Rabies in cattle: symptoms and treatment. Rabies - symptoms and treatment Rabies in cows symptoms and treatment

The first outbreak of mad cow disease was reported in 2003, and today it is back in the spotlight after several cows tested positive for the disease. If you eat red meat, you absolutely need to be aware of this disease. This article provides information about the causes and symptoms of this disease.

Did you know?

That people in New Guinea eat the brains of dead people as part of their funeral ritual. This resulted in a disease called Kuru (central nervous system disorder), which is associated with mad cow disease.

Medically known as Spongiform Encephalopathy, this disease affects the central nervous system (CNS) of cattle. Mad cow disease belongs to the group of Transmissible Spongiform Encephalopathies. This is a group of neurodegenerative diseases that affect animals and humans. In animals, other related diseases are scrapie (sheep) and feline spongiform encephalopathy (cats). In humans, Gerstmann-Sträussler-Scheinker syndrome (GSS) and fatal familial insomnia (FFI) have been reported. It is believed that mad cow disease is caused by the presence and actions of prions, which are infectious agents.

Transmission of these infectious agents occurs via protein misfolding. They are commonly found in the brain, spinal cord, small intestine, and blood of cattle. They can also be found in the lymph nodes, spleen, and bone marrow of the affected organism. Some scientists also believe that proteins present in the body are converted into prions due to the presence of the virus. However, this theory is not supported by research. Prions damage the CNS by making spongy holes in these edges. This leads to the degeneration of nerve cells, which ultimately leads to the death of the organism.

Symptoms in humans

Research and laboratory data demonstrate a striking association between BSE and Creutzfeldt-Jakob disease (vCJD) in humans. The cjd variant is a human neurodegenerative disease that is usually fatal. It is associated with the consumption of contaminated meat or meat products. The disease manifests itself as follows:

The earliest symptoms include depression, insomnia and anxiety.
The person may appear withdrawn and in a confused state of mind.
Significant changes in the personality and behavior of the individual.
The person may also experience muscle spasms, i.e. involuntary contractions of the muscles, which are very painful.
If the patient's condition worsens, he loses control over muscles and coordination, and problems with vision (blurred vision) and memory may also occur.
Temporary memory loss is another symptom that makes it difficult for the patient to recognize people.
The victim may feel tingling in the legs, arms, and face.
The patient may develop dementia, which will make him mentally and physically weak.
In the final stages of the disease, the patient may fall into a coma, which eventually leads to death. A person reaches the end stage within 6 months to one year after the onset of symptoms.

vCJD is named after the scientists Hans Gerhard Creutzfeldt, who first described the disease in humans, and Alfons Maria Jakob, who subsequently worked on the disease.

Symptoms in cattle

Mad cow disease is always a disease of cattle. Some of the clinical signs are listed below:

Difficulty standing and walking.
Problems with muscle coordination.
A small change in the behavior of the body.
Sudden weight loss.
Significant reduction in milk production.

It may take 2 to 8 years after infection.

The reasons

As mentioned earlier, the causative agent of this disease is a prion. It cannot be transmitted from one organism to another through physical contact. However, it can make its way from animals and humans:

In slaughterhouses, animal remains are removed without any tests. These waste/by-products are fed to livestock as a cheap source of protein. When they are fed infected (with prions) animal carcasses, the prions are passed on to them.
When people consume meat contaminated with spongiform encephalopathy, it puts them at risk of contracting the disease.
There have been cases where a variant of Creutzfeldt-Jakob disease has occurred in people with no known cause, including those who are vegetarians. A genetic mutation that is inherited can also cause this disease in a person.
In addition, transfusions of contaminated blood, grafts containing prions, and contact with infected surgical instruments can lead to the development of this disease in humans.

Diagnosis and treatment

There is no absolute method and physical test to diagnose this disease. However, a doctor may recommend a complete blood workup along with an MRI or PET scan. He may also recommend a brain biopsy to check for changes that are taking place in the brain.

Unfortunately, there is no effective treatment. Research is ongoing to find a drug that will help in the treatment of this disease in humans as well as animals. The patient may be prescribed certain medications to control the symptoms. Providing love, care, and moral support will help a person cope with illness.

It is recommended to take certain precautions to prevent this disease. Limit your intake of red meat. Heating, boiling, irradiation or chemical reagents failed to kill pathogenic prions. Therefore, cooking contaminated meat does not ensure safe consumption. Going vegetarian is a good idea to prevent this disease. If you notice any of the above symptoms, see your doctor as soon as possible.

Rabies is an acute infectious disease that occurs with severe damage to the nervous system, usually with a fatal outcome. Humans and all mammals are susceptible.

Rabies is ubiquitous. The causative agent of infection is transmitted by dogs, cats, wild rodents and predators, as well as blood-sucking bats - vampires.

The duration of the incubation period depends on the location and strength of the bite, the amount and virulence of the virus that has entered the wound, and the resistance of the bitten animal. The incubation period lasts from 1-3 weeks to a year or even more.

The disease is acute. Its clinical signs are basically the same in all animals, but they are most typical in dogs, in which both violent and quiet (paralytic) course of the disease can be observed. In cattle, rabies can occur atypically (loss of appetite, atony of the rumen, paralysis of the pharynx, salivation). There may be no stage of excitation. Pathological changes are not specific. In meat-eaters (mainly dogs), foreign objects can be found in the stomach.

The rabies virus has a pronounced neuroprobasia. Penetrating from the periphery (the bite site) along the nerve trunks into the central (centripetal nervous system), it spreads centrifugally in the body along the peripheral nerves and enters various organs, including the salivary glands.

The virus belongs to the family Rhabdoviridae, genus Lyssavirus. Virions are rod-shaped with a truncated end. Virion of the virus - RNA-containing with a helical type of symmetry, has a lipoprotein shell. Low temperatures preserve the virus. A temperature of 60°C kills it in 5-10 minutes, sunlight in 5-7 days. Solutions of formalin, phenol, hydrochloric acid (5%) inactivate the virus in 5-10 minutes.

The rabies virus virion contains glycoprotein (external) and nucleocapsid (internal) antigens. The glycoprotein antigen induces the formation of virus-neutralizing antibodies, and the nucleocapsid antigen induces the formation of complement-fixing and precipitating antibodies.

Epizootic strains of the rabies virus are immunobiologically related, but differ in virulence.

In the body, the virus is localized mainly in the central nervous system, as well as in the salivary glands and saliva. It is cultivated on mice, rabbits, guinea pigs and other animals, as well as in primary cell cultures (Syrian hamster kidneys, sheep embryos, calves, etc.) and transplanted cells (VNK-21, KEM-1, etc.). Reproduction of the virus in cell cultures is not always manifested by CPE. Chicken embryos are also susceptible to the rabies virus after preliminary adaptation. The virus induces the formation of cytoplasmic inclusion bodies, which are most often found in the cells of the ammon's horn, cerebellum, and cerebral cortex.

Sick animals are the source of infection. They transmit the virus when they bite. Carnivores can become infected by eating the brains and spinal cords of animals that have died of rabies. The possibility of infection with rabies by aerogenic route (in places where there are bats) has been proven. Until the 1960s, the main source of rabies was dogs and cats, later foxes, wolves, corsacs and other wild animals.

The diagnosis of rabies is made on the basis of epidemiological, clinical and laboratory data, which are of decisive importance.

When working with sick animals and infectious material, personal safety measures must be strictly observed: wear rubber gloves, gowns with oversleeves, a rubber or polyethylene apron, rubber boots, goggles, and a face mask.

It is prohibited to dissect suspicious animals with rabies in the field.

Laboratory diagnostics. It includes: detection of viral antigen in RIF and RDP, Babesh-Negri bodies and bioassay on white mice.

RIF setting technique.

Thin prints or smears are prepared on defatted glass slides from various parts of the brain on the left and right sides (Ammon's horn, cerebral cortex, cerebellum and medulla oblongata). Prepare at least two preparations of each part of the brain. You can also examine the spinal cord, submandibular salivary glands. For control, preparations are made from the brain of a healthy animal (usually a white mouse).

The preparations are dried in air, fixed in chilled acetone (minus 15-20 °C) for 4 to 12 hours, dried in air, fluorescent gamma globulin is applied, placed in a humid chamber at 37 °C for 25-30 minutes, then thoroughly washed saline or phosphate buffer pH 7.4, rinsed with distilled water, air dried, applied with a non-fluorescent immersion oil and viewed under a fluorescent microscope. In preparations containing the antigen of the rabies virus, various sizes and shapes of fluorescent yellow-green granules are observed in neurons, but more often outside the cells. In the control, there should be no such glow; the nervous tissue usually glows with a dull grayish or greenish color. The intensity of the glow is evaluated in crosses. A negative result is considered in the absence of specific fluorescence.

Material from animals vaccinated against rabies cannot be examined in the RIF for 3 months. after vaccination, as there may be fluorescence of the antigen of the vaccine virus.

In the RIF, tissues preserved with glycerin, formalin, alcohol, etc., as well as material that has signs of even slight decay, are not subject to examination.

RDP in agar gel. The method is based on the property of antibodies and antigens to diffuse in an agar gel and, upon meeting, form visually visible lines of precipitation (complex antigen ++ antibody). It is used to detect antigen in the brain of animals that died from the street rabies virus, or during an experimental infection (bioassay).

The reaction is placed on glass slides, on which 2.5-3 ml of molten 1.5% agar solution is poured. After solidification in agar, holes are made according to a stencil with a diameter of 4-5 mm, placed under a glass slide with agar. Agar columns are taken out with a student's pen. Wells in agar are filled with components according to the scheme.

From large animals, all parts of the brain (left and right sides) are examined, from medium animals (rats, hamsters, etc.) - any three parts of the brain, in mice - the entire brain. Using tweezers, a pasty mass is prepared from the brain, which is placed in the appropriate wells.

Controls with positive and negative antigens are placed on a separate glass according to the same stencil.

After filling the wells with the components, the preparations are placed in a humid chamber and placed in a thermostat at 37 ° C for 6 hours, then at room temperature for 18 hours. The results are recorded within 48 hours.

The reaction is considered positive when one or 2-3 precipitation lines of any intensity appear between the wells containing the brain suspension and anti-rabies gamma globulin.

Bacterial non-sterility and brain decay do not prevent its use for RDP. Material preserved with glycerin, formalin and other means is not suitable for RDP.

Identification of Babes-Negri bodies. Thin smears or prints are made on glass slides from all parts of the brain (as for RIF), at least two preparations from each part of the brain, stained according to one of the methods (according to Sellers, Muromtsev, Mann, Lenz, etc.).

An example of Sellers staining: a dye is applied to a fresh, not dried preparation, covering the entire preparation with it, incubated for 10-30 s and washed off with phosphate buffer (pH 7.0-7.5), dried in a vertical position at room temperature (in a dark place) and viewed under an oil immersion microscope.

A positive result is the presence of Babesh-Negri bodies - clearly defined oval or oblong granular formations of pink-red color, located in the cytoplasm of cells or outside them.

This method is of diagnostic value only when typical specific inclusions are detected.

Content:

Rabies (hydrophobia, rabies, spongy brain disease) is an acute, contagious, deadly disease of viral etiology. Belongs to the group of zooanthropozoonotic infections. Rabies is dangerous not only for warm-blooded animals, but also for humans. Treatment has not been developed, so farmers, pet breeders should pay attention to preventive measures. The mortality rate for this infection is 100%.

How infection occurs

Animal rabies (rabies) is a viral disease characterized by severe damage to the peripheral nervous system, signs of disseminated encephalomyelitis. The disease will inevitably lead to death. Refers to natural focal, periodic viral diseases. All types of warm-blooded, domestic, agricultural animals (cattle, horses, sheep, pigs), as well as most species of birds and humans, are susceptible to infection.

The disease is provoked by an RNA-containing bullet-shaped virus of the fam. Rhabdoviridae (rhabdoviruses). There are four serotypes of the pathogen that are widely distributed in the environment. The rabies virus is resistant to external environmental factors, some chemical disinfectants, and low temperatures. Under favorable conditions, it can be preserved in the corpses of animals from several months to several years. Instantly dies at a temperature of 100 degrees. UV rays inactivate it within 5–12 minutes.

Having penetrated into the body of animals, the rabies virus is initially localized in the salivary glands, lymph nodes, after which it penetrates with the bloodstream into other organs, in particular, into the spinal cord, brain (Ammon's horns, cerebellum), causing irreversible changes in the functioning of the central nervous system.

The reservoir of a dangerous virus in the natural environment are wild animals: wolves, foxes, jackals, raccoons, arctic foxes, raccoon dogs, bats, rodents (voles, rats), hedgehogs, and other types of domestic carnivores. The localization of natural foci of infection corresponds to the peculiarities of the distribution of wild animals, which are prone to long-distance migrations.

Taking into account the nature of the reservoir of the rabies pathogen, epizootics of this infection of urban and natural types are distinguished. In the city, the infection is spread by stray cats, dogs, latent virus carriers.

Important! Cases of infection of animals with rabies are currently registered in all countries of the world, including in the regions of our state.

Infection with the rabies virus in agricultural, domestic animals occurs through direct contact with an infected individual. Rabies virusIt is transmitted through a bite. The pathogen enters the body through damaged mucous membranes and skin. Infection of animals with a deadly infection is possible by aerogenic (airborne droplets), alimentary route.

The rabies virus is excreted into the external environment mainly with saliva, discharge from the nose, eyes.

Animal rabies is characterized by periodicity, seasonality. Most often, outbreaks of rabies of this disease are recorded in autumn, early spring, and also in winter. The risk group includes unvaccinated animals, weakened, emaciated individuals, young animals kept in adverse conditions.

Symptoms, course of the disease

From the moment of infection, the characteristic signs of rabies in animals can appear in 3–6 days to five to eight 5–8 weeks, depending on the general physiological state, the amount of virus in the body of infected individuals, the virulence of the pathogen, and the state of the immune system. In some cases, with animal rabies, the first manifestations may occur a year after infection. At the same time, infected infected individuals are latent virus carriers, representing a real danger to healthy individuals.

Rabies in domestic animals can occur in violent, silent, paralytic, abortive, atypical forms, each of which has its own characteristic symptoms.

In the pathogenesis of a viral disease, there are three main stages:

I - extraneural, without visible reproduction of the virus at the site of inoculation (lasts up to two weeks);
II - intraneural, in which centripetal spread of infection is noted.
III - dissemination of the virus throughout the body of infected animals. It is accompanied by the appearance of clinical symptoms of the disease and, as a rule, ends with their death.

As a rule, at the initial stage of the development of infection in sick animals, the general body temperature slightly increases. The state of apathy, oppressed. Some minor manifestations of damage to the central nervous system (muscle tremors, convulsions, spasms) are possible. As the infection progresses, the symptoms become more pronounced.

Violent form of rabies

The violent form of rabies is characterized by three stages of development:

prodromal;
arousal;
paralysis.

The duration of the prodromal period ranges from 12–15 hours to three to three days. In animals, minor changes in behavior are noted. Infected pets become lethargic, lethargic, depressed, try to hide in a dark secluded place. Attacks of apathy can alternate with periods of excitement. In some cases, dogs become very affectionate, try to lick their hands, the face of the owner, require increased attention.

As the disease progresses, anxiety and excitability gradually increase. Animals often lie down, jump up. There is an increased reflex excitability to any external stimuli (loud sounds, light, noise). Shortness of breath appears. The pupils are dilated, inadequately react to light.

Animals constantly comb, lick, gnaw out the bite site, scratches, wounds, scratches appear on the body. Sick pigs, horses, cattle Cattle begin to eat inedible objects (earth, wood, stones, their own feces). Gradually, paralysis of the muscular structures of the pharynx develops, which leads to difficulty swallowing. Animals refuse food and water. Abundant salivation, impaired coordination of movements, and sometimes strabismus are noted. The condition of the coat is deteriorating.

With the transition of the infection to the stage of excitation, which lasts about three to four days, the symptoms become more pronounced. Animals look excited, react inadequately to external stimuli, become aggressive. Dogs do not recognize their owners, show uncontrolled aggression. Attacks of violence are replaced by sudden apathy, oppression.

A slight increase in temperature is possible. Animals refuse to feed, quickly lose weight. The pupils are dilated and do not react to light. In dogs and other animals, the timbre of the voice changes, the lower jaw completely sags, and the lower jaw is paralyzed. The oral cavity is constantly open. There comes a paralysis of the tongue, pharyngeal muscles. Animals are disoriented in space, movement coordination is disturbed.

The paralytic period lasts one to six 1–6 days. For this stage, the characters are serious disturbances in the work of the central nervous system. In addition to paralysis of the lower jaw, the hind limbs, the muscles of the tail, bladder, and rectum are paralyzed, which leads to spontaneous urination and defecation. Animals cannot get up, rise to their feet. The sound of water causes severe panic.

The temperature can be increased by 1–2 degrees from the physiological norm. In the blood, polymorphonuclear leukocytosis, a change in the leukocyte formula are noted. Significantly reduced the number of leukocytes in the bloodstream. In the urine, the sugar content rises to 3–4%.

Paralytic (silent) form of rabies

With this form of viral disease, excitation is weakly expressed or may be completely absent. Animals do not show aggression, look oppressed, apathetic. A characteristic sign of the silent form of rabies is abundant salivation, dilated pupils, drooping of the lower jaw, paralysis of the pharynx and tongue. Swallowing is difficult.

Animals refuse food, water, quickly lose weight, look very emaciated, try to hide in a dark secluded place. Mucous membranes are pale. There comes paralysis of the muscles of the limbs, jaw, torso. The duration of the disease is two to four 2-4 days.

Atypical form of rabies

With this form of infection, the stage of excitation is completely absent. At the beginning of the disease, a slight increase in temperature is possible. Appetite is reduced. Animals refuse food, water, which leads to rapid weight loss.

Observe disturbances in the functioning of the digestive system. There are symptoms of hemorrhagic gastroenteritis. Fecal masses of a liquid consistency, contain a large amount of mucus, foam, bloody threads, clots.

In rare cases, agricultural animals are diagnosed with an abortive course of the disease. Some animals manage to recover. At the same time, this form often recurs, and after improvement, the condition of infected animals worsens again.

Rabies in farm animals

Rabies in cows occurs in a quiet and violent form. The duration of the incubation period can be from two 2 months to one 1 year.

With rabies in cows, if the disease proceeds in a violent form, increased excitability is noted. The animal shows aggression towards people, dogs, cats, other pets. The cow rushes to the walls, strikes with its horns, nervously beats with its tail.

The temperature is raised. Note salivation, sweating. Appetite is reduced. The lower jaw is pendulous. The pupils are dilated and do not react to light. The limbs are tense, stretched out.

With a silent form of infection, cattle have no chewing gum, no appetite. Animals are oppressed, lethargic, quickly lose weight, moo hoarsely. The cow stops secreting milk. There are signs of paralysis of the larynx, tongue, pharynx, front, hind limbs. The lower jaw is pendulous. Note abundant salivation, spontaneous defecation. Death occurs on the third or fifth, 3rd or 5th day after the onset of clinical symptoms.

goat rabies

In goats, sheep, the same symptoms are noted with a violent, quiet form of rabies, as in cattle, namely: aggression towards people, animals, especially cats, dogs, severe exhaustion, sexual excitability, paresis, paralysis. Goats, sheep trample in one place, butt heads, refuse water, feed. The disease develops rapidly. On the third or fifth day from the moment the first characteristic symptoms appear, the animals die.

Rabies in horses

Rabies in horses is manifested by increased excitability, inadequate reactions to external stimuli. Animals can show aggression towards people, their relatives. During periods of excitement, horses rush to the walls, gnaw on feeders, and begin to eat inedible objects. Excitation turns into complete apathy.

Muscle spasms, spasms of the cheeks, lips, and sternum are noted. The limbs are tense, stretched out. The coordination of movements is disturbed, paralysis of the pharynx, tongue, and lower jaw develops. The whinny becomes hoarse. Abundant salivation is noticeable. Animals look very emaciated, die on the third or sixth 3-6th day. In some cases, death is possible on the first day of the development of the disease.

swine rabies

In pigs, rabies occurs in acute and violent forms. The pigs are very excited, eat inedible objects, are afraid of water, refuse to feed, behave aggressively, inadequately. Sows can eat their piglets. a feeling of fear, strong anxiety, panic is manifested.

Paresis, paralysis of the extremities, lower jaw, and larynx develop on days 2–3. Animals become lethargic, apathetic, do not respond to external stimuli, constantly lie in one place. The duration of the viral disease is six to seven days, after which sick animals die.

Diagnostics

The diagnosis is made after a comprehensive examination, taking into account the general symptoms, the epizootological situation for rabies in the region, and the results of pathological anatomical autopsies. If necessary, differential diagnosis is carried out.

Treatment for rabies today does not exist, so the disease in 100% of cases ends in death.

When rabies occurs, quarantine is introduced. Animals, dogs, cats that have bitten people (except those obviously ill with rabies) are isolated for 10–12 days, placed in special boxes for veterinary observation. Animals with rabies are killed. The bodies are burned. The rest of the individuals are subjected to forced immunization. Suspicious wild animals are subject to destruction.

Important! Quarantine is removed after two 2 months from the date of the last case of animal disease with a viral disease.

In the event of an outbreak of rabies, settlements, as well as pastures, forests, fields are declared unfavorable. It is forbidden to export animals, hold exhibitions, competitions among dogs, cats, as well as trapping wild carnivores.

Farm animals of disadvantaged herds, flocks, herds are constantly monitored. Three times a day, a comprehensive veterinary examination is carried out. Suspicious animals are immediately quarantined.

The premises in which infected diseased animals were kept are disinfected using a 10% sodium hydroxide solution, a 4% formaldehyde solution. Inventory, care items, feed residues, manure are burned. The soil, which is contaminated with the secretions of sick individuals, is dug up, mixed with dry bleach, and then poured with disinfectant solutions.

It is also worth noting that people bitten, scratched, slobbered by any animal, even outwardly healthy, are considered suspicious for rabies infection. Therefore, it is very important to undergo a comprehensive examination at the medical center as soon as possible. Rabies in humans at the onset of the first symptoms is incurable.

Rabies Prevention

The most effective, effective way to prevent infection of domestic, farm animals can be called timely preventive immunization. In veterinary medicine, for these purposes, mono- and polyvalent anti-rabies tissue, cultural, live vaccines of domestic and foreign production are used.

Advice! The optimal scheme of vaccinations, subsequent revaccinations, preparations for immunization will be selected by a veterinarian.

An animal vaccine against rabies can be:

Brain - made from the brain tissue of animals infected with rabies;
Embryonic. Contains poultry embryos.
Cultural. It is made from the rabies virus reproduced in primary trypsinized or transplanted BNK-21/13 cells.

Against rabies in cats and dogs, the monovalent dry inactivated anti-rabies vaccine Rabikan is very often used. For preventive and therapeutic immunization of CRRS, horses, pigs, a liquid cultural anti-rabies vaccine "Rabikov" is used. For agricultural animals, universal polyvaccines (complex) veterinary preparations have also been developed for preventive immunizations.

In veterinary practice against rabies, they also use: Rabigen Mono, Nobivak Rabies, Defensor-3, Rabizin, Multikan-8. During revaccination, if there are no side symptoms, hypersensitivity to the components, the same vaccine is used.

Only clinically healthy animals are subject to vaccination. Pregnant, lactating females, malnourished, sick with viral infections, severely weakened individuals are not vaccinated.

Instructions are attached to veterinary preparations for immunization, so if you plan to vaccinate your pet on your own, carefully read the annotation to the medication. The first two or three days after vaccination, carefully monitor the behavior and health of animals.

In addition to preventive vaccination, farmers must monitor the cleanliness and hygiene in the premises in which animals are kept. Disinfection and deratization should be carried out regularly. Do not allow contact with wild, stray animals.

If a pet is suspected of having rabies, as well as if it has been bitten by stray, wild animals, it is necessary to immediately deliver the cat or dog to the veterinary clinic for examination and diagnostic tests.

It is also worth noting that animals not vaccinated against rabies are not allowed to participate in exhibitions, competitions, or hunting. Traveling abroad, to other regions is also prohibited without the presence in the veterinary passport, certificate of the necessary stamps, marks of immunization.

Rabies is an incurable, fatal disease. To avoid the loss of pets, it is necessary to be able to recognize this disease and know the principles of prevention. Let's consider them in more detail.

What is this disease

Rabies, or rabies, is a deadly viral disease of warm-blooded animals. The disease affects the central nervous system.

Did you know? An epidemic of rabies periodically awakens on all continents except Antarctica.

This disease is subject to:

wild animals (jackals, foxes, raccoons, bats);
domestic animals (cats, dogs);
livestock (sheep, cows, horses);
people.

How infection occurs

The causative agent of rabies is the Neuroryctes rabid virus. It is transmitted from a diseased object through saliva, primarily during a bite. It can also be transmitted through feed fed to an infected cow. First, the virus enters the spleen, after which it enters the nerve endings and diverges along them, affecting the nervous system.

In cattle, the incubation period of the disease lasts from two months to one year. The disease may not manifest itself for a long time - but, having manifested itself, it progresses within 5-6 days.

Forms and symptoms

If you suspect nervous system damage in cattle, pay attention to their behavior.

When infected with rabies, the following symptoms may appear:

Increase in body temperature.
Oppressed behavior.
The cow refuses to feed.
Sudden weight loss.
Periodic convulsions, staggering and muscle spasms.

Did you know? Rabies most often occurs in the winter or spring seasons.

The further manifestation of rabies develops in two directions: there are violent and calm varieties.

violent

During a violent form in a diseased animal, the following is observed:

sudden movements, attempts to break free, beat against the wall;
aggressive behavior, increased irritability towards other cows and dogs;
the cow makes a hoarse roar;
characteristic shortness of breath and inadequate reaction to light;
the cow combs the bite site to wounds, eats inedible (stones, wood).

With paralysis, which is the last stage of the disease, the lower jaw sags in a sick animal, the muscles of the pharynx and tongue atrophy. Further, the hind limbs cease to function, as a result of which movement practically stops.

Calm

The calm or paralytic form is most commonly seen in cattle. In a calm stage, cows do not show aggression, they are apathetic, lose weight sharply, and hide in a dark place.

The stage of paralysis quickly sets in and the cow fails in the jaw, throat and lower part of the croup. It becomes difficult to swallow, so the cow refuses to eat.

Important! Pay attention to the pupils: in a sick animal they are dilated.

Diagnostics

The diagnosis can be made by a veterinarian by ascertaining the characteristic painful signs of behavior and making a laboratory examination. All animals that are suspected of being infected, as well as those that have been in contact with sick people, should be isolated and subsequently transferred to a doctor for examination.
During the diagnosis, a high content of the virus is found in the cerebral cortex of agricultural cattle.

Is it possible to cure and what to do with corpses

Unfortunately, the probability of death for a person infected with rabies is one hundred percent. This disease is not treatable, so an isolated animal or the entire herd (if infection is suspected in the rest of the herd) is slaughtered. After slaughter, the corpses are burned, or taken to the laboratory for disposal.
The place where sick livestock is kept is disinfected with a solution of caustic soda and formaldehyde. After rabies is detected, quarantine is introduced.

They also check other cattle that were next to the infected: they are isolated for ten days and look at the symptoms of behavior. If there is no reason to worry about the health of the livestock, it is returned to the place of detention again.

Important! Quarantine in the region of infection due to rabies lasts at least two months.

Is it possible to eat meat and drink the milk of a sick animal

It is strictly forbidden to eat milk and meat from an infected animal, since this is how the disease can be transmitted to humans.

However, it is worth making a reservation: you can eat the meat of a cow suspected of having rabies and vaccinated against rabies. This can only be determined by a veterinarian. The same applies to milk - only if the fact of infection is not established, and the cow has received a vaccine, you can drink her milk.

Human infection from livestock can occur when eating the meat of a sick cow that has not undergone the necessary thermal treatment.

Vaccination schedule

Cattle are vaccinated against rabies to prevent and protect livestock from the virus.

The first vaccine is given to a calf at 6 months of age.
The next vaccination is carried out every 2 years. If a rabies quarantine is declared in the region, livestock can be vaccinated earlier.
The medicine is administered intramuscularly.
The amount of vaccine in one injection is 1 ml.
The vaccine should be stored in a dry, warm place. It cannot be frozen. In case of leakage, the bottle should be poured over with boiling water and left in boiling water for 5-10 minutes for disinfection.

Important! Only healthy livestock can be vaccinated.

Other preventive measures

In addition to vaccination, there are additional ways to control the development of rabies:

creation of safe conditions from the attack of wild animals;
destruction of wild animals;
vaccination of dogs used for livestock protection;
systematic inoculation of healthy livestock;
surveillance of a herd suspected of being infected to detect the virus as soon as possible.

Vaccination is the most reliable way to protect livestock from a sudden fatal disease. Be sure to consult your veterinarian about the required dose and frequency of livestock vaccinations in order to be calm for his health.

O. BELOKONEVA, Ph.D. chem. Sciences.

On January 25, 2001, a press conference for journalists was held at the Central House of Journalists on the topic "Mad Cow Disease - Does it exist in Russia? Reliable First-hand Information". It was organized by the scientific news agency "InformNauka" under the journal "Chemistry and Life". The press conference was attended by Doctor of Chemistry O. Volpina (M. M. Shemyakin and Yu. A. Ovchinnikov Institute of Bioorganic Chemistry RAS, Moscow), Doctor of Biology S. Rybakov (All-Russian Research Institute of Animal Welfare, Vladimir) and Head of the Veterinary Department of the Ministry of Agriculture of the Russian Federation M. Kravchuk. The main problems raised at this press conference are covered by the special correspondent of the journal "Science and Life", Candidate of Chemical Sciences O. Belokoneva.

The main problem of European farmers: "How to protect horned pets from a terrible disease?".

In patients with spongiform encephalopathy, cavities form in the brain.

The formation of protein filaments is one of the main signs of the presence of "wrong" prions in the brain. An electron micrograph shows a section of the brain of a sheep with scrapie.

The normal prion molecule (1) synthesized in the nerve cell moves to the surface membrane, where it participates in the transmission of the nerve impulse.

About 15 years ago in England, thousands of cows were stricken with a deadly disease. It mainly affected animals older than 4 years. The symptoms are varied. First - uneven limping gait. At the last stage of the disease, the cow cannot rise at all - the hind legs fail. Secondly, animals lose weight, milk yields decrease, but most importantly, the behavior of cows changes - they become restless, fearful (sick cows are especially afraid of narrow passages, corridors and pens), aggressive, gnash their teeth, tend to separate from the herd, react sharply light, sound, touch. In general, they behave like animals infected with the rabies virus. Hence the common name of the disease - mad cow disease. The "new" terrible disease turned out to be a long-known spongiform encephalopathy, which has nothing to do with "real" rabies. The "real" viral rabies - rabies and spongiform encephalopathy have in common - only the symptoms and the name, and the mechanism of the onset of the diseases is different.

Degenerative diseases in which the brain is destroyed, turning into a kind of sponge, have long been known. In sick animals, vacuoles - microscopic pores - are visible on a section of the brain under a microscope. The diseased brain resembles a porous sponge, hence the scientific name of this group of diseases - spongiform encephalopathy.

Cows, sheep (called scrapie disease), goats, rodents, and even cats are affected by spongiform encephalopathy. The animal dies from the complete destruction of the brain. Similar diseases, although extremely rare, are also found in humans: Kuru disease (common among the Papuans of New Guinea) and Creutzfel dta-Jakob disease. The latter has been known since the last century, and it affects approximately one in a million elderly people. First, the patient's coordination of movements is disturbed, then there is a complete loss of memory, the sufferer is overcome by convulsions. As a result, the patient dies.

Scientists have long understood that the causative agent of spongiform encephalopathy "lives" in the brain and bone marrow of animals and humans. The highest concentration of the infectious agent is in the oblong and middle sections of the brain. In meat, it is much lower.

Where did the epidemic come from

Why did a rare disease suddenly take on the character of a cow epidemic? About eight years ago, scientists suggested that the main source of cattle infection in England was meat and bone meal obtained from the carcasses of sheep (among which were animals sick with scrapie) and added to feed. True, bone meal was added to the cow's diet 50 years ago, and the mad cow epidemic broke out only recently. The thing is that 15 years ago in the UK the technology for processing sheep carcasses into bone meal was changed - some stages of high-temperature processing were omitted. As a result, the pathogen retained its activity and the cows became massively ill with spongiform encephalopathy. Most likely, mad cow disease is transmitted through food, and not directly from one animal to another. Therefore, in the herd sometimes only one or two cows get sick. But it is highly likely that the disease is transmitted to cow offspring - from parents to children.

Mad cow disease is an English disease, and predominantly English cows die from it. The incidence peaked in 1992, when tens of thousands of animals died in England. Measures were taken - bone meal was no longer added to the feed, sick animals were destroyed, their meat was not used. The disease has declined in England, but isolated cases of mad cow disease have been reported in other Western European countries.

Worse, in 1995, for the first time, people began to die from a new disease, very similar to Creutzfeldt-Jakob disease, in England. In contrast to the "classic" Creutzfeldt-Jakob disease, it mainly affected young people under 30 years of age. The official reason is the consumption of beef contaminated with the causative agent of mad cow disease. To date, more than 80 patients have died. However, there is no direct evidence that people became infected through meat and meat dishes.

The relatively small number of victims of spongiform encephalopathy is little consolation. Scientists fear that the number of cases may increase dramatically due to those who ate beef even before the introduction of sanitary examination at meat processing plants in Western Europe - the incubation period for mad cow disease in cows is from three to eight years. It is assumed that in humans it may be longer - up to 30 years. In some countries, those people who lived in England at the peak of the incidence of spongiform encephalopathy are under medical supervision, as they remain at risk of developing Creutzfeldt-Jakob disease.

The causative agent of mad cow disease is neither a virus nor a bacterium.

For a long time, despite the efforts of many scientific teams, it was not possible to find the causative agent of mad cow disease. Infectious diseases are caused either by viruses or microorganisms - bacteria, microbes, fungi. But in the case of mad cow disease, neither the virus nor the microbe was found. In 1982, the American biochemist Stanley Prusiner published a paper in which he first suggested that mad cow disease and other types of spongiform encephalopathy are caused by a protein molecule that folded in an unusual way. He named her "prion".

A prion is a normal protein. Each of us has it on the surface of nerve cells. In its normal state, its molecule is twisted in a certain way. For some reason, it can unwind and acquire an "incorrect" spatial configuration. "Wrong" straightened prion molecules easily stick together, protein plaques form on the nerve cell, and it dies. In place of the dead nerve cell, a void is formed - a vacuole filled with liquid. Gradually, the entire brain turns into a perforated substance, similar to a sponge, and the person or animal dies.

Where do the "wrong" prions come from? The cause of the disease (Creutzfeldt-Jakob, for example) may be a hereditary predisposition. A small mistake in the nucleotide sequence of the prion-encoding gene causes the synthesis of "incorrect" protein molecules with an "untwisted" configuration. It is likely that such abnormal prions in humans and animals with a genetic predisposition accumulate with age and eventually cause complete destruction of brain neurons.

It is believed that when at least one untwisted prion molecule enters the human or animal body, all other "normal" prions gradually begin to unfold in a similar way. How the "abnormal" prion molecule unfolds the normal one is unknown. Scientists are looking for an intermediary molecule in this chain of chemical reactions, but so far without success.

For the scientific community, all of the above still sounds implausible. Such that an ordinary molecule that does not contain genetic material transmits information to other proteins - causes an infectious disease - has not yet been observed. It was like a revolution in biological science, a revision of the basic ideas about the mechanism of infection transmission. Therefore, even despite the obvious lack of evidence for the prion model of spongiform encephalopathy, Prusiner received the Nobel Prize in 1997 for his discovery, which attracted new scientific forces and financial support to the problem of mad cow disease (Frolov Yu. Nobel Prizes 1997. Infectious protein. - " Science and Life" No. 1, 1998).

The mechanism of diseases, which, with the light hand of Prusiner, began to be called "prion", is being studied both in Russia and abroad (Zvyagina E. Protein heredity. A new chapter in genetics. - "Science and Life" No. 1, 2000). Unresolved scientific problems give rise to panic in society and provide food for the most incredible predictions. But although the study of abnormal prions is very difficult, since they are insoluble and resistant to enzymes, there is hope that soon the mysterious disease will be subject to humans. Or maybe we are in worse trouble than AIDS - not only can you not pick up a vaccine for a new infectious protein, it is also surprisingly resistant to any kind of influence, and the mechanism of transmission of the infection is not yet entirely clear.

Pathogenic prion - find and neutralize

After it was shown that spongiform encephalopathy is caused by prions, in order to make a diagnosis, it became possible not only to examine a section of certain parts of the brain for the presence of voids - vacuoles, but also to determine the causative agent of the disease itself. Prion proteins are isolated by biochemical methods and studied under an electron microscope - if their molecules are glued together, form threads, then the presence of pathogenic prions in the brain is beyond doubt. Immunological detection methods using specific antibodies to "hyped" pathogenic prions (immunohistochemical analysis of sections and immunoblotting) are more sensitive than electron microscopy. Their essence is as follows: if antibodies interact with proteins isolated from the brain, there are pathogenic prions in it, and if the reaction does not go on, there are no pathogens of spongiform encephalopathy in the brain. The biggest difficulty in determining is that the analysis is carried out exclusively on the brains of slaughtered cows. That is, it is not yet possible to conduct research on living animals.

In recent years, a method for diagnosing Keutzfeldt-Jakob disease in humans has been developed. This is also an immunoassay using antibodies to abnormal prions. The reaction is carried out by taking samples of cerebrospinal fluid or making a tissue section from the glands.

At large meat processing plants in Western Europe, immunological analysis is carried out in 10 hours, that is, during the time that the carcass is being prepared for processing. If, nevertheless, pathogenic prions are detected, the carcass is burned at a high temperature.

According to the latest data, for the complete destruction of the causative agent of mad cow disease, a temperature of at least 1000 degrees is needed! Meanwhile, any bacterium is easily destroyed by simple "boiling" in an autoclave for five minutes at 120 degrees. At first glance, the stability of "wrong" prions seems fantastic. Although from a scientific point of view, this fact can be explained. After all, the loss of activity by a protein means a change in its spatial configuration. But the pathogenic prion has already been "deployed", it has already lost its natural structure, so that more radical measures are required to neutralize its pathogenic activity than heating above 100 degrees.

How is the situation with the diagnosis of mad cow disease in our country? In 1998, by order of the Moscow government, the All-Russian Scientific Research Institute for Animal Welfare of the Ministry of Agriculture of the Russian Federation (Vladimir) received expensive equipment for analyzing sections of the brain of animals for the presence of spongiform encephalopathy. There is no such equipment yet either in the CIS countries or in most countries of the former socialist bloc. According to S. Rybakov, Doctor of Biology, the institute is currently conducting an immunological analysis of brain sections of cows obtained from different regions of Russia. It is quite lengthy - it takes 16 days to process one sample. The technique was developed jointly with the Institute of Bioorganic Chemistry. M. M. Shemyakin and Yu. A. Ovchinnikov RAS. Fortunately, no pathogenic prions have been found so far in any of the 800 samples received from 55 Russian regions.

Diagnosing a disease after the death of an animal is far from everything. It is also important to make sure that the causative agent of mad cow disease is absent in imported meat, feed and feed additives coming to us from abroad. And this is where the greatest difficulty lies. It is impossible to determine the presence of pathogenic prions in meat - the diagnosis is made exclusively by examining the brain immediately after the slaughter of the animal. Therefore, the control of meat and meat products can be reduced and is reduced only to prohibitive measures: to let them in - not to let them in.

All products, of course, are subject to mandatory border veterinary control at checkpoints, of which there are many in Russia - 291. The import of meat (beef and lamb) and meat products from England, France, Switzerland and some other countries of Western Europe to Russia was banned back in September 1996. If any meat products (for example, in the form of food for dogs and cats) nevertheless come to the Russians, then the supplier must guarantee the absence of meat of European origin in them.

Since this year, the import of pedigree cattle from many countries of Western Europe has also been banned.

According to the current rules, the brains of slaughtered animals are examined at the meat processing plant, and if pathogenic prions are not found, the supplier company issues a certificate allowing the export of meat and its processing. So we can only rely on the decency of suppliers from Western Europe and the conscientiousness of Russian expert veterinarians working there.

Our cows have diseases and worse

Again, mad cow disease is an English disease. But the British have already calmed down, they eat meat, as before, although the number of sick animals they have reached 176 thousand. But in Germany, where they heard about spongiform encephalopathy relatively recently and there were only a few cases of mad cow disease, there is a peak of hysteria: many simply refused meat. Fear has big eyes, and even in Russia people have become afraid of terrible mad cow disease: they do not eat beef, hamburgers in McDonald's restaurants and canned meat.

Are these concerns justified? Not yet. Indeed, in Russia to date, not a single case of mad cow disease has been recorded in cattle, and people with Creutzfeldt-Jakob syndrome, no more than one person per million inhabitants, which corresponds to the average population indicator, which does not depend on mad cow disease . Once again, Russian poverty served us well: there was no money for imported bone meal and compound feed, our cows and sheep ate safe silage and chewed hay, and therefore remained healthy.

According to the head of the Department of Veterinary Medicine of the Ministry of Agriculture of the Russian Federation, the chief veterinarian of Russia M. Kravchuk, we are not yet threatened with spongiform encephalopathy. And anthrax, viral rabies, brucellosis, swine fever, foot and mouth disease, trichinosis, tuberculosis, which are also dangerous for humans, alas, are widespread. So the government has something to think about even without exotic spongiform encephalopathy - the threat of these diseases to Russian animal husbandry is not imaginary, but quite real. State veterinary institutions are not funded by the state at all. 103 thousand Russian veterinarians do not receive a salary, what can we say about test systems and equipment for expensive tests. So far, the law on the budget for 2001 does not provide for financing of the Russian veterinary service.