

Answer 305

Mycobacterium avium subsp paratuberculosis (MAP): - Slow growing, fastiduous acid fast bacillus - Member of MAC - Cross reactivity with other mycobacteria including M. bovis: issues with TB testing (reduces sensitivity?), “False positives” to MAP ELISA after TB test - Long lived in environment: 12 months in water, 2 years in soil (low pH increases survival?), role of amoebae? Strain types: - Weak host specificity - Bovine (B) strains and strains from other species: major group: C17 - Sheep (S) strains: minor group: C1

Question 306

Pathology caused by MAP in Johne's?

Answer 306

MAP in macrophages (protected) Granulomata in distal ileum and LN: - Macrophages and lymphocytes - Spectrum of pathologies e.g. in sheep - Multibacilliary: cattle & sheep - Paucobacilliary: sheep - Cattle: diffuse thickening of gut wall (corrugated cardboard appearance)

Question 307

Which cattle respiratory viruses make up the Bovine Respiratory Disease Complex (BRDV) and which families do they belong to? Structure?

Answer 307

``` Paramyxoviridae: ssRNA - Bovine Respiratory Syncytial Virus (BRSV) = pneumovirus - Parainfluenza Virus 3 = paramyxovirus Herpesviridae: DNA viruses - Bovine Herpesvirus 1 (IBR) Flaviviridae: enveloped ssRNA - Bovine Viral Diarrhoea Virus (BVD) ```

Question 308

Pathogenesis of Paramyxoviridae?

Answer 308

Proteins required for attachment to the target cell: - Via G protein in RSV - Via HN glycoproteins in PI3 Fusion proteins induce fusion between the viral envelope and the target cell membrane Virus nucleocapsids are then released into the cytoplasm

Question 309

Bovine Respiratory Syncytial virus: Type of virus? Pathology?

Answer 309

Paramyxoviridae: pneumovirus Pathology: - interstitial pneumonia - interstitial emphysema - formation of multinucleated giant cells/syncytia, often containing eosinophilic inclusion bodies - thickened alveolar walls makes oxygenation more difficult

Question 310

Bovine Parainfluenza Virus type 3: Type of virus? Pathology?

Answer 310

Paramyxoviridae: paramyxovirus Pathology: - bronchitis and bronchiolitis - alveolar cell thickening and hyperplasia - possibly also giant cells - intracytoplasmic inclusion bodies in lungs

Question 311

Infectious Bovine Rhinotracheitis (IBR): Agent? Pathology? Age seen?

Answer 311

Bovine Herpes 1 Pathology: - Once infected, always infected - While healthy, CMI keeps virus from replicating so no clinical signs - Stress e.g. periparturient period when immunosuppressed -> recrudescence of virus -> replicates and sheds - virus causes sloughing of epithelial cells in URT -> necrosis -> leaves open to bacterial infection (shipping fever) - PM: haemorrhagic lining of trachea, lining sloughing off - neurotropic Commonly seen in cattle 6-18mo

Question 312

Bovine viral diarrhoea virus: Genus? Genotypes? Pathogenesis?

Answer 312

Genus: Pestivirus 2 Genotypes: BVDV-1 and BVDV-2 Pathogenesis: - Destroys alveolar macrophages - Depletes lymphoid tissue - Not specifically respiratory but immunosuppressed animal - Lymphotrophic: found in tonsils and then replicates in lymph nodes

Question 313

Mycoplasma bovis: Features? Where found? What can it cause?

Answer 313

``` No cell wall, gram positive Found in URT and LRT Can survive in epithelial and inflammatroy cells Can cause: - "Cuffing" pneumonia (enzootic pneumonia) - septic arthritis (joint ill) - otitis media (head tilts) - mastitis ```

Question 314

Which Pasteurellaceae affect cattle? Features/pathogenesis? What do they each cause?

Answer 314

Gram negative, facultative anaerobes Host specific RTX toxin: damages endothelial cells of capillaries -> haemorrhage into alveoli Fibrinous pleurisy and intra-alveolar fibrin deposition Mannheimia haemolytica: - shipping fever, classically follows IBR (but also primary pathogen) Pasteurella multocida: - similar to Mannheimia Histophilus somni: - commensal in genital tract - pathogenic in respiratory tract - LPS provoke inflammatory response -> can lead to thrombus formation in heart, joints, lungs, brain - TME = sudden death due to thrombus in brain - histamine release

Question 315

BSE: Clinical signs? Incubation period? Transmission? Strains?

Answer 315

``` Clinical signs: - ataxia - nervous or aggressive behaviour - loss of condition and death in 1-6 months Incubation period: 5+ years Transmission by oral route (meat and bone meal) Little evidence of host genetic effect 2 different strains ```

Question 316

What is atypical BSE?

Answer 316

Lower molecular weight PrPSc | Or higher molecular weight PrPSc

Question 317

Treatment for coughing calves?

Answer 317

Florfenicol (single sc) | Again 48h later if needed

Question 318

Diagnosis of cow trying to urinate, pyrexic, can't palpate bladder per rectum, raised tail, not eating?

Answer 318

Acute pyogenic cystitis

Question 319

What to do to diagnose the problem if: - multiple calves died in first 3 days of life - swabs from liver and spleen on PM reveal haemolytic E coli

Answer 319

Take peripheral blood samples from calves <14do and carry out zinc sulphate turbidity estimation

Question 320

What to do to diagnose the problem if: - In December, half of the calves born in spring develop severe scour 6 weeks after being weaned and moved into winter housing - fed big bale silage and 0.75kg coarse mix daily - organically farmed suckler cow herd

Answer 320

Investigate plasma pepsinogen values in a peripheral blood sample

Question 321

Diagnosis for: - 5 month old welsh black calf develops profuse diarrhoea - also mouth ulceration and crusty nasal discharge - dies despite therapy - severe enteritis with ulceration on PM and evidence of pneumonia and necrotic tracheitis - blood sample: severe neutropenia, BVD Ab positive

Answer 321

Necrotic enteritis and laryngitis of unknown aetiology (not BVD mucosal disease as Ab positive!)

Question 322

Diagnosis of: - Two 2-3 week old dairy heifers are both slightly depressed and salivating excessively - necrotic gingivitis on examination - severe halitosis

Answer 322

Calf diphtheria associated with Fusobacterium necrophorum

Question 323

Diagnosis of: - poor growth of 14 x 4 month old dairy calves - pot bellied - pasty diarrhoea - fairly bright, no coughing - treated with toltrazuril 2 weeks ago but no improvement - farmer suggests euthanasia of poorest calc for PM - housed in a pen with clean straw - receive 25kg calf nuts and straw daily

Answer 323

Peri-weaning scour syndrome

Question 324

Diagnosis of: - 10 week old calf with moderate watery diarrhoea with tenesmus and specks of fresh blood in it - ill thrift and not growing well compared to other calves in same pen - has received oral amoxicillin trihydrate and clavulonic acid for 2 days but no better - fed straw and 2kg calf resting pencils daily from a trough on floor in corner of pen - fresh water available from wall mounted drinker

Answer 324

Acute coccidiosis associated with Eimeria spp

Question 325

What treatment to give to: - 9 day old dairy heifer with profuse diarrhoea - faeces contain flecks of blood - dull, sunken eyes - slightly ataxic - moderate suck reflex

Answer 325

Oral rehydrating solution with a sodium concentration of 100mmol/L

Question 326

What treatment to give to: - 7 day old scouring calf - already received oral fluids with 100mmol/L sodium and 80mmol/L bicarbonate - told farmer to keep feeding milk at reduced rate of 1.5L twice daily - 3 days later farmer phones to say scour no better and may be worse, but calf is BAR with strong suck reflex

Answer 326

Continue with therapy

Question 327

Diagnosis of: - 6 year old Aberdeen angus cross suckler cow in february - due to calve in April - kept outside with 70 cows in 15 hectare rough grazing area - down and unable to get up - heavily poached ground especially around 2 ring feeders which farmer tops up with barley straw when cows have eaten up - water from stream - BCS 1, rumen fill 1 despite being given some straw which she eats and water - RR 32, rectal temp 38.4, HR 70, rumen mobility 4 every 2 mins - stiff faeces - normal demeanour - strong full remits in right posterior uterine artery per rectum and large metal forelimb within pelvic entrance

Answer 327

Low energy density of ration | E.g. feeding poor quality forages without other sources of dietary energy or protein during winter

Question 328

Diagnosis of: - 3rd lactation cow, calved 16 weeks ago - giving 24L milk/day - not in calf - last cow in for milking today (unusual) and gave no milk, cold to touch, didn't eat cake - next day dull and depressed, temp 38.3, RR 34, HR 96, absent rumen movements, scant firm faeces surrounded by mucus in rectum - percussion of right flank: gas/fluid interface noise heard in region of last 5 ribs

Answer 328

Right side abomasal dilation and torsion

Question 329

Diagnosis of: - first lactation heifer - calved around 140 days ago - 34L at peak lactation - calved down at BCS 3, but now 1.5 - milk yield fallen over past 3 weeks to 12L/day - doesn't eat parlour cake - poor rumen fill - temp 37, RR 36, HR 92 - rumen turnover 1 per 80 seconds and movement is weak - mm pale/dirty - scant, dark blackish, soft faeces

Answer 329

Abomasal ulceration

Question 330

Diagnosis of: - 4th lactation cow - calved 3 months ago in december - 7d ago went of food, milk yield halved - farmer put on ABs and improved but now bad again - dull, depressed, temp 39.7, RR 40, HR 85 - slightly arched back - rumen turnover 2 every 4 mins - - mm slightly congested, firm faeces

Answer 330

Traumatic reticula-peritonitis with localised peritonitis (positive Eric williams test)

Question 331

Diagnosis of: - 4th lactation holstein cow - calved 200 days ago - in calf 10 weeks - BCS 1.5 - gave 8L milk 24h previously - won't eat parlour cake - spends most of time lying down and doesn't want to eat - temp 37.2, RR 30, HR 66 - dull, depressed, 5% dehydrated - reduced rumen movements (one every minute) - ratio of primary to secondary contractions is chaotic with periods of almost complete absence of secondary contractions, followed by irregular periods dominated by secondary contractions - ventral abdominal distension of right flank - left sub lumbar fossa appears slightly distended and firm with a mild bloat - very few sounds heard of the right side but some gas-fluids interface sounds are heard when to low right side of the abdomen is balloted - rectum contains some scant faeces of normal consistency

Answer 331

Vagal indigestion

Question 332

Diagnosis of: - 6th lactation Friesian cow - calved around 5 months ago - unwilling to eat for 5d but continuing to give 8L milk/day - drinks water but refuses to eat both silage and concentrates - BCS 2, dull, depressed, HR 90, RR 24 - upper third of right lumbar fossa appears distended - left sub lumbar fossa shoe evidence of very poor rumen fill - rectal exam: swollen viscus in the right hand side of the pelvic entrance - percussion of right paralumbar fossa: gas-fluid interface

Answer 332

Abdominal catastrophe: caecal dilation and torsion

Question 333

What is the problem with too much protein or inadequate protein in the diet?

Answer 333

Too much protein: deaminated in the liver -> energy source -> fat cows Inadequate protein: reduces yield

Question 334

What are crude protein (CP) and digestible crude protein (DCP)?

Answer 334

``` CP = Measure of feed nitrogen content DCP = ERDP + UDP ```

Question 335

What starch and fat levels are needed to get a cow cycling after calving and then pregnant?

Answer 335

``` To get cycling: - high starch, low fat - dietary starch >160g/kg DM - dietary fat <44g/kg DM To get pregnant: - lower starch, higher fat - dietary starch 98g/kg DM - dietary fat <53g/kg DM ```

Question 336

What are dairy cows at risk for with a high or low milk protein:fat ratio?

Answer 336

Higher fat, lower protein: risk of ketosis as energy deficient Lower fat, higher protein: risk of acidosis as low fibre Ideal ratio: 0.7-1 : 1 (protein:fat)

Question 337

What is the 3.2% protein intercept?

Answer 337

= the point of kg milk per cow that can be sustained by the diet, maintaining 3.2% protein in the milk If low protein, then short of energy If high protein, then giving too much energy?

Question 338

What is the minimum data that will be available for a farm?

Answer 338

``` Legally required Farm Records: - BCMS - sheep movement licences From product purchaser: - number sold - dead weight - carcase grade - milk sales and Milk composition From Supplier: - feed input => feed rate - AI straw sales and medicine usage - vet cost? ```

Question 339

Signs of a diet which is short of energy?

Answer 339

BCS loss Poor fertility Low milk fat/protein ratio Low 3.2% protein intercept