Dairy Cattle Production

Metabolic disorders

Department of Animal Science

METABOLIC DISORDERS IN DAIRY COWS

Dairy Cattle Production 342-450A

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Metabolic disorders

Introduction: Management of the dry cow plays an important role in the control of
metabolic disorders near or at calving time. Calving and the first month after freshening
are critical times for the dairy cow. The major disorders affecting the fresh cow are
usually the result of nutrition and feed management problems. Metabolic disorders are
completely interrelated and tend to occur together

The main metabolic disorders of the fresh cow (at calving time) are:
- Milk fever
- Udder edema
- Ketosis
- Fat cow syndrome
- Retained placenta
- Displaced abomasum
- Rumen acidosis
- Laminitis

Milk Fever
Background
Milk fever or calving paralysis is a metabolic disorder usually occurs around calving
time. The name milk fever is misleading since the cow does not have a fever. Incidence
of milk fever is related to age. It is most common in older high producing cows while it
rarely occurs in first-calf heifers. About 75% of milk fever cases occur with 24 hours
after calving and less than 5% beyond 48 hours. Cows having milk fever once are apt to
repeat.

Symptoms
General symptoms.
- Loss of appetite.
- Inactive digestive tract.
- Cold ear and dry muzzle.
Specific symptoms
- In-coordination when walking
- Cow may fall or lay down and unable to rise.
This could happen in three stages;

I. Standing but wobbly

II. Down on chest and drowsy
III. Down on side and unresponsive

The major change in the blood of cows with milk fever is blood calcium. Normal level in
a dairy cow is 8-10 mg per 100 ml. The level drops to 8 mg per 100 ml at calving. In milk
fever cows, blood calcium level drops to 6.5, 5.5, and 4.5 mg per 100 ml in stage I, II,
and III, respectively. The drop in blood calcium level is usually accompanied by a drop
in blood P and increase in blood K and Mg levels.

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Blood calcium levels in cows with milk fever

Normal Lactating cow 8.4-10.2 mg/dl

Normal at calving 6.8-8.6 mg/dl
Slight milk fever 4.9-7.5 mg/dl
Moderate milk fever 4.2-6.8 mg/dl
Severe milk fever 3.5-5.7 mg/dl

Causes of milk fever

-Milk fever is likely to be caused by extra Ca drain from the blood into the milk at
calving coupled with the inability of the cow to change her metabolism rapidly enough to
keep blood Ca level up. The inability of the cow to change her Ca metabolism is likely
caused by imbalances of Ca, P, and Mg and overload of K as it relates to cation-anion
balance.

The dairy cow gets Ca from two sources; mobilization from bone and absorption from the
digestive tract. Calcium homeostasis in controlled by the parathyroid hormone. Low
blood Ca levels trigger its release. The hormone’s major effect is to mobilize Ca from
bone into blood. Although the parathyroid hormone becomes elevated in the milk fever
cow, the lag in the bone response prevents rapid enough replenishment of blood Ca. The
release of parathyroid hormone in hypocalcemic cows also stimulate the release of 1,25
dihydroxy vitamin D that in turn increases Ca absorption in the small intestine. The
active form of vitamin D is also elevated in the milk fever cow but the lag in response
prevents its active function.

Treatments
The method of choice for treating milk fever in intravenous injection of a solution of
calcium gluconate. Other treatments include oral administration of 100 g of ammonium
chloride for 204 days and high calcium boluses (75 g) within 8 hours of calving. Cows
than do not response to treatments can be given 700-800 g of Epsom in water to provide
available Mg and eliminate toxins from the intestinal tract.

Prevention
The traditional way of preventing milk fever is to limit Ca intake during the dry period.
This will allow the dry cow to adapt to Ca deficiency and make her better able to respond
to milk Ca demand in early lactation. In cows fed limited amount of Ca and P during the
dry period, bone and small intestine respond better to stimulation from parathyroid
hormone and active vitamin D.

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Guidelines for managing Ca intake during the dry period include:

- Limiting Ca intake to less than 50 g per day (less than 0.5% of the diet)
- Limiting P intake to less than 45 g per day (at 0.35% of the diet).

Feeding high Ca forages (alfalfa hay and silage) should be restricted during the dry
period. Replacing part or all of the alfalfa forages with grass hay or silage, cuts Ca
consumption during the dry period and helps prevent milk fever.

- Supplementation of the dry cow diets with anionic salts is another effective method of
preventing milk fever. Anionic salts reduce the incidence of milk fever by increasing the
mobilization of Ca from bones. They are helpful when there is a high incidence of milk
fever or when it is difficult to control Ca consumption during the dry period.

Anionic salts are effective in rations with high Ca levels (150 g per day). They should not
be fed when Ca intake is low. Therefore it is very important to analyze feed ingredients
especially forages, as book values on mineral content can be misleading.

Urine pH is affected by changes in the cow’s acid-base status and therefore, checking
urine pH can help producers monitor the effectiveness of a ration containing anionic salts

Ration DCAD Urine pH Acid-base status Ca status

(pre-fresh) (pre-fresh) (fresh)

Positive (>0 meg/kg) 8.0-7.0 alkalosis low blood Ca

Negative (<0 meg/kg) 6.5-5.5 mild metabolic normal blood Ca

Acidosis

<5.5 kidney overload

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Ketosis
Definition
A metabolic disorder, that results from inadequate nutrient intake (especially energy) by
the dairy cow in early lactation. When blood glucose level is too low, the cow mobilizes
body reserves, especially fat. Part of the mobilized body fat will be converted to ketones
in the liver (e.g. acetone), which results in elevated ketone levels in the blood.

Low Dry Matter (Energy) Intake

Fat Mobilization

Poor Immune Function Empty Rumen

Fatty Liver/Ketosis

Mastitis/Metritis D isplaced Abomasum

Impaired Liver Function

Occurrence
- Ten days to 6 weeks after calving in high producing cows. Peak incidence is about 3
weeks after freshening. Many high producing dairy cows go through a sub-clinical or
primary ketosis in early lactation when milk production exceeds nutrient uptake and body
reserve has to be used. Other problems such as retained placenta, hardware, displaced
abomasum can act as predisposing factors to ketosis.

Symptoms
- Loss of appetite especially to
Blood components of normal and ketotic cow
Normal Ketotic
grain.
Blood
- Rumen inactivity
Glucose 52 28
- Weight loss
Ketones 3 42
- Lower milk yield
Plasma
Two major changes occurs in
NEFA 3 32
the blood
Triglycerides 14 8

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- Drop in blood glucose level (initiation factor)

- A rise in blood ketone level

Normal blood glucose level in the dairy cow is about 50 mg/dl. Values below 40 mg/dl
are considered subnormal.

Diagnosis
Tests are available to check the ketone levels in the milk and urine. Milk has about half
the ketone level of blood whereas the ketone level in the urine exceeds the level in the
blood by 4 times. Since urine is about eight times more sensitive than milk, urine test for
ketone bodies is very sensitive with many cows in early lactation testing positive without
the need for treatment. However, a negative urine test will role-out ketosis. The milk test
will be a more accurate indication of the need for a treatment.

Treatment
All treatments of ketosis aim to increase blood glucose level and thus reduce tissue
mobilization
- Intravenous glucose injection: The most rapid and direct way of supplying blood
glucose. However, elapses occur when glucose infusion is used as the sole treatment.
Thus it should be followed by one of the longer acting treatments.

- Hormonal treatment:. Glucocorticoids (cortisone) cause the cow's body to produce

glucose from protein tissues. However, prolonged use of this hormone is not
recommended. Hormones that stimulate glucocorticoid secretion such as ACTH can also
be used.

- Oral sugar precursors: Sodium propionate and propylene glycol are two oral sugar
precursors that can be used by the cow to produce sugar in the liver. They can be fed or
drenched at a rate of 250-450 g per day usually following glucose or hormonal treatment.

Prevention
- Avoid over-conditioned cows in late lactation and dry period. Overconditioning causes
depressed appetite at freshening and may increase fatty liver problems. Body condition
score should be 3-3.5 at calving.
- Feed 2-4 kg of grain per cow during the close-up period (3 weeks before calving).
- Encourage maximum energy intake after calving by feeding high quality forages.
- Feed total mixed rations if possible. If not, limit grain intake to 2-4 kg per feeding.
- Feed niacin at 6 g per day for 2-10 days starting 2 weeks prior to calving.

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Fat Cow Syndrome (Fatty Liver Syndrome)

Definition
During early lactation many dairy cow are in negative energy balance. This leads to
excessive fat mobilization from body reserves and high levels of fatty acids in the blood
in the form of non-esterified fatty acids (NEFA). When fatty acids increase in the blood,
the liver increases its uptake of free fatty acids. Free fatty acids in the liver are converted
to triglycerides. Liver in ruminant animal has a very limited capacity of utilizing fat.
Therefore, fat (triglycerides) deposition and accumulation occurs in the liver (fatty liver).
The term fat cow syndrome is usually used to describe the condition of an over-
conditioned dairy cow within few days of calving.

Adipose
Liver
Tissue

NEFA
NEFA NEFA
Epi Insulin

TG
CO2

Gluco se

Ketone
Bodies
Milk
TG
Fat
Mammary VLDL
TG

Gland

Symptoms
Symptoms are similar to those of ketosis. The syndrome is usually associated with other
metabolic disorders such as milk fever, ketosis, mastitis. Symptoms include depression of
appetite and overall depression

Treatments
Cows with fatty liver syndrome do not respond very well to treatments. Treatments
similar to those used for ketosis can be tried (e.g. intravenous glucose). In many cases,
the most economic treatment is to cull extremely fat cows before they calve.

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Prevention
The best way to prevent fatty liver syndrome is to avoid excessive fatty acid
mobilization. Proper nutrition and feed management practices are critical to minimize
negative energy balance, especially in early lactation. The cow's body condition in late
lactation and during the dry period should be monitored to ensure that the cow is not
over-conditioned. During the dry period the cow should not lose or gain more than 0.5
body condition.

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Retained Placenta
Definition
Retained placenta refers to the failure of the placenta to separate from the uterine wall.
The cow normally cleans within an hour or so after calving. The placenta is considered
retained if the cow does not clean within 12 hours. Retained placenta is more common
in first-calf heifers and older cows. It is also more frequent in high producing cows, cows
the give birth to twins and in Holstein compared with Jerseys.

Causes
1- Interference with the process that loosens the connection between the placental
attachment and the uterus. Placenta goes through a maturation process in the last months
of pregnancy. The final maturing process depends on estrogen for at least 5 days before
the due date. Therefore when cows calve 5 days or more before the due date, they will
frequently retain the placenta.

2- Lack of, or weakened uterine contraction. Any thing that stops or weakens muscle
contractions, such as milk fever will interfere with the expulsion of the placenta.

- Diseases and infectious organisms that cause an infection in the reproductive

tract, produces a high fever or contribute to abortion, will increase the incidence
of retained placenta. Common disease problems include
- Brucellosis
- Bovine virus diarrhea
- Leptospirosis
- Infectious bovine rhinotrachetitis

- Severe deficiencies of vitamin A or beta carotene, selenium, iodine and improper

levels of Ca and P, all can increase incidence of retained placenta.

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- There is a tendency for overconditioned cows to be predisposed to retained

placenta. This predisposition can be a problem where excessive corn silage is
consumed and grain is overfed

Prevention
- Minimize stressful conditions such as heat, humidity, poor ventilation or crowding.
- Proper feeding program during the dry period (similar to milk fever and ketosis).
- Maintain a vaccination program against infectious diseases.
- Proper body condition score during the dry period.
- Selenium and vitamin E supplementation during the dry period.

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Displaced Abomasum

Definition
Displaced abomasum (DA) is a condition in which the abomasum (true stomach) is
twisted to the left or right from its normal position. The normal position of the abomasum
is near the belly floor on the right side.

About 80-90% of the abomasum

displacement is to the left. It moves
from the right side of the belly,
under the rumen and up to the left
body wall. There it is trapped
between the rumen and the left side
of the cow. Consequently, the
entrance and the exit of the
abomasum will be restricted
because of the pressure exerted on
them from stretching the abomasum
around to the other side of the
rumen. The abomasum will be gas
and bloats. About 90% of the
displacements occur within 6 weeks of calving affecting about 3% of the cows.

Symptoms
- Cows go off-feed
- Low milk yield
- Arched back
- Little manure or mild diarrhea at first, followed by dark and bad smelling feces or
diarrhea.

Causes
- Displacement of the abomasum by the fetus during pregnancy.
- Predisposing factors such as milk fever, fat cow syndrome, mastitis.
- Inadequate intake by the fresh cow or lack of bulky feed (e.g. long forages) may leave
more room for the abomasum to shift.
- Factors causing loss of muscle contraction and gas distention in the gut (e.g. high grain
rations) can lead to displacement.

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Treatments
- Rolling the cow on her back (useful in mild cases).
- Surgery (more effective but might not be economical).

Prevention
- Care in feeding programs before and after calving. Feed bulky feed to dry cows to keep
the rumen full.
- Gradual feed transition from dry cow ration to the milking cow ration (i.e. using close-
up rations).

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Laminitis

Definition
Laminitis can be defined as the inflammation of the vascular tissues. Laminitis is a non-
infectious disease involves degenerative changes in the sensitive and horny lamina of the
hoof. Phases of laminitis include acute, subacute, and chronic. Subacute laminitis
accounts for most of all lameness.

- Acute laminitis is sudden in onset with much pain.

- Subclinical laminitis will show no symptoms for 1-3 months.

- Chronic laminitis is the long-term result of this complex condition.

Causes
Causes of laminitis can be grouped into three groups
1- Nutritional imbalances
2- Inadequate rumen development
3- Overburdening of the hooves.

- High levels of fermentable carbohydrates in the ration combined with inadequate

effective fiber. This feeding practice will lead to rumen acidosis: lactic acid bacteria will
flourish in the rumen while gram-negative bacteria die and release endotoxins. In
response, the cow produces histamine, which causes constriction and then a dilation of
the capillaries in the sensitive corium of the foot. An edema and pooling of blood occurs,
with blood vessel destruction. The foot becomes painful and the resulting damage to the
capillaries will prevent normal synthesis of keratin in the hoof.

Types of Laminitis
Acute laminitis
- Increased respiration and heart beats
- Warm hoof walls and swelling over the coronary band of the hoof.
- Hemorrhaging is visible sometimes at the white line, or where the wall joins the
sole. Other times hemorrhaging is not visible until it causes a separation along the
white line, where dirt enters and forms an abscess.

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Subclinical laminitis
- No symptoms until lamenitis occurs 1-3 months later with lesions in the sole and the
wall of the hoof.
- Softer hoof and non-pigmented areas will yellowed or show hemorrhaging

Chronic laminitis
- Feet become elongated and overgrown.
- Horizontal ridges appear along the hoof walls, and feet become wide and flat with
no depth of heel.

Treatment
The rations must be corrected for improvement in all forms of this disease.
1- Chronic laminitis can be treated with corrective hoof trimming every 3-4 months.
Culling must be considered since the feet of these cows will never be normal.

2- Sub-clinical laminitis will require trimming to reveal the primary lesion. A

wooden block glued to the unaffected claw relieves pressure on the sore claw.

Prevention
Slug feeding of grains should be avoided. Fresh cows should be gradually brought to full
feed (e.g. over a 6-week period). Rations of transition cows should contain enough long
fibre for optimum ruminal fermentation.

Cows and heifers should have adequate exercise before and after calving. Pregnant
heifers should become accustomed to cement floor several weeks before calving. Plenty
of bedding should be used in stanchions and free stalls. The use of rubber mats should
also be considered.

For more information on metabolic disorders:

Transition Dairy Cow Management. A key to Profitability. (CD)

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