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
Bovine ketosis (acetonaemia of cattle)
Ketonuria test (Rothera)
- Comatose dairy cow with positive Rothera-test (nitrussid-Na) – a sign of energy deficiency
- Blood and milk should be checked for ketone bodies – both were positive
Bovine ketosis (acetonaemia of cattle)
Treatment of ketosis
Acute, nervous form
• Glucose/dextrose therapy:20-40% solution, 500ml iv repeatable (attention: glucose renal threshold in ruminants is very low)
• Stimulation of GNG: dexamethasone 5-10mg iv, im
• Glucoplastic compounds per os:
o Na-propionate 100-200 g/day, propylene glycol 100-200 g/day, commercial antiketogenic medicines are available in all countries
Digestive, wasting form
• As above + proper nutritional management, glucoplastic compounds, glucose therapy (20% solution, 200-300 ml iv/day)
Subclinical form
• Adequate nutritional management
Bovine ketosis (acetonaemia of cattle)
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)
Ovine ketosis (pregnancy toxaemia)
• Ketosis (during pregnancy) is so severe that they fall into metabolic acidosis
Ovine ketosis (pregnancy toxaemia)
Occurrence
- Last trimester of pregnancy (twins→require much more energy that mother falls into ketosis)
- Regularly heard-disease, prolonged outbreak
- Typical seasonal occurrence (late autumn-winter in northern part of Europe
Ovine ketosis (pregnancy toxaemia)
Predisposing factors
- Intensive housing
* Obesity
Ovine ketosis (pregnancy toxaemia)
Cause
- Energy deficiency
- Changes in nutrition and/or in housing
- Stress (endocrine basis of the condition)
Ovine ketosis (pregnancy toxaemia)
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, severe liver failure (fatty liver), coma, death
Ovine ketosis (pregnancy toxaemia)
Nitroprussid-Na reaction
• Milk-test is not used as milk is not available before lambing
Ovine ketosis (pregnancy toxaemia)
Treatment
• Regularly unsuccessful
• 100-200 ml glucose/dextrose 20% solution iv., ip.
• Treat ketosis
• Glucocorticoids → induce lambing/abortion
o Dexamethasone: large dose of 25mg/animal
• C-section has to be considered (1 week before expected lambing → okay to do C-section, but
date of mating is often unknown)
Ovine ketosis (pregnancy toxaemia)
Prevention
- More effective
* Avoid energy imbalance, stressors
Recumbency in the periparturient period due to metabolic problems
Downer cow syndrome Atypical milk fever (downer cow) Downer cow syndrome – musculoskeletal injury Parturient paresis (milk fever) Hypomagnesemic tetany
Recumbency in the periparturient period due to metabolic problems
Downer cow syndrome
Definition:
• There always is a primary cause
• Animals staying recumbend ager 24 hours of calving
• Cattle cannot stand long lasting recumbency well
• After a short time (36-48h) degenerative alterations occur in the musculoskeletal system due to weight of the cow→visualisable with microscope
• Worse chance of recovery when recumbent
• Fenwick et al, 1969
o Hypocalcaemic cows treated within 6 hours, only 2% became long lasting recumbent
o Treatment after 18 hours of the occurrences 50% of the animals did not stand up
• Secondary musculoskeletal disorders can cause long lasting recumbency
Recumbency in the periparturient period due to metabolic problems
Downer cow syndrome
Pathogenesis
- Long term lateral recumbency→muscle compression, ischaemia, hypoxia, necrosis, (inflammation)
- Compression of the nerves as well (n. ischiadicus, n. peronaeus)
- Repeated efforts to get up→rupture of muscles, haematoma
Recumbency in the periparturient period due to metabolic problems
Downer cow syndrome
Occurrence
- Usually periparturient
* But anywhere in lactation
Recumbency in the periparturient period due to metabolic problems
Downer cow syndrome
Incidence
- 2-5% of the herd
* 20% around calving time
Recumbency in the periparturient period due to metabolic problems
Atypical milk fever (downer cow)
Definition
• Primarily disorder of (hind) limb muscles (Extensors
• Due to their ischaemia myodegeneration, necrosis develops
• Ischaemia is caused by permanent compression
• Similar myodegeneration occurs in humans after long-term strangulation of the limb
(tourniquet-paralysis)
Recumbency in the periparturient period due to metabolic problems
Atypical milk fever (downer cow)
Aetiology
• Not uniform
• Any disease can be in the background causing lying of the cows.
• Always a secondary condition
• Potential background
o Milk fever
o Trauma (muscle, joints, bones, spinal cord)
o Fatty liver
o Hypomagnesaemia, hypokalaemia, hypophosphatemia o Lactacidaemia
o Mastitis (E.coli)
o Displaced abomasum
o Reticulo-peritonitis
o Infectious diseases (even BSE)
“5 M”
• Mastitis
• Metritis
• Metabolic
• Musculoskeletal/neurologic
• Massive sepsis (peritonitis)
→all cause recumbencyRecumbency in the periparturient period due to metabolic problems
Atypical milk fever (downer cow)
What should you do with a recumbent cow
• Slaughter
• Wait (if they are able to eat and drink)
→no strict rule because we cannot estimate the amount of muscle degeneration
→based on clinical signs
Recumbency in the periparturient period due to metabolic problems
Atypical milk fever (downer cow)
Clinical signs
• Sitting like a frog
Recumbency in the periparturient period due to metabolic problems
Atypical milk fever (downer cow)
Treatment without medicaments
- Pull/transport the cow to a smooth, soft surface
- Suspension of the cow
- Suspension with air bag
- Aqualift water bath
- Stimulation of circulation
Recumbency in the periparturient period due to metabolic problems
Atypical milk fever (downer cow)
Prognosis
• CK (creatinine kinase)
o >1000 IU/L – guarded
o Bad – elevated for two consecutive days
• AST (aspartate aminotransferase, GOT)
o >500 IU/L – bad
• Bad sign if both are elevated for 2 days
Recumbency in the periparturient period due to metabolic problems
Atypical milk fever (downer cow)
Laboratory findings
• Normal Ca-, Mg- and P-values in the blood
• Normal haematology (except when inflammation is present)
• Severe increase of enzyme activity (creatin-kinase=CK, AST=GOT,
LDH)
• Myoglobinaemia, myoglobinuria (proteinuria). Not visible
Recumbency in the periparturient period due to metabolic problems
Atypical milk fever (downer cow)
Medical treatment
- Electrolytes, vitamins, roborants
- Iv Ca-therapy: maximum 1-2 repeated doses
- Mg and P-therapy as well
- Vitamin D (increases Ca- and P-levels)
- In case of hypokalaemia K-therapy
Recumbency in the periparturient period due to metabolic problems
Downer cow syndrome – musculoskeletal injury
Sensorium decreased/kept?
• Decreased
o Metabolic, (hypocalcaemia, puerperalis coma, tremor, Mg loss, neurological ketosis)
• Kept
o Good status: certain metabolic disease, muscle disease, nerve damage, psychogenic
immobility
o Bad status: acute abdomen, shock/intoxication, abdominal pain
Recumbency in the periparturient period due to metabolic problems
Downer cow syndrome – musculoskeletal injury
Clinical examination
- Hoofs (laminitis)
- Joints
- Tendons and muscles (effusion, temperature, pain, swelling)
- Stifle
- Pelvis and upper limb
- Rectal exam
- Spine (palpation) T2-S
- Nerves
- Skin
- Anal tone/Anus-reflex
- Corona exam
- Patellar reflex
Secondary nerve damage due to prolonged recumbency
• Hind limb: n. ischiadicus
• Fore limb: n. radialis
Recumbency in the periparturient period due to metabolic problems
Parturient paresis (milk fever)
Occurrence
- High-producing, adult dairy cows (mainly in 5-10 years of age)
- Immediately after calving (1-3 days)
Recumbency in the periparturient period due to metabolic problems
Parturient paresis (milk fever)
Cause
- Increased neuro-muscular irritability (hypocalcaemia, hypophosphataemia)
- Simultaneous hypermagnesaemia (rarely normo- or hypomagnesaemia)
Recumbency in the periparturient period due to metabolic problems
Parturient paresis (milk fever)
Pathogenesis
• Relative/absolute hypoparathyroidism
• Loss of mobilizable Ca-stores in bones (age!)
• Decreased Ca-absorption from the GI tract
• Increased Ca-excretion with decreased Mg-excretion in milk
• 3 phases of clinical form
Mechanism affecting the calcium level
- 1L milk requires 1.2g Ca
- First 4-5 days are required until the animal is able to maintain normal Ca levels
Recumbency in the periparturient period due to metabolic problems
Parturient paresis (milk fever)
Symptoms
- Sternal, later lateral recumbency
- (tetany)
- Opisthotonos
- Coma
- Frequent consequence: “downer cow” syndrome
Recumbency in the periparturient period due to metabolic problems
Parturient paresis (milk fever)
In-office laboratory tests
• Ca-test, whole blood (Graeub, Switzerland)
o Semi-quantitative test
• Sulkowitch probe
o Composition
▪ 2.5 g oxalic acid
▪ 2.5 g ammonium-oxalate
▪ 5ml cc. acidum aceticum (“glacial acid”)
▪ Add 150 ml DW
o Hypothesis:
▪ Normocalcaemic cows excrete calcium via urine, precipitating in the presence
of oxalic acid
▪ Hypocalcaemic cows excrete less Ca (hypocalciuria), therefore less/no
precipitation is present
o Procedure
▪ Equal volume urine and reagent to be mixed
▪ After some 3 minutes the amount of precipitate is evaluated (+, ++, +++)
o Evaluation
▪ -/+: no Ca/hypocalciuira: most probable hypocalcaemia
▪ ++: normocalciuria, hypocalcaemia rare
▪ +++: normo/hypercalciuria, hypocalcaemia can be excluded
• Ionised calcium measurement possibilities
Measurement of blood Ca
• Total vs. ionised calcium (tCa vs. iCa)
o Ionised Ca
o Albumin bound Ca
o Other protein bound Ca
o Anioncomplex bound Ca
• Total calcium fractions in the sera
o Blood pH
o Blood albumin concentration
o Other proteins in blood
• Effecting the fractions
• The ration of ionised Ca changes 305% compared to total Ca as days go on after calving in the first five days
Recumbency in the periparturient period due to metabolic problems
Parturient paresis (milk fever)
Course
- Regularly good response to Ca-therapy
* (except: atypical from, downer cow syndrome)
Recumbency in the periparturient period due to metabolic problems
Parturient paresis (milk fever)
Treatment
• Ca-borogluconate 25% solution iv. or sc. (if Ca is not given iv not enough will be absorbed)
o If Calcium is given to non-hypocalcaemic cows→can be life threatening (can stop
the heart)
• 100-120ml/100kg iv. SLOWLU
• Calcium paste system
o 2-6h: CaCl2 61%, MgCl2 2%
o 5-7h: Ca-propionate 88%
o 16-20h
• Bovikalc – Ca bolus after calvingRecumbency in the periparturient period due to metabolic problems
Parturient paresis (milk fever)
Prevention
• P-rich, Ca-poor diet before calving, Vitamin D3 inj. 1 million units im. before calving. This condition rarely occurs in sheep (before lambing) and in goats (after parturition)
Avoid paravenous Ca-infusion→it causes (para-)phlebitis, sever tissue necrosis
Recumbency in the periparturient period due to metabolic problems
Hypomagnesemic tetany
Plasma MG drops from 0.8 mmol/L to 0.4 mmol/L→tetany
- Grass tetany: occurs in early spring at pasturing
o Cause:
▪ Grass: decreased Mg, increased K (fertilisers)
▪ Decreased Mg absorption (increased ruminal N)
▪ Stress (changes in Mg redistribution)
o Symptoms: weakness, anorexia, ataxia, tetany, excitation/coma - Transport tetany
o Pregnant cows are susceptible
o Cause: transport→stress (decreased magnesium uptake) - Calf tetany
o Caused by Mg-poor milk (“whole milk tetany”)
Recumbency in the periparturient period due to metabolic problems
Hypomagnesemic tetany
Treatment
- Commercial Mg(+Ca) compounds
* 15 MgCl2 + 40g CaCl2 solved in 500 ml water iv
Metabolic osteopathies in ruminants
Rickets Osteomalacia Osteoporosis/-penia Osteodystrophia fibrosa Spastic paresis
Metabolic osteopathies in ruminants
Rickets
Occurrence
• Calves, growing cattle, rare
Metabolic osteopathies in ruminants
Rickets
Cause
• Ca, P and Vit D deficiency
Metabolic osteopathies in ruminants
Rickets
Symptoms
• Allotriophagia (pica), ataxia, bone deformities
Metabolic osteopathies in ruminants
Rickets
Therapy
• Vitamin D, balanced Ca and P intake
Metabolic osteopathies in ruminants
Osteomalacia
Occurrence
• Milking cows. Endemic
Metabolic osteopathies in ruminants
Osteomalacia
Cause
• P and C deficiency
Metabolic osteopathies in ruminants
Osteomalacia
Symptoms
• Allotriophagia, ataxia, permanent recumbency, painful joints and bones, bone fractures, easily moveable teeth
Metabolic osteopathies in ruminants
Osteomalacia
Therapy, prevention
• As for rickets
Metabolic osteopathies in ruminants
Osteoporosis/-penia
Occurrence
• Mostly in sheep and in goats
Metabolic osteopathies in ruminants
Osteoporosis/-penia
Cause
- Extremely poor diet, endocrine background
* Not “pure” form of porosis (oseteoporomalacia)
Metabolic osteopathies in ruminants
Osteodystrophia fibrosa
Occurrence
- Goat (extremely rare)
* Mandible and maxilla involved
Metabolic osteopathies in ruminants
Osteodystrophia fibrosa
Cause
• Not clear
Metabolic osteopathies in ruminants
Osteodystrophia fibrosa
Symptoms
• Swelling and deformities of affected, rubber-like bones
Metabolic osteopathies in ruminants
Spastic paresis
Occurrence
• Calves (weeks – 6 months of age)
Metabolic osteopathies in ruminants
Spastic paresis
Cause
• Inherited (?) disease
Metabolic osteopathies in ruminants
Spastic paresis
Symptoms
- Increased tone of the gastrocnemius muscle, straightness of the hock, elevation of the tail
- Progressive lameness, recumbency
