Metabolic hypocalcaemia as one of the major field problem of heavy lactating cows

1. 1
Metabolic diseases of large
ruminant
1. Milk fever
2. Hypophosphataemia
3. Hypomagnesaemia
4. Ketosis
5. Fat cow syndrome
6. Downer cow syndrome
Prof Mohamed Ghanem
Professor of Veterinary Internal Medicine
Head of Department of Animal Medicine
Faculty of Veterinary Medicine Benha University

2. 2
Introduction
 1- Metabolic diseases usually associated
with pregnancy, parturition and lactation.
 2- Metabolic diseases usually associated
with high productivity and reproductivity
of the livestock animals.
 3- High productivity e.g: More than 20
Kg./day in Holistein-Fresian cows (total
cost of H.F. cow=14 kg milk/day.
 -High reproductivity e.g: Animals carry
more than one foetus (give twins,
triples...etc. e.g: ewes and goats).


3. 3
Introduction
 4- Metabolic diseases of our native breeds is mainly
attributed to "nutritional faults", more than associated with
high productivity and reproductivity.
 e.g:- Egyptian native breed balady cow give 700-900
kg/year.
 - Egyptian buffaloe give up 1200 kg milk per year.
 - Domiaty cows give up 1200 kg milk per year.
 - Fresian cows give 4000-5000 kg milk/year.
 - American Holestien cows give 6000-7000
kg/Year.
 5- The economic definition of the cow is udder plus uterus
and 60% of milk production from posterior 2 quarters of
udder.
 6-Metabolic disorders countered in food animals are, milk
fever, Hypophosphataemia, Hypomognesaemic tetany,
Ketosis, and fat Downer cow syndromes.

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(1) MILK FEVER
(Parturient paresis, parturient
hypocalcaemia)
 Definition:
 Milk fever is a metabolic neuretic disease
occurring most commonly about the time of
parturition and characterized clinically by
generalized paresis, circulatory collapse and
depression of consciousness and biochemically
by hypocalcaemia.

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Incidence, occurrence and
predisposing factors:
 1- Cattle most susceptible animals (particularly Jersy
breed 30%}.
 2- The disease may occur sporadically in buffaloes,
sheep;and goats (no records about the disease in camels).
 3- Aged or senile cattle mostly susceptible and age
incidence 5-10 years (3-8th calving).
 4- Heavy milkers cows (20kg/day and more milk
production).
 5- Usually 24 hours before or mostly 72 hr. post. partum
due to sudden evacuation of colostrum. (125 mg% in
cow).
 6- Incidence in winter more than other seasons.
 7- High protein diet before calving predispose to the
disease.
 8- Undue fatigue and excitment predispose to the

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Etiology
 1- The exact cause of milk fever is unknown.
 2- The known is that the basic biochemical
finding in the disease is hypocalcaemia.
 3- How the hypocalcaemia developed?
 a) At calving, there is a normal physiological fall
in blood calcium. But a more significant fall
occurs in cows, which develop the disease.
 b) There are 2 factors control-beside the
intrinsic endocrine factor calcium haemostasis
(blood calcium pool) in the body
 1- calcium inflow
 2-calcium outflow

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 Decreased calcium inflow: (due to)
 1- Impairment of calcium absorption from
gut due to bowel stasis during partition.
 2- Insufficient mobilization of calcium from
bone due to aging or senility.

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 Increased calcium outflow: (due to)
 1- Excessive loss of calcium in colostrum.
 2- Excessive calcium excretion in faeces
via gut due to for example profuse
diarrhea.
 3- Increased calcium bone mineralization.
 4- increased calcium excretion in urine
due to diuresis.

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Other theories suggested in the
pathogenesis of the disease:
 1- Parathyroid dysfunction which lead to
guanidine amino acid intoxication which inturn
result in hypocalcaemia.
 2- Thyroid dysfunction (which secrete calcitonin
hormone from C-cells) as histological section of
C-cells of the gland found to be depleted.
 3- sex harmons, as oestrogen antagonist to
parathyroid.

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Other biochemical changes
recorded with the constant
hypacalcaemia of paretic cows:
 1- Hypophosphataemia -- due to parathyroid
dysfunction.
 2- Hypo-or hypermagnesaemia.
 3- Hyperglycaemia:
 Hyperglycaemia (80-90 mg%) usually
accompany milk fever and severe
hyperglycaemia (up to about 160 mg%) occur
with severe paresis arid the cow become
diabetic-like, due to inhibition of insulin release
from B-cells of pancreas under the influence of
hypocalcaemia.

11. What is the role of Ca in the
neuromuscular transmission?
11

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Clinical signs:
 3 stages of the disease are known
including:
 A) prodromal stage (excitative short
phase)
 B) Stage of sternal recumbency
(semicomatosed stage). .
 C) Stage of lateral recumbency
(comatosed stage).

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A- Prodromal stage: (short
excitatory phase)
Characterized by:
 1- Excitement and restlessness (vigrous-
1icking of skin).
 2- Hypersensitivity and fine muscle
tremors.
 3- Disinclination to eat or move.

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(B) Stage of sternal recumbency
(Semicomatused stage):
Characterized by:
 1-Depression of consciousness.
 2- Animal in sternal recumbency and the head
turned laterally toward flank region resting on
the shoulder region.
 3- Dry muzzle dilated pupi1e cold extremities
and loss of anal reflex, as well as, atonic digest-
ive tract manifested by constipation.
 4- Temp. normal or even subnormal.

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Characteristic position in milk fever

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Characteristic position in milk fever

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(C) Stage of lateral recumbency
(comatosed stage):
Characterized by:
 1- Animal almost comatozed.
 2- Animal in lateral recumbency,
 3- Complete flaccidity of limbs and loss of
nervous reflexes.

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Lateral recumbency stage of milk
fever

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Diagnosis
 I) History.
 II) Clinical signs.
 III) Diagnostic therapy: Estimation of serum
calcium level usually below 6 mg %, sometimes,
as low as, 3 mg % (normal around 10 mg %).
 IV) Diagnostic therapy: (therapeutic diagnosis)
 Milk fever is a dramatic disease, due to
treatment with calcium borogluconate usually
followed by a dramatic recovery within few
minutes.

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Treatment:
 Most untreated cases die within 1-2 days.
(A) Nursing care:
 I- Stomach tube feeding to avoid aspiration pneumonia.
 2- Turning of animal from side to side to avoid tympany.
 3- Massage of limbs and bony prominants to avoid limb
dysfunction.
(B) Chemotherapy:
 Calcium borogluconate is the drug of choice or the
classical treatment.
 400-800 ml C-B-.G 25% slow I/V or S/C repeated after
12 hrs.if no r response, then repeated after 24 hrs. And
if no further response use alternative therapy containing
phosphorus and magnesium e.g calphomag (Virbac).

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Prevention:
 1- Feeding high phosphorus low calcium
ration in two last months of pregnancy
(dry period).
 2- Single 1/V or S/C-10 million I.U
crystalline vitamin-D 8-10 digs before
calvinng repeated if the cow not calving.
 3- Diet rich calcium after parturition only.

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Questions