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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!
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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!
0
0,5
1
1,5
2
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.
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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.
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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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