Hypovitaminosis and vitamin deficiency (deficiency / absence) of the necessary vitamins for the life of birds. The conditions that cause such deficits are very serious and can result in the death of a bird.
A deficiency condition can develop with a deficiency of one vitamin, and polyhypovitaminoses are also found when a pet grabs a whole group of these useful substances.
Most often, birds develop A, D, E - vitamin deficiencies.
Less often, vitamin C, K and group B are not enough in the diet.
Both poultry and decorative birds can suffer from a lack of vitamins.
With a lack of this vitamin, the skin, its appendages and the mucous membranes of the bird become dry and thin. This allows infectious agents to easily enter tissues.
Weakness of the limbs, coordination disorders are noted.
The bird does not see well at dusk.
The cornea of the eyes becomes inflamed (very often such changes are diagnosed in parrots and canaries).
Inflammation of the intestine develops, respiratory organs can be affected.
To prevent this condition, poultry can be fed nettle and dandelion leaves, as well as carrots in oil (vegetable).
It is allowed to add fruits (apricot, blackcurrant).
Decorative birds should receive vitamin preparations.
Hypovitaminosis - course and characteristics. Etiology, clinical signs, pathological changes, diagnosis of the disease, laboratory tests, determination of the vitamin in biological materials, relief, prevention and treatment.
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Hypovitaminosis of farm birds
A-hypovitaminosis - occurs chronically with a lack and poor absorption of vitamin A and provitamin carotene. It is characterized by a violation of the structures and functions of epithelial tissue.
Vitamin refers to fat soluble. A synonym for vitamin A is retinol. The action is multilateral: reducing the pathology of oxygen consumption by tissues, improving mineral (especially calcium and magnesium) and fat metabolism, accelerated release of benzoic acid, a beneficial effect on the function of endocrine glands, the formation of epithelial, cartilage and bone tissue and preservation of vision, and ultimately on growth , development and resistance of birds. All this contributes to the acceleration of broiler fattening, increase egg production, fertilization of eggs and hatchability in birds.
Etiology. The systematic shortage of poultry by carotenoids and vitamin A with food reduces the formation of acid mucopolysaccharides in the body, partially regulating the growth and development of cartilage. As a result of developing deformations, curvature and porosity of the bones of the skull and spine, dropsy of the brain forms and pressure on the spinal cord and central nervous system increases. This leads to ataxia, a continuously increasing discoordination of movement. With a disease of the digestive system (enteritis, hepatitis, cholecystitis), as well as with prolonged use of neomycin, polymyxin and nystatin, which bile bile and block the absorption of fats and fat-soluble vitamins, the absorption of vitamin A and its provitamin is impaired. Vitamin A antagonists are nitrates and nitrites, which should also be considered. A-hypovitaminosis develops after the chicken has been ill with pullorosis, helminth infections, mycoses and other diseases. The biological characteristics of the bird contribute to the development of A-hypovitaminosis - their high growth rate, rapid, due to their short length, feed advancement in the gastrointestinal tract, and limited absorption of endogenous vitamins in the digestive tract. Finally, they take into account the ratio of vitamins to the body: an excess of one vitamin often causes a shortage of another. For instance. with excessive intake of vitamin A in the intestine of the bird, the absorption of vitamin E is inhibited. Vitamin A, being oxidized, is excreted in the form of glucuronates with bile, which also increases the deficiency of vitamin E of endogenous origin.
Clinical signs. In chickens hatched from A-hypo vitamin eggs, the course of the disease is acute, especially when using feeds that are poor in vitamins. A-hypovitaminosis appears in this case at the end of the 1st week, in chickens hatched from eggs full of retinol - up to 45 -50th day of life. Observe drowsiness, stunted growth and disheveled feathers. Chickens refuse to feed due to keratinization of the oral mucosa and esophagus. Cheesy clusters appear in the corners of the eyes and the same cheesy plaques under the blinking membranes. The eyelids swell, stick together with the crusts of the mucous exudate. In the nasal cavity, dried exudate crusts, an increase in mucous scabs in the larynx. Shortness of breath, wheezing. Lodging. Complete exhaustion.
In adult chickens and turkeys, symptoms appear 2-5 months after feeding low carotenoid foods. The course is slower. Emaciation. Pen drop out. Lethargy, wrinkling and blanching, often to a white color, scallop. In the oral cavity, plaques are white-gray or gray-yellow. Food intake is difficult, especially the act of swallowing. In severe cases, lacrimation, dry mucous membranes and corneas, clouding and ulceration (xerophthalmia). Often perforation of the cornea. Hard breath. Depressed state. Egg production drops sharply or stops. The number of blood inclusions in the eggs is increasing. The hatchability of chickens is reduced by 3-5 times compared with the norm. Chickens die from exhaustion.
In males, the development of the ridge is delayed, the mass of the testes increases. The fertility of eggs is sharply reduced. Urate diathesis develops.
Pathological changes. Pallor of crest, catkins and mucous membranes are noted. The pen is dull, roughening the skin, primarily on the feet. Exhaustion. Xerophthalmia, cheesy plaques under the blinking membrane, fibrinous inflammation and softening of the cornea (keratomalacia), and then the eyeball (panophthalmitis). On the mucous membranes of the nasal passages, pharynx, larynx, esophagus, small white pustules up to 20 mm in diameter. Pustules enlarge, dents form in their center, and sores develop. The ducts of the mucous glands of the esophagus increase and keratinize. Often the epithelium of the renal tubules is affected, the excretion of uric acid with droppings is reduced. The amount of uric acid in the blood increases 5-10 times. Urate is deposited on a section of internal organs.
Diagnostics. A preliminary diagnosis is made taking into account clinical symptoms, autopsy results and previous studies of feed, eggs, liver and blood serum from a sick bird for the presence of vitamin A and carotene. Determine what is the main cause of A-hypovitaminosis: inadequate feed (poor in vitamin A) feed received at the poultry farm, or mistakes made on the spot when drawing up diets. In order to stop the disease, feed additives are immediately introduced into the diet. It is advisable to include in the diet of the bird - corn, acetate or palmitate in the form of a dry preparation with vitamin ds- In order to reduce the oxidation of vitamin A, an antioxidant (protective agent) - ethoxivine - is added to the feed mixture.
Differential diagnosis excludes smallpox, ILT, respiratory mycoplasmosis and A-hypervitaminosis. The latter develops when the bird is given excess vitamin A and carotene. A-hypervitaminosis is characterized by a decrease in egg production and body weight, catarrh of the mucous membranes of the oral and nasal cavities, severe hyperemia of the vessels and hemorrhages, osteoporosis and calcification of the epiphyseal cartilage of the tubular bones.
To determine vitamin A and β-carotene in biological materials, physicochemical methods (spectrophotometry with chromatographic separation), fluorometric, polarographic, and histochemical methods are used.
Prevention and treatment. Per tonne of dry feed is introduced (million IE of Vitamin A): for breeding birds 10-15, broilers 10, egg of an industrial herd 5-7, repair young stock 7. Use of combined silage (grass meal and chopped carrots or vitamin pumpkin) in feeding meat birds of the parent herd, ducks, turkeys, geese completely prevents diseases of vitamin deficiency, increases the usefulness of hatching eggs and the safety of young animals.
Treatment of sick birds is not economically effective.
D-hypovitaminosis is a chronic disease of young poultry of various species, in which the general and especially phosphorus-calcium metabolism is disturbed with a systemic violation of bone formation.
Fat soluble vitamin. There are varieties of vitamin D (calciferol), dz and D3; for birds, vitamin Dg or cholecalciferol is 20-30 times more active than vitamin U2. Vitamin ds comes from the intestines to the lymph with almost no change. Absorption is facilitated by fats, especially linoleic acid. In the liver, 25-hydroxylcholecalciferol (the most active form of vitamin) is formed from cholecalciferol. In the kidneys, vitamin Dg is converted to 1,25-hydroxyform, which is 3-4 times more active than its predecessor. Vitamin ds should receive young birds. Etiology. In plants and seeds, from which compound feeds for poultry are prepared, and in tissues and fluids (blood, blood serum, milk, melange, etc.) that are used to prepare dry (powdered) feed additives, there are physiologically inactive fat-like substances from the group of sterols - provitamins D. Under the influence of ultraviolet rays, they turn into active forms of vitamin D, which accumulates in the tissues of birds.
D-hypovitaminosis is of exogenous and endogenous origin. The first occurs during the period of increased growth of young poultry due to insufficient ultraviolet irradiation and diets unbalanced in terms of vitamin and mineral composition. Rickets of endogenous origin occurs in cases of malabsorption of vitamin D in the small intestine, which is a consequence of various diseases and predisposing factors: violation of veterinary and sanitary requirements for keeping the bird in cramped, dark, damp cell batteries, etc. The lack or absence of vitamin D in the body Contribute to: imbalance in the ratio of calcium and phosphorus, impaired intake of phosphate salts from the intestines into the blood and a sharp decrease in the concentration of phosphatase enzyme in the blood, which promotes transfer su phosphorus from organic compounds into bone tissue, the development of a deficiency of citric acid, in which potassium phosphate salts are excreted in the urine and droppings from the body, resulting in bone tissue depleted in minerals.
Clinical signs. In egg chickens, at 10-15 days of age, loss of appetite, weakness, feathers are tousled, and plumage is poor. After 2-3 weeks, chickens sharply reduced motor activity, impaired coordination of movements, diarrhea, beak, claws, keel and skull develop soft, easily miss. In 20-30 day old chicks, the hip joints twist. The final stage of rickets is osteomalacia: a complete breakdown, helplessness, chickens cannot move, lie with outstretched limbs.
In broiler chickens, rickets occurs earlier, at the age of 8-10. There is apathy, poor operability, walking on the heel (hock) joints, growth retardation and a decrease in body weight by up to 50%.
For turkeys and chickens, the ribs are curved at the junction with the dorsal trunk, bending them down and back, and very poor calcification of the epiphyses of the femur and tibia.
Layers lacking vitamin D lay eggs with a thin and deformed shell or no shell at all. Some take the “penguin” pose, which is fickle. The keel is curved, with a ribbed surface, the ribs are soft and sunken, the beak and claws become flexible. Oviposition stops.
Pathological changes. In chickens of different species of birds, ossification of the sutures of the cranial bones is delayed, the bones of the skull are soft, on the edges at the joints of the joints there are rickets and the same bone thickenings (osteophytes) in the pineal glands and on their surface. The chest and other bones are bent. Dropsy of the brain, anemia, stunting, and diarrhea develop. In sufferers, pronounced myxedema of the subcutaneous tissue of the nape is noted. Diagnostics. A preliminary diagnosis is made by specific pathological changes (curvature, softening, partial resorption of the ribs, fractures, breaks and corns on them). A nonspecific sign is taken into account - slow growth.
In order to stop the disease, measures are being taken to eliminate the causes of insufficient intake of vitamin D from food. Stop using vitamin D2, which the bird does not properly accumulate and use. Vitamin is added to the food only in the form of ds- At the same time, take into account that the need for turkeys in this vitamin is significantly higher compared to chickens. A temporary improvement in the condition of the bird is achieved by adding some synthetic antioxidants to the feed (for example, ascorbic acid). With further clarification of the diagnosis, D-hypervitaminosis, vitamin deficiency of another etiology and alimentary dystrophy are excluded. D-hypervitaminosis develops in poultry with uncontrolled excessive feeding of fish oil. In case of hypervitaminosis, an adult bird develops osteoporosis, hypercalcemia with metastatic calcification of the walls of large arterial vessels of the myocardium, lungs, stomach and kidneys, the formation of the shell is disturbed and exhaustion of the bird occurs.
Conduct laboratory tests. Vitamin D is determined in the blood and egg yolk. Blood serum is examined for the content of inorganic and total phosphorus, calcium, phosphatase and citric acid. The early manifestations of D-hypovitaminosis include a decrease in the concentration of phosphorus in the blood to 1.0-2.0 mg% (normal 5.0-6.0 mg%), as well as alkaline phosphatase. The level of calcium in the blood decreases. As a result, a salt ratio is especially characteristic of rickets: an extremely low content of serum phosphorus and subnormal - calcium, the concentration of citric acid in the blood decreases sharply.
Prevention and treatment. It is carried out by adding vitamin D preparations to feed mixtures (million IE): for adult birds with high egg production of 3-3.5 per 1 ton of feed, and for young animals - 1.5-1.8.
To prevent hypovitaminosis, chickens are irradiated with PRK-2 and PRK-7 lamps: the first time after being removed from the incubator, the second time before being transferred to the growing workshop. Boxes with young animals are placed at a distance of 1 m from the PRK-2 lamp, the exposure time is 3-5 minutes. PRK-7 is placed at a distance of 1.7 m from the boxes, the irradiation time is 1-1.5 minutes.
E-hypovitaminosis - a disease develops when the body systematically does not receive fat-soluble vitamin E, represented by related analogues of a-, r-, y-tocopherols (Greek tocos - childbirth, pher - to support).
Vitamin. Natural tocopherol is a derivative of tocol and has a biological activity of 1.49 IE per 1 mg, its seven natural compounds with biological activity of vitamin E are less active. The drug is thermostable.
Vitamin E antagonists are aldehydes and ketones, formed during the rancidity of fats, i.e.with the accumulation of fatty acids and stearins. Vitamin E is widely distributed in unicellular organisms, yeast, algae. In the body of birds it is not synthesized. A cheap source of this vitamin is hay flour, which contains up to 200-250 mg of vitamin E per kg of flour, in alfalfa flour - up to 160-180 mg per 1 kg, in legumes and cereal grains - up to 30-50 mg per 1 kg. Other sources: vegetable oils and cereal germ. Compound feeds are enriched with a synthetic preparation granuvit E25. Diseases of birds of E-vitamin deficiency occupy one of the leading places among diseases of non-communicable pathology. Tocopherol deficiency in farm birds is manifested by encephalomalacia, exudative diathesis, white muscle disease and toxic liver dystrophy.
These diseases are especially widespread in turkey, utensil and broiler farms.
Etiology. The main cause of E-vitamin deficiency diseases in farm birds is the lack of vitamin E in the feed, and, consequently, its deficiency in the body of birds. Contributing factors in the development of pathology are: a high content of antagonists of E-vitamin metabolism in feeds: the presence of lipid peroxides, nitrates, nitrites, unsaturated hydrocarbons, gossypol, mycotoxins, a lack of selenium, methionine, cystine, lysine in feed.
A lack of vitamin E leads to a weakening of redox processes, oxidation of free radicals, impaired absorption and metabolism of microelements, increased permeability of the vascular wall of the capillary, impaired integrity of cell membranes, and the appearance of various diseases that differ in clinical presentation and pathological changes.
Encephalomalacia Along with a deficiency of tocopherol, a contributing factor in the occurrence of this disease is an increase in the body of birds of unsaturated fatty acids, mainly linoleic, arachidonic.
Exudative diathesis. This is a violation of vitamin metabolism, a constant companion of which is a deficiency of selenium,
White muscle disease (myodystrophy). In the etiology of this disease, along with a deficiency of tocopherol, a lack of selenium is of great importance. Contributing factors in the development of this pathology are a deficiency of sulfur-containing amino acids (cystine, lysine, methionine) and a high content of lipid peroxides in animal and vegetable feeds.
Toxic dystrophy of the liver. The main cause of this pathology is the effect on the body of meat birds (ducklings and broilers of the first age) of toxins of exogenous and endogenous origin, i.e. feeding of animal and vegetable feed containing high amounts of mycotoxins, lipid peroxides and unsaturated hydrocarbons, which are tocopherol inhibitors.
Clinical signs. Diseases of E-vitamin deficiency in young farm birds are manifested by a wide variety of clinical signs and pathological changes.
Encephalomalacia Chickens of 3-6 weeks of age are affected, the disease is accompanied by depression, uncoordinated movements, convulsive twitching of the head, its eversion and throwing back.
A sick bird dies 1-3 days after the onset of clinical symptoms of the disease. Mortality among patients reaches 30-35%.
Exudative diathesis. Chickens and turkey poults of 3-7 weeks of age are mostly ill. A sick bird loses its appetite, becomes lethargic, lags behind in development. Swelling in the head and neck results in difficulty breathing. Poultry, chickens usually sit choked, while frightening remain motionless. Mortality among patients reaches 40%.
White muscle disease. Young animals of 2-4 weeks of age of all types of birds get sick. In turkeys, white muscle disease also occurs in the embryonic stage, in which morphological changes are found in 24-25-day-old embryos. White muscle disease in young birds is manifested by depression, inactivity, decreased appetite, and a slowdown in growth and development. In the future, general exhaustion occurs, muscle atrophy develops, when a sick bird moves, a tired bird quickly gets tired, some develop limb paralysis, and the mortality rate among patients reaches 95%.
Toxic dystrophy of the liver. Broilers and ducklings of 2-5 weeks of age are sick, young growth is depressed, inactive, gait is shaky, head and wings are lowered, swimming movements are observed in many. The duration of the disease is 4-5 days, mortality among patients is 70-80%.
Encephalomalacia Changes are localized mainly in the cerebellum and are manifested by hemorrhages, swelling and softening of the cells of the cerebellum, followed by the formation of a focus of gray-yellow necrosis.
Exudative diathesis. The main pathological signs are extensive subcutaneous straw-colored infiltrates in the head, neck, chest, limbs. In a severe form of the disease, when, along with a deficiency of tocopherol, there is also a deficiency of vitamin K, subcutaneous edema becomes hemorrhagic. In addition to edema in the subcutaneous tissue, changes are found in the myocardium (dystrophy) and in the pancreas (focal necrosis), followed by fibrosis of the gland.
White muscle disease. In turkey poultry, pathological changes are constantly detected in the muscle stomach, much less frequently in the myocardium and skeletal muscle. The muscular stomach is reduced in volume, slightly flattened, slightly elastic consistency. On the section of the stomach, gray-white areas of the affected muscle tissue are found, giving it a mosaic pattern.
The heart muscle is flabby, sometimes gray-white stripes and cords are found against a dark pink background. In chickens and goslings, morphological changes are localized in the skeletal muscles of the sternum and limbs. The affected areas of the musculature are dystrophic and look like cooked meat.
Toxic dystrophy of the liver. In ducklings, the liver is sharply enlarged, fills the entire abdominal cavity, full-blooded, dark cherry in color, smeared with consistency. The capsule is easily removed, the incision surface is bleeding, the blood is dark cherry in color, not clotted.
In broilers, the liver is enlarged, with rounded edges, gray-brown in color, flabby, paste-like consistency.
The heart muscle is flabby, pear-shaped and penetrated by thin gray-white stripes that give the heart muscle a gigroid pattern.
Diagnostics. Diagnose diseases of E-vitamin deficiency according to the clinical signs of the disease, according to the autopsy results and data of morphological and biochemical studies. Along with morphological methods, the most informative are biochemical studies.
These are: a) determination of tocopherol in the liver and blood serum, b) determination of the content of malondialdehyde blood, c) test for erythrocyte hemolysis, d) determination of selenium in the liver and muscles.
Determination of vitamin E content and acid number of egg yolk allows predicting the disease and effectively preventing it in the early stages of development.
Diseases of E-vitamin deficiency, which occur with a clinic of nervous phenomena and liver damage, differentiate from Newcastle disease, viral hepatitis, encephalomyelitis, aflotoxicosis by appropriate virological, toxicological and mycological studies.
The norm of vitamin E supplements in the diets of poultry is from 5 to 30 g per 1 ton of feed.
Sodium selenide is added to bird feed at the rate of 1-2 g of the drug per 1 ton of feed for 45-60 days, and for birds of the parent herd during the entire period of collection of hatching eggs. A good prophylactic effect in feed encephalomalacation of broiler chickens is provided by a water-dispersed 33% vitamin E preparation - aquavit E, which is introduced into the feed at the rate of 33 ml per 1 ton of feed from the 3rd to the 50-60th day of life.
For the prevention of toxic liver dystrophy in young meat and poultry, dipromonium is recommended at the rate of 7.5-10 mg / kg body weight with feed from 3-5 days of age for 45-50 days. To adjust the preventive measures in the fight against diseases of E-vitamin deficiency, it is important to study the feed, dead birds and hatching eggs, which must be done at least 1-2 times a month.
K-hypovitaminosis is a rarely diagnosed disease state, manifested by hemorrhagic diathesis, normo- and hypochromic anemia, as well as edema of the subcutaneous tissue. Vitamin. Refers to derivatives of naphthoquinones. Vitamin ki is synthesized by plants, Kg - by bacteria in the intestine, K3 - are synthetic preparations, of which menadione disulfite is soluble in fat, menadione sodium bisulfate is soluble in water.
Vitamin K stimulates the synthesis of prothrombin in the blood and thrombotropin in the liver, which are necessary for normal blood coagulation. It activates the function of the endothelium of the capillaries and mucous membranes. With a deficiency of this vitamin, thrombopenia and bleeding (hemorrhagic diathesis) occur. Vitamin K stimulates the synthesis of coagulation factors in the liver. It takes part in the formation of accelerin and convertin, catalyzing the conversion of prothrombin to thrombin. It is known that feed contains anti-vitamins, in particular dicumarin, which is formed when oats are damaged and destroys vitamin K.
Etiology. The need for birds in vitamin K increases when feeding them an increased amount of fat compared to the norm (over 5%). K-hypovitaminosis can occur due to a decrease in the absorption of vitamin K in the intestine, which is observed with insufficient liver function (bile production deficiency).
K-hypovitaminosis of endogenous origin develops with the excessive use of chemotherapy drugs (chloramphenicol, nitrofurans and sulfonamides), a lack of B vitamins and an excess of trace elements that inhibit the development of beneficial intestinal microflora.
Clinical signs. General oppression, ruffled plumage, poor blood coagulation. Patients with chickens, chickens, turkeys, ducks, geese, pheasants under the skin of the trunk and wings develop hemorrhages in the form of blue spots, anemia of the crest and earrings, depletion are observed. The indicated symptoms in an intensively growing bird appear after 2-3 weeks from the beginning of feeding a diet deficient in K-vitamin. Often, K-hypovitaminosis is complicated by eimeriosis.
With a lack of vitamin K in feeds, laying hens increase embryonic mortality. Frozen embryos have multiple hemorrhages. Bred chickens are weak, often die due to heavy bleeding.
Pathological changes. In chickens, diapedetic hemorrhages in the subcutaneous tissue, mainly on the limbs, in the pectoral muscles, peeling of the cuticle of the muscle stomach and general anemia are very characteristic. Sometimes dystrophic and necrobiotic changes in the myocardium. Dead chicken embryos have severe hemorrhagic diathesis. With exudative diathesis, inflammatory edema in the tissues and effusion in the body cavities are formed. The exudate consists of blood plasma with proteins and cells of the surrounding tissue included in it. With exudative diathesis and edematous disease, the muscles are moist, saturated with water-like exudate. With hemorrhagic syndrome, the muscles are degenerated, has a dry appearance.
Diagnostics. In poultry farming, the diagnosis can only be assumed.
K-hypovitaminosis should be differentiated from acute septic diseases, hypovitaminosis A, C and E and mixed hypoavitaminosis.
In specialized laboratories conduct histological studies.
Prevention and treatment. Reduce the amount of fat in the diet. Corrupted oats and other grain feeds are excluded from feed. An effective treatment for eimeriosis is carried out.
N-hypovitaminosis, or biotin deficiency
N-hypovitaminosis is a disease that occurs in poultry during prolonged feeding unbalanced in vitamins and keeping it on wheat-barley diets with the addition of boiled or autoclaved protein components, especially meat and whale flour. The disease is characterized by a violation of the metabolism of acids - fatty, ascorbic, pantothenic and folic, which is manifested by growth retardation and plumage in young animals, first with dermatitis on the extremities, then in other parts of the body and a picture of perosis.
Vitamin. Water-soluble vitamin, easily destroyed by peroxides. Participates in the body in the carboxylation reaction, in the synthesis of fatty acids and stearins. It is synthesized by microorganisms in the cecum. Vitamin synthesis is inhibited by antibiotics and sulfonamides. Vitamin is a regulator of skin nutrition, protects it from the appearance of itching, strengthens redox processes in the bird's body and promotes feather growth. Vitamin H deficiency worsens the activity of endocrine glands, metabolism and promotes the development of intoxication in the body due to the rapid reproduction of putrefactive microflora in the intestines of birds.
Etiology. The development of N-hypovitaminosis is facilitated by violations in the rationing of nutrients in diets. When rationing nutrients, the correct ratio of energy to protein is definitely established. This takes into account not only the level of protein, but also the content of amino acids in it. Strictly control the usefulness of feed by mineral and vitamin sources. The norm of vitamin H supplements g / t of feed: for 60-day-old chickens, laying hens and meat hens - 0.1 and for turkeys, guinea fowls, quails - 0.2.
Vitamin H norms are designed for optimal conditions for feeding and keeping poultry. If the necessary regimen is not observed, the vitamin H norm should be higher. This is due, for example, to the fact that feed intake decreases by an average of 1% with an increase in temperature of 1 ° C compared to the optimum. A critical signal of vitamin H deficiency is its blood level of 100 mcg% or less.
Clinical signs. In chickens and turkey poults, lethargy, drowsiness, growth retardation, skin lesions in the metatarsus and sole of the feet on which bleeding ulcers and cracks form are observed. A little later, dermatitis occurs around the eyes and beak and on the crest. The picture of perosis develops. General oppression intensifies. Paresis and paralysis of the legs are possible.
High mortality of embryos during incubation. At the opening of the embryos, there is a violation of skeletal growth - shortening or thickening of the leg bones, especially the lower leg and wings, the "parrots" of the beak. In hatched chickens, the above pathological changes and congenital perosis, ataxia and mass mortality in the first days after hatching are noted.
Pathological changes. The pallor of the crest v, catkins, baldness of some skin areas, the presence of scabs on it, bruising and hematoma in the subcutaneous tissue, muscles, hemorrhage in the intestinal mucosa and erosion on the cuticle of the muscle stomach. Fatty degeneration of the liver with the presence of point hemorrhages on its surface. The strength of the skeleton with N-hypovitaminosis does not change. There is no violation of endochondral ossification, there are no rickets in the places of bone-cartilage joints of the ribs, there is no excessive formation of osteoid tissue in the zones of endo- and periosteum, which is typical for D-hypovitaminosis.
Diagnostics. The veterinarian makes a diagnosis presumably based on clinical symptoms, autopsy findings, and analysis of egg incubation results.
Differentiate N-hypovitaminosis from dermatitis, developing due to the lack of other B vitamins, which is very difficult to do.It is necessary to conduct a thorough analysis of poultry diets for the energy protein ratio (EPO) and the quality of the fed protein by amino acid and vitamin composition. With a low protein content in the diet and a high energy protein ratio (with the expansion of EPO) obesity of the bird and the termination of egg laying are observed. In addition, the herds additionally analyze the results of egg incubation. With a low vitamin tl content (0.1 mg / kg) in the feed of the hen rations, a high mortality rate of the embryos is observed.
Prevention and treatment. Revise the diets of poultry feeding. As a source of N-vitamin, fodder yeast, green leguminous plants, grass and meat-bone or fish meal, PABA and ABA preparations are added to feed.
When dermatitis appears on the limbs, the dose of vitamin in the diet is increased to 0.3 mg / kg of feed. When obesity of the liver and kidneys is established, supplements of this vitamin in the amount of 0.15-0.2 mg / kg are also introduced into the feed. When feeding turkeys, up to 70% of wheat-soybean feeds do the same: vitamin H supplements are administered at a dose of 0.15-0.3 mg / kg of feed.
Laboratory studies are not developed.
C-hypovitaminosis is predominantly a chronic disease of birds with the phenomena of hemorrhagic diathesis.
Vitamin. Vitamin C (ascorbic acid, anti-scotting or anti-scribing factor) activates and supports the activity of endocrine glands, blood formation, collagen formation, assimilation of manganese, copper, protects adrenaline from premature oxidation, is associated with the synthesis of glycogen from glucose, and is involved in the inactivation of endogenous toxins and exogenous self , contributes to the accumulation of vitamin A in the liver, smoothes out the symptoms of vitamin B deficiency.
Vitamin C is synthesized by higher plants, bacteria and body tissues. In birds, it is synthesized in the kidneys.
The absorption of vitamin is carried out in the small intestine mainly in the duodenum and jejunum, partially in the ileum. For vitamin C to enter the cells, the transition (oxidation) of ascorbic acid (AA) to DAA (dehydroascorbic acid) is important. DAK easily diffuses into red blood cells. This became the basis to consider DAK as a transport form of vitamin C.
A deficiency of vitamin C, in which the AK = DAK system, which is capable of reversibly oxidizing, i.e., donating and attaching hydrogen atoms, causes a pronounced violation of the redox processes of cellular respiration in the bird's body.
Etiology. Under normal conditions of maintenance and with full feeding, the need for poultry in vitamin C is ensured by endogenous synthesis. With a high, compared to the norm, planting density, serious stresses: low and high air temperature in the houses, moving the bird from one room to another, and strong noises, the bird increases the consumption of vitamin C, which causes its insufficiency. With an unbalanced feeding on protein, essential amino acids, vitamins (especially group B) and minerals in birds, a violation of the endogenous synthesis of vitamin C is observed in the bird. Vitamin C deficiency can cause symptoms of secondary deficiency of vitamins A, E and group B, with which it is in close metabolic communication.
Excessive doses of vitamin A contribute to the depletion of the body in ascorbic acid. The relationship between vitamins C and Bc (folic acid) deserves serious attention. With prolonged vitamin C deficiency, megaloblastic hematopoiesis inherent in vitamin B deficiency may develop.
With a deficiency of vitamin C, the processes of using carbohydrates in the body of the bird are disrupted. In diseases of the gastrointestinal tract, the release of vitamin C with litter increases dramatically. Ascorbic acid has a cost-saving effect on reducing the need for vitamins A, bi, B2, Vd, Vs and E.
Clinical signs. Lag in growth of young growth: the mass of C-hypovitaminous is 30-80% lower than the curves of the standard mass of control chickens. In chickens, the skeleton is not mineralized enough. The strength of the shell decreases, especially in the summer, at high temperature (+27. + 35 ° C) the reproductive function of males worsens. Cases of cannibalism are increasing. In protracted cases - anemia, exhaustion and death.
Pathological changes. Hemorrhages in the skin, subcutaneous tissue, mucous membranes, internal organs, muscles, joints, under the periosteum, in cartilage and even in joint cavities. In places of hemorrhage under the influence of penetrating microflora, ulcerative necrotic foci develop. Hemorrhages in the cartilage and periosteum are accompanied by dystrophic and necrobiotic changes in them, while the formation of sequesters and the separation of diaphysis from the pineal glands is possible. Often in young birds, the skeleton changes (bone plates are destroyed). The bone marrow, which replaces the fibrous tissue, is destroyed,
Diagnostics. The veterinarian makes a preliminary diagnosis by analyzing the quality and level of feeding, clinical and pathological data.
With differential diagnosis, diseases such as E- and K-hypovitaminosis, A-hypovitaminosis, polyhypovitaminosis, i.e., a deficiency of the vitamin group, are excluded.
In the conditions of a veterinary laboratory, AK and DAC are determined. Examine the plasma, blood, liver and pancreas. The plasma of laying hens contains 15-23 μg / ml AK. In chickens, the content of vitamin C in the liver increases with age: in diurnals - 170 mcg / g, in 60-day-old animals - 380 mcg / g and in adult poultry - 750 mcg / g, during intensive laying - 1970 mcg / g and when molting is reduced to 1010 μg / g.
Prevention and treatment. Vitamin C often decomposes during prolonged storage of feed. Therefore, supplements in the form of vitamin C and flour from the leaves of green plants are added to such feeds. Increase at the same time the supply of vitamin E, which helps accelerate the synthesis of vitamin C.
IN 1-hypovitaminosis, or polyneuritis
B1-hypovitaminosis --- a disease with a predominant lesion of the nervous system.
Vitamin. Thiamine is synthetically prepared. It is highly soluble in water and acetic acid, worse in ethyl and methyl alcohols and insoluble in ether, chloroform, acetone and benzene.
The vitamin content in poultry feeds varies widely. During technological processing of feed, up to 30-40% of vitamin is destroyed. High temperature and high blood pressure destroy up to 80-90% of the vitamin. In cereal and plant seeds, thiamine is contained in the shell and germ. Under the influence of digestive enzymes, thiamine is released from the feed and absorbed in the small intestine. Most of the thiamine received in the blood is phosphorylated in the liver, the other is distributed to organs and tissues and again enters the gastrointestinal tract. Vitamin antimetabolites are artificially prepared thiamine analogues, which have powerful antiprotozoal properties, as well as some antibiotics and sulfa drugs.
Etiology. The development of bi-hypovitaminosis is facilitated by excessive feeding of legumes containing anti-vitamin-oxythiamine, the presence of vitamin-thiaminase antagonists in such feeds as fish entrails (carp, bream, etc.), in mollusks and some plants, heating and autoclaving of carbohydrate feeds.
Clinical signs. In an adult bird, limb weakness, diarrhea, decreased body temperature, decreased weight, blue comb (in chickens), paralysis. In chickens and ducklings, the symptoms appear suddenly: a difficult gait, a head thrown back (opisthotonus), weakness of the extremities, fragility of the feather, paresis of the extremities, and a decrease in general resistance to other diseases.
Pathological changes. The corpses of birds are exhausted. Congestive hyperemia of the gray matter of the brain. Atrophy of skeletal and muscle fibers, heart muscle, stomach, genitals, necrotic foci in the musculature, proliferation of connective tissue. Swelling of the subcutaneous tissue. Sometimes inflammation of the air sacs. Hemodynamic and dystrophic changes in parenchymal organs. The suffocates have curly plumage.
Diagnostics. A preliminary diagnosis is made taking into account the history, analysis of the level and quality of poultry feeding, pathology and clinical features (characterized by opisthotonus).
Assess the adequacy of vitamin bi in poultry diets to the recommended standards. Eliminate the negative impact of technological (thermal, high pressure during autoclaving, etc.) feed treatments to reduce the level of vitamin bi in feed. When violations are identified in order to stop the disease, the feed preparation technology is immediately changed. Fodder yeast, milk, milk whey, sprouted grain, herbs and high-quality herbal flour are included in the diet, especially when treating poultry with antibiotics and sulfonamides. Bi-vitamin deficiency is differentiated from encephalomalacia, E-vitamin deficiency, various viral diseases with nerve symptoms (BM, bird plague, IEM, etc.).
Serum and plasma are examined for the presence of vitamin bi using fluorimetry, colorimetry, and microbiological methods, using the microorganism Lactobacillus fermentum-36, which is most sensitive to the deficiency of this vitamin.
The presence of vitamin bi is indirectly judged by the amount of pyruvic acid with a normal thiamine content in the body. The amount of pyruvic acid in the liver of birds is in the range of 1.4-1.9 μg / g mass, and in the blood - 1.5-2.5 mg%. In the initial stage of hypovitaminosis, the content of pyruvic acid in the blood rises to 3.5-4.5 mg%, which corresponds to 0.9-1.1 μg / g of thiamine in the liver. For the prevention of bi-hypovitaminosis, it is added in the form of thiamine, bromide or thiamine chloride to poultry of all ages and productive orientation at the rate of 2-4 g per 1 ton of feed.
IN 2-hypovitaminosis, or riboflavin deficiency
B2-hypovitaminosis is a disease characterized by growth retardation of young animals, impaired tissue respiration, metabolism of amino acids - methionine, tryptophan, lysine and vitamins - pantothenic acid, choline, pyripokoin, folic and orotonic acids, a decrease in the synthesis of vitamin Bi2 in the intestine and the development of ulcers in the oral cavity and gastrointestinal tract of the bird.
Vitamin isolated from egg yolk. The needle-shaped orange-yellow riboflavin crystals in a neutral aqueous solution exhibit bright yellow-green fluorescence with a maximum of about 545 microns. Riboflavin is very sensitive to light. When illuminated in an alkaline medium, its molecule loses 4 carbon atoms from the side chain and turns into lumiflavin. When illuminating riboflavin in a neutral or acidic environment, it turns into lumichrome.
The riboflavin molecule has redox properties. These properties of riboflavin determine its wide biological activity.
Riboflavin antagonists are galactoflakine, antimalarial drugs (Akrikhin), acridine dye - ethacridine lactate and phenazine analogues of riboflavin.
Some analogues of riboflavin antagonists are able to temporarily replace riboflavin and support bird growth, but its death is accelerated. It is believed that antagonists used in small doses displace riboflavin from its compounds and increase its content in the blood, which contributes to a temporary improvement in the state of the bird. At the same time, riboflavin reserves are consumed faster and the bird dies earlier.
Etiology. Gastrointestinal upsets adversely affect riboflavin absorption. Riboflavin deficiency increases due to its large loss in urine and, of course, with dropping of a liquid consistency.
Temperature extremes, low temperatures, and drafts in houses increase riboflavin intake and consumption.
Clinical signs. Signs of riboflavin deficiency are sometimes observed in embryos and day old chickens, but more often in older chickens - on days 14-21. Growth slows down, poor susceptibility, anemia, lethargy, depression, gait shakiness, emaciation, corneal vascularization.
With the development of the disease, paresis of the wings, the bird, relying on the hock joints, moves with difficulty, the toes are twisted, paralyzed or semi-paralyzed, dermatitis develops. In turkey poults, similar symptoms are observed: a violation of the hematopoiesis process, a decrease in the hemoglobin content and the number of red blood cells.
Pathological changes. The corpses are exhausted. Bad plumage, dermatitis. Vascularization of the cornea (red eye), cataract. Toes twisted, assembled inward.
Internal organs changed: hyperemia and swelling of the thymus, adrenal hypertrophy, degenerative changes in the kidneys, liver, thickening and at the same time softening of the nerve trunks (shoulder and sciatic).
Diagnostics. The veterinarian makes a preliminary diagnosis of 62-hypovitaminosis based on an analysis of the level and quality of feeding the bird, the clinical symptoms of the disease, and the results of the postmortem examination of the fallen and forcibly killed birds. To clarify the diagnosis, blood serum and samples of organs are sent to the laboratory: liver, kidneys, small intestine, peripheral nerves.
During differential diagnosis, A-, B- and E-hypovitaminoses, the classical form of BM and perosis are excluded.
The enzymatic method is used to determine the various forms of riboflavin, using purified apoenzymes (D-amino acids), the fluorescence method, and hydrolysis with trichloroacetic acid.
Normally, the content of riboflavin in the liver of young birds is 14-15 μg / g, in adults 14.5-17.5 μg / g, in the yolk of a full-fledged egg 4-6 μg / g.
Prevention and treatment. They take measures to eliminate the causes of vitamin B2 deficiency in the body of the bird, associated with a lack of it in feed and destruction in the intestine after taking antibiotics and sulfonamides. For treatment and prevention, crystalline riboflavin (B2-vitamin) is given before feeding. For the same purpose, use alcohol or acetone-butyl lacquer vinasse, which contains up to 30 μg / g riboflavin and up to 30% protein. The poultry diet is enriched with additives such as fodder yeast, sprouted grain (oats, wheat), alfalfa and nettle flour, dairy waste, fish and meat and bone meal, tested for the absence of virulent and conditionally pathogenic microflora.
AT 4-hypovitaminosis, or choline deficiency(deficiency of balineurin or amatin, "manganese" failure)
B4-hypovitaminosis is a disease in which a lack of a leading nutritional factor, choline, dramatically reduces the formation of acetylcholine, a mediator of transmission of nerve impulses, reduces the biosynthesis of protein and the starting products for the formation of choline, methyl groups of betaine and methionine, and disrupts the transport of triglycerides from liver, the concentration of residual nitrogen in the blood and the structure of the kidneys.
Vitamin. Choline is classified as vitamin-like substances. It is part of lecithin as a permanent structural component. The exclusion of choline from the compound feed recipe leads to the development of liver obesity in birds receiving such compound feed. Choline is an aminoethyl alcohol. This is a colorless, highly hygroscopic compound that hardly crystallizes. Choline is part of many feeds: in larger quantities - in animal feed and in much smaller - vegetable (legume and green leaves). Being an integral part of phospholipids, choline is a part of all body cells. Blood contains approximately 35 mg% choline.The physiological role of choline in the body is diverse: it enters the structure of biological membranes, is a structural component of acetylcholine, which provides excitation through the nervous system, a lipotropic factor that enhances phosphorylation, esterifies lipids and involves them in the metabolic processes of the birds.
Etiology. Due to the possibility of synthesis of choline in the body of birds and participation of methionine and vitamins Big and Bs (folic acid) in this process, B4-hypovitaminosis cannot be considered as a usual consequence of choline deficiency. Therefore, the occurrence of primary choline deficiency is excluded in a larger number of poultry farms. Secondary choline deficiency occurs with a lack of protein in the diet of poultry. Young growth is more sensitive to lack of choline than an adult bird. The need for vitamin 64 arises when feeding a bird high-calorie diets, especially in cases where they include supplements of fat, with the additional use of vitamin bs (nicotinic acid), with high egg production. A sufficient balance of diets for protein, vitamins B6, Bi2, Bc and manganese significantly reduces the need for poultry in the choline. However, protein deficiency can be of an exogenous nature when, during pathological conditions in the body, absorption and assimilation of the protein are impaired. Choline deficiency in the diet has a dramatic effect on reducing the productivity of laying hens and the fertilization of eggs.
Clinical signs. In young animals, mainly turkeys and meat chickens, depression of growth and difficulty in moving. The limbs are shortened, the tibia-tarsal joints are greatly thickened and deformed, the joints turn out. In an adult bird, a decrease in egg production, perosis, weight loss, ruffled plumage, loss of feather shine. Pathological changes. The liver is enlarged, its color varies from tan to light yellow with a muscatel pattern. The texture is flabby, the fabric is torn. The surface of the incision of the liver is sebaceous. Muscular atrophy in the chest and legs. Sometimes vitelline peritonitis. Deformation of the tibia-tarsal joint. Enlarged kidneys with deposition of fat in the tubules. Dystrophic and atrophic changes in the tissues of the parenchymal organs. Metaplasia of liver lobules into adipose tissue. from the periphery (perivascular obesity) and ending with the center of the lobules - large-drop obesity.
Diagnostics. A preliminary diagnosis in poultry farming is made taking into account anamnestic, clinical and pathomorphological data (fatty liver and other changes), as well as the results of monitoring the level and quality of bird feeding.
Considering that B4-vitamin deficiency is a consequence of polyetiological reasons, it is necessary to exclude biotin (vitamin H) and nicotinic acid (vitamin bs), calcium, phosphorus and the classical form of BM during differentiation. In laboratory conditions, the choline determination method according to H. M. Eidin et al. Is quite widely used. (1969). It is based on the formation of a chloroform extractable compound of choline with bromothymol blue,
Prevention and treatment. In order to eliminate the deficiency of vitamin 64, components with a high content of choline are introduced into the diet: feed yeast, oilcake, animal feed, grass meal. Diet balance on all indicators of usefulness, including a complex of vitamins - Sun, Be, Bi2, as well as methionine and manganese. When using high-calorie compound feeds, including corn, fodder animal fat and other energy components, increased additives of synthetic choline chloride are introduced - 1000-1200 g per 1 ton of compound feed.
Wb-hypovitaminosis, or nicotinic acid deficiency(pellagra (ital, “rough skin”),PP factor, black language)
B5-hypovitaminosis or pellagra (lat. Pellas - skin, agros - rough) is a chronic disease in which the regulation of carbohydrate, protein and fat metabolism, skin trophism are impaired and inflammatory and ulcerative necrotic processes develop in the gastrointestinal tract.
Vitamin. Niacin is widely distributed in vegetable and especially in animal feed. Brewer's yeast (40 mg%) and pressed baker's yeast (28 mg%) are rich in vitamin. In corn and grain of other cereals, nicotinic acid is 95-98% in a bound, non-digestible form (ether, cyacitin).
Niacin is one of the most persistent vitamins. There are practically no losses during freezing or drying. Nicotinic acid solutions undergo autoclaving at + 120 ° C for 20 minutes. Nicotinic acid tolerates boiling in 1 n and 2 n solutions of mineral acids and alkalis.
Tryptophan is the source of nicotinic acid. Animal proteins contain up to 1.4%, and plant proteins do not exceed 1% tryptophan.
Etiology. The disease develops due to a lack of nicotinic acid and its amide, nicotinamide, in the diet of poultry. The inclusion of corn in compound feeds increases the likelihood of a lack of nicotinic acid, since its concentration in corn is low, and it contains: it is inaccessible form. Moreover, in corn there is an insignificant amount of tryptophan (0.08-0.1), a provitamin of nicotinic acid, and an anti-vitamin component, a structural analogue of nicotinic acid (3-acetylpyridine), has been established. Bs-hypovitaminosis is aggravated by a lack of tryptophan-rich feed in the diet.
Nicotinic acid deficiency develops in infectious diseases of birds, accompanied by damage to the gastrointestinal tract. Nicotinic acid deficiency causes the use of sulfonamide drugs and antibiotics for the treatment.
Clinical signs. Decreased appetite. Boring, insecure movement, trembling head. Anemia and cyanosis of the mucous membranes. Dry skin, appearance of symmetrical red spots on bare skin from feathers (pellagric erythemia). Emaciation, alternating diarrhea with constipation.
Pathological changes. In chickens and turkey poults, growth is delayed, plumage worsens. Dermatitis develops in young and adult birds, scales (hyperkeratosis), crusts (scaly dermatitis) form on the skin of the legs, around the eyes and beak. The mucosa of the oral cavity, the tongue is dark cherry in color ("black tongue"). The intestinal mucosa is inflamed, covered with ulcers and scattered necrotic sites. However, turkeys do not have a “black tongue” and dermatitis. The remaining pathology is the same as in chickens.
Symptoms of vitamin deficiencies
Vitamin A deficiency
Most often, a deficiency of retinol occurs in birds. This leads to damage to the mucous membranes, respiratory system (sometimes a runny nose occurs), indigestion and impaired reproductive function. The eyelids swell in the bird and the eyes watery, and in advanced cases, a whitish coating may appear on the cornea of the eyes. Retinol deficiency can also be indicated by long, non-healing wounds. Vitamin A deficient chicks lag behind in growth and development.
Since dry food contains very little vitamin A, the parrot must receive it from plants, fruits, or dairy products. A good supplier of vitamin A is carrots.
Vitamin B deficiency
B vitamins play a large role in metabolic processes and are especially important for the nervous system of birds. Their deficit leads to uncoordinated movements, limited flying capabilities, the bird is not able to reliably stay on the perch. In advanced cases, cramps appear, in which the head of the parrot jerks jerking back. The last sign suggests that if the treatment is not started immediately, the parrot will die.
Vitamin B deficiency usually occurs if the diet is poor and monotonous or the feed has been expired.
It is not always possible to understand what type of vitamin B is lacking in a feathered diet. In this case, it is best to give brewer's yeast (they can be bought at a regular pharmacy).
Vitamin C deficiency
The lack of ascorbic acid in the diet of a parrot is indicated by the vulnerability of the mucous membranes, poor growth, and a decrease in egg production. Deficiency of this vitamin occurs relatively rarely, and only if the parrot does not receive fruit or green food at all.
For prevention, the bird is given fruits, cabbage, bell peppers and other vegetables.
Vitamin D deficiency
Calciferol deficiency leads to impaired motor function, curvature of the spine, limbs and sternum, and deformation of the beak. Chicks especially often suffer from a deficiency of calciferol: their plumage becomes disheveled, their appetite decreases, and rickets develop. Recovering young growth remains underdeveloped.
Vitamin D should be in the right ratio with phosphorus and calcium.
Good natural suppliers of vitamin D are fish oil. It should be added to the grain feed for 1-2 drops daily.
Vitamin E deficiency
With a deficiency of tocopherol, the bird becomes weak, the plumage looks tousled, the parrot can rotate its head, tremble, and lay its head on the floor of the cage. In addition, in adult birds, fertility decreases, and the embryo can die even in the egg.
For prevention, it is necessary to give fresh herbs, and in the winter months - germinated wheat. Vitamin E is also found in cereal seedlings, eggs, and many vegetable oils.
Vitamin H deficiency
With a lack or absence of biotin, the parrot becomes lethargic, drowsy, the skin around the eyes may peel off, bleeding wounds appear on the soles of the legs.
For prevention, the diet includes yeast, corn, cabbage, cottage cheese, whey.
Prevention of vitamin deficiency
If your pet’s diet consists not only of a high-quality grain mixture, but also greens, vegetables, fruits, chicken eggs, cottage cheese, then, most likely, a parrot is not threatened with such an attack as vitamin deficiency. But sometimes the vitamins obtained from food may not be enough for normal life and strong immunity, for example, in winter.
Controversy often arises among parrot owners over whether to give pets synthetic vitamins. In our opinion, if the feathered one receives food enriched with fruits and herbs, then it is not advisable to introduce purchased vitamins into the diet on a regular basis. In any case, vitamin mixtures can only be given to healthy birds in a two-week course, after which a break for 2 months should be taken. If the pet receives too many vitamins, then it may develop hypervitaminosis (a disorder due to an overabundance of vitamins), which is even worse than vitamin deficiency.
For the treatment and prevention of vitamin deficiency in the spring-autumn period, it is useful for parrots to give some medicinal plants fresh - dandelion or plantain leaves, meadow clover, dill, etc. It is important to observe the basic hygiene rules. Firstly, it is recommended to collect plants away from the city - in the garden, in the country, in the field, and secondly, before giving the plant to the bird, it must be thoroughly washed and dried on a paper towel. A twig is pinned with a clothespin to the cage, and the bird itself plucks the plant. If the plant is not completely eaten and begins to wilt, it should be removed.
Useful for vitamin deficiency branches and rowan berries. They can be given fresh or dried for the winter. Harvesting rowan berries should be in late autumn at the first frost.
In winter, nettle infusion is very useful. Stinging nettle can be bought at a pharmacy, but it is better to prepare it yourself (the leaves are collected and dried from mid-May to the end of July). The infusion is prepared as follows: pour a tablespoon of dried nettle leaves with 1.5 cups of boiling water, leave for 2-3 hours, strain through a fine sieve or gauze. Give the parrot 3 times a day, 2-10 ml, depending on the size of the bird, drinking from a syringe without a needle.
Vitamin D deficiency
A correct and healthy skeleton cannot form in chicks with a deficiency of this vitamin. With a deficiency of vitamin D, the bird suffers from rickets, joints become thicker, skeleton growth slows down, limbs bend, the spine and sternum bones are deformed, and the beak softens. The functions of the apparatus of movement are impaired. The bird moves with difficulty.
With a deficiency of this vitamin, anemia develops in birds.
Male parrots and canaries lose the ability to fertilize their partners. If fertilization succeeds, the embryos are weak and often die.
The muscular system is weakened, the myocardium is affected, the vessels become brittle.
A twitching of the head is observed, less often - its tipping over, hemorrhages appear on the hips of adult birds.
To prevent a deficiency, you need to add more plant foods to the diet of birds. It is proposed to give them the pulp of avocado, wheat germ, greens and carrots.
Phylloquinone or vitamin K is an active participant in the formation of prothrombin. This is one of the significant coagulation factors. With its deficiency in birds, yellowness of the sclera and visible mucous membranes, diarrhea with blood and lack of reaction to irritants are observed.
Poultry is fed alfalfa, legumes and young nettles, as well as cabbage to prevent this type of vitamin deficiency.
Decorative feathered veterinarians recommend the necessary vitamin complexes.
Hypo- and vitamin deficiency with proper nutrition in birds is extremely rare. But doctors advise introducing this vitamin into the diet of poultry in order to enhance the non-specific resistance of the feathered organism to infections. With a deficiency of this vitamin in young birds, bone mineralization slows down. In females, the amount of calcium in the eggshell decreases, in males spermatogenesis worsens.
Clinically, a deficiency of this vitamin is manifested in the form of periodic muscle twitches, tipping the head back. With prolonged vitamin deficiency, paralysis of the limbs is possible.
Poultry needs to be fed bran, corn grains, you can add potatoes and carrots to the diet to prevent this deficiency.
B2 vitamin deficiency
In young birds, vitamin deficiency is accompanied by diarrhea, growth retardation is noted, they cannot fly up. Adult birds suffer from infertility. The embryos, if they appear, are very weak and die. The feather cover is brittle, dry. The skin also becomes dry. Resistance to infectious diseases drops significantly. The eyelids become inflamed.
Egg white, corn, potatoes, dandelion leaves, peas - such a vitamin deficiency in poultry is perfectly prevented.
Another name for the vitamin is choline.
In young birds, its deficiency leads to bone deformation, in adults, to fatty liver. Against the background of the latter, peritonitis may develop. It threatens the case of feathered.
To solve the problem for poultry, peas, dandelion (leaves), oats and wheat help.
A more familiar name for poultry houses is pantothenic acid.
With its lack, the embryos often die, the chicks grow poorly, the feathers do not develop, the babies are exhausted, and dermatitis develops. The mucous membrane of the eyelids is inflamed, a viscous secret glues the eyelids. A brown clump forms around the cloaca and near the beak.
Corn grain and bran, the ubiquitous carrots and nuts, and nettle leaf can help solve the problem of vitamin deficiency for poultry.
With a lack of vitamin B12, anemia develops in birds, the skin loses firmness and elasticity, and becomes dry. In female parrots that lack this vitamin, most embryos die. The nervous system suffers, there may be convulsions of different muscle groups.
It is believed that for the prevention of this vitamin deficiency, birds need cottage cheese or milk.
It can be in any birds, despite the fact that a certain amount of vitamin is synthesized by the bird's body.
In birds with a deficiency of this vitamin, diarrhea opens, the mucous membranes of the oral cavity and goiter are hyperemic, weakness appears, and dermatitis develops.
It is possible to enrich the diet of poultry with nicotinic acid (vitamin PP) by including carrots, corn, chokeberry, dandelion leaves.
Group B vitamin called biotin (vitamin H) is involved in metabolic processes.
With its deficiency, coordination is disturbed in birds (it is noticeably laid on the chest or side), feathers develop poorly, and dermatitis appears.
Nettle leaves, beets, carrots and potatoes can solve this problem for poultry.
Doctors usually recommend decorative birds to supplement the diet with special balanced complexes to avoid vitamin deficiencies.
Vitamin A (Retinol) responsible for the state of the epithelium and is called growth vitamin. And the poultry organism vitamin A comes in the form of carotene from plant foods, fruits, vegetables and dairy products. Moreover, the body's need for a parrot in vitamin A increases dramatically if it consumes a lot of protein feed.
Lack of retinol in the body of a parrot leads to damage to the mucous membranes, digestive organs, reproduction (deterioration of reproductive abilities, decrease in the number of eggs in the clutch, increase in the number of unfertilized eggs) and breathing, as a result of which the bird has disorders of the upper respiratory tract and digestion. If a parrot, which has a deficiency of vitamin A, gets sick, then his disease is very difficult.
- damage to the mucous membranes,
- visual impairment
- digestive upset
- impaired reproductive ability,
- reduce the number of eggs in the clutch,
- an increase in the number of unfertilized eggs,
- feather quality deterioration,
- claw curvature and fragility,
- disorders of the upper respiratory tract.
- weak legs.
The normal development of an embryo of birds depends on the content of vitamin A in the egg yolk. And in chicks, a lack of retinol can lead to a violation of the motor functions of the body.
Treatment of vitamin A deficiency is reduced to the introduction of a diet rich in this vitamin (corn, millet, carrots, herbs, grass meal), as well as regular feeding of an oil solution of vitamin A.
No less harmful is the excess in the body of the bird of vitamin A. An overdose of retinol can lead to improper development of the skeleton and accelerated bone growth.
In young birds, normal bone development is only possible if there is a sufficient amount of vitamin D or calciferol in the body, which is responsible for calcium-phosphorus metabolism. In addition, vitamin D prevents the development of rickets in chicks and bone decalcification in adult birds. The consequences of a deficiency of calciferol can be impaired function of the motor apparatus, curvature of the limbs, spinal column and sternum, thickening of the joints, and growth retardation.
Signs of Vitamin D Deficiency:
- impaired function of the motor apparatus,
- limb curvature,
- deformation of the spinal column and sternum,
- joint thickening
- growth and development retardation,
- decrease in egg production.
- beak softening
- difficulty in moving.
Excess vitamin D can cause tissue calcification in parrots.
With a lack of vitamin E (tocopherol), the plumage of the parrot looks disheveled, the bird becomes lethargic, often lays its head on the floor of the cage. In a parrot, coordination of movements is often disturbed and irreversible changes occur in the cerebellum and muscles.
Vitamin E is found in green fodder, germinated grain, milk, as well as in boiled eggs. In addition, tocopherol is part of the Trivit and Tetravit preparations.
- weakening of sexual desire,
- decrease in egg production,
- a large number of unfertilized eggs,
- congenital malformations,
- nutritional encephalomalacia,
- exudative diathesis,
- genetic muscular dystrophy,
- increased embryo mortality,
- underdevelopment of embryos,
- delayed chicks in growth and development.
- subcutaneous edema (usually in the area of goiter).
Tocopherol deficiency weakens the sexual attraction of parrots, reduces fertility, and also negatively affects the development of embryos.
Vitamin K, or phylloquinone, is involved in the production of prothrombin by the liver, thereby affecting the rate of blood coagulation.
Vitamin K deficiency usually occurs with long-term treatment of poultry with antibiotics, as well as with regular addition of coal preparations to the feed.
With a lack of phylloquinone, the parrot weakens, almost does not respond to external stimuli, and loses appetite. In a bird, blood coagulation is impaired and a tendency to bleeding appears.
- lack of response to external stimuli,
- loss of appetite,
- bleeding tendency
- jaundice and dry skin
- diarrhea with blood in the litter.
Vitamin K deficiency is compensated by introducing young nettles, cabbage and beans into the diet.
VITAMIN COMPLEX IN
With a deficiency of vitamin B, (thiamine), the budgie's appetite worsens, as a result of which digestion is disturbed and general weakness is observed. After a while, the bird cramps and paralysis of the extremities develops.
It is worth noting that even with a slight thiamine deficiency, parrots cannot reliably stay on the perch. In severe cases, serious disturbances in the activity of the central nervous system are observed in birds, leading to death.
Obvious signs of a deficiency of the vitamin B complex (riboflavin, nicotinamide, pantothenic and folic acid) in the bird's body are a violation of feather growth and an upset bowel. Deficiency of nicotinic acid in the bird's body leads, as a rule, to constant cramps of the limbs, and in severe cases to paralysis.
- disturbance of feather growth,
- bowel disorder
- constant cramps of the limbs,
- liver dysfunction
- eyelid granulation
- crusting on the edges of the beak and legs,
- plumage depigmentation,
- paralysis (in severe cases),
- weight loss
- lowering body temperature
- atrophy of the muscles of the legs,
- inflammation of the mucous membranes,
- embryonic death.
"Parrots receiving a complete, varied diet do not lack folic acid, since it is synthesized in sufficient quantities in their bodies."
Pantothenic acid deficiency leads to liver dysfunction, tissue death, eyelid granulation and crusting on the edges of the beak and legs.
Folic acid deficiency causes anemia and plumage depigmentation in birds.