Controlling ketosis in cows Flashcards
Background
- 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
Subclinical ketosis
- (newer terminology = hyperketonaemia)
- Blood BHB > 1.2mmol/L
- No clinical signs
Clinical ketosis
- Blood BHB > 3.0 mmol/L
- Clinical signs
Type 1 ketosis
- 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)
Type 2 ketosis
- Occurs soon after calving and is associated with excessive fat mobilisation
- This is often associated with hepatic lipidosis
Type 3 ketosis
- (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.
Comparisons
- 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
Prevention
- 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
Prevention - why bother? (figures based on cows with subclinical ketosis
- 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
What is BHB?
- beta hydroxybutyrate
Why are cows at risk?
Energy requirements
- Maintenance ~ 10%bwt MJ ME/d
- Lactation ~ 5MJ ME/L
When are cows at risk?
- 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
Pathophysiology - type I ketosis
= 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
Pathophysiology - type II ketosis and fatty liver
- 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
Pathophysiology - Hepatic lipidosis (fatty liver)
- 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
Pathophysiology - Type 3 ketosis
= 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
Type 1 simplified
- energy intake < energy demand
- affects cows at peak lactation
- usually seen 4-8w after calving
Type 2 simplified
- excessive fat mobilisation
- affects cows in NEB
- usually seen in the 1st 1-2w after calving
Type 3 simplified
- excessive butyrate consumption -> BHB produced
- affects cows fed poor quality silage that’s high in butyric acid
- seen at any time
Clinical signs of ketosis
- 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
Clinical signs of hepatic lipidosis
- often vague and non-specific
- off food
- milk drop
- immunosuppression
- collapse, liver failure
- death
Relevant history
- Recent calving (Type 2)
- Peak lactation (Type 1)
- Fed poor silage (Type 3)
- Milk drop
- BCS loss (Type 2)
- Off feed
What to test?
- Ketone bodies
- NEFAs
Testing ketone bodies
- 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
Testing NEFAs
- Serum/plasma
- Needs referral to external lab
- Useful before and after calving
- More expensive
Types of tests available
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
Ketone measurement - whole blood
- 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
Ketone measurement - urine
- 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
Ketone measurement - milk
- Strips measure BHB
- 1-2mins
- Powder measures acetone or acetoacetic acid
– Purple colour
NEFA measurement
- 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)
Hepatic lipidosis diagnosis
- 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)
Note on fat:protein ratio (FPR)
- 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
Tx
- Propylene glycol
- Dextrose
- Glucocorticoids
- Vitamin B12/phosphorus
Propylene glycol
- 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
Dextrose
- 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
Glucocorticoids
- 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
Vitamin B12/phosphorus
- 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
Evidence based recommended treatment protocols
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.
