What is a stale element in selenium

Careful diagnostics in sheep and goats is essential. The first signs are difficult to recognize and are often overlooked, the indicators are diverse. The veterinarian should be asked for advice in order to counteract the deficiency of trace elements in a targeted manner.

Vitamin E and selenium are building blocks of an important enzyme system in the body. If the enzyme is missing, the muscles are damaged and the immune system is weakened. In the adult animal, the muscle damage is not as severe as in the young animal. If the mother animal has a hidden deficiency, then the lambs are also poorly cared for in the womb or with colostrum. Animals born in this way are either incapable of living from the outset or they die during the first days of life (early form). Sometimes these lambs can drink, but not get up.

Check the status with blood samples
If the initial deficiency symptoms are not quite as pronounced, the problems begin with noticeable movement disorders in the somewhat older lambs (late form): tired, unsteady gait. Inability to stand up, shortness of breath. Fatalities can also occur here. These images cannot be seen in the adult animals. In fact, despite a good supply of food, they do not gain weight properly and are more susceptible to worm infestation or other diseases. Goats often have a shaggy coat of hair. Often the element is selenium not enough in the soil. The plants do not need selenium to grow. So it is difficult to offer a sufficient selenium content in the feed (requirement: 0.5 mg / kg TS selenium / 50 mg / kg TS vitamin E). If you suspect a vitamin E / selenium deficiency, it is advisable to check the supply by analyzing blood samples. In the event of an insufficient supply, an injection treatment with a corresponding vitamin E / selenium preparation must be carried out and a mineral feed containing selenium must be consistently offered. To monitor the process, you should first check the status regularly using blood samples.

That too copper is a vital trace element that has to be taken in with food. If there is not enough copper in the diet, what is known as primary copper deficiency occurs. However, it is also possible that other substances occurring in the soil or in feed, such as molybdenum and sulfur, prevent the body from absorbing copper; then one speaks of secondary copper deficiency.
The clinical picture of copper deficiency is very similar to that of vitamin E and selenium deficiency. Often both occur in parallel. Lambs with weak life are often born. Lambs mortality is increased. The animals show movement disorders and cannot stand up. Mostly this is due to a clear weakness behind. This in turn arises from the fact that the formation of the nerve tissue is disturbed. In lambs that seem to grow up without any problems at first, so-called swayback can occur after three to four months. You develop an increasing weakness in the hind quarters, the gait is increasingly unsteady, finally movement coordination is no longer possible. The older animals do not look well fed, fleece or fur are dull. They suffer from wool loss and are susceptible to infection. The milk yield drops. Skin changes can also occur. The mucous membranes are often yellow in color.
The diagnosis of Copper deficiency in a living animal is difficult. Determinations of copper in the blood are possible. However, they only provide information about how much copper is currently in the blood. The liver is the actual storage location. The diagnosis is only confirmed if it is found to be too low (liver of slaughtered animals or dead animals). It should be, because the treatment of the deficiency takes place through oral administration of copper and carries the risk of copper poisoning.

There is a risk of oversupply
The acute Copper poisoning is not that common. However, it should be mentioned at this point in order to make the risk of oversupply clearer. Because it is the case that the trace elements are chemical elements with high toxicity (poisonous effect). And overdosed treatment can cause symptoms of intoxication. The balance between undersupply and oversupply is a tightrope walk, especially with sheep. The goat is a little more generous. So you should put together a ration in which the content of 12 to 15 mg copper / kg dry matter (DM) of the total ration is not exceeded in order to provide the animals with sufficient trace element copper without provoking symptoms of poisoning.

If the sheep receives too much copper either through a single dose or in smaller quantities over a longer period of time, this can have devastating effects and the picture of copper poisoning arises. The symptoms of chronic copper poisoning in adult animals roughly correspond to those of copper deficiency. They are often not recognized. However, if you suspect an oversupply, the liver analysis will also provide information in this case. An analysis of the suspicious feed also helps here.
Too much copper can be found in concentrate for cattle or on areas that have been fertilized with pig manure, for example. If, after a certain period of time, the animals have absorbed absolutely too much copper and stored it in the liver, the liver becomes depleted and thus acute copper poisoning occurs. In its acute form, the poisoning takes a dramatic course. The impressive clinical picture of acute copper poisoning may have resulted in the absence of copper in many sheep minerals. In the foreground are the symptoms caused by a type of liver failure. The animals no longer eat and are short of breath. The mucous membranes take on a yellow color and blood urine is possible. Mortality is high and treatment is practically impossible.

The Cerebral necrosis is primarily a disease of lambs and is caused by a deficiency in a vitamin of the B group of vitamin B1, also known as thiamine. The thiamine is partly ingested with food and partly formed by bacteria in the rumen. There are three ways in which a deficiency can occur. It is missing in the diet, it is broken down by the constituents of plants (thiaminases) or the rumen does not work properly, so that the bacteria that settle there when the rumen function is impaired also produce thiaminases. If the vitamin is missing, body cells cannot be supplied with sufficient energy. Since the brain cells have the greatest need for energy intake, they are most affected. And they die first in the cerebral cortex. This death of the cerebral cortex leads to the typical phenomena. With their heads extremely stretched backwards / upwards, the animals lie on their side with muscle tremors and cramps, which can intensify depending on the noise. If left untreated, they usually die. The disease can also occur in older animals, and then looks exactly the same. The treatment is best carried out by repeated injections of thiamine directly into the blood and is quite successful if it is done early enough. Depending on the triggering cause, which cannot be clearly identified, a change in diet or an improved intake of thiamine should be made.

In the Rumen acidosis it is, as the name suggests, an overacidification of the rumen. The small ruminants have several stomachs and in the largest of them, the rumen, the digestion of food, the formation of vitamins etc. take place with the help of the rumen bacteria. The rumen bacteria need an alkaline environment for this. If the acid content in the rumen changes, for example due to the intake of too large amounts of sugar (carbohydrates), the balance of the rumen bacteria is upset. This can gradually develop if the diet is too high in carbohydrates for long periods of time.
This chronic acidification can, for example, promote the development of cerebral necrosis (CCN). The animals no longer eat well, have a stiff gait, fever and diarrhea. Then it is usually sufficient to first stop the carbohydrate-rich feed and offer feed and water rich in crude fiber for several days. This should be followed by a slow adjustment to the ration.

If the acidification happens acutely, i.e. if an "eaten up" animal messes with a lonely bucket of beet pulp or if it goes to a pasture with fruit trees in late summer, the whole thing happens very quickly. Within a few days, the rumen mucous membrane comes off due to the aggressive action of the acid. The animal is in severe pain, stops eating, has watery diarrhea, and often gets stuck and dies. During treatment, it is important to neutralize the acid as quickly as possible and restore the rumen environment: stopping the sugar-rich feed, changing areas, giving straw and water, adding buffering drugs and supplying vitamin B. Also adding rumen juice (obtained from slaughtered animals) has proven itself. In the case of severe symptoms, treatment usually comes too late. The healing process takes a long time. If the illness has been overcome, generalized wool loss often occurs later.