Bovine Ketosis p1252-1258

Question 1

The three ketone bodies are?

Answer 1

Acetone
Acetoacetate
Betahydroxybutyrate

Question 2

Type I vs Type II ketosis?

Clinical vs subclinical ketosis?

Answer 2

Type I - classic, seen during early lactation from reduced glucose in blood and liver, thus causing mobilization of fat and elevating ketones; all due to negative energy balance

Type II - seen in overconditioned cattle and fatty liver, when blood insulin is high and a transient hyperglycemia is present

Clinical - elevated blood ketones and clinical signs; when absorption and production of ketone bodies extend their use as an energy source

Subclinical - elevated ketone bodies, few clinical signs, high RISK of low milk production, assoc. dzs and early culling

Question 3

First clinical signs of ketosis? When is this occurring? Differential diagnosis?

Answer 3

Decreased feed intake and milk production. Type I occurs 3-6 weeks after parturition, with Type II occurring shortly after calving. Other c/s include scant feces, lethargy, reluctance to move, pica, nervous ketosis, odor on breath and in milk

DAs, metritis, mastitis, and peritonitis are common differentials

Question 4

How is ketosis diagnosed? What from the body should be tested? Which ketones/other values are the best to detect?

Answer 4

In clinical ketosis - BG 20-40 mg/dL, blood ketones > 30 mg/dL, total urine ketones > 84 mg/dL and milk ketones > 10 mg/dL

Subclinical ketosis - lower than normal BG, blood ketones 10-30 mg/dL, milk ketones of 2 mg/dL

Blood BHB 1.2-2.9 mmol/L for subclinical and > 3 mmol/L for clinical. 1.4 mmol/L is the consensus to diagnosis subclincial.

Urine ketones are concentrated 2-20 more than blood, while milk ketones closely reflect blood levels and are a better indicator of ketosis

AcAc is not to be used, as it is unstable and difficult to detect. BHB in milk has an acceptable Se and Sp for screening herds with subclinical ketosis. Can use blood levels of NEFAs, greater than 0.5 mEq/L is detecting subclinical ketosis. BUT NEFAs vary greatly in diurnal variation, and timing can be difficult.

Liver values can be increased, (AST and SDH). Liver bx would be the gold standard for accurately assessing degree of hepatic lipidosis.

Question 5

In the normal lactating cow, how is energy handled by the liver and what are the outcomes? How does this change during negative energy balance?

Answer 5

Energy = VFAs (acetate, butyrate, propionate), bacterial protein and glucose protein that has not been degraded in the rumen
Acetate is used for fat synthesis and may be used at acetylcoenzyme A (CoA).
Butyrate is converted to acetate and thus does the same.
Propionate enters the TCA cycle at the level of succinyl CoA, and aids in glucose production.

During negative energy balance, there is a reduction in oxaloacetate (which comes from gluconeogenic precursors, like propionate) and this leads to a slow down of the TCA cycle and a build up of CoA. CoA turns into ketones.

Question 6

Subclinical cases of ketosis, with BHB > 1.2 mmol/L within 3-5 DIM are more likely have what problems?

Answer 6

6.1 x more likely to develop a DA
4.5 x more likely to be removed from the herd
Produced 2.2 kg less milk/day

Question 7

What is the main goal behind treatment of ketosis?

Answer 7

Increasing blood glucose, providing glucose precursors, stopping the mobilization of fat and increasing uptake of glucose by cells.

Question 8

List 2 forms of replacment therapy for ketosis.

Answer 8

1. IV dextrose, 100-500 mL of 50%
   Remember this is a transient treatment and blood ketones will rise again in < 12 hrs
2. Oral propylene glycol, 225 mL BID x2d then 110 mL BID x2d; 300 SID x5d
   Want to decrease glucose demand by peripheral tissues, and allow blood glucose to rise, in turn stimulating insulin release. This slows release of triglycerides from adipose tissues and decreases NEFAs and BHBs.

Question 9

List 2 forms of hormonal therapy for ketosis.

Answer 9

1. Glucocorticoids, dexamethasone 0.04 mg/kg or 20-25 mg/animal, once.
   This helps maintain a hyperglycemic state. This can cause reduced feed intake and exacerbate the fatty liver syndrome.
2. Insulin, long acting, 200-300 IU/animal protamine zinc SQ q48hrs
   This suppresses fatty acid mobilization and increases tissue uptake of glucose, still stimulating hepatic glycolysis. Not commonly used, but should be administered with glucose or glucocorticoid to prevent hypoglycemia.

Question 10

List 3 novel treatments for ketosis.

Answer 10

1. Cobalt and Vit B12. Deficiency in these supplements can be a cause of ketosis. Vit B12 is necessary for the metabolism of propionate, which is essential to the TCA cycle. Cobalt is vital to the formation of Vit B12 in the rumen.
2. Niacin or nicotinamide decrease blood ketones and FFA, and increases blood glucose. Used in conjunction with propylene glycol, but studies have shown inefficacy.
3. Ionophores can increase the rate of propionate formation in the rumen.

Question 11

What are ways a producer can try to prevent ketosis?

Answer 11

Feeding and management of cows during late lactation and dry period should produce cows with good BCS at calving. Introduce the lactation diet gradually. The early lactation diet should be highly palatable and with an appropriate energy density.