Internal MedicineLectures for students, 8th semester

Department of Internal MedicineFaculty of Veterinary Science

Szent István University

Metabolic disorders of ruminants - ketosis

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BOVINE KETOSIS (ACETONAEMIA OF CATTLE)Typical production disease. Ketogenesis > ketolysisIncreased keton body production → ketonaemia, ketonuria, ketolactia

Occurrence: high-producing dairy cows, during postparturient period (within 6O days, average: 3 weeks after calving).Little evidence for a heritable predisposition.

Keton bodies:aceto-acetate (AcAc) → 3-OH-butyrate → acetoneNa-nitroprussid: sensitive to AcAc and partially to acetone, not sensitive to 3-OH-butirate

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KETON BODIES IN BIOLOGICAL FLUIDS

Physiological keton body ratio post partum in plasma:3-OH-B : (AcAc +acetone) = 1O : 1

Pathological ratio in a ketotic cow’s plasma:3-OH-B : (AcAc + acetone) = 3-5 : 1

Keton body distribution in biological fluids of a ketoticcow:

urine keton : plasma keton : milk keton = 1O : 2 : 1PU/PD deeply influences urine keton body concentration!

Ketone bodies in blood plasma(aceton, mmol/l)

Nitroprusszid-Na (Rothera- and Ross-test, Ketostix-strip etc.) reacts mainly with AcAc and aceton, does not react with 3-OH-B!

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0,5

1

1,5

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Monog.species

Healthy Subcl. ketosis Ketosis

AcetonAcAc3-OH-B

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ETIOLOGY OF KETOSIS

1. Nutritional factorslow carbohydrate and high protein content in the ration

↓low propionate level, increased butyrate (poor quality silage)

2. Endocrine factorsketogenic hormones: thyroxin, GH, glucagonantiketogenic: glucocorticoids, insulin

Endocrine imbalance around calving is a predisposing factor.3. Liver malfunction

"Overload" of liver metabolic capacityFatty infiltration (hepatic failure, -coma)

4. Decreased muscle function Ketone bodies can not be utilized (oxidized) in inactive muscles

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CLASSIFICATION OF BOVINE KETOSIS

• Primary (production) ketosis

(caused by high milk yield)

• Secondary (starvation, deficiency) ketosis

(caused by low energy supply or anorexia)• Nutritional

(caused by bad quality food, ie. butyrate-containing silage)

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FORMS OF PRIMARY (PRODUCTION) KETOSIS 1.

Other classifications also exist!

1. Acute, nervous form

Highly elevated (10-fold) keton body increase in the blood plasma (ketonaemia), hypoglycaemia, ketonuria, ketolactia.

Signs:Excitation, unconsciousness, convulsions, grinding of the teeth,apathy, ataxia. Finally lateral recumbency, blindness, coma. Sweet, typical smell of the expired air and urine (caused by acetone).

Course: Sometimes sudden death. Quick recovery following treatment. Relapses are rare.

Ketonuria-test (Rothera)

Comatosus dairy cow with positive Rothera-test(nitrorussid-Na) – a sign of energy deficiency.Blood and milk should be checked for keton bodies – both were positive

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FORMS OF PRIMARY (PRODUCTION) KETOSIS 2.

2. Subacute, digestive, wasting form (most common)

Mild ketonaemia (3-5-fold increase) + hepato-steatosis, ketonuria, less severe ketolactia

Signs:maldigestion, loss of condition, diarrhoea, abdominal pain, decreased milk production. GI signs dominate with or without nervous symptoms.

Course: depending on the liver function.

Treatable, but the response is frequently transient.

Ketonuria-test with test-strips and with Ross-reagent

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EVALUATION OF KETOLACTIA 1.

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EVALUATION OF KETOLACTIA 2.

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FORMS OF PRIMARY (PRODUCTION) KETOSIS 3.

3. Subclinical form

Slight ketonaemia (2-fold increase)

Signs: Not typical. Drop in milk yield, loss of body condition

Similar to the subacute form of fatty liver syndromeCourse: Never fatal. Main consequences: reproductive disorders, secondary diseases.Potential manifestation of acute form at the succeeding calving

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TREATMENT OF KETOSIS

1. Acute, nervous form:• Glucose/dextrose therapy: 20-40% solution, 500 ml iv. Repeatable.

(Attention: Glucose renal threshold in ruminants is very low)• Stimulation of GNG: dexamethasone 5-10 mg iv, im.• Glucoplastic compounds per os:

Na-propionate 100-200 g/day, propylene glycol 100-200 g/day, commercial antiketogenic medicines are available in all countries

2. Digestive, wasting form:As above + proper nutritional management, glucoplasticcompounds, glucose therapy (20% solution, 200-30 ml iv/day)

3. Subclinical form: adequate nutritional management

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PREVENTION

• Carbohydrate-rich diet (easily fermentable) after

calving. Avoid butyrate in the ration (good quality

silage)

• Appropriate N-supply

• Exercise (stimulates ketolytic procedures in muscles)

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OVINE KETOSIS (PREGNANCY TOXAEMIA) 1.

Occurrence: last trimester of pregnancy (twins!).Regularly herd-disease, prolonged outbreak. Typical seasonal occurence (late autumn – winter innorthern part of Europe)

Predisposing factors: intensive housing, obesity

Cause: energy deficiency,changes in nutrition and/or in housing,stress (endocrine basis of the condition)

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OVINE KETOSIS (PREGNANCY TOXAEMIA) 2.

Symptoms: 2-6 days course. Similar to the nervous form of ketosis in cows.Apathy/lethargy, anorexia, ataxia, blindness, grinding of the teeth.Ketonuria, ketonaemia, hypoglycaemia, severeliver failure (fatty liver), coma, death Ketotic ewe, positive urine

and plasma keton-test

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OVINE KETOSIS nitroprussid-Na reaction

Milk-test is not used asmilk is notavailablebeforelambing

Dark pink colour

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OVINE KETOSIS (PREGNANCY TOXAEMIA) 3.

Therapy: regularly unsuccessful100-200 ml glucose/dextrose 20% solution iv, ip.propylene glycol, glycerol drenchDexamethasone. Large dose of 25 mg/animal!Induces even abortion/premature parturition.

Prevention: more effective. Avoid energy imbalance, stressors

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