Vitamin A in plants mainly exists in the form of provitamin A (carotene). Various green feeds, including fermented green feeds, especially green hay, carrots, pumpkins, and yellow corn, are rich in provitamin A, which can be converted into vitamin A. However, there is almost no provitamin A in cotton seeds, linseeds, radish, dry beans, dry cereals, potatoes, and beetroots. Diarrhea, rumen hypokeratosis or hyperkeratosis in calves can lead to vitamin A deficiency. Because a large amount of carotene is converted into vitamin A in the intestinal epithelium, and vitamin A is mainly stored in the liver, chronic intestinal disease and liver disease are most likely to cause secondary vitamin A deficiency.
Vitamin A deficiency most commonly occurs in calves and poultry. It can also occur in other animals, but it rarely occurs in horses.
Pathogenesis
Vitamin A deficiency mainly affects the normal metabolism of animal visual pigments (affecting rhodopsin in cattle), the growth of epiphysis and the maintenance of epithelial tissue. Severely deficient female animals may even affect the normal development of the fetus.
(1) The effect of vitamin A on bovine visual pigment
Vitamin A in the retina of normal animals is oxidized under the action of enzymes and converted into retinaldehyde. The outer segments of the retinal visual cells of cattle are almost all visual pigments, the chromophore part of which is retinal, the protein part of which is rod opsin, and the visual pigment part of which is rhodopsin. Optic cells are dark photoreceptors that contain visual pigments. When exposed to light, visual pigments are decomposed into retinal and opsin. In the dark, they react in reverse to synthesize visual pigments. When vitamin A is lacking or insufficient, the regeneration and replacement of rhodopsin is interfered with, and animals suffer from weakened vision and blindness in dark light.
(2) Vitamin A deficiency leads to abnormal bone development
Due to the change in the normal position and destruction of the activity of osteoblasts and osteoclasts, the growth of endochondral bone and bone structure are affected. Finely sculpted. Skeletal growth retardation and abnormal bone formation are mainly manifested in the nervous system. Due to overcrowding of brain tissue in the cranial cavity, brain torsion and herniation occur, and cerebrospinal fluid pressure increases, followed by characteristic neurological symptoms such as papilledema, ataxia, and syncope. Due to compression, torsion and elongation of cranial nerves, the cerebellum enters the foramen magnum, causing hypofunction and ataxia. The notochord enters the intervertebral foramen, causing nerve root damage and local symptoms of individual peripheral nerves. In the later stages of the disease, typical blindness occurs due to facial nerve paralysis and optic nerve atrophy.
(3) Vitamin A deficiency can cause atrophy of all epithelial cells
But it is mainly the epithelial tissue that has both secretory and covering functions that is affected. Due to the failure of secretory cells to divide and generate on the basal epithelium, in deficiency, these secretory cells are gradually replaced by laminated keratinized epithelial cells, becoming non-secretory epithelial tissue. This condition is mainly seen in the salivary glands, the urogenital tract (including the placenta, but not the ovaries and renal tubules), and the accessory eye glands and teeth (loss of dentinoblasts in the enamel). Thyroxine secretion is significantly reduced. The effect on gastric mucosa is not obvious. Clinically, placental degeneration, dry eye disease, and corneal changes occur as a result of these epithelial changes.
In addition, since vitamin A is an essential substance for organ formation during fetal growth, vitamin A deficiency in maternal animals can lead to multiple congenital defects in the fetus, especially cerebral edema, eye damage, etc. .
Clinical symptoms
The clinical symptoms of various animals are basically similar, but there are some differences in the degree of manifestation in tissues and organs.
The skin of animals suffering from deficiency can show seborrhea and dermatitis, and the skin of cattle has bran-like scabs. However, the deficiency can affect the reproductive capacity of both male and female animals. Although male animals can still retain their sexual desire, the reproductive epithelium of the seminiferous tubules is degenerated, sperm motility is reduced, and the testicles of young bulls are significantly smaller than normal. Although the conception function of the female animal is not affected, the placenta degeneration can lead to miscarriage, stillbirth or fetal weakness after birth and retained placenta of the female animal.
Newborn calves may suffer from congenital blindness and encephalopathy, internal hydrocephalus, notochord hernia, and generalized edema; other congenital defects such as renal ectopia, heart defect, and diaphragmatic hernia may also occur.
Night blindness is a prominent symptom, and it is also the earliest important symptom to appear in pigs. Especially in calves, when other symptoms are not obvious, it can be found that they move blindly, move slowly, and collide with obstacles in the morning, evening or moonlit night when the light is hazy. As for the so-called "dry eye disease", it refers to the thickening and cloudy formation of the cornea, which is only seen in dogs and calves. In other animals, the eyes secrete a serous secretion, and then the cornea becomes keratinized, forming a cloudy shape. , sometimes ulcers and blindness occur. Due to compression of the optic nerve, papilledema and blindness can occur. Blindness is caused by retinal degeneration and should be distinguished by ophthalmoscopy.
In addition, animals suffering from deficiency may also show symptoms of central nervous system damage, such as encephalopathy caused by increased intracranial pressure, blindness caused by narrowing of the optic canal, and skeletal muscle damage caused by peripheral nerve root damage. paralysis. Movement disorder due to paralysis of skeletal muscles. As for encephalopathy caused by increased cerebrospinal fluid pressure, it is usually seen in calves and is characterized by tonic and paroxysmal convulsions and hyperesthesia.
Diagnosis
Based on the feeding history and clinical characteristics as a preliminary diagnosis, the diagnosis must refer to the pathological damage characteristics, vitamin A and carotene levels in plasma and liver, and changes in cerebrospinal fluid pressure. Weight loss, slowed growth, and reduced fertility are general symptoms and are not limited to those seen in vitamin A deficiency. Seizures in calves and hindquarter paralysis in growing pigs are seen among many other diseases. Clinically, it is difficult to distinguish encephalopathy caused by vitamin A deficiency from hypomagnesemic convulsions, leucomalacia, enterotoxemia caused by Clostridium perfringens type D, and lead poisoning. The difference between rabies and sporadic bovine encephalomyelitis is based on the former being accompanied by disturbance of consciousness and loss of sensation, and the latter being accompanied by high fever and serositis.
Prevention
Since vitamin A or carotene exists in oil and is easily oxidized, if the feed is left for too long or if lipovitamin A is mixed into the feed in advance, it will It may be oxidized and deteriorate, especially in an environment where a large amount of unsaturated fatty acids exist. Carotenease can also destroy carotene. When supplementing vitamin A, the use of alcoholic vitamin A is beneficial to animal absorption and can pass through the placental barrier. The use of capsules can reduce the oxidation of vitamin A. Silage and fertile pasture containing high levels of nitrates and nitrites can interfere with the conversion of carotene into vitamin A. The fermentation of ruminant forestomach microorganisms and the action of abomasal chemistry and enzymes can also lead to the loss of carotene. Phosphorus deficiency can reduce the conversion of carotene, but low-phosphorus feed is beneficial to the storage of vitamin A.
The minimum normal daily requirement of vitamin A for various animals is 30 international units per kilogram of body weight, and the minimum normal daily requirement of carotene is 75 international units per kilogram of body weight. To store it in the liver, the above intake must be doubled. During the pregnancy and lactation stages of dairy cows, the dose can be increased by 50. In the diet of fattening cattle, 10,000 IU of vitamin A should be added every day in winter and 40,000 IU every day in autumn. Because too high a dose can interfere with the role of vitamin D in bone development, care should be taken when using it. As for clinical cases, the normal requirement can be increased by 10 to 20 times, but it should not be too high. Usually it is 440 international units per kilogram of body weight. Treatment does not require oral administration but injection. The injection is an alcoholic form of vitamin A rather than a lipid form.