What is selenium, cobalt and zinc deficiency disease in deer?
Uneven geographical distribution of trace elements and substandard feeding management can both cause trace element deficiency diseases. Targeted and appropriate supplementation of the trace elements essential for deer is the most effective method for preventing and treating trace element deficiency diseases in deer.
In the deer body, trace elements act as catalysts for various enzymes and as activity regulators of proteins, fats, polysaccharides, nucleic acids, vitamins, hormones and so on. Trace elements cannot be synthesized in the deer body and must be obtained from feed, while their excretion is continuous; therefore, supplementation according to the actual situation is very necessary.
The causes of trace element deficiency disease are roughly as follows: (1) The geographical distribution of trace elements in soil is uneven, so that one or several trace elements are lacking in feed and drinking water. (2) The content of a certain trace element is normal, but because the intake of other elements that antagonize this element is too high, the absorption and utilization of this trace element are affected. (3) During pregnancy of does or during vigorous growth and development of fawns, the demand for certain trace elements exceeds the ordinary level, but these cannot be obtained from feed. (4) Deer suffer from chronic diarrhea or indigestion, which affects the absorption of trace elements, thereby causing secondary trace element deficiency disease.
There are many kinds of trace element deficiency; this article will focus on the deficiency diseases of 3 elements that are seriously harmful to deer: selenium, cobalt and zinc.
1 Selenium deficiency disease
Selenium deficiency can cause many diseases, such as white muscle disease and mulberry heart disease in fawns. Surveys show that a very large area of China has geographical selenium deficiency; this area is a belt-shaped selenium-deficient zone extending from Heilongjiang in the northeast to Yunnan, involving Heilongjiang, Jilin, Liaoning, Inner Mongolia, Shanxi, Hebei, Henan, Hubei, Shaanxi, Gansu, Sichuan, Yunnan, Tibet and other places. In addition, some cities and counties in Shandong, Jiangsu, Zhejiang, Fujian and other provinces are also severely selenium-deficient. In severely selenium-deficient areas, the soil selenium content is only 0.06mg/kg. People in these areas are prone to Keshan disease and Kashin-Beck disease. Fawns and other young animals raised in these places are also prone to white muscle disease, so selenium supplementation is very necessary.
By contrast, Enshi in Hubei and Ziyang in Shaanxi in China are rare selenium-rich areas, where chronic selenium poisoning of young animals occurs locally. In feed, fish meal has a relatively high selenium content, followed by pasture grass, then oilseed cakes and meals, and cereal grains the least, for example corn is only 0.02mg/kg. Antioxidant capacity is the basis of the biochemical action of selenium, and selenium and VE have a synergistic effect in antioxidation. Selenium supplementation can improve non-specific immune functions such as cellular immunity and humoral immunity. In addition to regional occurrence, VE insufficiency can induce selenium deficiency disease, and it is also related to season; May to July is the peak period of onset, mainly harming fawns and other young animals, because young animals have weaker disease resistance and are more sensitive to special nutrients.
1.1 Clinical symptoms (1) Motor dysfunction: affected deer prefer to lie down and have difficulty standing up, with stiff limbs; (2) Cardiac dysfunction: rapid heartbeat, irregular rhythm, and sudden death while running; (3) Digestive dysfunction: indigestion and poor appetite; (4) Neurological dysfunction; (5) Reproductive dysfunction: poor semen in bucks, does are not easy to conceive or are prone to miscarriage; after death of fawns, necropsy shows obvious symptoms of white muscle disease, namely degenerated affected muscles that are pale in color, with grayish-white and pale yellow streaks on the cross-section.
1.2 Diagnostic method Diagnosis is made in combination with epidemiology (history of selenium deficiency), clinical features, analysis of selenium content in feed and tissues, pathological necropsy, related blood enzymes - glutamic-oxaloacetic transaminase (GOT), lactate dehydrogenase (LDH), plasma peroxidase (GSH-PX) - and relief of symptoms after selenium supplementation.
1.3 Prevention and treatment methods After onset, 0.1% sodium selenite can be injected subcutaneously or intramuscularly, 3-5ml per time for fawns, repeated once after 10 days, while VE supplementation is used in combination, with 15mg added for fawns. Injection of 0.1% sodium selenite, adding selenium to feed, providing selenium-added salt lick blocks, placing rumen selenium boluses, and subcutaneous embedding of sodium selenite can all effectively prevent it. Selenium is a toxic element, so when using it attention should be paid to even mixing and the dose should be scientifically controlled; it is best to have a professional feed enterprise provide the service.
2 Cobalt deficiency disease
Cobalt deficiency disease is a chronic endemic disease caused by insufficient cobalt in soil and feed, characterized by reduced appetite, pica, anemia and gradual emaciation.
Cobalt is an essential trace element for animals, especially for ruminants such as deer. The growth and reproduction of bacteria in the deer rumen require cobalt, and some of these bacteria can use cobalt to synthesize VB12; the synthesized VB12 is a vitamin essential for ruminants such as deer, which can not only ensure the growth and reproduction of rumen ciliates, but also help improve the digestibility of cellulose. If cobalt is lacking, VB12 synthesis is insufficient, which directly affects the growth and reproduction of bacteria and rumen ciliates, and directly affects cellulose digestion. If rumen digestion is abnormal, it directly affects the energy supply of the deer body, leading to emaciation and weakness. Cobalt can accelerate the mobilization of iron in the body and cooperate in the realization of hematopoietic function. In addition, cobalt can improve the absorption of zinc; zinc is related to gustin, and cobalt deficiency can cause decreased appetite and even pica.
2.1 Clinical symptoms Cobalt-deficient deer show progressive emaciation and anemia, pale visible mucous membranes, and decreased hemoglobin concentration, and the condition can last about 1 year; diarrhea and decreased reproductive function occur. Necropsy shows extreme emaciation of affected deer, hemosiderin deposition in the liver and spleen, increased iron content and decreased cobalt content in the liver and spleen.
2.2 Diagnostic method A preliminary diagnosis can be made based on history and clinical symptoms, but confirmation still requires testing of cobalt content and other biochemical indicators in soil, feed, blood and tissues: (1) Cobalt content in soil and feed When cobalt in soil is below 3mg/kg and cobalt in feed is below 0.07mg/kg, this can be used as an indicator for diagnosing cobalt deficiency. (2) Blood cobalt When the content is below 15% of the normal level, cobalt deficiency disease can be considered to have occurred. (3) Amount of cobalt and VB12 in tissues When VB12 in the liver is below 0.1mg/kg and cobalt content is below 0.07mg/kg, cobalt deficiency disease can be considered to have occurred. (4) Detection of blood glucose concentration and alkaline phosphatase concentration, etc. If below normal values, cobalt deficiency disease can be considered to have occurred.
2.3 Prevention and treatment methods For treatment of this disease, oral cobalt salt preparations should be used, combined with VB12 supplementation, with obvious efficacy; generally cobalt preparations are not injected. Cobalt oxide, cobalt sulfate, cobalt chloride and the like can all serve as sources for oral cobalt supplementation. For prevention of this disease, cobalt salts can be added directly to feed, or made into additives or lick bricks for deer to lick freely. Cobalt is added in trace amounts, and the dosage must be well controlled, otherwise cobalt poisoning will occur.
3 Zinc deficiency disease
Most provinces in China are zinc-poor or zinc-deficient; for example, in Hebei, Beijing, Hubei, Jiangxi, Jiangsu, Sichuan, ** and other places, 30%-50% of the area is zinc-deficient. Among feedstuffs, plant-based feeds generally have low zinc content or low biological effectiveness, while animal-derived feeds such as bone meal and fish meal have high zinc content and are easy to absorb. In addition, bran and chaff also contain relatively more zinc. Antagonistic factors in feed can also affect the absorption and utilization of zinc. Excessive calcium and phosphorus, or excessive copper, iron, manganese, molybdenum and other elements, can all affect zinc absorption.
3.1 Symptoms Growth and development are hindered, skin shows incomplete keratinization or hyperkeratosis, and skeletal development is abnormal, manifested as shortened and thickened long bones, swollen and stiff joints, reproductive dysfunction, dull hair and large-area shedding in inappropriate seasons, and wounds that are difficult to heal. A confirmed diagnosis can be made by combining measurement of zinc content in local soil and feed and zinc content in the serum of affected deer, as well as measurement of the content of other elements in feed that easily cause zinc deficiency. After zinc supplementation, symptoms lessen in about half a month.
3.2 Prevention and treatment methods The content and ratio of zinc and zinc-antagonistic elements in feed should be adjusted according to the actual zinc deficiency situation. Zinc sulfate, zinc carbonate, zinc oxide and the like can be used as zinc sources for zinc supplementation. Prevention of this disease focuses on ensuring the zinc content in feed, while also adjusting the ratio of other elements to zinc in feed, so as to avoid antagonism affecting zinc absorption and causing absorption-disorder zinc deficiency. Zinc is basically non-toxic and the risk of use is not great, but it should still be used under the guidance of professionals.
In short, due to the uneven geographical distribution of elements, mistakes in feeding management, and the induction of some other diseases, the @#@253@#@ industry in China has serious trace element deficiency diseases, and the losses caused are enormous. Some breeders are not aware of it, or do not know how to handle it and therefore do not supplement; some know only a little relevant knowledge and then prepare and supplement trace elements themselves, resulting in excessive use of trace elements or inappropriate ratios among elements, causing man-made deficiency or poisoning. My suggestion is: after becoming aware of trace element deficiency, one should ask a research institution or high-tech enterprise with good technical conditions, mature methods and reliable reputation to make a targeted diagnosis before appropriate supplementation.