Feeding to prevent NEBAL Flashcards
1
Q
Reminder of dairy cow year?
A
2
Q
When is peak lactation? Energy needed at that time?
A
60 DIM -> 3 x maintenance (3 kg of glucose per day)
3
Q
Reminder of NEBAL cycle
A
4
Q
Ketosis Clinical case
A
- Classic 20-50 days after calving (<1 month).
- Decreased milk yield.
- Rapid BCS loss.
- Loss of appetite (refusal of concentrates).
- Dark, firm, waxy faeces.
- Ketone breath - pear drops.
- Underlying concurrent disease LDA, metritis, lameness
5
Q
‘Nervous form’ of ketosis (hypoglycaemic encephalopathy)
A
- Signs can be intermittent.
- Excessive salivation.
- Abnormal chewing.
- Licking objects VIDEO
- Inco-ordination, circling, head pressing VIDEO
- Apparent blindness.
6
Q
Type 2 ketosis ?
A
- Similar to type II diabetes.
- High circulating glucose with peripheral insulin resistance.
- Not well understood.
- Fatty liver involvement?
- Excess energy in dry cow period?
7
Q
Describe Fatty Liver syndrome
A
- Mobilisation of body fat reserves occurs
during the first month of lactation - This leads to the deposition of fat in liver. * Relatively normal in high yielding cows.
8
Q
What happens in severe prolonged NBAL?
A
20% liver fat deposition
9
Q
Interference with liver function exacerbates…?
A
-NEBAL & ketosis
- Poor fertility
- Depressed milk prod
10
Q
Above 34% ?
A
Severely affected
- This may lead to fat cow syndrome. Fat cows with rapid weight loss & poor response to treatment
11
Q
What biochem diagnostics ?
A
– Mobilisation of body fat NEFA.
– Ketone body formation BHB. Cases of clinical
ketosis BHB levels over 3 mmol/l.
– +/- Hypoglycaemia ¯ glucose.
12
Q
Cow side tests?
A
– Smell of ketone bodies.
– Ketostix urine
– Rother
– Ketone metres
13
Q
Tx of ketosis?
A
- 400ml of 40% glucose solution IV.
- Oral propylene glycol Ketol ~200ml BID
- oral glucose precursors.
- Glucocorticoids stimulate
gluconeogenesis & appetite -
Dexamethasone - Dexadresson. - Vitamin B12 / cobalt preparations -
required for metabolism of propionate.
14
Q
What is Monensin?
A
Mechanism of action:
* Ionophore antimicrobial (and anticoccidial).
* AMR??
* Alters microbial fermentation in rumen in favour propionate production.
15
Q
Who should get Monensin?
A
Target ‘at risk’ cows pre-calving
- Fat dry cows
- Twins
16
Q
Risk factors for ketosis?
A
- Inadequate energy content of the ration.
- Inadequate DEC DMI .
- High BCS before calving DEC DMI (target 2.5-3 at calving).
- Ketogenic butyric silage.
- Secondary to other disease which DEC DMI (LDA, lameness)
- Poor feed utilisation –poor adjustment to new diet / SARA.
17
Q
What aims for FAR off vs Transition Cow Feeding?
A
18
Q
What cow factors affect intake?
A
- BCS (fat cows have reduced VFI)
- Social interactions
- Health: lameness, metritis ..
19
Q
What feed factors affecting intake?
A
-> Palatability
- Taste, moisture content, quality (inc NDF -> inc time to digest -> inc rumen fill -> inc VFI)
-> Presentation
- Chop length (VFI inc if short shop length)
- Complete / mixes forages => VFI inc
- Little & often
20
Q
Management & environmental factors?
A
=> Access - 24 hr access, how often put out? space allowance? how many cows feed at same time?
=> Water - 24 h acess
=> environmental temp hit V DMI
=> Day length: artificial light / light quality
21
Q
describe pregnancy tox in ewes?
A
Pregnancy toxaemia in sheep is a common metabolic disease of undernourished
ewes caused by inability to adapt to increasing energy demands in late pregnancy
22
Q
Classic presentation?
A
- Ewes carrying multiple foetuses - 2+ lambs.
- In thin body < BCS 2 or very fat body condition
- Last 6 weeks of pregnancy.
- Poor nutritional - poor forage quality, inadequate concentrates.
- Stress – interrupted feeding – gathering / weather / dogs
- Older ewes – broken mouthed.
23
Q
What can preg tox look a lot like?
A
HYPOCALCAEMIA
24
Q
Prognosis for preg tox?
A
poor even with aggressive tx
25
What appearance of preg tox animal?
Dull, inappetent & progressivelt more depressed, isolated
26
What neuro signs might we see with preg tox?
* Apparent blindness Video
* Hyperaesthesia.
* Head pressing.
* Star gazing.
* Teeth grinding
27
Diagnosis of Preg Tox?
* Based on clinical signs and history.
* Lack of response to treatment
* Blood BHB > 3mmol/l.
* PME -Fatty infiltration of liver
28
Tx Preg Tox?
* IV glucose 100ml of 40% glucose intravenously.
* Oral electrolyte, glucose solutions & propylene glycol 50ml X4 day.
* Induction of parturition/abortion – steroids?
* Caesarean – remove the glucose drain save the ewe.
* Supportive care?
* Euthanasia.
29
Pg with Preg Tox?
50-70% mortality rates
30
Prevention categories?
- Forage analysis, dietary ration advice
- BCS
-Grouped according to nutritional need
- Metabolic profiling
- Individual level BHB (<1.1mmol)
- At flock level
31
Describe forage analysis prevention
Toward the end of pregnancy (last 6 weeks),even on excellent quality forage, forage alone is unlikely to meet their energy needs & ewes will
require introduction of supplementary feeds.
32
BCS for prevention?
BCS 2.5-3 during pregnancy until 6 weeks before lambing.
BCS 3 of 3.5 before partition.
Scored at 6 weeks before lambing and every 2 weeks.
Supplementary feeding be adjusted accordingly
33
Grouping for prevention?
Keel marking ewes at tupping time - accurate lambing dates.
Scanning ewes to determine foetal number.
Grouping ewes by age.
Grouping by BCS.
34
Detail metabolic profiling?
6 weeks before lambing to ‘check’ that the ration ewes meets their nutritional requirements.
>1.6mmol/l and over indicate a severe lack of energy in the diet.
35
What are the calcium requirements ?
* Maintenance: 700Kg cow Ca ~ 30 g/day.
* Lactation:
– Ca demand increases x3 Ca above maintenance.
– Ca 2g per litre of milk..
* At calving 10 litres = 20g/day.
* Peak lactation 40 litres = 80g/day!
36
Clinical signs of milk fever?
* Downer cow.
* Uterine inertia.
* Uterine prolapse.
* Retained Fetal membranes.
37
T/F Hypocalcaemia is an iceberg disease ?
True -> loads of subclinical cases and subsequent dec productivity
38
Diagnosis of milk fever?
* Response to treatment.
* Take blood before treatment
* Calcium below 1.5mmol/l
* Phosphate below 1.0mmol/
39
Tx of HypoCa?
- IV calcium borogluconate / SC +/- Phosphorous
-Oral Ca containing product / sachet / gels / boluses
40
Prevention of HypoCa?
* Calcium restriction
* Calcium-binding agents (X-Zelit)
* Magnesium supplementation
* DCAD / DCAB manipulation
41
Describe Calcium restriction
– Aim to limit Ca below 30-50g/day
– <20g/day ideal
42
What is typical calcium content of grass in uk ?
10mg/kg DM-> makes restriction diffictult if much grass/silage in diet
43
How can we decrease Ca content?
inc maize silage, whole crop, or straw in ration
Use Ca-binding agents
44
Mg supplementation - why?
Mg needed for Ca mobilisation
45
Feeding strategies for Mg supp?
– Magnesium levels >40g/day
– Usually supplied via Magnesium Chloride (helpful for DCAB)
– MgCl2 in drinking water (dry cows at grass).
46
What to be aware of when supplementing Mg?
– It is bitter! Must be the only water source.
– Concentrated MgCl2 fatal.
– Mg salts in TMR ration can also affect palatability and DMI.
47
Describe DCAD / DCAB
48
Diets with ....... induce mild metabolic acidosis
low DCAB (<0mEq/kg DM)
49
What si the point of DCAB manip
* Acid/base status influences Ca homeostasis.
* Metabolic acidosis increases tissue receptivity to PTH - D3 activation, Ca
mobilisation and Ca gut absorption.
50
How do we acheive DCAB?
* Addition of anionic salts e.g. MgCl2, NH4Cl, MgSO4 .
* Fed 2-3 weeks pre-calving (at least 10 days).
* Full DCAB only if the base ration is already < 250meq/kg DM.
51
Full vs Partial DCAB?
* Full DCAB aiming for -100mEq/kg DM.
* Partial DCAB aiming for 0 to 100mEq/kg DM.
52
What to do alongside DCAB
Monitor urine to check systemic acidification pH 5.5-6.5 (norm pH 7.5-8).
* These bitter anionic salts can ¯ DMI pre-partum.
* When DCAB is negative ration needs to supply Ca 130g/day.
* No calcium restriction at the same time.
53
Role of magnesium
* Activation of enzymes and biological processes e.g. Ca mobilisation.
* Neurological function – synaptic transmission.
54
Mg absorption?
* No storage / no homeostatic process.
* Dependant on daily Mg dietary intakes.
– dietary Mg content and amount eaten.
- K+ / ammonia fertiliser on pastures disrupts
absorption.
– Absorption from the gut (rapid digestive transit =
less absorption)
55
Typical presentation of Grass Staggers (HypoMg)
Typical: 4 week calved, older cow, lush spring / autumn
* Increased Mg demands in lactation
56
Prevention of Grass Staggers?
* 60g magnesium oxide per cow per day in highmagnesium cobs / increase fibre in diet.
* Magnesium salts via water.
57
Lush Grass CLS
* Down cows.
* Dead cows – thrashing.
* Weird behaviour Excitable
/aggressive.
58
What macrominerals, trace elements, vitamins do we manipulate in cattle
59
Copper toxicity in sheep?
– Typically intensively fed / overzealous supplementation.
– Liver has a high capacity for storage.
– Once critical levels are reached, massive haemolytic crisis occurs.
60
Clinical signs of toxicity in sheep?
- Jaundice
- Black urine
- Depression, recumbency, death
61
Diagnosis of Copper Tox?
– Serum copper levels - not always useful.
– Massively raised AST / GGT.
62
Management for copper tox?
– Molybdenum antagonist reduce further uptake?
– Ammonium tetrathiomolybdate? NOT FOOD PRODUCING ANIMALS!
– Phone the nearest APHA lab for advice.
63
Roel. ofSelenium / vit E?
– Both powerful antioxidants produced in normal cell metabolism.
– Deficiency allows cellular membrane damage ® tissue necrosis
– Reduced immune function
64
Clinical signs of selenium & vit E?
Clinical signs
– Reduced fertility / retained fetal membranes.
– risk of mastitis and metritis.
– White muscle disease (WMD) -> skeletal, respiratory, cardiac
65
Diagnosis of Selenium & Vit E?
– History of selenium deficient soils.
– Blood Glutathione peroxidase GSH-PX. WMD raised AST and CK.
– PME - Liver selenium levels / WMD white necrotic lesions in the myocardium,
diaphragm, thigh, shoulder muscles
66
Management Selenium def?
Inclusion in compound feeds / adlib minerals.
– Injectable selenium combined with Vitamin E (eg.Vitesel / Deposel).
– Oral selenium drenches.
– Intra-ruminal boluses.
– Selenium is potentially toxic, take care not to over supplement.
67
Role of iodine?
– Thyroid hormones: thyroxine (T4) and triiodothyronine (T3).
– Control of basal metabolic rate.
– Primary deficiency.
– Secondary deficiency due to goitrogens found in brassicas & white clover.
68
CLS of Iodine def
Clinical signs – deficiency in pregnant animals
– Still birth / Sick and weakly calves/lambs that do not thrive.
– Classic goitre is not necessarily seen.
– Reduced fertility / retained fetal membranes.
69
Diagnosis of iodine def?
– History of Iodine deficient soils. Goitrogenic forages.
– Plasma inorganic I2 (PII) or T4.
– PME of still born calves - Thyroid histopathology / weight.
– Supplementation trial.
70
Management of Iodine def?
Inclusion in a compound feed.
– Adlib minerals (= variable intakes / effectiveness).
– Intra-ruminal boluses provide slow release of iodine for 6 months.
– Painting cows flanks in 5 per cent tincture of iodine once a week!
71
Role of Cobalt/ Vit B12?
– Cobalt is required by rumen bugs ® Vitamin B12.
– Vitamin B12 is key in metabolic processes including:
* Gluconeogenesis via propionate
* Specific amino acid formation
* Liver lipid metabolism ® fatty liver.
72
deficiency of cobalt?
– Cobalt deficiency rare in cattle.
– Growing lambs have a high requirement for Vitamin B12.
73
CLs of Deficiency cobalt?
– Pine - ill thrift in weaned lambs.
– Impaired immunity - increased susceptibility to infection e.g. PGE.
– Anorexia, anaemia, conjunctivitis, infertility.
74
Diagnosis of Cobalt. vit 12
– History of cobalt deficient or manganese rich soils. Limed pastures.
– Rapid pasture growth. No concentrate supplementation.
– PME – Liver B12 levels / Ovine White Liver Disease (Fatty liver).
– Blood B12 levels
– Supplementation trial. Drench and see!
75
Management of Cobalt/ Vit B12?
– Oral drenching / Intra-ruminal boluses / Injectable B12, long acting SMARTShot.
– Inclusion in a compound feed / Adlib minerals
76
Why do we get acidosis?
* Normal rumen pH: 6.5 – 7
* Buffered by saliva (HCO3 / PO3)
* INC CHO diets -> INC acid + DEC saliva =>DEC pH
* Lactic acid producing bacteria ® DEC pH
77
Risk factors for ruminal acidosis
* Size of conc feeds
* Feeding frequency
* Overall starch levels
* Forage access
* Ration sorting
* Transition Sudden change in diet
/ poor no transition to milk cow
diet.
* Concentrate:forage DM ratio >
60:40!
* Overall lack of fibre.
* Lack of effective long fibre (short
chop length)
* Poor Cow comfort - ¯ rumenation
78
Further investigations ?
* Rumination. <60% chewing their cud at rest.
* Rumenocentesis (3/12 cows
79
Prevention of SARA pt1?
limit depression of rumen pH =>
– Forage : concentrate ratio >40:60
– Dietary NDF content >35%
– NDF from forage >20-25% of DMI
– Total sugar & starch content <25%
– In parlour feeding Max 4Kg / feed
80
Prevention. of SARA pt2?
* Improve rumen function
– physically effective fibre – which stimulates chewing!
– Avoid rapidly released starch
– Good transition management (max DMI)
– Good mixing of rations
– Include yeasts
– Include buffers
81
A good transition diet?
MAximise DMI
-> Correct BCS
--> good transition diet:
- Avoid sudden changes in the ration
– Optimising rumen health
– good quality forage to these cows.
– protein and energy supply in the diet is balanced.
– Balance rations for cows requirements of minerals, trace element and vitamins
82
AIMS of transition period?
