Milk Fever
This is the beginning of a new series of letter to and for the Pro-Ag of Australia Consultants.
Volume II No. 1
From time to time all consultants need to have a way to explain to their clients about certain diseases of cattle sheep and other animals. Mr Bryan McLeod and I have been friends for many years and he has asked me to begin a series of short articles that you may use when the need arises. My goal is to make these articles written in everyday language so you may give copies to your clients. Of course I am hoping that these will help you. If they do and you have a disease you would like to have me write about please let me know. I also welcome any additions or comments any of you have because the combination of our skills is one great advantage of working together.
Milk Fever also called Post Parturient Hypocalcemia
Those three words mean that it happens right after calving and there is inadequate Calcium in the blood.
One of the functions of Calcium in our bodies is to build bones and milk. Another is to assist in the transmission of nerve messages to muscle. When your system doesn’t have adequate Calcium one of the symptoms is the individual’s inability to move muscles properly. That means when the farmer goes out and finds a recently fresh cow unable to stand often flat on her side that one of the problems may be milk fever. If a cow is down flat on her side and cannot get up she will be unable to belch. Because the rumen bacteria are still doing their thing gas is being produced in the rumen and often if a cow has milk fever and is let unattended she will die of bloat.
Etiology: Etiology is defined as the study or theory of the factors that cause disease.
Milk fever is usually associated with the sudden onset of profuse lactation in dairy cows. Today’s modern cow can give well over a hundred pounds of milk in a day. The average composition of Calcium in milk is 0.9%That means for every 100 pound of milk there is almost a pound of Calcium taken from the bones to put into the milk. In Australia if she gives 45 Kilograms of milk she will take about 405 grams or
A cupful of that powdery white mineral from her storehouse to put into the milk.
This may help you understand mineral metabolism. If a baby calf weighs 50 Kilograms about 4 % 0r it’s body weight is mineral. The minerals came from what the cow ate. This discussion may help you understand why we need a mineral analysis of your feeds in order properly balance a ration.
When a cow eats a food like alfalfa hay she gets her Calcium from the hay. Alfalfa is a very good source of Calcium. The Calcium content of good alfalfa hay is 1.5%. All food that is eaten by any animal is first ground up by the teeth, then soaked in stomach enzymes and sent to the gut where it is in a soupy suspension. The particle size of the food must be small enough so it can be absorbed through the wall of the gut and enter the blood stream. At this point the Calcium is deposited in the storage system of the animal or the skeleton. All minerals that any of us eat follow this pathway. The first place to store most minerals like Calcium and Phosphorus is the skeleton.
When a cow makes milk she takes the minerals from the bones and the blood carries it to the udder where it is put in the milk. It takes about 1300 kilos of blood to make one kilo of milk. Imagine the marvel of milk production. Now when a cow is living in a diet of luxury consumption of Calcium, in other words she always has enough Calcium in her diet to meet her bodily needs. With this diet her retrieval system to get the Calcium out of the "bank" or the skeleton is not called on to get Calcium. Couple that with the fact the she suddenly is putting a large amount of Calcium into the milk and the Calcium level in the blood stream drops below the normal level and she goes down with milk fever.
There is a simple law in nature, use it or lose it. Athletes who want strong muscles lift weights. If we want the cow’s calcium retrieval system to be operating at optimum efficiency we do not feed her luxury consumption of Calcium during the last three weeks of her pregnancy. At that time she is putting the final touches of Calcium on the skeleton of her baby. If she has to withdraw Calcium from her skeleton in order to get the level high enough so she can supply the const4ruction requirements for the baby. This action then is sufficient stimulus to keep the retrieval system in optimum operational condition.
When she comes fresh we then can return to giving her Calcium at the level it is present in Alfalfa.
The entire thread of thought in this paper is designed to make you understand that a cow is simply a factory. If you want milk you give her the raw materials needed for milk production. If you aren’t making milk you do not need the same level of Calcium consumption.
The entire process of dairy cow nutrition is one of balancing the needs of the job we have for the cow with materials we put in the diet. This discussion is to emphasize the need for laboratory analysis of the raw materials we have on hand. We know what is in the forages and grains we produce, then we know what sort of a blend we need to incorporate in the minerals we feed.
The job of the consultant is to help the farmer with thee decisions.
Clinical findings and diagnosis
Parturient paresis or milk fever usually occurs within 72 hours of calving. It can occur during or sometimes even a bit before calving. The disease is sometimes responsible for dystocia because of inadequate muscular effort to expel the fetus.
Early in the onset the cow may exhibit some unsteadiness as she walks. More frequently she is unable to rise and will be found lying on her sternum with her head around to the side with her head in her flank with a kink in her neck. The eyes are dull and staring and the pupils dilated. Anorexia is complete. That means she has stopped eating. The muzzle tends to be dry and the extremities are cool. The pulse rate is likely to elevated and the temperature will be normal or subnormal. The digestive tract is atonic with suppressed defecation and a relaxed anus.
If treatment is delayed for several hours, the dullness gives way to coma, which becomes progressively deeper leading to death. With approaching coma the animal assumes lateral recumbancy which predisposes to bloating, regurgitation, and aspiration pneumonia.
Treatment in the early stages is more successful and fewer relapses occur. Those cases that occur at or within a few hours f calving appear to develop more rapidly and be more severe than those that develop at other times. .
Diseases that may be confused with milk fever are, metritis, mastitis, grass tetany, acute indigestion, traumatic gastritis, coxofemoral luxations, obturator paralysis, lymphosarcoma, spinal compression and fracture of the pelvis. Some of these diseases and, in addition aspiration pneumonia and degenerative myopathy may also occur concurrently with milk fever or as complications of the disease.
Prophylaxis
We have already talked much about the concept that diet is the key to prevention. Simple guidelines are to save the best alfalfa hay for the milking cows. Do not feed it to the dry cows. Use forages like Oat hay or haylage. This is the place where the consultant can have the greatest value. What feeds are available? How can they be combined for the optimum levels of the required diet guidelines?
Massive doses of Vitamin D (20 to 30 million units daily), given 5 to 7 days before calving may help that individual that is known to have the problem every year. The hazard here is that if the administration is stopped more than 4 days before calving the cow is more susceptible. The other problem is that too much of the vitamin can have toxic consequences. It is much better to work with managing the diet with testing and ration formulation. There are newer compounds on the market today and there are pastes that can be given orally with a caulking gun that are helpful with prevention. There are also ways to use gel forms of calcium again with the caulking gun. Doses of 150 grams of calcium can be given the day before and the day after calving.
Your local vet may have some of these products. I encourage all producers to utilize their local vet as well as the consultant and it is often a good idea for the consultant to cultivate friendship with the veterinarians.
Treatment
Effort is directed toward restoring the serum Calcium level to the normal range. This must be done at the earliest possible opportunity to avoid nervous and muscular damage. Some caws can injure themselves by thrashing around trying to get up.
Calcium borogluconate is most commonly used (250 to 500 cc of 25% solution). This is preferably given intravenously. I have seen bad sloughing and damage to the neck when large quantities have been accidentally put under the skin by careless injection. . Remember that too rapid injection is a way to kill a cow. Use a sixteen or eighteen gauge needle. I do not recommend a 12 gauge for IV use for Calcium. If you listen to the heart rate as you are giving the medication you are more apt to be cautious.
It seems almost unnecessary but I would remind you to attempt to be clean and aim for aseptic technique. When you are giving IV medications wash you equipment immediately after use. There is no excuse for being dirty or sloppy with surgical equipment.
Animals that relapse or fail to get up after 8 to 12 hours should be treated again. In those cases use a formula with some Magnesium added. There are many different brands and I tried to use a different one if I was giving a second treatment. If the case is complicated with ketosis it is helpful to give 250 to 500 CC of 50% dextrose.
Parturient Paresis in Ewes
This is a similar problem to that in cows. The Merk Manual states it this way. A disturbance of metabolism in pregnant and lactating ewes characterized by acute hypocalcemia and rapid development of hyperexcitability, ataxia, paresis, coma and death.
Etiology: The exact cause is unknown, but the conditions under which field outbreaks take place are fairly well defined. The disease occurs a few weeks before lambing and may happen several weeks after principally in highly conditioned older ewes at pasture. The onset is sudden and almost invariably follows –within 24 hours – and abrupt change of feed, a sudden change in weather or short periods of fasting imposed by circumstances such as shearing, or transportation.
This may be the place to mention Transport Tetany in Ruminants or sometimes called Railroad Disease, Railroad sickness or Staggers. These conditions are similar. It can affect well-fed cows and ewes in the advanced stages of pregnancy during and immediately after extended transportation and stress.
Clinical Findings: Characteristically the disease occurs in outbreaks. The incidence is usually less than 5% but in severe outbreaks up to 30% of the flock can be affected at one time. The earliest signs are slight hyperexcitability, muscle tremors and a stilted gait. Are soon followed by dullness, sternal decubitus, often with the hind legs extended backward, mild ruminal tympany and regurgitation of the food through the nostrils, staring eyes, shallow respiration, coma and death within 6 to 36 hours.
Diagnosis: This is based on the history and clinical signs. In outbreaks occurring before lambing, pregnancy toxemia offers the main problem in differential diagnosis. A tentative diagnosis of acute hypocalcemia can be confirmed readily by a dramatic and usually lasting response to Calcium therapy.
Prophylaxis and Treatment: Treatment consists of IV or subcutaneous administration of 100 cc of 25% w/v Calcium borogluconate preferably with Magnesium added. Affected sheep should be handled with care, lest sudden deaths occur with heart failure. Prevention is largely a matter of avoiding the predisposing causes.
I enjoyed writing this for you and if you have questions, don’t hesitate to email me a question. I learn more from my friends than I did in school.
One more thing, believe in yourself with all your might.
Doc Bob