2. MILK FEVER is an important production disease
occurring most commonly in adult cows within 48-72
hours after parturition, which is characterized
clinically by hypocalcemia, general muscular
weakness, circulatory collapse and depression of
consciousness (Radostits et al., 2000).
3. ETIOLOGY
A depression in the levels of ionized calcium in the
extracellular space, including plasma, is the basic
biochemical disturbance in milk fever.
The onset of lactation places such a large demand on
the calcium homeostatic mechanisms of the body that
most cows develop some degree of hypocalcemia at
calving.
4. A cow producing 10 kg of colostrum (2.3g of Ca/kg)
will loss 23g of Ca in a single milking. This is about 9
times as much Ca as that present in the entire plasma
Ca pool of the cow.
5. Occurrence
Age - Hypocalcemia at calving is age related and most
marked in cows at their third to seventh parturition.
Aging also results in a decline in the ability to mobilize
Ca from bone stores and a decline in the active
transport of Ca in the intestine, as well as impaired
production of 1,25(OH)2D3.
6. Breed- Jersey, Swedish Red and White, and Norwegian
Red breeds develop clinical milk fever more frequently
than Holstein–Friesian cows.
The higher Ca concentration in milk from Jersey
compared with Holstein cows has been proposed as
possible explanation.Differences in the number of
intestinal vitamin D receptors regulating the intestinal
Ca uptake have been reported in some studies.
7. Calcium Homeostasis
The following three factors affect Ca homeostasis, and
variations in one or more of them may contribute to
the development of clinical disease in any individual:
1. Excessive loss of calcium in colostrum beyond the
capacity of absorption from the intestines and
mobilization from the bones to replace it.
2. Impairment of absorption of Ca from the intestine at
parturition.
3. Mobilization of Ca from storage in the skeleton may
not be sufficiently rapid or efficient to maintain
normal plasma Ca levels
8.
9. Clinical signs
The main clinical manifestations are divided into three stages
First stage or Stage of excitement: -
Anorexia (decreased appetite)
Nervousness or hypersensitivity
Mixed excitement or tetany without recumbency
Weakness or weight shifting
Stiffness of hind legs
Rapid heart rate
Rectal temperature is usually normal or above normal (>39
C).
10. Second stage or Stage of sternal recumbency: -
Sternal recumbency comprising down on chest and
drowsiness - Characteristic “S” shaped posture
sitting with lateral kink in neck or head turned to lateral
flank.
Depression
Fine muscle tremors
Rapid heart rate with decreased intensity of heart sounds
Cold extremities
Decreased rectal temperature (35.6 to 37.8 C)
Decreased gastrointestinal activity
Pupils dilated and unresponsive to light
11. Third stage or Stage of lateral recumbency: -
Lateral recumbency, comprising of almost comatose
condition, progressing to loss of consciousness
Severe bloat
Flaccid muscles
Profound gastrointestinal atony
Rapid heart rate
Impalpable pulse and almost inaudible heart sounds.
12.
13. PATHOGENESIS
Calcium has several functions relevant for the
pathophysiology of periparturient hypocalcemia,
which include the following:
Cell membrane stability: Calcium bound to cell
membranes contributes to the maintenance of
adequate membrane stability. In excitable cells the
decreased availability of ionized Ca results in higher
cell membrane permeability, thereby altering the
resting membrane potential and making nerve cells
more excitable.
14. Muscle contractility: Calcium is required to clear the
binding site for myosin on the actin molecule inside
the muscle fibers. The cross-bridging between actin
and myosin is the basis for the contraction of muscle
fibers. Decreased availability of Ca can therefore affect
muscle contractility.
15. Release of acetylcholine: Calcium is required for the
neuronal release of the neurotransmitter acetylcholine
into the synaptic cleft of the neuromuscular junctions.
Calcium depletion can thus hamper the signal
transmission at the level of the neuromuscular
endplate
16. Cows developing milk fever have higher plasma
cortisol concentrations than do non-milk fever cows
(Goff et al., 1989).
Muscle tone decreases in most body systems,
particularly in the cardiovascular, reproductive, and
digestive systems, and possibly in the mammary
system. Blood flow to the extremities is reduced,
causing the characteristic cold ears of a cow suffering
from milk fever.
17. Diagnosis
1. History taking
Occurs in mature cows usually 5-9 years old, within 72
hours after parturition.
Occurs in highest milk producing period.
Higher incidence in the Jersey breed.
18. 2. Clinical examination Under this though examine the
animal after collecting the detail history.
Clinical signs include early excitement and tetany,
hypothermia, flaccidity pupil dilation, impalpable
pulse, no rumen movement, soft heart sounds, fast
heartbeats are fast (80-100 per minutes), decreased
reflex, depression coma, bloated and death.
19. 3. Laboratory diagnosis
Hypocalcemia- Milk fever can be defined as low blood
total calcium (8.0 mg/dl) or low blood ionized calcium
(4.0 mg/dl), with or without clinical signs of
hypocalcemia.
Normal level in a dairy cow is 8-10 mg/dl. Direct
determination of blood calcium is the more accurate
method to diagnose a case of milk fever.
20. Differential diagnosis
Differential diagnosis include toxic mastitis, toxic
metritis, other systemic toxic conditions, traumatic
injury (eg, stifle injury, coxofemoral luxation, fractured
pelvis, spinal compression), calving paralysis
syndrome (damage to the L6 lumbar roots of sciatic
and obturator nerves), or compartment syndrome.
Some of these diseases, in addition to aspiration
pneumonia, may also occur concurrently with
parturient paresis or as complications.
21. Treatment
The treatment of choice for milk fever is slow,
intravenous infusion of 8-12 g of calcium as soon as
possible after the onset of clinical signs. Heart rate
should be closely monitored for toxic effects.
Calcium borogluconate containing products with or
without added magnesium and phosphorus are mostly
used in the India: usually 400 ml of 40% calcium
borogluconate. For cattle 400-800 ml of 25% solution
is the usual dose.
22. Recommended treatment is IV injection of a calcium
gluconate salt, although SC and IP routes are also
used. A general rule for dosing is 1 g calcium/45 kg
(100 lb) body wt. Most solutions are available in single-
dose, 500-mL bottles that contain 8–11 g of calcium.
In large, heavily lactating cows, a second bottle given
SC may be helpful, because it is thought to provide a
prolonged release of calcium into the circulation.
23. Solution containing dextrose should not be given
subcutaneously because of abscess formation.
During cold weather the solution should be warmed to
body temperature. Warming the calcium solution
seems to reduce toxic effects also.
Approximately 85% of cases will respond to one
treatment, in many cases cows recumbent from milk
fever will rise within 10 minutes of treatment and
others will get up 2-4 hours later.
24. Prevention:
prevention of parturient paresis has been approached
by feeding low-calcium diets during the dry period.
The negative calcium balance results in a minor
decline in blood calcium concentrations.
This stimulates PTH secretion, which in turn
stimulates bone resorption and renal production of
1,25 dihydroxyvitamin D. Increased 1,25
dihydroxyvitamin D increases bone calcium release
and increases the efficiency of intestinal calcium
absorption.
25. Strategies for prevention of periparturient hypocalcemia
in general are based on one of following approaches:
Reduction of dietary Ca available for intestinal
absorption during the dry period
Induction of mild to moderate acidosis during the last
weeks of gestation
Supplementation of vitamin D during the dry period
Oral Ca supplementation around parturition
Parenteral Ca administration around parturition
Partial milking
26. Large doses of vitamin D (20–30 million U/day), given
in the feed for 5–7 days before parturition, reduces the
incidence. However, if administration is stopped >4
days before calving, the cow is more susceptible.
Doses of 150 g of calcium gel are given 1 day before, the
day of, and 1 day after calving.
27. Dietary Cation-Anion Difference (DCAD)
Most recently, the prevention of parturient paresis has been
revolutionized by use of the DCAD, a method that decreases the
blood pH of cows during the late prepartum and early
postpartum period.
The DCAD approach is based on the finding that most dairy
cows are in a state of metabolic alkalosis due to the high
potassium content of their diets.
This state of metabolic alkalosis with increased blood pH
predisposes cows to hypocalcemia by altering the conformation
of the PTH receptor, resulting in tissues less sensitive to PTH.
Lack of PTH responsiveness prevents effective use of bone
calcium, prevents activation of osteoclastic bone resorption,
reduces renal reabsorption of calcium from the glomerulus, and
inhibits renal conversion to its active form.
28. DCAD is expressed in milliequivalents per kilogram of dry
matter (mEq/kg DM) or in some instances in mEq/100 g
DM.
The most commonly used is DCAD4 = (Na+ + K+) − (Cl− +
S–2), which only considers the four (thus DCAD4)
quantitatively most important dietary ions.
29. Cations have a positive charge like sodium (Na),
potassium (K), calcium (Ca), and magnesium (Mg).
Cations in the diet promote a more alkaline (higher
blood pH) metabolic state which has been associated
with an increased incidence of milk fever.
Anions have a negative charge such as chloride (Cl),
sulfur (S) and phosphorus (P). Anions promote a more
acidic metabolic state (lower blood pH) that is
associated with a reduced incidence of milk fever.
30. ECONOMIC IMPORTANCE
Hypocalcemia is considered to be a socalled “gateway
disease” that predisposes to a number of common
fresh-cow disorders, such as dystocia, uterine prolapse,
retained fetal membranes, mastitis, ketosis, abomasal
displacement, ketosis, and immune suppression.
