Metabolic Disorders

David Marcinkowski
Dairy Cattle Technology
AVS346
Metabolic Disorders of Dairy Cattle

 Milk Fever
 Udder Edema
 Ketosis
 Fat Cow Syndrome
 Retained Placenta
 Displaced Abomasum
 Rumen Acidosis
 Laminitis
DMI at Calving
Milk Fever - Occurrence
 Wisconsin SRS - 8% of cows, 67% of herds
 1990 Hoard's survey - 8% cows, 82% herds
 Older cows, - 10% or more
 Jerseys - greater tendency
 Lowly heritable, can be managed!
 75% of cases occur between 1 and 24 hours
post calving
 Less than 5% beyond 48 hr
Calcium Movement in High
Producing Cow

Milk Production
Milk Fever - Symptoms
 Fever is not a symptom
 Lack of appetite, inactive GI tract, dull, listless, cold ears, dry
muzzle
 In coordination while walking, down and unable to rise
 Canadian staging system:
 Standing but wobbly
 Down on chest and drowsy
 Down on side and unresponsive
 Blood calcium:
 Normal is 8-10 mg/100 ml
 6.5, 5.5 and 4.5 mg/100 ml in stages 1,2,and 3 from above
 Also causes imbalance of P, K, Mg
Milk Fever – Cause
 Milk production causes extra drain on blood Calcium
 Compensatory metabolic pathways don’t react fast
enough
 Two sources of Ca
 Dietary
 Bone stores – action of Parathyroid Hormone
 Prefresh diet affects speed of PTH response
 Low Ca in prefresh diet stimulates PTH
 Alkaline diets inhibit PTH
 Acidic diets stimulate PTH
 Diets high in K alkaline
Milk Fever Treatment
 IV Calcium Gluconate – slowly
 Different types high in P, Mg, K
 Can be given sub-Q
 30% of treatment relapse
 Oral Calcium gels not good once cow is down but
good preventative and may help with relapses.
 Calcium Chloride in some gels may cause throat
abcesses if not given carefully
 Partial milking not only useless it predisposes the
animal to mastitis
DCAD
 Dietary Cation Anion Difference
 (Na + K) – (S + Cl)
 Positive DCAD
 Urine pH 7.0-8.0
 Alkalosis – Prone to Milk Fever
 Negative DCAD
 Urine pH 5.5-6.5
 Mild Metabolic Acidosis – Mobilize Ca better from bone
 Test urine pH to evaluate dry cow ration
 Urine pH under 5.5 – Metabolic acidosis - Kidney overload
Anionic Salts
 Ammonium Chloride
 Ammonium Sulfate
 Calcium Chloride
 Magnesium Sulfate
 Magnesium Chloride
Milk Fever - Prevention
 MANAGE the dry cow feeding program!
 Calcium < 50 grams/day or 0.5% of DM
 Phosphorus <45 g/day or 0.35% of DM
 This severely limits alfalfa inclusion!
 If forced by circumstance - anionic salts
 Work best when dietary Ca > 150 g/day
 Very unpalatable - must be masked
 Solicit help of competent nutritionist
Milk Fever Disease Complex
Ketosis
 Disorder results from inadequate energy
intake
 When blood glucose low cow mobilizes fat
stores
 Fat breakdown results in ketone production
 Ketones build up in blood and liver
Ketosis - Causes
 Acetonemia
 acetoacetic acid
 Beta-Hydroxybutyric acid
 Energy needs exceed dietary intake
 Milk production - primary
 Illness - secondary
 Cow draws on body fat stores
 Fat cows
 Poor feeds
 Affects 3-17% of cows
Energy Imbalance
Ketosis - Clinical Signs
 10-60 da. PP (avg = 28)
 Sweet smell
 Breath, urine, milk
 Loss of appetite especially concentrates
 Rumen inactivity
 Dull and listless
 Loss in body weight
 Decreased milk production
 Lack of coordination
 Nervous ketosis
 Milk/Urine test strips
 Urine is 4X higher in ketones than milk
 Normal cows may show high on a urine test
 Milk better
Blood Components of Normal and
Ketotic Cows (mg/dl)
Normal Ketotic
Blood
Glucose 52 28
Ketones 3 42
Plasma
NEFA 3 32
Triglycerides 14 8

McGill University – 324-450A

Ketosis - Treatments
 IV glucose
 Very short lived effect
 Hormonal Treatment
 Corticosteroids
 Produce glucose from protein stores

 Oral sugar precursors

 Propylene glycol
 Drenches
 Gels
 Add to fresh cow ration
 Sodium propionate
Ketosis - Prevention
 Avoid over conditioned cows
 Balance diet
 Avoid dietary changes at calving
 Maximize feed intake
 Feed palatable feeds
 Feed high quality forages
 Limit competition between cows
 Lead feed concentrates
 Up to 10 lb
 Feed TMR to prevent sorting
 Feed niacin (6g/day) 2 weeks before calving
Fat Cow Syndrome
Fat Cow Syndrome
 Also known as Fatty Liver Syndrome
 Symptoms similar to ketosis
 Add poor response to treatments
 Mastitis and poor immune function
 So is cause
 Negative energy balance leads to fat mobilization
 Ruminant livers have limited capacity of utilizing fat
 Triglycerides build up in liver
 Treatment same as ketosis
 Cull
Prevention
 Minimize negative energy balance
postcalving
 Manage BCS of late lactation and dry cows
 Avoid fat cows
 Late Lactation <=3.5
 Dry <=4.0
 Don’t change BCS during the dry period
Retained Placenta
 Selenium
 Vitamin E
 Proper BCS
 Avoid Milk Fevers
Displaced Abomasum
 DA, LDA, twisted stomach
 Occurs around calving
 Normally on right
 Two types
 left - 85%
 right - very serious
 Theories
 mechanical
 metabolic
 Incidence 3-15% of cows
 Heritability .24
DA
Factors Affecting DA’s
DA - Clinical Signs
 Off feed
 Depression
 Dehydration
 Secondary ketosis
 Asymmetrical bloating
 Little manure produced
 Arched back
 Other illness
 Milk fever, mastitis, fat cow syndrome
DA - Treatment and Prevention
 Treatments
 Do nothing
 Rolling
 Blind stitching
 Surgery
 Fiber in diet - particle size
 Dry cow and close up rations
 Prevention
 Lead feeding
 Slug feeding vs. TMR
 Prevention of other disorders
Acidosis
 Nutritional imbalances causing low ph in rumen
 Caused by
 Low fiber
 High concentrate
 Slug feeding of grain

 Clinical and Subclinical - SARA

 Two types
 Periparturient
 Under 30 DIM
 Ration formulation and delivery
 30+ dim
Metabolic
Acidosis
Rumen Adaptations Due to ph
Acidosis Prevention
 No good treatment – Prevention Key!
 Lead feeding of concentrates
 Encourage DMI
 Maintain adequate fiber in ration
 Feed TMR
 Add buffers to ration
 Bicarb
 Magox
Laminitis
 Non infectious inflammation of the vascular
tissue lamina of the hoof
 Acute – sudden onset, painful
 Subclinical – no symptoms for 1-3 months
 Chronic – long term
Causes
 Acidosis
 Gram negative bacteria in rumen die and
release endotoxins
 Histamine released
 Constriction and dilation of capillaries
 Edema
 Damaged capillaries destroyed
 Synthesis of keratin affected
General Prevention of
Metabolic Diseases
 Keep DMI high
 Keep adequate forage/fiber in diet
 Avoid ration changes
 Lead feed concentrates