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Y4 Farm - Production diseases > Controlling ketosis in cows > Flashcards

Controlling ketosis in cows Flashcards

1
Q

Background

A
  • High herd and cow level prevalence
    – Particularly in high producing dairy farms
  • Subclinical form of Type 2 ketosis most common
    – Increased risk of clinical ketosis, RFM, LDA, metritis, lameness, mastitis, culling, death
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2
Q

Subclinical ketosis

A
  • (newer terminology = hyperketonaemia)
  • Blood BHB > 1.2mmol/L
  • No clinical signs
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3
Q

Clinical ketosis

A
  • Blood BHB > 3.0 mmol/L
  • Clinical signs
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4
Q

Type 1 ketosis

A
  • Occurs at peak lactation and related to failure to meet energy demands of milk production
  • This occurs due to insufficient gluconeogenic pre-cursors (i.e. underfeeding)
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5
Q

Type 2 ketosis

A
  • Occurs soon after calving and is associated with excessive fat mobilisation
  • This is often associated with hepatic lipidosis
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6
Q

Type 3 ketosis

A
  • (also called silage ketosis or butyric ketosis)
  • Feeding of poor-quality butyric silage (carbohydrates are fermented to butyric acid rather than lactic acid) results in butyric acid being converted to BHB in the rumen.
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7
Q

Comparisons

A
  • Ketosis in cattle is not the same as DKA (diabetic ketoacidosis) in small animals
  • Ketosis in cattle is not called ketoacidosis
  • Ketosis in cattle is not the same as acidosis (SARA or acute) in cattle
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8
Q

Prevention

A
  • Preventing ketosis is key

Achieved through appropriate nutritional management
- Type 1 = management of nutrition during lactation to ensure demands are met
- Type 2 = management of nutrition in transition period to maximise DMI and minimise NEB
- Type 3 = management of silage to ensure adequate fermentation
- Pregnancy toxaemia = management of nutrition in late gestation

  • Monensin
    – questions re it’s use, but is beneficial
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9
Q

Prevention - why bother? (figures based on cows with subclinical ketosis

A
  • 6x increased risk of displaced abomasum
  • 4.5x increased risk of early cull
  • 30% less likely to conceive to 1st service
  • 2.2kg less milk per day in 1st 30 DIM
  • For every 0.1 mmol/L increase in BHB
    – 1.1x increased LDA risk
    – 1.4x increased risk of cull
    – 0.5kg/d less milk
  • Increased risk of developing clinical ketosis
  • Increased risk of death
  • Increased risk of progressing to hepatic lipidosis
  • Pregnancy toxaemia
    – High risk of death
    – Increased risk of abortion
  • Subclinical disease should be treated when identified to prevent progression to more severe disease and development of associated co-morbidities
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10
Q

What is BHB?

A
  • beta hydroxybutyrate
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11
Q

Why are cows at risk?

A

Energy requirements
- Maintenance ~ 10%bwt MJ ME/d
- Lactation ~ 5MJ ME/L

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12
Q

When are cows at risk?

A
  • Just after calving yield is increasing much faster than food intake (type 2)
  • In high yielding cows it can also be difficult to provide enough energy for peak lactation (Type1)
  • particularly at risk around calving
  • appetite drops cows in the late dry period, so day of calving feed intake drops
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13
Q

Pathophysiology - type I ketosis

A

= failure to meet peak lactation demand
- Reduction in production of glucose precursors in rumen
- Results in a reduction in hepatic glucose production
- Liver metabolises fatty acids -> ketones produced, also NEFAs are not taken up by hepatocytes
- Clinically this can be detected by elevated measurements of BHB and NEFA in blood and other fluids

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14
Q

Pathophysiology - type II ketosis and fatty liver

A
  • Altered glucose metabolism results in negative effects on milk yield, reproductive performance and increases the risk of metabolic disorders
  • Oxidation of NEFAs favours ketone bodies when blood glucose is low -> hyperketonaemia
  • Large amount of NEFA exceed liver capacity for oxidisation and NEFAs starts to be esterified to TAG. Export is very slow in ruminants -> TAG accumulates in hepatocytes -> hepatic lipidosis
  • NEFAs absorbed by liver and can be processed one of 2 ways:
    – Oxidation -> ketone bodies or ATP
    – Esterification -> triacylglyceride (once the concentrations are high it exceeds the livers capacity to oxidise them and they’re esterified)
  • In NEB NEFAs are released from adipose tissue
  • End stage: liver failure
    – due to so many triglycerides being accumulated, the hepatocytes don’t work
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15
Q

Pathophysiology - Hepatic lipidosis (fatty liver)

A
  • Associated with type 2 ketosis
    – Likely part of a spectrum
  • Circulating NEFAs exceed liver capacity for processing
    – Re-esterified and deposited in hepatocytes as triacylglycerol (TAG)
    (“liver lipid accumulation”)
    – Larger deposits of TAG can interfere with hepatic function
    – Exacerbates NEB
  • Can be fatal
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16
Q

Pathophysiology - Type 3 ketosis

A

= consumption of ketogenic compounds
- Poor quality silage
- Wet grass (late season)
- Low sugar content
- High nitrate content

  • Clostridial bacteria predominate -> ferment carbohydrate to butyric acid (not lactic acid)
  • Butyric acid converted to BHB in rumen -> hyperketonaemia
  • Not very common, esp in comparison to the other types
17
Q

Type 1 simplified

A
  • energy intake < energy demand
  • affects cows at peak lactation
  • usually seen 4-8w after calving
18
Q

Type 2 simplified

A
  • excessive fat mobilisation
  • affects cows in NEB
  • usually seen in the 1st 1-2w after calving
19
Q

Type 3 simplified

A
  • excessive butyrate consumption -> BHB produced
  • affects cows fed poor quality silage that’s high in butyric acid
  • seen at any time
20
Q

Clinical signs of ketosis

A
  • vague and non-specific
  • off food
  • milk drop
  • can smell ketones (some people)
  • nervous ketosis
    – rare
    – care: animals can be aggressive
    – intensive licking of leg(s)
  • all types present in the same way
21
Q

Clinical signs of hepatic lipidosis

A
  • often vague and non-specific
  • off food
  • milk drop
  • immunosuppression
  • collapse, liver failure
  • death
22
Q

Relevant history

A
  • Recent calving (Type 2)
  • Peak lactation (Type 1)
  • Fed poor silage (Type 3)
  • Milk drop
  • BCS loss (Type 2)
  • Off feed
23
Q

What to test?

A
  • Ketone bodies
  • NEFAs
24
Q

Testing ketone bodies

A
  • Usually BHB
  • More variety of tests available:
    – Blood/serum/plasma/milk/urine
    – Cowside/laboratory
    – Quantitative/semi-quantitative
  • Can be done on farm
  • Most useful after calving
  • Lots of cows have slightly elevated BHB before calving, so not useful before calving
25
Q

Testing NEFAs

A
  • Serum/plasma
  • Needs referral to external lab
  • Useful before and after calving
  • More expensive
26
Q

Types of tests available

A

Whole blood: Ketometer:
- e.g. Precision Xtra meter (Abbott Labs)
- Sn = 88-96%
- Sp = 96-97%
- cow side
- quantitative
- validated meters available

Serum/plasma: External lab
- NEFAs or ketone bodies can be tested externally

Milk:
- Ketone test strips
– e.g. Ketotest (Santa Kagaku Co. Ltd)
– Sn = 27.73%
– Sp = 96-99%
– Cow side
– Can be done by farmers
- Powdered reagent
– E.g. Rothera’s reagent/KetoCheck powder
– purple powder develops if ketones present
– Sn = 2-41%
– Sp = 99-100%
– powders have very low sensitivity; fallen out of favor

Urine: Ketone test strips
- e.g. Ketostix (Bayer)
- Sn = 78-90%
- Sp = 86-96%
- Cow side
- Semi-quantitative
- Economical for herd level use

27
Q

Ketone measurement - whole blood

A
  • Measures blood concentration of BHB
  • Most commonly used thresholds:
    – Subclinical ketosis > 1.2 mmol/L (range 1.0 – 1.4mmol/L)*
    – Clinical ketosis > 3.0 mmol/L
28
Q

Ketone measurement - urine

A
  • Measures urine concentration of acetoacetic acid
    – Note this is not BHB
    – Accuracy is reasonable
  • Cheap and easy to use
  • Read at manufacturer recommended time -> usually 10-15s
  • Can be difficult/time consuming to wait for cows to urinate
    – Consider catheterisation
29
Q

Ketone measurement - milk

A
  • Strips measure BHB
  • 1-2mins
  • Powder measures acetone or acetoacetic acid
    – Purple colour
30
Q

NEFA measurement

A
  • Measurement of blood NEFA concentration
  • External lab needed
  • Most often used for herd level monitoring of NEB rather than diagnosis of sick cows
    – Slower to get results
  • More useful than BHB pre-calving
  • Generally accepted thresholds
    – Last 2 weeks of gestation < 400 mmol/L (< 300 mmol/L in some texts)
    – Other times < 700 mmol/L (< 600 mmol/L in some texts)
31
Q

Hepatic lipidosis diagnosis

A
  • Often presumptive based on severity and duration of ketosis present
  • Absolute diagnosis needs determination of hepatic triglyceride content
    – Not routinely tested
  • Liver biopsy
    – Can indicate severity of lipidosis
    – Difficult to assess effect on function
  • Refractory to tx (therefore, decent presumptive diagnosis made from this)
32
Q

Note on fat:protein ratio (FPR)

A
  • Milk fat % ÷ milk protein %
  • Readily available metric
  • Ratios > 1.4:1 can indicate cows at increased risk of developing ketosis -> useful screening test
  • Can be useful to get an idea of energy status at herd/group level
  • Not recommended for diagnosis of individual cows
  • Robotic milkers often flag cows they think are ketotic
  • Ketotic: more fat being released into the milk
33
Q

Tx

A
  • Propylene glycol
  • Dextrose
  • Glucocorticoids
  • Vitamin B12/phosphorus
34
Q

Propylene glycol

A
  • Gluconeogenic precursor
  • Most evidence-based treatment
    – Shorter recovery time
    – Reduce negative outcomes
  • 300g once daily for 3-5 days (by mouth)
    – Check concentration to make sure volume = 300g
  • Increases the amount of propionate in the rumen
  • By mouth rather than in food
35
Q

Dextrose

A
  • Limited evidence
  • Short-term effect
  • High dose dextrose possibly detrimental to abomasal function?
  • Indicated for more severe cases
    – e.g. nervous ketosis (IV)
  • Get rebound effect if don’t also use propylene glycol
  • Not valuable for subclinical cases
36
Q

Glucocorticoids

A
  • Stimulate hyperglycaemia and inhibit insulin effects
    – ?stimulate gluconeogenesis -> well established in monogastrics, not demonstrated in ruminants
  • Stimulate appetite
  • Reduced glucose uptake by udder
  • Evidence for effect is limited
  • May impede recovery
  • No longer recommended for routine use
    –Sometimes used in severe cases - controversial
37
Q

Vitamin B12/phosphorus

A
  • Limited evidence
  • Involved in gluconeogenesis pathway
  • Efficacy unclear
    – Not currently recommended for routine use
  • Needs to be given parenterally
    – Oral compounds degraded in rumen
  • Probably doesn’t do harm but unsure of its real value
38
Q

Evidence based recommended treatment protocols

A

Subclinical ketosis
- Propylene glycol 300g for 3-5 days per os

Clinical ketosis and hepatic lipidosis
- Propylene glycol 300g for 3-5 days per os (clinical with mild signs)
+
- 500 mL 50% dextrose IV in severely affected cases (e.g. nervous ketosis)

Tx for all types of ketosis regardless of original aetiology.

Y4 Farm - Production diseases (18 decks)

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