World Veterinarian Prize Quiz - 2

 

Introduction

⇒ Normally milk containing approximately 2 g of Ca per kg and colostrum 2.3 g of Ca per kg, so the production of 10 kg of milk or colostrum requires the equivalent of the entire amount of Ca available in the extracellular space of adult cow.

⇒ Normally the calcium requirements of a cow during late gestation are minimal at about 30 g/day and after parturition cow need more than 30 g/day requirement of calcium

⇒ Maintenance of Calcium lost from the extracellular pool must be replaced by increasing intestinal absorption and bone resorption of calcium.

⇒ Sub-clinical hypocalcemia seen when total plasma calcium [Ca] < 2.0 mmol/L or 8 mg/dL occurs at the onset of lactation caused by an imbalance between calcium influx to the extracellular pool from gut and bone and output in colostrum and milk. 

⇒ Subclinical milk fever with serum Ca concentrations between 1.4-2.0 mmol/L (5.5 to 8.0 mg/ dL) in multiparous periparturient cows has been estimated at 50%.

⇒ Clinical milk fever is estimated to occur in 5% of periparturient dairy cows in the United States

⇒ There is depression in the levels of ionized calcium in the extracellular space including plasma.

⇒ The sudden increase of Ca losses through the mammary gland at the onset of lactation disturbing in regulating of Ca homeostasis.

⇒ Most cows adapt within 48 hours after calving by increases in plasma concentrations of parathyroid hormone (PTH) and 1,25- (OH)2D, the biologically active form of vitamin D3.

Epidemiology 

✔️ Incidence: Cattle are more susceptible than the Buffaloes. 

✔️ Age: Most of cattle seen at 3^rd to 7^th parturition than the 1^st or 2^nd calving.

✔️ Breed: Jersey, Swedish red more seen than other breeds.

✔️ Time of occurrence: Most cases occur within the first 48 hours after calving. Some of prepartum cases occur in the last few days of pregnancy and during parturition but rare cases seen several weeks before calving.

✔️ Feed intake: After the parturition feeding poor quality of roughage which lead to depression of serum level calcium and produce milk fever.

Sheep & Goat:

⇒ Mature ewes are the most susceptible in the period from 6 weeks before to 10 weeks after lambing.

⇒ Disease occurs in ewes exposed by forced exercise, long-distance transport, sudden feed deprivation, and grazing on oxalate-containing plants or green cereal crops.

⇒ The disease is manifested by paresis (A condition of muscular weakness caused by disease or nerve damage) but poor growth, lameness, and bone fragility can be detected in Sheep and Goat.

⇒ Feeding of hay when they are supplemented with an energy-rich concentrate which increases their calcium intake which lead to milk fever and when the pasture growth is lush and very low in Ca content also occur milk fever.

⇒ Milking goats become affected mostly during the 4-6-year old age.

⇒ Before and after kidding some later than 3 weeks after parturition. 

⇒ Clinical syndromes are like cattle two stages of ataxia and recumbent.

Calcium Homeostasis

There are mainly 3 factors are affecting Ca homeostasis and if there is change or variation in anyone so its develop milk fever.

1.     1.  Excessive loss of calcium in colostrum

2.      2.  Impairment of absorption of Ca from intestine at parturition.

3.   3. Mobilization of Calcium from the storage in the skeleton may not be sufficiently rapid maintain normal plasma Ca levels.

⇒ Osteoblasts which are the only bone cell to express the 1,25-(OH)2D receptor protein.  Here, the decrease in the numbers of osteoblasts with old age cows could delay the ability of bone to contribute Calcium to the plasma Calcium pool. 

⇒ Failure to secrete sufficient levels of PTH or insufficient availability of 1,25-(OH)2D was the primary defect to produce the milk fever.

Dietary Factors

Dietary Calcium: Feeding more than 100 g of calcium daily during the dry period which is associated with increased incidence of milk fever. Daily requirement of dietary Ca for an adult cow is 30g/day in late gestation.

✔️ If we provide more than 100g Ca so active absorption from GIT take place and there is drepression of mobilization from bone. After calving there is sudden increase calcium requirement and because of mobilization system has been depressed the calcium requirement are not fulfill thus lead to milk fever     

✔️ So, during prepartum period provide low Ca concentration which is less than 20 g/day to induce a negative Ca balance is already before calving and prevents milk fever by activating Ca transport mechanisms in the intestine and bone before parturition and allowing the animal to adapt more rapidly Ca.

Dietary Potassium: High potassium concentrations >2% of the ingested dry matter in the ration fed to cows in their last weeks of gestation can increase the incidence of periparturient hypocalcemia.

Dietary Magnesium: Magnesium deficiency in late gestation is a major risk factor for periparturient hypocalcemia and hypomagnesemia and it is most common cause of milk fever in midlactating dairy cows.

✔️ Because magnesium is required for the release PTH from the parathyroid glands and influences the tissue sensitivity to PTH and the efficacy of PTH is require for the correction of hypocalcemia.

Dietary Phosphorus: During the prepartum high diets in phosphorus (P > 80 g P/d) greatly increase the incidence of milk fever and the severity of hypocalcemia.

✔️ Because increase P à Inhibit the renal enzyme à which catalyze the conversion of vitamin D to its active form 1,25-(OH)2D à Decreased amounts of 1,25- (OH)2D will reduce the intestinal absorption of P and Ca à periparturient hypocalcemia.

Normal pathophysiology

1. Cell membrane stability: Calcium bound to cell membranes contributes to the maintenance of adequate membrane stability. Decreased availability of ionized Ca results in higher cell membrane permeability resting in membrane potential and making nerve cells more excitable.

2. Muscle contractility: Calcium is required to clear the binding site for myosin on the actin molecule inside the muscle fibers and this cross-bridging between actin and myosin is the basis for the contraction of muscle. Decreased availability of Ca can therefore affect muscle contractility.

3. Release of acetylcholine: Calcium is required for the neuronal release of the neurotransmitter acetylcholine into the synaptic cleft of the neuromuscular junctions. If Calcium depletion can thus hamper the signal transmission at the level of the neuromuscular end plate. 

⇒ The plasma Ca concentration is normally maintained between 8.4 to 10.4 mg/dL.

⇒ Almost all multiparous dairy cows will experience at least transient and subclinical hypocalcemia is less than 7.5 mg/dL within 24 hours after calving.

⇒ In some cows, hypocalcemia is more pronounced, causing neuromuscular dysfunction resulting in clinical milk fever.

⇒ If not treatment so it is 2 mg/dL which is usually incompatible with life. 

Clinical signs 

I Stage - Prodromal stage

II Stage - Sternal recumbency

III Stage - Lateral recumbency

 

 STAGE I OF MILK FEVER

✔️ Excitement and tetany

✔️ Hypersensitiveness

✔️ Muscular tremor of head and limbs

✔️ Disinclined to eat and move

✔️ Grinding of teeth

✔️ Protruding tongue

✔️ Stiff hind limb

✔️ Animals ataxic and falls easily

STAGE II OF MILK FEVER

✔️ Sternal recumbency with lateral kink

✔️ No tetany but unable to get up

✔️ Muzzle – dry

✔️ Skin and extremities – cold

✔️ Temperature .Pupil – dilated – no reflex

✔️ Eyes – disparity in the size of pupils staring and dry – pupillary light reflex decrease or absent

✔️ Relaxation of anus and loss of anal reflex-dung in rectum

✔️ Circulatory system - decrease heart sound – veins cannot be raised Weak pulse, ruminal stasis, forced expiratory grunt  

STAGE III OF MILK FEVER

✔️ Lateral recumbency

✔️ Coma

✔️ Limbs – flaccid, unable to get up

✔️Pulse – impalpable

✔️ Heart sounds – inaudible 120/min

✔️Unable to raise the vein

✔️Bloat if without treatment – animal dies within a period of 12 – 24 hr

✔️ Milk fever with hypomagnesaemia and hyperphosphatemia 

✔️ Tetany and hypersensitiveness beyond 1st stage

✔️ Excitement and fibrillary and twitching of the eyelids

✔️ Tetanic convulsion by touch or sound

✔️ Trismus

✔️ Heat and respiratory rate-accelerated Heart sound – increased

✔️ Death occurs due to respiratory failure.

Diagnosis

✔️ Base on clinical sign

✔️ Clinical pathology 

1.   Total serum Ca levels are reduced to below 8 mg/dL to 5 mg/dL and sometimes its 2 mg/dL.

2.   Serum magnesium levels are usually moderately elevated to 4 to 5 mg/dL.

3.   Serum inorganic phosphorus (Pi) levels are usually decrease to 1.5 to 3.0 mg/dL.

4.    Blood glucose levels are usually normal

If depressed it is ketosis and if higher in long duration because calcium is require for release insulin from pancreas.

5.  Serum Enzyme activity like creatine kinase (CK) and aspartate aminotransferase (AST) are increase because prolong recumabncy lead trauma to muscles.

6.  Hemogram:  Eosinopenia, Neutrophilia, and Lymphopenia which suggest the adrenal cortical hyperactivity. High plasma cortisol levels and PCVs occur in cows with milk fever and they are higher still the cows that do not respond to treatment.

Differential diagnosis

✔️  Injuries to the pelvis and pelvic limbs

✔️  Degenerative myopathy

✔️  Downer-cow syndrome

✔️  Other metabolic diseases

✔️  Diseases associated with toxemia and shock

TREATMENT

✔️Treatment during I stage – ideal

✔️Longer the interval between recumbency and treatment, greater the incidence of downer cow due to ischemic muscle necrosis

✔️Temperature > 39oC – indication of existing complication – higher mortality rate

✔️To be placed in sternal recumbency until the treatment ends to avoid aspiration pneumonia.

✔️Calciumborogluconate 500 ml to 1 liter – 3 g/10 lb  50% i/v and  50% s/c

✔️Shifting to non-slippery ground or pure rubber mat

✔️ Do not milk for 6 hours.

✔️ Do not urge the cow to stand too soon

Dose of Calcium

⇒ 1 gm Ca / 45kg (100 lb)

⇒ 25 % calcium borogluconate = 10.4 gm /500ml

⇒ Cattle – 400-500 ml  slow i/v & 100-200 ml s/c

⇒ Goat- 150-200 ml i/v, 50-100 ml s/c

Response to Calcium therapy

✔️ Belching

✔️ Muscle tremor – flanks→ whole body

✔️ Pulse rate decreases and amplitude improves

✔️ Heart sound intensity is increased

✔️ Sweating of muzzle

✔️ Defecation – firm stool with mucous

✔️ Urination does not follow until cow rises wait for 5-8 hrs until it stands. If not repeat the dose If it doesn’t stand after 24 hrs – use hip lifters.

Unfavorable Response to Calcium therapy

✔️ Cardiac irregularities

✔️ Heart rate increased

✔️ Shallow respiration.

The result of failure treatment of milk fever are following…

✔️ Downer-Cow Complications

✔️ Dystocia and Reproductive Disease

✔️ Retained Placenta

✔️ Decrease Milk Production

✔️ Mastitis