Rumen alkalosis in animals. Acid-base balance in animals. What happens to the body of a cow when sick

Short description

Target. Conduct an analytical review of the literature.
Tasks.
1. Define diseases.
2. Indicate the etiology of diseases.
3. Explain the pathogenesis.
4. Describe the clinical signs.
5. Give information about diagnostics.
6. Provide forecast data.
7.Describe the treatment.
8. Give information about prevention.

Introduction………………………………………………………………………………….3
1. Rumen alkalosis………………………………. …………….…………………...4
1.1.Definition of disease………………………………………… ....…………4
1.2. Etiology…………………………………………………………….…………………...4
1.3. Pathogenesis…………………..………………………………………………………...……...4
4. Clinical signs ………………………………………………….. ....6
5. Diagnostics………………..…….……………….…………………...…......6
6. Forecast…….……………....................................... .....................................7
7. Treatment…………..…………………………….……………………..…...7
8. Prevention…………………………………………………………….....8
2. Rumen acidosis………………………………………………………………...9
2.1.Definition of disease……………………..……………………. ....…………9
2.2. Etiology…………………………………………………………….…………………...9
2.3. Pathogenesis…………………..……………………………………...…….10
2.4. Clinical signs……………………………………………………………….. ....12
2.5. Diagnostics………………..…….……………………………..…...…....12
2.6. Forecast…….…………................................................... ..................................13
2.7. Treatment……..……………………….……………………..………………....13
2.8. Prevention……………………………………………………………..15
Conclusion…….....……………………………..………..……………………..16
References…………………………………..……………………….17

Attached files: 1 file

According to I. S. Shalatonov, recently the structure of diets for cows with a milk yield of 4-6 thousand kg of milk has changed dramatically. Concentrates account for 50–60% of the diet; silage and haylage are fed with an imbalanced ratio of acetic (normally 10–15%), lactic (normally 85%) and butyric acids; the diet contains virtually no good quality hay and root crops. Against this background, acidosis of rumen contents has become widespread.

2.3.Pathogenesis

Starch and sugar, found in large quantities in the above-mentioned feeds, are fermented in the rumen under the influence of enzymes secreted by bacteria to form excess amounts of lactic acid and volatile fatty acids (acetic, propionic, butyric). Microflora (lactic acid bacteria, the number of which increases in the rumen due to improper feeding) also takes part in the formation of lactic acid. These products of ruminal fermentation are common metabolites of ruminal digestion. When animals are properly fed, a small amount of them is formed, and they are quickly used by the body as sources of energy or for the synthesis of fat and protein.

Pathology occurs when the body does not have time to utilize the increased amount of formed fermentation products. Lactic acid accumulates in the rumen, and the pH of the rumen fluid becomes acidic (pH below 6). The more significant the pH shift occurs, the more severe the disease. There is no strict relationship between the severity of the disease and the amount of food eaten. With a significant decrease in pH, rumen motility is inhibited.

A shift in pH to the acidic side is unfavorable for the life of rumen organisms. The number of ciliates decreases or they die completely. The number of gram-negative bacilli (normal inhabitants of the rumen) also decreases, but the number of gram-positive bacteria increases, Streptococcus bovis and Lactobacillus acidophilus appear. The enzymatic activity of still surviving microorganisms decreases. Therefore, the methylene blue discoloration time increases or discoloration does not occur at all, which is an indicator of severe digestive disorders in the rumen.

Clinically, the cessation of fermentation in the rumen is determined by the disappearance of noise in it.

The accumulation of acids in the rumen creates high osmotic pressure in the rumen fluid. This causes fluid to flow from the extracellular environment (blood) into the rumen. As a result, hemoconcentration (blood thickening) occurs in the blood, the hematocrit increases, and liquid contents accumulate in the rumen. With a significant increase in the volume of fluid in the rumen, its level may be higher than the inlet of the esophagus. In this case, the act of belching is disrupted and the clinical picture of acidosis is complemented by the occurrence of varying degrees of tympany.

Lactic acid and other toxic substances (histamine, tyramine, tryptamine, ethanol) have a harmful effect on the rumen epithelium. Its papillae become swollen, hemorrhagic, and may be necrotic. Toxic products from the contents of the rumen are absorbed through the damaged epithelium. These include histamine, which is formed from dead microorganisms and some feed ingredients. The formation of histamine and its absorption into the blood is associated with the occurrence of laminitis (aseptic pododermatitis) in patients, clinically manifested by lameness, most often of the pelvic limbs. Animals fall behind the herd or even fall down on the way from the pasture.

As a result of high osmotic pressure in the rumen, fluid flows from the blood into the rumen. Together with the fluid from the blood, alkaline substances also enter the rumen; the latter enter the rumen and with saliva. In this way, the environment in the rumen is leveled, the activity of microflora and motility is restored and, as a result, digestive activity in the rumen is restored. The first sign of resurgent fermentation is the appearance of noise in the rumen.

2.4. Clinical signs

The earliest signs of the disease are refusal to feed and suppression of rumen motility (hypotonia, atony). The rumen is moderately or heavily filled with food masses.

The latter is especially typical for overfeeding cows with corn at the stage of milky-wax ripeness. In this case, the scar is slightly enlarged and has a dense consistency, the left hungry fossa is leveled, the contents are dense, and when pressed, a dent is formed. A moderate amount of gas accumulates in the upper part of the rumen. The animal is depressed and moves reluctantly. Muscle tremors are noted in the area of ​​the anconeus and posterior femoral muscles. The stool is of a liquid consistency, there may be diarrhea. In severe cases of the disease, the animal cannot stand and lies with its head on its chest. The nasal planum is dry, moderate salivation occurs. Increased breathing and heart rate are observed; Body temperature rises briefly on days 4-5.

Clinical symptoms of chronic rumen acidosis are not typical. Animals experience slight depression, a weakened reaction to external stimuli, variable appetite, eating less than normal grain and sugary feeds or periodically refusing them, weakened rumen motility, anemic mucous membranes, diarrhea, signs of laminitis. The fat content of milk is low, milk yield is reduced. Chronic rumen acidosis over a long period of time can be complicated by laminitis, ruminitis, liver abscesses, fatty hepatosis, myocardial dystrophy, kidney damage and other pathologies.

2.5. Diagnostics

In diagnosing the disease, it is of great importance to establish the fact of overeating by animals of feed that causes rumen acidosis, as well as analyzes of the contents of the rumen, blood, and urine.

Scar contents acquire an unusual color and a strong odor. In severe forms of acidosis, the concentration of lactic acid in the rumen fluid increases above 58 mg%, the pH decreases below 5-4 (the norm in cows is 6.5-7.2), the number of ciliates sharply decreases (less than 62.5 thousand / ml) and their mobility . In the blood, the content of lactic acid increases to 40 mg% and higher (the norm is 9-13 mg%), reserve alkalinity drops to 35 vol.% CO2, the hemoglobin level decreases to 67 g/l, the sugar concentration increases slightly (up to 62.3 mg%, or up to 3.46 mmol/l). In the urine, the active reaction (pH) decreases to 5.6, and protein is sometimes detected. In sheep with acute rumen acidosis, the pH of the contents decreases to 4.5-4.4 (normal 6.2-7.3), the amount of lactic acid increases to 75 mg%.

Rumen acidosis should be distinguished from ketosis, primary atony and hypotension of the proventriculus. With rumen acidosis, there is no ketonemia, ketonuria, low blood sugar, or ketonolactia. Primary and secondary hypotension and ruminal atony occur in a milder form than acute rumen acidosis, without significant symptoms: diuresis is not impaired, tachycardia and rapid breathing are not manifested or are mild, laminitis does not occur. Rumen acidosis often becomes widespread; primary and secondary hypotension and rumen atony occur mainly sporadically.

2.6. Forecast

A severe form of rumen acidosis often ends in death within 24-48 hours. With moderate and mild severity of the disease, recovery is possible after appropriate treatment. With the development of laminitis, liver abscesses, hepatosis, glomerulonephritis, myocardial dystrophy, the economic value of animals decreases, which leads to their culling.

2.7.Treatment

Treatment of rumen acidosis varies at different stages of the disease, during which various changes occur in the internal environment of the body.

1. Use of alkali internally to neutralize the acidic environment in the rumen. Such treatment is indicated only in the early stages of the disease, when alkaline products enter the rumen along with fluid from the blood. The use of alkaline preparations (soda) during this phase of the disease will help maintain the pH in the internal environment of the body and neutralize acidic products in the rumen itself. Soda is usually used orally in a dose of 100-150 g per 0.5 - 1 liter of water 2 times a day, on the first day of illness.

2. Treatment can also be started by washing the scar. The success of this procedure depends on the nature of the contents of the scar. The grain feed is removed by washing the rumen. 36 hours after the end of washing, normal fermentation is restored in the rumen. Administration into the rumen after washing rumen contents from healthy cows speeds up recovery.

In addition to washing the rumen, when overfeeding occurred more than 24 hours ago, 1 liter of 7% sodium bicarbonate solution is used intravenously. This will reduce acidosis in the internal environment of the body and help restore liver function.

3. If the rumen is full of feed and washing is likely to be unsuccessful, it is necessary to perform a rumenotomy and remove the contents of the rumen through an incision in the abdominal wall. If there is a delay in the operation, the scar epithelium becomes loose and suturing the inner layer of the scar wall will be difficult.

4. V. A. Lochkarev, with acidosis from overfeeding cows with corn at the stage of milk-wax ripeness or overfeeding sugar beets, successfully used potassium permanganate in a dose of 5 g in 5 liters of water. Potassium permanganate, as an oxidizing agent, destroyed toxic products in the rumen.

There are reports of the beneficial use of intramuscular thiamine in rumen acidosis. It is also recommended to give the animal oral antibiotics up to 200 g, yeast and milk.

2.8. Prevention

Balance the diet according to the sugar-protein ratio, which should be 1-1.5:1. Exclude access of animals to an unlimited amount of feed with a high content of soluble carbohydrates. The daily diet of cows should include no more than 25 kg of fodder beet, which is fed in two doses; The sugar content should not exceed 4.5-5 g/kg body weight. Grain feed should be included in the diet gradually, not all at once. The diet should always contain a sufficient amount of high-quality roughage (hay, straw). Reducing roughage in the diet can cause acidosis even with the usual amount of grain feed. Avoid long breaks in feeding animals.

To prevent rumen acidosis in cows, the drug macerobacillin has been proposed, which in a dose of 0.3 g per 100 kg of body weight is given with concentrated or other feeds once a day for 30-60 days. For this purpose, enzyme preparations amylosubtilin, protosubtilin, pectofoetidin are used at the rate of 0.3-0.5 g per 1 feed. units diet, which are given with food for 30 days. To prevent rumen acidosis, ewes are prescribed amylosubtilin at a dose of 0.05 g per 1 kg of body weight.

Conclusion

Alkalosis and rumen acidosis are diseases of ruminants that can lead to fatal consequences. The reason for them is human negligence in feeding and maintaining farm animals. To prevent alkalosis and acidosis of the rumen, it is necessary to observe the diet of ruminants and improve the sanitary and hygienic condition of livestock premises.

Bibliography

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Rumen alkalosis(alcalosis ruminis acuta)

Rumen alkalosis called indigestion, characterized by a change in the pH of the contents of the rumen to the alkaline side. Clinically, the disease is manifested by a weakening of the motor function of the rumen (hypotension, atony) and sometimes at the same time by the overflow of the rumen with fodder masses. Compared to rumen acidosis, alkalosis is much less common.

Etiology. Scar alkalosis occurs when using excessive doses of nitrogen-containing additives (urea) or their incorrect use. The disease has been described in buffaloes fed large amounts of peanuts (Nagarajan and Rajamani, 1973). Sometimes alkalosis occurs when eating a large amount of legumes in the pasture. We have established the occurrence of alkalosis when eating rotten food residues from the bottom of the feeders, a long-term absence of salt in the diets of animals. This causes salt starvation and the desire of animals to lick the floor and walls contaminated with feces.
Alkalinization of the rumen contents also occurs in hungry animals.

Pathogenesis. The microflora of the rumen is able to hydrolyze various nitrogen-containing substances. Feed substances containing a lot of nitrogen include protein, and chemical substances include urea and nitrates. The main product formed in this case is ammonia. It serves as the main source for the growth and reproduction of microorganisms. The resulting microbial protein is subjected to enzymatic action in the abomasum, where it is broken down into amino acids, which are absorbed in the small intestine. The enzyme urease, which is necessary for protein breakdown, is found in the cell wall of some microorganisms. The unused amount of ammonia released during protein hydrolysis quickly diffuses through the epithelial surface of the rumen and enters the blood, where it can have a toxic effect on the body. However, under natural conditions this does not happen due to the small amount of ammonia formed in the rumen and absorbed into the blood, its rapid conversion in the liver into urea, which is excreted from the body in the urine. The rate of protein hydrolysis and the amount of ammonia produced depend on the composition of the diet and the amount of protein or nitrogen-containing additives in it. When feeding animals feed containing large amounts of protein or urea, ammonia is formed in large quantities, which cannot be completely and quickly absorbed by the microflora. Ammonia enters the blood in quantities exceeding the norm. In the liver, it is not converted into urea, and poisoning of the body occurs. All this creates a clinical picture of the disease, which manifests itself if the level of ammonia in the blood reaches 1 - 4 mg.
Ammonia has the properties of a base and has a pH of 8.8. The accumulation of ammonia in the rumen causes a shift in the pH of the medium in it to the alkaline side. The pH level of ruminal fluid depends on the rate of ammonia formation and its absorption into the blood. The higher the pH level of the rumen fluid, the higher the amount of ammonia in it, which is in an easily absorbable state, that is, in free form, and not in the form of cations. With liver damage, the sensitivity of animals to ammonia concentration increases.
Changes in the pH of rumen fluid when feeding spoiled feed, mineral starvation, or keeping animals in unsanitary conditions occurs due to decay processes when putrefactive microflora from the external environment enters the rumen.
A change in the pH of the environment in the rumen towards the alkaline side causes changes in the quantitative and species composition of ciliates and beneficial microorganisms. Their number decreases or they disappear completely. Discoloration of methylene blue added to such rumen contents is dramatically delayed or does not occur at all.

Symptoms When a large amount of urea is ingested, signs of abdominal pain are observed: restlessness, teeth grinding. The secretion of foamy saliva and polyuria are noted. Later, tremors, weakness, loss of coordination of movements, rapid breathing, mooing, and muscle spasms occur. Death occurs 0.5 - 4 hours after poisoning.
When overfeeding with protein-containing feed, the disease lasts longer and with a calmer external state of the animal. Persistent refusal of food, lack of chewing gum, lack of rumen motility, severe depression up to the point of coma or drowsiness are observed. The nasal mucosa is dry, the mucous membranes are hyperemic. The stool is initially formed and then may be liquid. A putrid or unpleasant odor is felt from the oral cavity. There is moderate tympany (Setareman and Rather, 1979). With jerky palpation of the scar, a splash of liquid is sometimes noted.
The prognosis for rumen alkalosis depends on the timeliness and effectiveness of treatment measures, without the use of which death inevitably occurs.
Alkalosis resulting from an overdose of urea is acute; from overfeeding with protein-containing feed, even with medical assistance, it lasts up to 7-8 days.

Pathological and anatomical changes. In case of alkalosis caused by urea poisoning, hyperemia and pulmonary edema, hemorrhages in the mucous membrane of the digestive canal are detected.
When overfeeding with protein feeds, the rumen contents look like a semi-thick mass; when consuming feed contaminated with slurry, the contents of the rumen are liquid, dark in color, with an unpleasant manure odor.
Diagnosis. Analysis of feeding and feed quality, living conditions, and feeding hygiene is important. The diagnosis can be clarified by determining the pH of the liquid contents of the rumen. When alkalosis pH is above 7, no live ciliates are found in the contents.

Treatment. In case of overdose or poisoning with urea, the most effective treatment is to infuse the rumen with up to 40 degrees of cold water with the addition of 4 liters of a 5% solution of acetic acid. Cold water lowers the temperature in the rumen and slows down the rate of urea metabolism. This also reduces the concentration of ammonia and the rate of its absorption. Acetic acid, in addition, forms neutral salts with ammonia. The animal is monitored, since after 2 - 3 hours a relapse of the disease is possible and treatment must be repeated (Mullen, 1976).
In severe cases of urea poisoning and illnesses from eating feed rich in protein or contaminated with E. coli, rumen rinsing is an effective treatment. In the absence of dense contents in the rumen, this therapeutic measure will be successful and useful. Restoration of ruminal digestion is accelerated by the introduction of contents from healthy cows into the rumen in an amount of 2 liters or more.
In milder cases of the disease, the effect occurs from the introduction of acetic acid into the rumen in a dose of 30 - 50 ml in 200 - 300 ml of water or a 6% solution of acetic acid in a dose of 200 ml. Recovery occurs within 5 - 8 days. Some authors supplement this treatment by introducing an antibiotic into the scar to suppress putrefactive microflora and intramuscular administration of thiamine and an antihistamine. Thiamine in this case is administered to prevent possible clinical manifestations of vitamin deficiency Bi (corticocerebral necrosis) due to the death of microflora in the rumen and the long course of the disease.
The use of laxatives in the form of Glauber's salt for alkalosis is contraindicated. Glauber's salt, having an alkaline reaction, aggravates alkalosis.

Prevention. Rumen alkalosis can be prevented by the correct use of nitrogen-containing supplements and at the same time
significant use of feed containing easily digestible carbohydrates (starch, sugar). The resulting acidic fermentation products reduce the alkalinity of the environment in the rumen, the rate of breakdown of urea and the formation of ammonia.
It is important to monitor feeding hygiene, feed quality, and living conditions for animals. It is necessary to regularly clear the feeders from the remnants of uneaten food, and provide the animals with free access to table salt.

1. Hypotension and atony of the forestomach

2. Overfilling, scar paresis

3. Rumen tympany

4. Parakeratosis

5. Rumen acidosis

6. Rumen alkalosis

7. Traumatic reticulitis

8. Blockage of the book (blockage, obstruction)

9. Abomasitis (inflammation of the abomasum)

The volume of all sections of the proventriculus and abomasum is 250 liters.

The volume of the scar is 80% of the total volume. The scar (rumen) is located in the left half of the abdominal cavity. Function: primary processing of feed through maceration (soaking) and symbiotic flora. Normally, the number of contractions of the scar is 3-5 in 2 minutes. The rumen pH is neutral.

Hypotension and atony (the common name for these diseases is dystonia) is a violation of the motility of the proventriculus, accompanied by indigestion.

Etiology: feeding disorder:

Prolonged feeding of difficult-to-digest feed (for example, stale hay);

Concentrated feeding with a shortage of roughage;

Spoiled or substandard feed;

Frozen feed (more often root crops);

Feed contaminated with soil or sand.

Secondarily - with injuries of the proventriculus, intoxication, infections and invasions.

Pathogenesis(for all diseases of the scar). In the rumen pH 6.9±0.2 (neutral).

An acidic environment is formed by organic acids (butyric, acetic, pyruvic). Alkaline saliva constantly neutralizes acids (400 g of sodium bicarbonate (a pack of salt) is produced per day along with saliva; when eating dry feed, a cow produces up to 50 liters of saliva per day).

If the pH is disturbed, changes in the microbial environment of the rumen occur.

Acidification of the contents (acidosis) occurs with a decrease in appetite (due to a decrease in saliva production) with predominantly carbohydrate foods (potatoes, apples, cereals). At the same time, useful flora dies and gram-positive (pathogenic) develops.

Alkalosis (alkalinization) of rumen contents occurs with an excess of protein feed and a lack of carbohydrates; when giving too large a dose of urea. In this case, gram-negative flora (Proteus, Escherichia coli) develops.

In both cases, the symbionts die, rotting and fermentation occurs in the rumen (the feed decomposes), toxins enter the bloodstream and cause intoxication of the animals.

Symptoms.

Refusal of feed, decrease in milk yield, belching and feed chewing are absent (but gas belching is preserved, the animal does not bloat). Contractions of the rumen are weak and rare with hypotension or completely absent with atony. The contents of the rumen are semi-liquid. Depression due to intoxication. Over a long period of time, constipation gives way to foul-smelling diarrhea.

. The contents of the proventriculus have a putrid odor. There are hemorrhages on the mucous membrane, the mucous membrane is red. Over a long period of time, the keratinized mucous membrane peels off (easily scraped off with the back of a knife).

When setting diagnosis Traumatic reticulitis is excluded; hypotension often occurs with ketosis. With timely treatment, the outcome is favorable; without treatment, the disease drags on for weeks and the animal dies.

Treatment.

The rumen is freed from its contents: either we wash the rumen with a Cherkasov probe, or we give a laxative (4-6% Glauber's salt - a bucket, 1.5 liters of vegetable oil).

Ruminators are prescribed (hellebore tincture from 14 to 16 ml). In this case, you must first determine whether the cow has acidosis or alkalosis. You can add 0.5 l of milk. – if there is alkalosis.

40% glucose 200 ml, gluconate or calcium chloride - 200 ml are administered intravenously.

If the illness is prolonged, pour in the ASD-2 fraction - 20 ml into 100-200 ml of water.

To stimulate appetite, bitterness is prescribed (wormwood, yarrow), and succulent food is given.

Incorporation of symbionts into the rumen: 0.5-1 l of rumen contents of a healthy cow + 0.5 kg of sugar + 50 g of yeast; or pour in 3 liters of yogurt.

You can do animal wiring and infrared thermal procedures.

Move your fist counterclockwise in the area of ​​the hungry pit.

Traditional methods of treating hypotension: laxative - vegetable oil, instead of hellebore as a ruminator - a head of garlic + 250 g of vodka and add to 0.5 liters with water. To whet the appetite: pickles, pickled apples, sauerkraut. Bridling: a wide bandage is placed in the cow's mouth and tied behind the teeth. The animal constantly tries to remove the foreign object with the help of its tongue, salivation increases and the proventriculus reflexively begins to work).

Overfilling, scar paresis (dilatacia ruminis ab ingestis) is an overflow and stretching of the rumen with dense feed masses, accompanied by impaired motor skills, pain and paresis.

Etiology: eating large quantities of grain, flour, straw and other feed that can bind water and swell.

Rumen paresis is often the result of exposure to pesticides, fertilizers or drugs in the food.

Symptoms Refusal to feed, restlessness (shifts from foot to foot), stopping chewing gum and belching (even gas burps stop due to overstretched muscles). The animal groans. There is a large number of doughy masses in the rumen, the left hungry hole is bulging, the hole from the fist is slowly leveling out. Breathing and pulse are increased. Subsequently, cyanosis of the mucous membranes (the lung is compressed through the diaphragm). Defecation is rare. With paresis, scar contractions are completely absent, the contents of the scar are dense.

Treatment. The animal is on a starvation diet for 1-2 days. We release the scar from the contents (rinsing through a Khokhlov probe, or laxatives - Vaseline, castor, vegetable oil or Glauber's salt). 5-7 ml of hellebore are injected subcutaneously. Caffeine is injected subcutaneously (preferably cordiamine or sulfacamphocaine, since caffeine will further increase the heartbeat). Depending on the condition of the animal - driving or escorting the animal. When the condition improves - succulent feed, silage, soft hay.

With a threat to life, a ruminotomy is prescribed.

Tympany of the rumen – an increase in the volume of the scar due to the formation of gases or foam in it, as well as when their discharge is disrupted (when the esophagus is blocked).

There are simple gas and foamy tympany, as well as acute and chronic (periodic), primary and secondary. The disease can become widespread.

Etiology: eating easily fermented feed (wet legumes - clover, alfalfa, or sour feed) followed by abundant watering. The cause of foamy tympania is fermented grain feed and gluten, which is contained in flour feed, form a dense sticky soufflé foam. Secondarily – with blockage of the esophagus and poisoning accompanied by paresis of the proventriculus.

Pathogenesis. Normally, gas escapes from ruminants through gaseous belching. When excessive pressure in the scar occurs, a spasm of the cardiac sphincter occurs. With foamy tympany, foam blocks the belching mechanism.

Symptoms. Stopping feeding, drooling. Increased abdominal volume, protrusion of the left hungry fossa. The animals are worried and hit you in the stomach with their limbs. Superficial rapid breathing, cyanosis of mucous membranes. Percussion of the area of ​​the left hungry fossa produces a tympanic sound with gas tympania and an atympanic (pulmonary) sound with foamy tympania. When pressing with gas tympany, crepitus is heard (gas bubbles burst). When probing or puncturing, the result is negative with foamy tympania (the lumen is clogged with foam).

Forecast favorable with timely help. The death of the animal is possible after 1-3 hours from asphyxia or rumen rupture.

Treatment.

If the tympania is foamy, it is converted to gas (you need to extinguish the foam): fresh milk in the amount of 2-3 liters, 1 liter of vegetable oil, you can administer the drug sikadel (50 g diluted in 3 liters of water), tympanol, timpachol, atimpanol.

Place the animal with the front part elevated to relieve the condition and facilitate belching.

A probe is inserted to remove gases.

After the gas has been removed (it cannot be removed quickly), antifermentation drugs (2% ichthyol solution) and absorbents (activated carbon, enterosgel) are administered through the probe.

If there was gas tympany, tympanol, atympanol, timpachol are administered.

If there is a threat to life, puncture the scar with a needle or trocar.

Parakeratosis – compaction of the papillae of the rumen mucosa with impaired rumen digestion.

Fattening cattle bulls are sick.

Etiology: feeding finely ground grain flour while limiting roughage.

Pathogenesis. The rumen papillae are stuck together with gluten, are constantly irritated, and hypertrophy over time. The microbial background of the contents changes, and inflammation of the mucous membrane occurs.

Symptoms. Decreased appetite, drooling, periodic hypotension, teeth grinding. In addition, diarrhea, dehydration, weakness.

Treatment. Balance the ratio of roughage and concentrates. Burnt magnesia 30 g per 1 liter of water is prescribed internally. Brewer's yeast in the diet. Colonization of symbionts in the rumen (vetom-1.1, 1.3).

Rumen acidosis – acidification of the rumen contents (pH = 6 or less) develops when ruminants eat large quantities of carbohydrate feed (potatoes, apples, grains) or too acidic silage. It becomes widespread when grazing grains (grass) against the background of a deficiency of protein in the diet.

Symptoms: poor appetite, hypotension or atony, increased salivation (salivation), weakness and diarrhea.

Diagnosis confirm the study of the pH of the rumen contents (with acidosis 4-6). The contents of the scar can be extracted using a probe or by puncture of the scar in the area of ​​the hungry fossa. You can take a sample during the rumination period, when the cow has regurgitated the contents of the rumen (but the technique in this case is not accurate, since the feed masses are mixed with alkaline saliva).

Treatment. Rinsing the rumen with a 2% soda solution or pouring about 1-2 liters of a 2% soda solution inside, and then populating the symbionts (pour in the contents of the rumen of a healthy cow + sugar + yeast, or 3 liters of yogurt).

Rumen alkalosis – alkalization of the rumen contents as a result of feeding a large amount of protein feed (clover, alfalfa) or feed with a nitrogenous component (natural - lupine seeds, or synthetic - urea or urea) against the background of carbohydrate deficiency. Protein in the diet should be no more than 20%.

Symptoms: with protein overfeeding, hypotension or atony, tympany, sweating in the animal, salivation, grinding of teeth, and loose stools are observed. When overeating urea, there is a lack of coordination of movement and frequent urination. In practice, rumen alkalosis very often occurs if a cow is given half a pack or a pack of soda.

Treatment: washing the rumen with 2% acetic acid; either acetic or lactic acid 1-2% solutions are given orally in an amount of 2-3 liters. In addition, carbohydrates are needed for treatment: diluted 0.5-1 kg of sugar is added. Inhabited by symbionts.

The mesh is the second proventriculus. Located in the area of ​​the xiphoid process. The net receives food from the rumen, which has already gone through the process of regurgitation and chewing. The purpose of the net is to sort the food (it passes what is well chewed further into the book, and it returns poorly chewed food to the rumen). Due to the fact that sorting occurs there, heavy metal objects also settle there. Traumatic reticulitis - a question for the state examination.

Traumatic reticulitis – damage to the mesh and perforation (puncture) of internal organs with sharp metal objects, followed by putrefactive inflammation. As a rule, cattle are sick.

Etiology. The structural features of the oral mucosa of cattle contribute to the capture of foreign bodies with feed. Predisposes to the disease are mineral deficiency (as a result of which the cow develops mucus), underfeeding of the animal (the cow is outwardly normal, but begins to eat atypical objects). The prevalence of the disease is associated with littered pastures and careless feeding.

Pathogenesis. Foreign bodies, lingering in the mesh, can pierce it during contractions, damaging the peritoneum, diaphragm, liver, heart and other organs. In this case, purulent-fibrinous or necrotic inflammation develops.

Symptoms. There is a distinction between metal carriers - the accumulation of non-sharp metal objects in the mesh, in this case chronic hypotension develops. Sharp metal bodies, and over time they can sharpen, moving, can cause reticulitis (when stuck only in the mesh), reticuloperitonitis (peritoneum), reticulopeuritis (pleura), reticulosternitis (sternum), reticulomasitis (book). Abscesses, adhesions, and putrefactive inflammations appear. In this case, reticulitis is accompanied by non-specific clinical signs.

Acute form: appetite decreases, temperature rises (strongly), atony, hypotension, decreased milk yield are noted, the animal loses weight, stands hunched over, cows rise like horses (swing of the head, rises to the forelimbs, then the hind limbs). Fibrillar twitching of the muscles of the elbow and thigh is noted (individual fibers twitch). Painful reaction during clinical studies of the mesh, swelling of the dewlap, intermaxillary space, jugular veins are full.

Diagnosis

Conduct clinical researches . In addition to the anamnesis and a full clinical examination, there are three tests for traumatic reticulitis: 1) grab the fold of the withers, the cow’s skin in the area of ​​the xiphoid cartilage will become tense and the cow will exhibit a sharp pain reaction; 2) downhill wiring; 3) pressure in the area of ​​the xiphoid process (the doctor squats down and places his elbow on his knee, his fist under the xiphoid process and presses hard, helping with his knee).

Pharmacological tests : hellebore 2 ml intravenously, or orally laxatives (Glauber's salt in recommended dosages) - this will cause increased pain in the animal.

Special samples . Metal detectors, X-rays, magnetic probing – both diagnostics (can be applied to the xiphoid process) and treatment. Magnetic sounding is carried out after a 12-hour diet without restriction of water. Preventively pull out everything potentially dangerous.

Treatment. Conservative: provide the animal with rest, a half-starved diet (slimy feed, steamed hay). Antibiotics are prescribed medicinally and, to relieve pain, 40% glucose (200 ml) + 30% alcohol (300 ml) (there is a drug called glucethyl). With a threat to life, a ruminotomy is prescribed.

According to the account, the book (omasum) is the third proventriculus, small in volume, inside it has outgrowths - leaves (large, medium and small). The role of the book is grinding (grinding) of fodder masses. Topography: lies in the right hypochondrium at the level of the lower third of the 8-10th rib.

Blocked book (blockage, clogging) - overflowing of the interleaf niches of the book with dried food masses. Often these feed masses contain large quantities of earth or sand, which are the cause of this disease. Cattle and small cattle are affected. The disease is often found in dry regions.

Etiology. Feeding with soil-contaminated feed (root crops), feeding with chaff, husks (waste from grain production), grazing with dry grass, insufficient watering, as a result of hypotension. Goats sometimes have a tendency to chew the rag, which will later cause a blockage.

Pathogenesis. In the book, when grinding the feed masses, up to 70% of the water is absorbed (this is necessary to begin the enzymatic processing of the feed, and in the rennet the water is returned to the feed masses). When removal from the book is delayed, the food dries out, the interleaflet niches are filled with dry, dense contents, the leaves are compressed, become necrotic over time, digestion is disrupted and intoxication of the body occurs.

Symptoms. Decreased appetite (virtually absent), depression, atony, book noises disappear (normally, the noises resemble the rustling of hay), intestinal motility is weakened, stool is dry with mucus, in small quantities. Percussion volume of the book is increased.

Pathological changes. The book is hard, in the niches in the form of dry plates there is food mixed with earth and sand, or foreign objects (rags). The mucous membrane on the leaves is necrotic, rejected, with hemorrhages.

Treatment. It is necessary to eliminate the causes of the disease. They are trying to liquefy the contents of the book: oil or salt solutions are poured inside (1.5 l of vegetable oil, 4% solution of Glauber's salt 10-15 l, 5-7 l of mucous decoctions (decoction of flax seed, oat seed - in the ratio to a glass of oatmeal 3 liters of water, with starch jelly). At the same time, a 10% sodium chloride solution is prescribed intravenously to induce thirst and enhance peristalsis. Only after the contents have liquefied, 5-7 ml of hellebore tincture is administered subcutaneously (if 2-15 ml orally). Next, cleansing enemas are performed (about a bucket) Then you can use deep enemas.

If conservative methods do not help, then saline and oil laxatives are injected directly into the cavity of the book. The earlier treatment is started, the easier it is to achieve results.

After digestion has been restored, it is necessary to stimulate appetite with lactic acid, bitterness, or pickled apples, pickles, and sauerkraut. Restoration of symbionts.

The abomasum (abomasum) is the only true stomach and has the appearance of an elongated pear. On the mucous membrane there are longitudinal spiral folds that do not straighten out. Topography: lower third of the right hypochondrium.

There are diseases of the abomasum: inflammation of the abomasum, displacement and inversion of the abomasum, ulcers of the abomasum.

Abomasite - inflammation of the abomasum. Calves and lambs are sick.

Symptoms not typical, depression, decreased and perverted appetite, thirst, diarrhea, pain in the abomasum (lower third of the right hypochondrium on palpation), emaciation are noted. A diagnosis during life can only be made tentatively.

Treatment. Prescribe laxatives (vegetable oil), drinking mucous decoctions, dietary food (small soft hay, succulent good food, not dirty). If necessary, in case of severe disease, the abomasum is washed with a pink solution of potassium permanganate. In case of intoxication, electrolytes are administered intravenously or intraperitoneally: 5% glucose solution with ascorbic acid, Ringer's solution, Ringer-Locke solution, saline solution, preferably + vitamin C. Antimicrobial therapy (norsulfazole, baytril, gentamicin, chloramphenicol, farmazin). Inhabited by symbionts.

Essay

Topic: Acid-base balance in the body of animals

Maintaining a constant internal environment is a necessary condition for normal metabolism. The most important indicators characterizing the constancy of the internal environment include acid-base balance, that is, the ratio between the amount of cations and anions in the tissues of the body, which is expressed by pH indicators. In mammals, blood plasma has a slightly alkaline reaction and remains within the range of 7.30-7.45.

The state of acid-base balance is influenced by the intake and formation in the body of both acidic products (organic acids are formed from proteins and fats, and also appear as products of interstitial metabolism in tissues) and alkaline substances (formed from plant foods rich in alkaline salts of organic acids and alkaline earth salts, metabolic products - ammonia, amines, basic salts of phosphoric acid). Acidic and alkaline products are also formed during various pathological processes.

Due to the fact that shifts in acid-base equilibrium are compensated, the concentration of hydrogen ions changes only in rare cases. Therefore, blood pH is determined infrequently. The state of acid-base balance is assessed by studying those regulatory mechanisms that ensure pH constancy.

5 main types of acid-base balance disorders and their main causes

The main causes of metabolic acidosis:

A. renal failure;

b. diarrhea;

V. chronic vomiting;

d. severe shock;

d. diabetes mellitus;

e. hypoadrenocorticism.

The main causes of metabolic alkalosis:

A. profuse vomiting develops acutely;

b. pyloric stenosis;

V. excessive use of diuretics;

d. therapy with bicarbonate solution.

The main causes of respiratory acidosis:

A. anesthesia;

b. obesity;

V. chronic obstructive pulmonary disease;

d. brain damage or injury;

d. drugs that depress the respiratory center.

The main causes of respiratory alkalosis:

A. fever;

d. hypoxemia.

Rumen acidosis. Rumen acidosis (Acidosis ruminis) - lactic acidosis, acute acidosis of rumen digestion, acidosis, grain intoxication, ruminohypotonic acidosis - is characterized by the accumulation of lactic acid in the rumen, a decrease in the pH of the rumen contents, digestive disorders and the acidotic state of the body (a shift in the pH of the rumen contents to the acidic side ). Cattle and sheep get sick, especially in the autumn and summer.

Etiology. It develops when ruminants eat large quantities of feed with a high content of soluble carbohydrates. These are corn, oats, barley, wheat, sugar beets, potatoes, apples, green grass.

Symptoms The disease is accompanied by a decrease or cessation of animal feed intake, hypotension or atony of the rumen, general weakness, muscle tremors, and salivation. In severe cases, patients lie down, pulse and breathing become more frequent.

Treatment. In order to free the rumen from toxic feed mass and neutralize acidic products, it is washed with a 1% solution of sodium chloride, a 2% solution of sodium bicarbonate, or 0.5-1 liter of a 3% solution is administered, as well as antibiotics. up to 200 g of yeast, 1.2 liters of milk and rumen contents obtained from healthy animals, with the aim of populating it with symbionts.

Prevention. Balance the feeding ration according to the sugar-protein ratio, which should be 1-1, 5:1. Ensure that animals are constantly fed high-quality roughage.

During the period of feeding feeds rich in sugars and starch, the diets should contain a sufficient amount of fiber due to long-stem hay, hay cuttings, straw, haylage in good quantities.

Rumen alkalosis. Rumen alkalosis. (Alcalosis ruminis) is a disease characterized by a shift in the pH of rumen contents to the alkaline side, disruption of ruminal digestion, metabolism, liver function and other organs. Rumen alkalosis is also called alkaline indigestion, alkaline indigestion.

Etiology. The cause of the disease is eating large amounts of legumes, green vetch-oat mass, pea-oat mixture and other protein-rich foods. Cows develop rumen alkalosis when they eat rotten feed residues or a long-term absence of table salt in their diets.

Symptoms An increase in ammonia concentration in the blood of more than 20% is accompanied by clinical signs of poisoning. With a strong degree of alkalosis, for example, with urea (urea) poisoning, anxiety, teeth grinding, salivation, frequent urination, weakness, and shortness of breath are observed. With conventional protein overfeeding, clinical signs are less smoothed out.

If the cause of the disease is excessive feeding of high-protein feeds, the disease develops slowly. Depression, drowsiness, decreased appetite or persistent refusal to feed, and lack of chewing gum are observed. The nasal mucosa is dry, the mucous membranes are hyperemic. An unpleasant, putrid odor is felt from the oral cavity.

With the development of rumen alkalosis, the pH reaches 7.2 and higher, the ammonia concentration is more than 25.1 mm%, the number of ciliates decreases to 66.13 thousand/mm, and their mobility decreases. Reserve blood alkalinity increases to 64 vol.% CO2 and higher, urine pH is above 8.4.

Treatment. Aimed at reducing the pH of rumen contents, restoring the vital activity of ciliates and rumen bacteria. Feeds that caused the disease are excluded from the diet, and urea is stopped. To reduce the pH of the ruminal contents, 1.5-2.5 m of a 1% acetic acid solution is injected 2 times a day.

To reduce the pH of the rumen contents, animals are given 1-2 liters of 0.3% hydrochloric acid and 2-5 liters of sour milk. Sugar 0.5-1.0 kg in 1 liter of water. Sugar in the rumen is fermented to form lactic acid, which lowers the pH.

In severe cases of urea poisoning, bloodletting should be done immediately. In large animals, 2-3 liters of blood are released at one time. Followed by replacement of saline solution, 400-500 ml of 10-20% glucose.

In case of acute urea poisoning, you can immediately try to wash the rumen.

Prevention. They regulate the feeding of legumes, promptly clean feeders from leftover feed, and do not allow the use of spoiled or rotten feed. Urea and other nitrogen-containing non-protein substances are fed to animals under strict veterinary control, preventing overdose.

To improve the absorption of urea nitrogen and other nitrogen-containing non-protein substances and maintain the pH of the rumen contents at an optimal level, it is advisable to feed them along with feeds rich in sugars and starch (cereals, cereals, beets).

Bibliography

1. Vitfind V.E. Secrets of emergency care.-M.; "Publishing house BINOM" - "Nevsky Dialect", 2000.

2. Zaitsev S.Yu., Konopatov Yu.V. Biochemistry of animals.-M.; SP.; Krasnodar: 2004

3. Kondrakhin I.P. Nutritional and endocrine diseases of animals - M: Agropromizdat, 1989.

4. Kondrakhin I.P. Clinical laboratory diagnostics in veterinary medicine – M.: Agropromizdat, 1985.

5. Osipova A.A., Mager S.N., Popov Yu.G. Laboratory blood tests in animals. Novosibirsk 2003

6. Smirnov A.M., Konopelka P.P., Pushkarev R.P. Clinical diagnosis of internal non-contagious animal diseases -: Agropromizdat, 1988.

7. Shcherbakova G.G., Korobova A.V. Internal diseases of animals. – St. Petersburg: Lan Publishing House, 2002.

Rumen alkalosis is caused by bacteria of the coliproteus group, which displace the normal flora of the rumen, or occurs when animals are fed large amounts of protein-rich concentrated feed, which causes increased formation of ammonia in the rumen.

Alkalosis is also observed when animals eat excessive feed containing non-protein nitrogen compounds (ammonium bicarbonate or urea). Bacteria of the coliproteus group are found in large quantities in autumn in contaminated feed (in the tops of root crops, root crops and silage) or in putrefactive, musty feed (beets, potatoes, silage, hay).

It is especially dangerous to give animals large amounts of urea in addition to silage of reduced quality, but still rich in proteins. In this case, the rapid release of NH3 in the rumen leads to accelerated growth of the coliproteus.

Symptoms. First of all, indigestion, a violation of the general condition and diarrhea are noted. The course of the disease can be hyperacute, acute or subacute-chronic. The cicatricial juice has a gray-brown or dark gray color, a putrid odor and a pH over 7.5. 80-90% of dead ciliates are found in it.

Therapy. Treatment is aimed at restoring the physiological balance in the rumen and intestines. To do this, appoint 3-5 g of streptomycin, 1/2 l of 40% vinegar or 50-70 ml of lactic acid per 8-10 l of water or 7-8 l of linseed mucous decoction and 3-5 l of fresh cicatricial juice from a healthy animal. The rumen juice is injected using a nasopharyngeal tube.

It is very effective to introduce 100 g of agramin (“new”) or glutamic acid granules into the rumen and 400-500 g of Glauber’s salt, soluble in 10 liters of water, into the abomasum. 500-1000 ml of 5% glucose solution, 2 ml of strophanthin and 100 ml of methionine are used intravenously. In subacute and chronic forms of the disease, you can temporarily feed large quantities of easily digestible carbohydrates (sugar beet pulp, molasses or sucrose; maximum allowance is 4 g/kg body weight per day).

In severe and subacute forms of the disease, you can resort to rumenotomy to remove all the contents of the scar. After the operation, 8-10 liters of fresh rumen juice from a healthy animal and 500 g of glucose are injected into the rumen. The animal is given some hay.

Prevention.
Please keep the following in mind:
- if the diet contains more than 13% crude protein, animals should not be fed urea as a supplement;
- protein-rich silage should be fed in combination with feed containing little protein and high energy;
- Nitrate-rich food should be excluded from the diet if animals have insufficient energy metabolism (subclinical ketosis).