Acidosis and alkalosis of the rumen in animals. Symptoms and treatment of acidosis in cows

20.06.2020 -

Rumen lactic acidosis in cows is a non-contagious disease. However, a sick animal loses weight, stops producing milk and may even die if treatment is not started in time. The disease occurs quite often, so it has been well studied. Its main reason is flaws in the cow’s diet, followed by metabolic disorders. Most often, highly productive animals that are important for the farm suffer. It is for this reason that you need to know as much as possible about acidosis in order to recognize it in time and treat it.

Causes of acidosis

There may be several of them. Sometimes just one is enough to make a cow get sick, and sometimes they occur in combination. IN the latter case It is more difficult to treat an animal. As a rule, the causes of acidosis are:

too crushed food;
shortage coarse fibers in food;
excessive levels of quickly digestible carbohydrates in the diet;
disturbance of the rumen microflora;
too wet food;
low-quality silage with high acidity.

As you can see, all the troubles come from illiterate or careless management of cattle nutrition.

So, a cow can get sick with a sudden change in diet or with an excessive amount of seemingly ordinary products - grains, beets, potatoes, apples, silage. The favorite “food made from anything” - a boiled mixture of any plant waste: pulp, vegetables and others - also leads to bad consequences.

What happens to a cow’s body when it’s sick?

With acidosis, lactic acid accumulates in the rumen (the first section of the stomach), and natural substances become less than normal. The animal’s digestion is disrupted, and along with this, immunity decreases. Lactic acid begins to enter the blood, causing destructive processes in the liver. The microflora in the rumen changes.

Organisms that process cellulose and lactic acid give way to those that “specialize” in starch. The consequence is the inability to digest roughage, an imbalance of substances in the ruminant’s body, and a change in pH levels. Sometimes when accumulated in the rumen harmful bacteria may come sudden death animal.

Acidosis is extremely dangerous for pregnant cows. The reason is a change in the placenta. She is losing her protective functions, passing to the fetus all substances circulating in the mother’s body, including harmful products disrupted exchange. They, in turn, affect the metabolism of the fetus and undermine its immune system.

Very often, calves born by sick cows die in the first days of life - their body is not able to cope with the threats environment. If the calf survives, it will lag behind its peers in development.

Symptoms of the acute form of the disease

Acidosis in cows is associated with malfunction digestive system, so it can be easily confused with other gastrointestinal diseases. It is necessary to carefully monitor the condition and behavior of the sick animal.

There are three forms of the disease: acute, subacute (subclinical) and chronic.

In acute cases, the disease develops very quickly and is easiest to recognize. It is also quite easy to understand what caused the acidosis. Symptoms appear very quickly after eating the food that triggered the disease, literally within a few hours.

The animal suddenly becomes lethargic, stops eating, and lies motionless all the time. Breathing is difficult and the cow may also grind her teeth. If you feel her stomach, there will be a clear lump in the area of the gastric scar. The body temperature usually does not rise.

A little later, the animal begins to tremble, chewing cud stops, and stool becomes frequent and loose. Convulsions and coma are possible. This is the most dangerous form. If active treatment is not started immediately, the cow may die within a day.

Subacute or subclinical acidosis

It is not as scary as the acute form, but it is also dangerous. Most often, subclinical acidosis affects recently calved cows, as their diet is changed after calving. If the owner is not literate enough, he changes the animal’s diet dramatically, not allowing the rumen microflora to rebuild. This is what causes the disease.

The symptoms here develop gradually. In general they are the same as for acute form, but the body temperature may rise, the animal loses weight, and the muscles noticeably weaken.

If a cow is left untreated, her immunity decreases and mastitis develops. Over time, subclinical acidosis becomes chronic. Complications of the subacute stage with the transition to the chronic stage are all kinds of hoof diseases, reproductive dysfunctions, ruminitis (inflammation of the mucous membrane of the rumen), myocardial dystrophy, liver abscess and other diseases.

Chronic lactic acidosis

At this stage, signs of the disease become moderate apathy, indifference to external stimuli, fluctuations in appetite. The animal eats grain and sugary foods poorly or refuses them altogether. The mucous membranes are paler than usual due to anemia caused by the disease.

Sometimes the chronic form does not manifest itself at all. Unless the animal gets tired faster or seems lethargic. Therefore, it is important to closely monitor the condition of the cows in the herd.

Cows suffering from chronic acidosis with complications lose their value for the farm because they produce very little milk, and it also loses its fat content. They are also not suitable for reproduction, since either they cannot bear offspring, or they will be born sick. For this reason, such individuals are culled; they do not participate in the life of the herd and in economic work.

Although acidosis is not contagious, it can affect several animals or the entire herd at once, because the diet is usually the same for the entire herd.

Making a diagnosis: what tests will be needed

All symptoms and treatment of acidosis in cows should be analyzed and monitored by a veterinarian. Primary diagnosis placed if the fact of overfeeding the animal with products that provoke the disease is proven.

Then you need to exclude similar diseases - atony and hypotension of the forestomach, ketosis. A study of the contents of the rumen is required, and, if necessary, a urine and blood test. If a cow, for example, has ketosis, which is similar in symptoms to acidosis, there will be ketone bodies in the urine and blood. Sugar levels will also not be reduced.

With atony and hypotension of the forestomach, the course of the disease is not so severe, there is no tachycardia, breathing is normal, and the condition of the hooves does not change.

Acidosis is also often confused with alkalosis. Analysis of rumen fluid can help differentiate between these two diseases. With acidosis, it acquires an unusual color and smell, and the concentration of lactic acid is greatly increased.

In addition, its amount in the animal’s blood increases, and alkalinity decreases. Protein is sometimes found in the urine.

Treatment: the sooner the better

The most important thing for cattle acidosis is to start providing assistance as early as possible. The animal's life depends on it.

The first thing you need to do is remove the junk food. In the acute form, the veterinarian performs washing of the scar using special probes, or ruminotomy. During the second procedure, the scar is opened and the contents are removed.

When the scar is cleaned, alkali is introduced into it - 5 liters of soda solution. Proportion – 150 grams per 1 liter of water. Additionally add flaxseed decoction, or 500 grams of ordinary baker's yeast dissolved in clean water. Later, the rumen of the sick cow is filled with rumen contents from healthy animals - 3-4 liters. The procedure is carried out through a probe.

The animal is injected intravenously with 1 liter of sodium bicarbonate solution (7%). This can be done 8 times a day or less, depending on the condition of the cow. If there are convulsions, prednisolone and B vitamins are injected intramuscularly.

In addition, it is necessary to give the animal orally enzyme preparation Macerobacillin: 10-12 grams per day for at least three days.

Self-service ambulance

There are some methods that livestock farmers use themselves after seeing characteristic features acidosis in a cow. They are from the category folk remedies, therefore, you should use them at your own peril and risk and only when it is absolutely impossible to quickly deliver them to a veterinarian.

As soon as the cow feels ill, dilute ½ pack of regular baking soda in 3 liters of water and pour it over the cow. The head must be held so that it swallows the solution. Then give from 0.5 to 1 liter vegetable oil(sunflower) and massage the scar. The oil should be warm.

A good sign is the appearance of gurgling in the cow's stomach. This means that digestion has started. If the animal starts vomiting, this is very good - the scar will clear.

Prevention of acidosis in cattle

Since the cause of this disease is a careless attitude to animal nutrition, prevention consists of the opposite - careful control of the diet.

It is imperative to take into account the ratio of proteins and carbohydrates in the livestock menu. If there are too many concentrates and not enough fiber-containing foods, this is a direct path to acidosis. Concentrates should be no more than 40%, but it is better to completely remove the bare dirt (crushed, unrefined grain) of barley and wheat. It is better to give concentrates containing rapeseed, extruded soybeans, and ground corn.

Fodder beets can be given, but not more than 25 kilograms per day. Moreover, it is necessary to divide it into at least two doses.

Macerobacillin is given in a proportion of 0.3 grams per 100 kilograms of weight. The rest - at the rate of 0.3-0.5 grams per feed unit. All drugs must be mixed with food once a day. Prevention is carried out in courses of 30-60 days.

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Brief description

Target. Conduct an analytical review of the literature.
Tasks.
1. Define diseases.
2.Indicate the etiology of the diseases.
3. Explain the pathogenesis.
4.Describe the clinical signs.
5.Give information about diagnostics.
6. Provide data about the forecast.
7.Describe the treatment.
8. Provide 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, for lately The structure of rations 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 a disturbed ratio of acetic (normally 10 - 15%), lactic (normally 85%) and butyric acids; there is practically no hay in the diet good quality and root vegetables. 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 no discoloration occurs 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 appearance of varying degrees tympania.

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 most early signs illness - refusal to feed and inhibition 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 show 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 acidosis of the rumen with long term may 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 concentration of sugar slightly increases (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 rumen atony occur in a milder form than acute ruminal 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 ruminal acidosis varies in different stages of the disease, during which various changes occur in internal environment 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 feeding ration according to the sugar-protein ratio, which should be 1-1.5:1. Prevent animals from having access 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 this is human negligence in feeding and maintaining farm animals. To prevent alkalosis and acidosis of the rumen, it is necessary to comply with the diet of ruminants and improve the sanitary and hygienic condition of livestock premises.

References

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2. Grushkin, A.G. On the morphofunctional features of the rumen microbiota of ruminants and the role of cellulolytic bacteria in ruminal digestion / A.G. Grushkin, N.S. Shevelev // Agricultural biology. 2008. - No. 2. - P. 12 - 19.

3. Kalashnikov, A.P. Achievement of the science of animal feeding // Zootechnics. 2003. - No. 11. - P. 4-9.

4. Kalashnikov, V.V. Modern approaches to the development of animal nutrition systems and the implementation of biological potential and their productivity / V.V. Kalashnikov // Bulletin Russian Academy agricultural Sci. 2006. - No. 2. - P. 78-80.

5. Kalyuzhny I.I. Rumen acidosis / I.I. Kalyuzhny // Veterinary medicine. -1998.-No. 7. -WITH. 42-47.

6. Kassil G.N. Internal environment of the body / T.N. Kassil. M.: Nauka, 1983.- P.24-34.

7. Kondrakhin I.P. Rumen alkalosis // Veterinary medicine. 1998. - No. 10. - P.37-39.

8. Korostelev A.I. The influence of concentrated feeding on the development of bulls / A.I. Korostelev // Animal Science. - 2008. - No. 10. - p. 12-13.

9. Laptev, G. Lactic acidosis? The reason is in the diet / G. Laptev // Animal husbandry of Russia. - 2007. - No. 4- P. 41-42.

10. New technologies in the diagnosis, prevention and treatment of agricultural diseases. animals. Sat. scientific tr. State Scientific Research Institute of National Health of the Russian Federation. - Nizhny Novgorod, 2006.-P. 141-148.

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12. Pykhtina L.A. Increasing the efficiency of feed use in milk and meat production in the Middle Volga region / L.A. Pykhtina // Author's abstract. diss. doctors, agricultural Sci. Nizhny Novgorod- 2002. - P. 12-15.

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Pathology of the digestive organs ranks first among all forms of internal non-communicable diseases. Changes in feeding regimen and rapid changes in feed have a negative impact on digestion. Great importance in maintaining functions and normal condition metabolism have the quality of feed, the completeness and structure of the feed ration.

The entire large group of diseases of the digestive system is divided into four groups:

illnesses oral cavity, pharynx and esophagus;

diseases of the proventriculus and abomasum of ruminants;

diseases of the stomach and intestines;

gastrointestinal colic.

Stomatitis- inflammation of the oral mucosa. It usually occurs under the influence of mechanical, thermal, chemical, biological and other factors.

Symptoms An unpleasant putrid odor appears from the patients' mouth, and the act of eating and chewing is disrupted.

Treatment. The oral cavity is washed several times a day with solutions boric acid, potassium permanganate, etocridine lactate, furacilin.

Pharyngitis- inflammation of the tissues of the pharynx. Most common reasons: drinking hot animals with cold water, grazing on grass covered with frost, as well as infectious diseases(washed, anthrax, swine fever, pasteurellosis, etc.).

Symptoms. Due to the soreness of the pharynx, animals stretch their heads when swallowing, and the pharynx area is painful on palpation.

Treatment. Externally - warming compresses, wrapping. Appointed sulfa drugs.

Esophageal blockage- one of frequent illnesses cattle, less often other types of animals.

Cause- feeding unchopped root vegetables (beets, potatoes, carrots, turnips, corn on the cob, etc.).

Symptoms Salivation increases, shaking the head, moaning, fanning the tail, kicking the stomach, convulsive coughing, and empty chewing movements are noted.

Treatment. Therapeutic measures depend on the location of the esophageal obstruction, from removing the foreign body by hand to pushing the probe into the scar with the infusion of Vaseline or vegetable oil. To relieve spasms, a 1% solution of novocaine, atropine, and platiphylline are administered subcutaneously.

Diseases of the proventriculus and abomasum. The forestomach plays a major role in the digestion of ruminants, since proteins are broken down in them, carbohydrates are fermented, and volatiles are formed and absorbed. fatty acids, due to the rumen microflora, vitamins B, K and some other substances are synthesized.

The basis of these diseases is mainly a violation of the motor function of the proventriculus. The diagnosis of atony and rumen overfilling is made by external manifestations diseases. However, the latest scientific achievements allowed us to take a slightly different look at impaired motor function, taking into account changes in the biochemical processes of rumen digestion.

A disease characterized by a shift of ruminal contents to the acidic side is called rumen acidosis, and to the alkaline side - rumen alkalosis.

Rumen acidosis- one of the common forms of forestomach pathology.

Etiology. Rumen acidosis occurs when feeding a large amount of feed containing easily digestible carbohydrates: barley, rye, oats, corn in the stage of milky-wax ripeness, sugar beets, potatoes, watermelons, grain concentrates.

According to I.S. Shalatonov, over the past 10 years 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.

Symptoms. General depression, loss of appetite, chewing gum is sluggish and sparse, rumen contractions are weakened. Milk yield decreases. Pulse and breathing are increased. If the animal has consumed a large amount of food, the disease is complemented by symptoms of rumen overflow: the left hungry hole is leveled, the contents are dense, and when pressed, a dent forms. Body temperature in some sick animals increases, which indicates the development inflammatory process in the rumen, mesh, book or intestines.

Treatment. Oral administration of baking soda 150 - 200 g 2 times a day, Glauber's salt 200 - 300 g 2 times a day. The best results are obtained by washing the rumen and then injecting 3 liters of rumen contents from a healthy cow into it.

Rumen alkalosis- pH shift to the alkaline side (above 7.3). The disease is rare.

Etiology. Overdose of urea, feeding legumes (vetch, peas, soybeans).

Clinical signs the same as with acidosis of the rumen contents.

Treatment. A 5% solution of acetic acid is prescribed orally, 300 - 500 ml 2 times a day.

Atony and fullness of the rumen. They are often of secondary origin.

Etiology. Mastitis, metritis, reticulopericarditis, osteodystrophy, infectious, invasive and other diseases.

According to I.S. Shalatonov, hypotension and atony of the rumen become widespread with prolonged feeding of acidic feed (concentrates, silage, haylage) with a lack of alkaline feed (hay, root crops), with a shift in the pH of the contents to the acidic side (below 6.0).

Symptoms Hypotension and depression of the animal are usually observed. Other clinical symptoms depend on the underlying disease. The left hungry pit has a dense or even hard consistency.

Treatment. Rumenatory - tincture of white hellebore (10 - 15 ml per 0.5 liter of water orally), massage, wiring, 10% solution of table salt (200 ml intravenously).

Tympany- accumulation of gases in the rumen.

Etiology. Abundant feeding of freshly cut grass, potato and beet tops, cabbage leaves, grazing on dew. Abundant consumption of mash from ground concentrates by calves.

Symptoms The scar is stretched by gases (enlargement of the left side abdominal cavity), animal anxiety: wagging its tail, looking at its stomach. Difficulty breathing: neck stretched, movements chest tense. Postures for defecation and urination are repeated frequently, with little excretion of feces and urine.

Treatment. 150 - 300 ml of sunflower, castor or vaseline oil is prescribed orally. Timpanol 0.4 - 0.5 ml per 1 kg of body weight with water in a ratio of 1:10 orally. If necessary, urgently remove gases from the scar - by probing or puncturing the scar with a trocar.

Traumatic reticulitis- inflammation of the mesh caused by injury to it by foreign bodies.

Etiology. Ingestion of sharp metal objects with food (pieces of wire, nails, pins, needles, etc.).

Symptoms diseases can be different, so it is not always easy to determine whether the mesh or other organs are affected. IN acute cases note: short-term increase temperature, depression of the animal, loss of appetite, decrease in milk yield, pain when pressing in the area xiphoid process.

Treatment. A magnetic probe has been proposed to remove foreign bodies from the mesh, but treatment is effective when foreign body has not yet gone beyond the wall of the net. It is advisable to introduce magnetic rings into the forestomach. The prognosis is often unfavorable.

Gastroenteritis- mainly acute inflammation stomach and small intestine.

Animals of all kinds get sick age groups, often young animals. The disease can affect up to 80 - 100% of the population.

Etiology. Mass diseases can occur due to violations of the technology for manufacturing and feeding compound feed, premixes, additives, feed preservatives, waste from meat and dairy, sugar, alcohol, fish, canning and other processing industries. Many poisonings with mineral and plant poisons, infectious and invasive diseases, and radiation sickness occur with gastroenteritis syndromes.

Symptoms Depression of the animal, loss of appetite, increase in body temperature by 0.5 - 1 °C or more, increased heart rate and breathing, the animal is restless, the stomach is tucked.

The most important feature are changes in stool. It is softened, mucus and undigested food particles are found in it. There is profuse diarrhea with a foul odor. Due to constant straining, the mucous membrane of the rectum comes out. The animal loses its fatness, its eyes become sunken, its skin loses elasticity, and its hair becomes dull. The animal lies down more.

Treatment. They start with a fasting regime. Rinse the stomach with 1% solutions of sodium bicarbonate or sodium chloride. Saline laxatives (1% solution of sodium sulfate or magnesium sulfate) are prescribed. A course of treatment is prescribed with antibiotics, sulfonamides (furoxin, trimethosul, trimerazin, tribrissen), painkillers (analgin, anesthesin), decoctions and infusions medicinal herbs and their collections (St. John's wort, yarrow, hops, immortelle, etc.).

Diseases of the stomach and intestines, occurring with symptoms of colic. Colic- symptom complex indicating the presence pain in the abdominal organs: stomach, intestines, liver, kidneys. Gastrointestinal colic is more often observed in horses, less often in other animals. There are about 40 diseases of different etiologies that are accompanied by a symptom complex of colic.

The pain is caused by strong spasmodic contractions of organs, stretching of the walls of the stomach and intestines by gases, feed masses, helminths accumulated in them, tension of the mesentery as a result of the unnatural position of the intestines, inflammation of the serous integuments of the abdominal cavity, damage nerve plexuses, blood supply disturbance.

Depending on the causes, colic is divided into two types: colic with dynamic and colic with mechanical obstruction.

Dynamic obstruction can be spastic (gastric dilatation, enteralgia, intestinal flatulence) and paralytic (chemostasis and intestinal coprostasis).

Rumen alkalosis(alcalosis ruminis acuta)

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

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

Pathogenesis. The rumen microflora is capable of hydrolyzing 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 enzymatically affected in the abomasum, where it is broken down into amino acids, which are absorbed in the small intestine. The enzyme urease, necessary for protein breakdown, is found in cell wall 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 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 clinical picture a disease that manifests itself if the level of ammonia in the blood reaches 1 - 4 mg.
Ammonia is a base and has a pH of 8.8. The accumulation of ammonia in the rumen causes a shift in the pH of the environment 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 the 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 feeds, the disease lasts longer and with a calmer external condition animal. They observe persistent refusal to feed, lack of chewing gum, rumen motility, severe depression up to comatose state or drowsiness. The nasal mucosa is dry, the mucous membranes are hyperemic. The stool is initially formed and then may be liquid. The mouth feels putrid or bad smell. 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 therapeutic measures, without the use of which death inevitably occurs.
Alkalosis arising from an overdose of urea occurs acutely, from overfeeding with protein-containing feed, even when medical care, last 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 up to 40 I cold water into the rumen 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, effective measure The treatment is rumen rinsing. In the absence of dense contents in the rumen, this curative 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 rumen to suppress putrefactive microflora and intramuscular injection thiamine and antihistamine. Thiamine in this case is administered to prevent the possible death of microflora in the rumen and the long course of the disease clinical manifestation vitamin deficiency Bi (corticocerebral necrosis).
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.