Metabolic diseases in ruminants Flashcards
Fatty Liver syndrome
Contents of 30 kg milk
• Energy demand
o Dry period: 80MJ/500kg BW
o Lactation
▪ 30kg milk/day: 200 MJ
▪ 50kg milk/day: >350MJ
Crucial point in metabolic changes: calvingFatty Liver syndrome
Metabolic characteristics of a dairy cow
• Factors influencing metabolism around calving
o Nutritional changes (adaptation of the ruminal flora and fauna)
o Changes in housing (stress!)
• Expected (physiological) increase of body weight (suspected BW in peak lactation: 500kg i.e. 100%)
o At start of dry period: +10%, i.e. some 550kg
o Just before calving: further 10% i.e. some 605kg
• Expected (physiological) loss of the body weight
o At calving: 60-70kg
o Due to catabolic processes in early lactation:40-60kg (mainly due to lipid mobilisation)
Fatty Liver syndrome
Characteristic features of the energy status in a dairy cow
- Catabolic in the 1st month
* Anabolic following the 2nd month of lactation
Fatty Liver syndrome
Fat mobilisation (fatty liver) syndrome – development
• A typical “production disease” – occurs over 5000kg milk production/year
• Main cause:
o Energy demand does not meet energy supply
o Rate of morbidity depends on milk production
Fatty Liver syndrome
Factors influencing the energy metabolism around calving – summary
• Dry period
o Cause: overfeeding (concentrate!, changes in housing)
o Consequences: obesity→fat stores
• At calving
o Cause: physiological loss of appetite housing and nutritional changes, intercurrent
diseases, obesity)
o Consequences: lipid mobilisation , fatty liver
• Puerperium
o Cause: energy deficiency, too long catabolic period
o Consequences: loss of condition, ketone body production , fatty liver
• Lactation
o Cause: energy overload, too long anabolic state
o Consequences: disposition to obesity
Fatty Liver syndrome
Nomenclature
• During dry period/early postpartal period: Fat Cow Syndrome
• At calving/early postpartal period: Fatty Liver Syndrome, hepatic coma
• Midlactation: Thin Cow Syndrome, secondary (mainly inflammatory) diseases, reproduction
disorders
Fatty Liver syndrome
Forms of fatty liver/fat mobilisation syndrome
- Acute/peracute
- Subacute – during lactation
- Subclinical (chronic disorder)
Fatty Liver syndrome
Forms of fatty liver/fat mobilisation syndrome
• Acute/peracute
o After (rarely before) calving
o Clinical signs
▪ Obesity, anorexia, sudden loss of condition, abdominal pain, hepatomegaly,
apathy, coma, death o Liver lipid >255
o Prognosis: very poor
o Differential diagnosis
▪ Ketosis, milk fever (both are easily treatable)
Fatty Liver syndrome
Forms of fatty liver/fat mobilisation syndrome
• Subacute – during lactation
o Clinical signs: “thin cow”, anorexia and apathy o Intercurrent diseases (lameness, mastitis etc.)
o Ketonuria (ketonanaemia, ketolactia is rare)
o Liver lipid: slightly elevated (around 15%)
o Course might be fatal
Fatty Liver syndrome
Forms of fatty liver/fat mobilisation syndrome
• Subclinical (chronic disorder)
o Clinical signs
▪ Not typical, poor body condition, decreased milk production, high frequency of post-parturient diseases (ketosis, mastitis, retained placenta)
▪ Ketonuria
o Liver lipid 10-12%
o Disorders in reproduction (anovulation, infertility)
o Course: not fatal
Fatty Liver syndrome
Consequences of fatty liver syndrome
• Sudden death of the cow
• Decreased milk production
• Loss of condition
• Development of secondary diseases (increase susceptibility to retained placenta, abomasal
displacement)
• Reproduction disorders (poor oestrus signs, anovulation, increase in the number of days
between two calving)
Fatty Liver syndrome
Diagnostic methods
• Clinical signs (not typical)
• Ultrasound (rarely used)
• Liver biopsy (blind or US-guided)
o Visual evaluation
o Floating test
• Laboratory tests
o In-office (not specific – show energy deficiency)
o Referral laboratory (too slow)Fatty Liver syndrome
Laboratory diagnosis of energy deficiency
• Ketone body (acetone, aceto-acetate) checking by nitroprusside-Na: o Ross-test
o Rothera’s test
o Test strips (urine, plasma, milk)
• Urea determination
o Test strips or photometric measurements: plasma, milk
o Physiological range: 3-6mmol/L
o Energy deficiency: >5 mmol/L
o (N-deficiency: <2.5mmol/L)Fatty Liver syndrome
Plasma/serum parameters
- FFA/NEFA
- Total cholesterin, albumin
- Glucose
- Ketones: BHB
Fatty Liver syndrome
• Enzyme activity
o AST, ALT, LDH
o SDH, GLDH, OCT
Fatty Liver syndrome
Laboratory diagnosis in referral laboratories
- Histology
- Chemical analysis for total lipids and/or triglycerides
- Results of these methods often arrive too late
- Useful to monitor subclinical forms at herd level
Fatty Liver syndrome
Prevention and treatment
- Avoid overcondition of dry cows
- Stimulate energy supply following parturition
- Immediate treatment of any other diseases decreasing the appetite of the cow
- A typical condition that can be more easily prevented than treated
Bovine ketosis (acetonaemia of cattle)
- Typical production diseases
- Ketogenesis > ketolysis
- Increased ketone body production→ketonaemia, ketonuria, ketolactia
Bovine ketosis (acetonaemia of cattle)
Occurrence
- High-producing dairy cows, during postparturient period (within 60 days, average: 3 weeks after calving)
- Little evidence for a heritable predisposition
Bovine ketosis (acetonaemia of cattle)
Ketone bodies
- Aceto-acetate (AcAc)→3-OH-butyrate→acetone
* Na-nitroprusside: sensitive to AcAc and partially to acetone, not sensitive to 3-Oh-butyrate
Bovine ketosis (acetonaemia of cattle)
Ketone bodies in biological fluids
• Physiological ketone body ratio post partum in plasma: o 3-OH-butyrate : (AcAc + acetone) = 10:1
• Pathological ration in a ketonic cow’s plasma
o 3-OH-butyrate : (AcAc + acetone) = 3.5:1
• Ketone body distribution in biological fluids of a ketonic cow o Urine ketone : plasma ketone : milk ketone = 10:2:1
• PU/Pd deeply influences urine ketone body concentration
• Nitroprussid-Na (Rothera- and Ross-test, ketosis-strip etc.) reacts mainly with AcAC and acetone, does not react with 3-OH-butyrate
Bovine ketosis (acetonaemia of cattle)
Aetiology of ketosis
• Nutritional factors
o Low carbohydrate and high protein content in the ration
o Low propionate level, increased butyrate (poor quality silage)
• Endocrine factors
o Ketogenic hormones: thyroxin, GH, glucagon
o Antiketogenic: glucocorticoids, insulin
o Endocrine balance around calving is a predisposing factors
• Liver malfunction
o “Overload” of liver metabolic capacity
o Fatty infiltration (hepatic failure, - coma)
• Decreased muscle function
o Ketone bodies cannot be utilised (oxidised) in inactive muscles
Bovine ketosis (acetonaemia of cattle)
Classification of bovine ketosis
• Primary (production) ketosis
o Caused by high milk yield
• Secondary (starvation, deficiency) ketosis
o Caused by low energy supply or anorexia
• Nutritional
o Caused by bad quality food i.e. butyrate-containing silage
Bovine ketosis (acetonaemia of cattle)
Forms of primary (production) ketosis
• Acute nervous form
o Highly elevated (10-fold) ketone bodies increase in the blood plasma (ketonemia),
hypoglycaemia, ketonuria, ketolactia
o Signs
▪ Excitation, unconsciousness, convulsion, grinding or the teeth, apathy, ataxia, finally lateral recumbency, blindness, coma
▪ Sweet, typical smell of the expired air and urine (caused by acetone)
o Course
▪ Sometimes sudden death
▪ Quick recovery following treatment
▪ Relapses are rare
• Subacute, digestive, wasting form
o Mild ketonemia (3-5 fold increase) + hepato-steatosis, ketonuria, less severe ketolactia
o Signs
▪ Maldigestion, loss of condition, diarrhoea, abdominal pain, decreased milk production
▪ GI signs dominate with or without nervous symptoms
o Course
▪ Depending on the liver function
▪ Treatable, but the response is frequently transient
• Subclinical form
o Slight ketonemia (2-fold increase)
o Signs
▪ Not typical
▪ Drop in milk yield, loss of body condition
▪ Similar to the subacute form of fatty liver syndrome
o Course
▪ Never fatal
▪ Main consequences: reproductive disorders, secondary diseases
▪ Potential manifestation of acute form at the succeeding clave
