Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

4th year > Cattle > Flashcards

Cattle Flashcards

1
Q

What design issues do bovine lungs have?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Consequences of bovine respiratory disease?

A 
Death
Poor growth
Drug costs
Delay in age at first calving
Reduction in subsequent milk yield
Related diseases
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Estimated UK prevalence of enzootic pneumonia of calves?

A

Dairy - 30%

Beef - 80-90%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Infectious causes of pneumonia in cattle?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What should the plasma and serum TP be for calves?

A

Plasma TP > 56g/l

Serum TP > 52g/l

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Why is Bovine respiratory disease most common in winter?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

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?

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

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How long can a calf gut absorb antibodies from colostrum?

A

12 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How close in age should calf groups be? Why?

A

<2 weeks spread between youngest and oldest

Older calves act as pathogen multipliers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Cattle Lungworm life cycle?

A 
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the prepatent period for cattle lungworm?

A

3 weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Max humidity for cattle housing?

A

80% (65% better)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is Fog fever?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

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

A

Channel Island

Fresian

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

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

A

Belgian blue

Lung volume:body weight lowest for any breed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Which respiratory diseases are fattening cattle most prone to?

A

Mannheimiosis/Pasteurellosis

Histophilus somni

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

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

A

Parasitic pneumonia: Dictyocaulus viviparus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What bovine respiratory diseases are associated with an allergic response?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What usually causes stertorous upper respiratory noise in cattle?

A

Laryngeal pathology - commonly laryngeal chondritis

  • secondary to calf diphtheria (necrotic smell from mouth)
  • breed predispositions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Treatment for laryngeal chondritis in cows?

A

May respond to penicillin/anti-inflammatories

May require tracheotomy/-ostomy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Causes of a profuse nosebleed in cows?

A

Vena caval thrombo-embolism - hopeless

Foreign body - blackthorn prickles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What to do for respiratory clinical exam of cattle?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

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

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

How to assess the environment when investigating bovine respiratory disease?

A 
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Short term/immediate treatment for bovine respiratory disease?

A

Antibiotics in an outbreak
NSAIDs
Nursing Isolation/reduce numbers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Longterm prevention of bovine respiratory disease?

A

Improve environment
Colostrum and nutrition
Vaccination

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Difference between IBR live and dead vaccines?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Non cardiac signs of bovine cardiac disease?

A 
Reduced production
Exercise intolerance
Increased urine output
Syncope
Poor appetite when failing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Causes of pale mucous membranes in bovines?

A 
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Causes of red mucous membranes in bovines?

A 
Toxaemia
Salmonellosis
Pasteurellosis
Malignant catarrhal fever
Infectious Bovine Kerato-conjunctivitis
IBR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Causes of cyanosis of mucous membranes in bovines?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Causes of jaundice of mucous membranes in bovines?

A 
Hepatitis
Haemolytic anaemia (Babesia-red water)
Photosensitisation
Ragwort, kale, lupin, copper poisoning
Post-partum haemoglobinuria
Leptospirosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Causes of haemorrhage mucous membranes in bovines?

A 
Anthrax
Bracken
Sweet vernal grass posioning
Copper toxicity (acute)
Leptospirosis
Mycotoxicosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Normal pulse rate in calves and cattle?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

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

A

Distension in right sided failure

Increased venous pressure in cardiac failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

How to assess the jugular pulse in a bovine?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Which cardiac sounds can be heard in bovines?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

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

A

Loud S1: increased force of contraction

Loud S2: increased pressure in vessels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Causes of heart murmurs in bovines?

A 
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

When are valvular stenosis and incompetence murmurs heard in bovines?

A 
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What causes endocarditis?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Clinical signs of endocarditis in bovines?

A 
Persistent fever
Pain on pinch test
HR 100+
Shifting polyarthritis due to emboli
Pulsation of mammary veins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Diagnosis of bovine endocarditis?

A

Take 20ml blood for culture

Neutrophilia with left shift, increased fibrinogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

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

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Clinical signs of ventricular septal defects in calves?

A

Range from no effect to stunted growth to sudden death

No cyanosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Clinical signs of PDA in calves?

A

Exercise intolerance and weakness

No cyanosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What makes up tetralogy of fallot?

A

VSD
Pulmonary stenosis
Dextroposed aorta
Secondary ventricular hypertrophy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

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

A

Milk regurgitation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What can cause myocardial weakness in bovines?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What is pericarditis usually associated with?

A

Traumatic reticulitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Clinical signs of traumatic reticulitis and pericarditis?

A

Shallow abdominal breathing

Abducted elbows

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Tests for traumatic reticulitis and pericarditis?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Treatment for traumatic reticulitis and pericarditis?

A

Surgery
Magnets
Antibiotics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Clinical signs of dilated cardiomyopathy in bovines? Age seen?

A 
Peripheral oedema
Jugular distension
Fluid accumulations in body cavities
Enlargement of heart with rounded 'globose' shape
Well grown 2-3yo Holsteins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

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

A

Secondary to liver abscess

1-3yo cattle - acidosis, rumenitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Clinical signs of caudal vena cava thrombosis in bovines?

A

Peracute - dead in pool of blood

Acute - respiratory distress, pain, pyrexia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Clinical signs of respiratory effects of cardiac disease in bovines?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Clinical signs of adomen effects of cardiac disease in bovines?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Why is GI disease a common cause of cardiac arrhythmias?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

What cardiac degenerative changes can bovines have?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

What are vitamin E and selenium important for?

A

Needed by certain enzymes as antagonists of free radicals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

What syndromes can myocardial degeneration and necrosis cause?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Sudden death differential diagnosis for bovines?

A 
Haemorrhage - calving injury, abomasa ulceration from NSAIDs
Plant toxicity - yew
Lightening
Electrocution
Hypomagnesaemia
Hypocalcaemia
Toxaemia - mastitis, metritis
Bloat
Blackleg
Black disease
Anthrax
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

What is the Older Cattle Disposal Scheme (OCDS)?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

What is the Over Thirty Months Scheme (OTMS)?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

What is the rule for emergency slaughter?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Clean livestock policy?

A

Category 3 = dirty

Category 3 and obove - unable to proceed for normal slaughter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

How must fallen stock (cattle) be disposed of?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

What is NFSCo?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Anthrax procedure?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

What is ERDP? What happens to it?

A

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 FME, NH4+ absorbed across rumen wall -> urea in blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

What is RUDP? What happens to it?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

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

A

16% if yield <8000L
18% if yield >8000L?
Grass silage = 12-18% protein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

What is metabolisable energy?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

What is the rumen capacity?

A

200L+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

What are carbohydrates fermented to in the rumen?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

What happens to VFAs?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

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

A

Dry/normal 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 30L/day: 3% BW
- Lactating 50L/day: 4% BW (aim is 4% at peak yield)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

What influences ruminant DMI?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

How much energy does a dairy cow require?

A

Maintenance: 65-70MJ
Production: 5MJ/L milk
Weight gain/loss: 30MJ/kg BW
Late pregnancy: 20MJ for early dry period, 40MJ for transition period

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

What does milk yield depend on?

A

Genetic merit
Nutrition
Health

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

What is M/D?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

When is peak milk yield reached?

A

At around 8 weeks of lactation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

How to maximise DMI in lactating cows?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

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

A

Lactating cow M/D: 11.5-12.3
Dry cow M/D: 8-8.5
Pasture DMI: no more than 14kg/day

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

What different feeding systems are there for lactating cows?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

Features of TMR for lactating cows?

A 
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

Features of traditional feeding systems for lactating cows?

A 
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

Features of a hybrid feeding system for lactating cows?

A

TMR at barrier and cake in parlour

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

How to monitor a cow’’s nutritional status?

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

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

A 
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

How to assess a feed?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

What is the four diet model?

A

Should all be the same:

  • diet formulated by nutritionist
  • diet mixed by farmer
  • diet received by cows
  • diet cows require
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

What factors affect the four diet model?

A 
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

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

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

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

A

Will depress appetite

Aim to calve at BCS 2.5-3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

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

A

Mammary regeneration

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

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

A 
Low energy, high fibre
About 1.5-2% BW DMI (10-14kg)
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

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

A

= 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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

What is the ‘Keenan’ diet?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

Dry cow management? What is done? Housing?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

Fat distribution in cows?

A 
Subcutaneous fat - more in beef cows, fresians
Visceral fat (hidden) - more in holsteins, channel island
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

Problem with overfeeding during dry period?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

BCS interpretation?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

Problems associated with post natal depression?

A 
Milk fever
RFM/metritis/endometritis
Mastitis
Displaced abomasum
Ketosis
Fertility
Lameness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

What bugs are in the rumen?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q

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

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
125
Q

Factors affecting rumen pH?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
126
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
127
Q

What causes rumen acidosis?

A

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

128
Q

Why is long fibre good?

A

Encourages cudding - bicarbonate buffers acid

Forms a rumen mat - keeps food particles in rumen to be digested, home to bug biofilms

129
Q

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

A

‘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

130
Q

Effects of SARA?

A

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

131
Q

Diagnosis of SARA?

A

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

132
Q

Selecting cows for sampling rumen pH?

A

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

133
Q

Technique for sampling cow’s rumen pH?

A 
Restrain cow - nose and tail
Site = level of stifle &amp; 6-8in behind last rib
Clip and scrub
Local anaesthetic
3-5in needle, 16-18G
Read sample immediately
134
Q

What does grass silage quality depend on?

A 
Grass type
First or second cut
Time of day (pm best for sugars)
Moisture content
Chop length
Compaction in clamp
Fermentation
135
Q

Pathophysiology of acute ruminal acidosis?

A 
Excessive acid production
pH falls below 5
Lactic acid production predominates
Lactic acid eating bugs killed off
Cow cannot metabolise D lactate
136
Q

When does acute ruminal acidosis occur?

A

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

137
Q

Signs of acute ruminal acidosis?

A 
Often group problem
Varying severity 
Ataxia
Distended rumen +/- bloat
Diarrhoea - profuse and smelly
Depression
Recumbency and shock
Mild: almost normal
138
Q

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

A

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

139
Q

Treatment for ruminal acidosis?

A

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

140
Q

Prevention of ruminal acidosis?

A

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

141
Q

Rumenotomy?

A 
Life saving emergency surgery
Recumbent animal
18in incision at least
Pack towels around
Open rumen and empty all contents
Not a sterile operation
142
Q

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

A

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’

143
Q

Who is at risk of trace element deficiencies?

A

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
144
Q

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

A

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

145
Q

Do dairy cows need copper supplementing?

A

No - not associated with fertility (myth causing problems!)

Can cause toxicity if over-dosing

146
Q

Diagnosis of trace element deficiencies?

A

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)

147
Q

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

A 
Very easy and safe
Right flank
Biopsy needle
Rib space 11
20cm below lumbar process
148
Q

Methods of supplementing trace elements for cows?

A 
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
149
Q

Age Johne’s seen? When? Clinical signs?

A 
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
150
Q

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

A 
>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
151
Q

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

A

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)

152
Q

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?

A

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)

153
Q

Immunology of Johne’s?

A

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

154
Q

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

A 
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
155
Q

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

A

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

156
Q

Control of Johne’s?

A

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
157
Q

Control of Johne’s for beef suckler herds?

A

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)

158
Q

Options to avoid Johne’s when purchasing stock?

A

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?)

159
Q

Johne’s vaccination? Pros and cons? When?

A 
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
160
Q

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

A

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

161
Q

How do MAP and M.bovis affect each other?

A

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

162
Q

What is milk fever? When seen? Why happens?

A

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

163
Q

Homeostatic control of Ca?

A

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

164
Q

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

A

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

165
Q

Roles of Ca2+ in the body?

A

Muscle function
Nerve impulses
Immune response

166
Q

Clinical signs of acute milk fever?

A

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

167
Q

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

A

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!

168
Q

How does hypophosphataemia complicate milk fever?

A

‘Downer cows’

Unable to rise fully unless given P - can add Foston IV to Ca boroglucoronate

169
Q

Treatment of hypocalcaemia (milk fever) in cows?

A

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

170
Q

Problems with subclinical hypocalcaemia?

A

Risk factor for other diseases:

  • immune function depressed
  • coliform mastitis
  • metritis/endometritis
  • post-partum depression
171
Q

Prevention of milk fever?

A 
"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
172
Q

What is hypocalcaemia associated with in sheep? Main sign?

A

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

173
Q

Where is Mg stored in the body?

A

No body stores

174
Q

Output and inputs of Mg?

A

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

175
Q

Clinical signs of hypomagnesaemia in cows?

A 
= 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
176
Q

Risk factors for hypomagnesaemia?

A

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

177
Q

Treatment for hypomagnesaemia?

A

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)

178
Q

Prevention of hypomagnesaemia?

A 
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
179
Q

What does lipolysis of adipose tissue produce?

A

NEFA (energy source)

Glycerol

180
Q

Where are ketones produced? What for?

A

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

181
Q

What does insulin cause?

A

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

182
Q

How do adrenaline/noradrenaline affect fat?

A

Stress -> stimulates lipolysis and NEFA release

183
Q

How is lactose synthesised in the udder?

A

From glucose from propionate and oxalo-acetate

184
Q

What causes increased production of ketones -> ketosis?

A

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)

185
Q

Clinical signs of clinical ketosis?

A

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)

186
Q

Treatment of clinical ketosis?

A 
Propylene glycol (oral)
Corticosteroids - dexaforte
Glucose 40% IV
Combination of above
Vitamin B12 (supportive)
187
Q

When is subclinical ketosis seen? Diagnosis?

A

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

188
Q

Key periods to monitor BCS changes?

A 
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
189
Q

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

A

Dry period: 2.5 (-3)
Drying off: 2.5 (-3)
Mid lactation: 2.5 (-3)
Early lactation: 2-2.5

190
Q

Prevention of FMS/ketosis?

A 
Feeding in dry period:
Low energy
Maximise DMI - comfort, palatable food, food at all times
Monitor BCS
Avoid fat cows
191
Q

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

A

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

192
Q

Risk factors for abomasal disorders?

A 
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
193
Q

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

A

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

194
Q

Differential diagnoses for signs caused by LDA?

A

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

195
Q

What happens to cause an LDA?

A

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

196
Q

Rolling for LDA - how? Advantages and disadvantages?

A

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

197
Q

Toggling for LDA - how?

A

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

198
Q

Advantages and disadvantages of toggling for LDAs?

A

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

199
Q

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

A 
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
200
Q

Right side (omentopexy) surgery for LDA - how?

A

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

201
Q

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

A

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

202
Q

Ventral abdominal paramedian surgery for LDA - how?

A 
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
203
Q

Post-op care for LDA surgery?

A 
Antibiotics? Pen/Strep OTC
Treat underlying conditions
- ketosis: propylene glycol
- endometritis etc
High fibre diet
204
Q

Which method to use for LDA?

A

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

205
Q

Aetiology of RDA? Pathogenesis?

A

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

206
Q

Metabolic sequelae of right abomasal dilatation?

A

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

207
Q

Metabolic sequelae of right abomasal displacement and torsion?

A

Mucosal damage
Cytokine release and endotoxaemia
Metabolic acidosis
Severe dehydration

208
Q

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

A 
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
209
Q

Differential diagnoses for signs seen with RDA?

A

Abomasal impaction
Caecal torsion
Traumatic reticulitis
Intestinal obstruction

210
Q

Treatment for RDA?

A 
Dilatation and displacement:
- medical: Ca 40%, metaclopramide, fluids
- surgery: drain and replace
Torsion:
- slaughter
- surgery
211
Q

Surgery for RDA - how?

A 
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
212
Q

Post op care after RDA surgery?

A 
Hartmanns fluids 50-100L
NSAIDs
Antibiotics
Oral KCl (50g daily)
Ca 40%
Propylene glycol
213
Q

Prevention of LDAs/RDAs?

A

Better dry cow management!

214
Q

History for caecal dilation and volvulus?

A 
Dairy cows
1st few months of lactation
Inappetant
Decreased milk yield
Ping in upper right flank
Rectally: distended, recognisable viscus
215
Q

Aetiology of caecal dilatation and volvulus? Pathogenesis?

A

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

216
Q

Clinical signs of caecalo dilatation? And volvulus?

A 
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
217
Q

Rectal exam findings for caecal dilatation and volvulus?

A

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

218
Q

Treatment for caecal dilatation and volvulus?

A

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

219
Q

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

A 
Antibiotics
Feed long fibre
TLC
Good prognosis
11-13% recurrence rate in first week
25% recurrence rate long term
220
Q

Causes of abomasal ulcer?

A 
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
221
Q

Pathogenesis of abomasal ulcers?

A

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

222
Q

Abomasal ulcer types?

A 
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
223
Q

Where are ulcers most likely found in the abomasum?

A

Cattle: fundic
Calves: pyloric

224
Q

Clinical signs of abomasal ulcers?

A 
Abdominal pain
Melaena
Pale mm
Sudden onset anorexia
Tachycardia
Perforation - hypovolaemia, unable to stand
225
Q

Treatment for abomasal ulcers?

A

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

226
Q

Signs of oesophageal obstruction?

A 
Cervical oesophagus above larynx, base or heart/cardia,
Inability to swallow
Regurgitation of feed and H20
Salivation
Bloat
Stop eating
Anxiety/retlessness
227
Q

Aetiology of oesophageal obstruction?

A

Intra-luminal - potatoes, turnips

Extra-luminal - pressure by surrounding organs (mediastinal abscesses, tuberculous LN)

228
Q

Treatment for oesophageal obstruction?

A 
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
229
Q

History/signs of traumatic reticulitis? Progression?

A 
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
230
Q

Where does the reticulum lie?

A

Opposite 6-8th rib on LHS

231
Q

Rumen contraction timings? Types? How does it sound?

A

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)

232
Q

Diagnosis of traumatic reticulitis?

A

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

233
Q

Causes of traumatic reticulitis?

A 
From tyres - fall into feeder wagons
Perished tyres
Baling sheep netting
Nails fall into mixer wagons etc
Old fencing wire
(not fussy eaters!)
234
Q

Consequences of swallowing a wire?

A 
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
235
Q

Exploratory rumenotomy for traumatic reticulitis?

A 
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
236
Q

After care for exploratory rumenotomy for traumatic reticulitis?

A 
Antibiotics
NSAIDs
Return to milk yield
Magnets for others
Stop using tyres
237
Q

Aetiology of vagus indigestion?

A

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

238
Q

Clinical signs of vagus indigestion?

A 
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
239
Q

Pathology seen with vagus indigestion?

A

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

240
Q

Pathogenesis of vagus indigestion?

A

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’

241
Q

Differential diagnoses for signs caused by vagal indigestion?

A

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

242
Q

Treatment for vagus indigestion?

A

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

243
Q

What is bloat? types?

A

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

244
Q

Diagnosis and treatment of frothy bloat?

A

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

245
Q

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

A

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

246
Q

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

A

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
247
Q

What host defences are involved in calf diarrhoea?

A

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

248
Q

How to minimise calf scour?

A 
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
249
Q

Should you keeping feeding milk to a calf with scour?

A

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

250
Q

What is the Sandhills system for beef cattle|?

A 
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
251
Q

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

A 
Usually in older calves (>21do)
Poor hygiene - especially near feeding troughs
Dark scour ± blood
Tenesmus
Usually bright
Treatment: Sulfonamides, Vecoxan
Diagnosis - faecal oocyst count
252
Q

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

A

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

253
Q

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

A

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

254
Q

Which pathogens can cause diarrhoea in calves? When?

A 
Young calf (0-6do):
- Enterotoxogenic E coli
Older calf (6d+)
- Rotavirus
- Coronavirus
- Cryptosporidium
- Salmonella dublin, typhimurium
255
Q

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

A

Reoviridae
Double stranded RNA virus
Calves: group A surface antigen

256
Q

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

A

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

257
Q

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

A

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

258
Q

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

A

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

259
Q

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

A

Scour
Mastitis
Endometritis

260
Q

How are the E.colis affecting the intestine classified?

A 
ETEC = enterotoxigenic, diarrhoea in calves
VTEC = verocytotoxinogenic, E.coli 0157:H7
EIEC = enter-invasive
EPEC = entero-pathogenic
EAggEC = entero-aggregative
DAEC = diffusely adherent
261
Q

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

A

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

262
Q

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

A 
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
263
Q

Define diarrhoea

A

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

264
Q

Pathophysiology of diarrhoea?

A

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

265
Q

Treatment for calf diarrhoea?

A

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

266
Q

What can cause metabolic acidosis?

A

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

267
Q

How acidotic do diarrhoeaic calves get?

A

Majority are severely acidotic

>6do tend to more acidotic than younger calves

268
Q

What stimulates a calf to breathe at birth?

A

Respiratory acidosis from build up of CO2

269
Q

What problems can calves have as a result of dystocia?

A

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

270
Q

Diagnosis of hypoxaemia and acidaemia in newborn calf?

A

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

271
Q

How to rescuscitate a calf?

A 
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
272
Q

What is in colostrum?

A

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

273
Q

Causes of inadequate colostrum intake and absorption by calves?

A

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

274
Q

Factors affecting quality and quantity of colostrum?

A 
When collected (decrease in Ig quantity with time)
Breed of cow
Parity?
Pre-partum nutrition
Length of dry period
Pre-milking
Abortion/induction
Mastitis
275
Q

What passive immunity do young calves have?

A

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

276
Q

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

A 
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
277
Q

Definition of herd with FPT?

A

> 20% of calves with TP <55g/L

Take random sample of calves <10do

278
Q

How to assess colostrum quality?

A

Brix refractometer: cut off 22%

Colostrometer

279
Q

How to prevent FPT?

A

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

280
Q

What is the current best dairy calf practice for colostrum?

A 
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
281
Q

Which colostrum chosen for frozen colostrum? Storage?

A 
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
282
Q

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

A

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)

283
Q

Diagnosis and treatment of navel ill in calves?

A 
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
284
Q

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

A 
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
285
Q

Define bacteraemia and septicaemia?

A 
Bacteraemia = bacteria in blood, secondary to mucosal damage e.g. rumen acidosis, mastitis
Septicaemia = bacteria multiplying in blood, concurrent endotoxaemia, fatal
286
Q

Aetiology of septicaemia in calves? When? Risk factors?

A

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)

287
Q

Clinical signs of septicaemia in calves?

A

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

288
Q

Treatment of septicaemia in calves?

A 
Very rarely successful
Antibiotics
NSAIDs - flunixin
Corticosteroids
Fluids - care not to over do
Supportive nursing, warmth, feeding
289
Q

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

A 
Fusiformis necrophorum
Oral lesions:
- sore mouth
- salivation and foul smell
- ulcerative lesions
Dirty buckets - poor hygiene
Treat with penicillin
290
Q

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

A 
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
291
Q

What causes rumen bloat in calves?

A

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

292
Q

Treatment of calf bloat?

A

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

293
Q

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

A 
Mortality <5%
Weaning weight >65kg
3 months weight >120kg
Service weight at 13-14 months >380kg (withers height >125cm)
Calving age 24mo
294
Q

What constraints on calf growth are there?

A

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

295
Q

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

A

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

296
Q

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

A

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
297
Q

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

A 
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
298
Q

Options for housing of dairy calves? Advs? Disadvs?

A 
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
299
Q

Rules for group housing of calves?

A

8 calves maximum

14 days maximum age range

300
Q

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

A

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

301
Q

When are calves weaned?

A

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

302
Q

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

A 
Weaning = 11MJ/kg
Puberty = 9MJ/kg (falls as consumes more forage)
303
Q

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

A 
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
304
Q

How can we feed more milk replacer to calves?

A

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

305
Q

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

A

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

306
Q

Pathology caused by MAP in Johne’s?

A

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)

307
Q

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

A 
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)
308
Q

Pathogenesis of Paramyxoviridae?

A

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

309
Q

Bovine Respiratory Syncytial virus: Type of virus? Pathology?

A

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

310
Q

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

A

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

311
Q

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

A

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

312
Q

Bovine viral diarrhoea virus: Genus? Genotypes? Pathogenesis?

A

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

313
Q

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

A 
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
314
Q

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

A

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

315
Q

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

A 
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
316
Q

What is atypical BSE?

A

Lower molecular weight PrPSc

Or higher molecular weight PrPSc

4th year (44 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions