Kira Stoletova

Some people raise broiler chickens not only on an agricultural farm, but also in the city on their own loggia. For many farmers, raising broiler birds at home is not just a hobby; for them it is both a food product and an income. Diseases of small broiler chickens are not uncommon nowadays. In order for chicken diseases to go away without complications, you need to know what symptoms of diseases can attack broilers and how to deal with various infections. Many novice poultry farmers are often lost and don’t know what to do and how to deal with chicken diseases. Diseases in chickens most often occur in very young chickens and this should be prevented.

In chickens, three stages of maturation can be noted during which the bird’s immunity has not yet strengthened: from the 1st to the 5th day after birth, from the 20th to the 25th and from the 35th day for 5 days. At this time, from the first days of life in broiler birds dangerous period when they are most vulnerable to infections. Diseases of chickens, their symptoms and treatment are the special concern of the owner. When about 1.5 months have passed after birth, you can relax a little. After this period, the immunity of day-old chicks and future laying hens settles down and the individuals grow a little. No special differences from ordinary adult laying hens and broiler birds were found. What diseases of broiler chickens are there?

Aspergillosis in chickens

Diseases of baby chickens and their treatment. Aspergillosis is fungal infection which amazes respiratory system chickens Birds develop wheezing, coughing, and uneven breathing. The pathogens enter the embryos through the shell. To avoid such a disease, you should avoid the development of fungal diseases in the litter of chickens. You should clean the areas around drinking bowls and feeders as often as possible. Aspergillosis occurs due to a fungus, but it can also be caused by other pathogenic microorganisms.

The infection can be transmitted within a few days through infected individuals and equipment. The young animals become apathetic and have no appetite. To treat this disease, you should contact a veterinarian who will prescribe necessary medications. At home, aspergillosis should be prevented from the first days of life. The poultry house must be kept clean and stocked regularly.

Salmonella

Everyone has heard about this disease, even those who are completely unfamiliar with chicken breeding. Salmonellosis is an infectious disease that can be transmitted by airborne droplets through contact between healthy birds and infected individuals. Her signs are as follows:

• The eyes are swollen and watery.
• There is no appetite at all.
• Swollen feet.
• Slow growth.

If you find signs of salmonellosis even in one individual, you should feed the entire livestock with chloramphenicol. In some cases, signs of salmonellosis may be completely absent or very vague, which makes it difficult to identify such a disease. Most often, the first manifestations occur a few days after infection. Prevention against salmonellosis should be carried out regularly. To increase immunity, broiler chickens are given mineral supplements. Sometimes a drug such as enroflon is prescribed. More details about diseases of broiler chickens and their treatment can be found in the photo or video.

Gumboro disease

Gumboro disease in broilers at home is not uncommon. Gumboro is also often called infectious bursal disease. Gumboro primarily affects young animals between 2 and 20 weeks of age. Symptoms of this disease are accompanied by damage to the bursa of Fabricius, and to a lesser extent to other lymphoid organs and the kidneys. Gumboro broiler diseases and its treatment regimen should be prescribed by a veterinarian at the first symptoms.

The infected individual should be transplanted to another room, and the chicken coop should be quarantined. Such a disease can be transmitted through one infected individual to another. Gumboro disease makes birds' immune systems vulnerable. There is no cure for this disease, but regular prevention is an effective method. Many farmers are vaccinating. For these purposes, live and inactivated vaccines are used to prevent chicken diseases and symptoms.

Dyspepsia in broiler chickens

The smallest chickens are susceptible to this disease. This disease occurs quite often among young animals. In simple terms, dyspepsia is the most common indigestion in chickens and the signs that they are sick are immediately visible. The reason for this may be poor nutrition does not contain mineral additives. With this disease, individuals lose all interest in food, they become incredibly lethargic and inactive. The main symptom of this disease is liquid droppings containing particles of undigested food. The cause of this disease can be the abuse of feed, a change in diet, as well as poor quality feed.

To prevent this disease, you should follow several rules.

• The temperature in the chicken coop should be warm at all times. A lot depends on temperature, but many novice poultry farmers forget about this.
• To combat the processes of decay in the bird’s body, the most ordinary ascorbic acid. You can also use a solution of manganese and baking soda.

These simple manipulations will help your pets fight the disease.

• Give to chickens every four hours. The food should not contain fats or complex proteins. Only a strict diet, and nothing else. Make sure that there are no grains with rot or mold in the feed. Also, babies always need clean and fresh water.
• Think carefully about the arrangement of the area where your birds eat. Under no circumstances should chickens crowd together, fighting and scattering and soiling their feed, as often happens.

Feeding will help chickens with indigestion medicinal herbs. The method is simple, but that doesn’t make it any less effective.

Broiler diseases

Why do chickens fall on their feet?

How to treat chickens sneezing and wheezing?

Bronchopneumonia

Bronchopneumonia is really something to be afraid of, as this disease is dangerous for broilers. It entails a huge variety of different diseases, in some cases even fatal. If this disease is not treated in time, then bronchopneumonia can develop into other, more serious diseases, such as pneumonia, sinusitis, rhinitis, tracheitis.

Birds with this disease will have a painfully unkempt appearance, severe weight loss, a complete lack of appetite, and a depressed state. If the bird begins to cough and mucous fluid comes out of the nose, the disease is obvious. Although this is not an infection, mass mortality of birds is possible. Unfortunately, you cannot find a special drug for treatment in pharmacies. Therefore, you should immediately make the medicine yourself.

Here is the recipe for the most common medicine

One and a half glasses of soda ash must be dissolved in three liters hot water. Next, add a solution of bleach (one glass per seven liters of water). The resulting composition must be allowed to brew, bring to a volume of twenty liters and treat the room. Birds do not go anywhere at this time. Nothing harmful will happen to them from this. To treat chickens, you can use penicillin, norfloxacin, and terramycin is also suitable. You can also use an infusion of mumiyo with honey, tinctures of ginseng and nettle. After a month, the chickens will begin to feel much better.

Hypovitaminosis

Chickens, like people, also need vitamins, and serious diseases can also occur due to a lack of microelements. These diseases are represented in large numbers. Like vitamins, hypovitaminosis is named after the letters of the Latin alphabet. If there is not enough vitamin A in the body of birds, pathology is formed in the embryo. Such birds have no appetite, growth stops, growth and development do not occur, the chicks are characterized by weakness and inactivity.

If the disease develops, there may be a lack of digestion, as well as damage to the nervous system.

Poultry farmers often notice a lack of vitamin A when night blindness occurs. To compensate for the lack of vitamin A, you can use herbal flour, carrots and greens. If there are not enough vitamins of group D in the bird's body, calcium-phosphorus metabolism is disrupted. This affects the health of their bones. The birds are weak, have diarrhea, their legs are shaking, and the birds may limp severely. At home, you need to follow proper feeding, rearing and maintenance of birds. If there is a deficiency of the vitamin, veterinarians advise adding it to the main food. In addition, walking will be very useful. Fresh air, grass, warm sun.

A lack of B vitamins causes the following problems in birds:

• Various apathies
• Gastrointestinal upset may occur
• Conjunctivitis
• Developmental delay

Green food, sprouted grains, meat, fish, and grass meal are full of this vitamin. It is a good idea to give birds complex vitamins.

Newcastle disease

Russian scientists more often call this disease “whirlwind”. Birds develop a cough, apathy, strange coordination movements, drooping wings, a sickly appearance, ruffled feathers, and weight loss. There is something else that is characteristic of this disease. Sick individuals can stagnate in the same place. Newcastle disease is considered infectious and infected individuals must be isolated from healthy chickens.

If measures are not taken, the entire population may be affected by this disease. There are currently no special medications for Newcastle disease. Sick birds should be immediately placed in a separate room to avoid spreading the infection. You can study Newcastle disease in more detail in the video.

Mycoplasmosis

Mycoplasmosis manifests itself in broilers with cough, runny nose and lacrimation. If the disease continues for a long time, pus accumulates in the eyelid area and tumors may appear. Even after treatment, recovered birds continue to be considered a source of infection and can infect healthy birds simply by being nearby. It is necessary to treat sick birds with an antibiotic called Tylosin and, in addition, it is worth using medications of the tetracycline group.

It is worth considering that your birds will not be completely cured, because mycoplasmosis still remains in the body for life. The best way out is timely vaccination of all birds and isolation of sick ones. To avoid problems with young animals in the future, you should carry out proper care and regularly clean the chicken coop. How to treat broiler chickens with mycoplasmosis can be studied in detail in the photo or video.

Marek's disease

Marek's disease affects individuals from birth to 5-6 months. At an early stage, this disease does not manifest itself in any way, but later the birds develop uncoordination, curling of the fingers, and damage to the joints of the legs. A month after the disease, the birds die. Treatment of this disease is impossible, however, the carcasses of these birds after heat treatment can be used for food.

To prevent Marek's disease, it is necessary to vaccinate in a timely manner, improve the maintenance, feeding and care of broilers. Joints can be affected due to calcium deficiency in the body. Review the diet of broiler chickens.

Chicken pox

Distinctive symptoms of chicken pox

• Strange red spots appear, which then turn into scabs.
• Individuals may experience an unpleasant odor.
• Apathy in chickens.
• Chicks have difficulty breathing and swallowing.

This disease can only be treated with initial stage when symptoms first appear, so don’t waste time. For treatment, you can use galazolin, boric acid and furatsilin solution. But there are farmers who prefer not to bother with treatment, slaughtering sick birds so that the disease does not spread to the rest of the birds.

Constipation in broilers

Constipation in young animals is quite common if the feeding regime is not followed and prohibited foods are used. The causes of constipation in young animals can be the consumption of flour feed and the lack of gravel in the feeder. Constipation can be caused by factors such as: overheating or, conversely, hypothermia of the chicks. Failure to comply with the conditions of detention can cause a lot of problems for young animals. It is very important to monitor the temperature of newborn chicks to prevent constipation.

To keep day-old chicks, a special box is used, which is covered with cloth to retain heat, leaving only a small hole for air to pass through. The first days after birth, the young are illuminated around the clock to maintain daylight and warmth. If chickens are sick and rearing becomes difficult, then their diet needs to be reconsidered; it may be deficient in potassium or other microelements.

Disease Prevention

It is easier to prevent a disease than to treat it later. Follow a few rules for caring for and keeping birds at home, then raising young animals will become an easy process.

• Cleanliness of your broilers. Birds must be clean, well-groomed, and well-fed. Feed mixtures should not stick to the paws. Feeding should be done with high-quality and fresh food. If the feed is moldy, it should not be given to broilers. For active growth, special additives can be added to feeding.
• Disinfection of the chicken coop. Don't forget that your broilers need a clear area for eating and drinking and a clean sleeping area. The feeder is changed as needed. Perches are cleaned at least once a week. It is necessary to treat the walls and floor against mold so that the individuals do not get sick, then the cultivation will be carried out according to all the rules.
• Timely quarantine of all sick chickens. This way the infection will not spread to other healthy individuals. Patient care broiler chicken must be regular.
• Vaccination of all individuals. Many vaccines are given on the first and second days after the appearance of young animals.
• Newborn chickens should be placed on a heated bedding in a room where the air contains at least 17% oxygen and the temperature is about 30-32 degrees.
• If individuals are cramped in a small room, then in such conditions there is a greater likelihood of contracting infectious diseases.
• You can feed the young animals saturated drinking water with vitamin C and glucose (ascorbic acid - 2 g/l, glucose - 50 g/l), this measure helps chickens well against diarrhea.
• To make newborn chicks feel great, you can use special feeding, about 6 times a day. Present in the diet low-fat cottage cheese, curdled milk and whey. At the same time, all these products should not mix with each other.

If you follow all these measures, raising chickens will not seem difficult to you and you will avoid many problems.

General information about the disease

Infectious bursal disease (IBD, Gumboro disease, chicken infectious bursitis) is a highly contagious viral little-studied disease of chickens 2-15 weeks of age, characterized by damage to the bursa of Fabricius, nephroso-nephritis, intramuscular hemorrhages and diarrhea. The disease, first registered in Gumboro County (Delaware, USA) in 1957, has become widespread in many countries of America, Asia, Africa, including the CIS countries. Since 1991, the disease has been registered in the Republic of Belarus.

Infectious bursal disease is common mainly in industrial poultry farms. The reason for this is considered to be the constant import of poultry. Birds 3-6 weeks of age are most often affected. The earliest outbreaks reported were in 11-day-old chicks and the latest at 84 days of age. Morbidity reaches 100%, mortality averages 20-40%. The source of infection is sick and recovered birds; the main route of spread of the virus is aerogenic. Transmission factors: poultry slaughter products, contaminated feed, water, clothing and footwear of service personnel. There are acute, subacute and chronic course of the disease. When chickens 3-6 weeks of age are infected, the disease, as a rule, is acute and subacute. When the disease occurs in chickens under 3 weeks of age that do not contain maternal antibodies, a latent (subclinical) form of the disease develops.

The economic damage caused by the disease is caused by the death of chickens, a decrease in body weight gain, and an increase in the percentage of rejection of birds and carcasses. The virus has a pronounced immunosuppressive effect, selectively affecting one of the central organs immune system birds - Fabrician bursa. As a result, the effectiveness of vaccinations against infectious laryngotracheitis, Newcastle disease, infectious bronchitis, Marek's disease decreases, and secondary infections become more active.

Most chickens infected with the infectious bursal disease virus show signs of liver damage, and during bacteriological examination of the organ, the causative agent of salmonellosis is isolated. Economic losses in farms unfavorable for IBD increase significantly due to complications: dermatitis with extensive necrotic lesions of feather follicles and skin in the back and wings, hepatitis and necrotic enteritis are often observed, and the incidence of chicken colibacillosis, Marek's disease, and eimeriosis increases. The danger of immunosuppression of this virus lies not only in the reduction of the immune response of the bird's body, but also in the fact that the antibodies produced to various antigens during and after the disease are functionally defective.

Infectious bursal disease virus

The virus was first discovered and described as an independent pathogen in 1962. According to modern classification, it belongs to the family Birnaviridae.

Sustainability.

The virus is resistant to ether, chloroform and UV irradiation. At a temperature of +56°C it lasts for 5 hours, at +60°C for 30 minutes, and at 30°C in the presence of 0.5% phenol for 1 hour. When exposed to a 0.5% formalin solution, it is inactivated in 6 hours, iodine preparations - in 2 minutes, 0.5% chloramine - in 10 minutes.

Antigenic variability and relatedness.

Two serotypes of the virus have been identified: Cu-1 (contains proteins VP-1, VP-2, VP-3, VP-4 and VPX), isolated from chickens, and 23/82 (contains proteins VP-1, VPX, VP-3 and VP- 4), isolated from turkey poults. The antigenic relatedness of these serotypes does not exceed 10-30%.

Spectrum of pathogenicity.

IN natural conditions The IBD virus affects chickens of all breeds, but White Leghorn chickens are most seriously ill. Birds are most sensitive at 3-6 weeks of age. When laying hens, as well as 1-10-day-old chickens, are infected, no symptoms of the disease are observed.

Localization of the virus.

On the 3rd day after experimental infection of 3-5 week old chickens, the virus accumulates in the bursa of Fabricius, spleen and, in lower concentrations, in the brain and blood. In one-day-old chickens, 3 days after inoculation of the virus, its high concentration was noted in the bursa of Fabricius, liver and kidneys. During experimental infection of chickens, the virus can be isolated within 10 days, but pathomorphological changes in the bursa of Fabricius persist for 10 weeks after infection.

Antigenic activity.

Already on the 21st day after infection of chickens 3-5 weeks old with the virus, virus-neutralizing antibodies (in titers up to 1:718) and precipitating antibodies (in titers up to 1:640) are detected in the blood serum. Antibodies in laying hens are transmitted transovarially to their offspring. In the blood serum of chickens obtained from immune chickens, specific antiviral antibodies are detected within 3-4 weeks after hatching.

Experimental infection.

Experimental infection is carried out on 20-30-day-old chickens by inoculating the viral material onto the conjunctiva, as well as orally. Infection is accompanied by the development in birds of clinical signs and pathological changes characteristic of this disease.

During intraperitoneal and intracerebral infection of 1-3-day-old white mice with the Becht strain, itching, ataxia, coma were noted, and in the brain - non-purulent lymphocytic encephalitis. Intracerebral infection of rats and hamsters is possible.

Infection with the turkey virus is accompanied by the formation of virus-neutralizing and precipitating antibodies in the absence of clinical signs of the disease. Pigeons, geese, quail and ducks are not susceptible to this infection.

Cultivation.

The virus is cultivated in chicken embryos (CE), free from maternal antibodies, when they are infected into the allantoic cavity or onto the chorion-allantoic membrane. The death of embryos occurs on the 3-8th day after infection.

The virus reproduces well in culture kidney cells chick embryo, causing on the 3-5th day after infection with CPD. In cultured FE fibroblasts, the virus forms plaques. The possibility of cultivating the virus in a continuous cell culture MA-104, Vero has been demonstrated.

Hemagglutinating properties.

IN normal conditions, without prior special processing, the virus does not have hemagglutinating properties.

Pathogenesis

The pathogenesis of infectious bursal disease has not been fully studied. It has been established that the target cells for virus reproduction are lymphocytes of the bursa of Fabricius of chickens. B-lymphocytes carrying class M immunoglobulins on their surface turned out to be highly sensitive to the virus. The virus has a pronounced cytopathic effect, causing necrosis of lymphoid nodules and inflammatory processes in the interstitial tissue of the bursa of Fabricius. The death of a large number of lymphoid elements causes the development of secondary immunodeficiency in recovered birds.

It has also been shown that the latent course of IBD is accompanied by the phenomena of atrophy and delymphatization of the bursa of Fabricius against the background of the absence or very weak manifestation of an inflammatory micro- and macrophage reaction in the interstitium of the organ. This form of the disease is also characterized by the development of an immunosuppressive state in chickens associated with the phenomena of B-lymphocyte necrosis.

Morphologically, lymphocyte necrosis is revealed by the phenomena of karyopyknosis, karyorrhexis, vacuolization of the cytoplasm with the formation of apoptotic bodies. Apoptosis, unlike necrosis, does not cause a pronounced inflammatory response. The phenomena of B-lymphocyte necrosis in chickens with the subclinical form of Gumboro disease are found not only in the bursa of Fabricius, but also in the spleen, cecal tonsils and peripheral blood.

The pathogenesis of the disease also depends on the influence of immune complexes circulating infected lymphocytes. Hemorrhages in skeletal muscles ah, liver and other organs are caused by damage to the walls of blood vessels. The presence of urates in the kidneys and an increase in uric acid levels in the blood indicate kidney damage. Increased activity of lactate dehydrogenase and glutamate oxalate transaminase in the blood serum confirms liver damage.

Clinical signs

Incubation period infectious bursal disease short. During experimental infection of chickens clinical signs appear after 2-3 days. The disease can occur acutely, subacutely and latently, depending on the immune status of the livestock. In susceptible groups, as a rule, the incidence rate can reach 100%. In acute cases, the disease usually lasts 4-8 days.

The characteristic symptom of IBD is diarrhea, accompanied by the discharge of watery, whitish-yellow droppings. In sick chickens, depression is observed, and in a later stage - trembling of the head and neck, coma. Morbidity and mortality increase rapidly and reach a maximum on the 3-4th day of illness. The distinctive signs of the disease are suddenness and high incidence, rapid recovery of the livestock. Mortality can reach 20-40%. In subsequent chick hatchings, occasional outbreaks are less severe and often go unnoticed.

IN recent years The number of outbreaks of latent Gumboro disease has increased significantly. In this case, infection of chickens leads to the development of an immunodeficiency state in birds due to necrosis of B-lymphocytes. As a result, the effectiveness of vaccinations against a number of viral diseases decreases. There have been outbreaks of chronic respiratory diseases leading to the development of swollen head syndrome. Saprophytic microflora are often isolated from the affected tissues: cocci, pseudomonads, etc.

Pathomorphological changes

The corpses of dead chickens are usually well fed. At autopsy, signs of dehydration and anemia are noted. The goiter is empty. Changes in the bursa of Fabricius are pronounced and very natural, lesions of which are also found in cases of asymptomatic infection. The organ is enlarged 1.5-2.5 times. The serous membrane is gray-yellow. The mucous membrane is swollen, reddened, with hemorrhages. In the lumen of the bursa between the folds of the mucous membrane, serous-fibrinous exudate is found, in severe cases - hemorrhagic exudate and cheese-like fibrin clots. Atrophy of the thymus, aplasia of the red bone marrow, esophageal and cecal tonsils, and serous-hemorrhagic inflammation of the spleen are noted.

Dotted and spotty hemorrhages are found in the pectoral muscles, on the medial side of the thighs and wings. The liver may be slightly enlarged, with marks from the ribs visible on the surface. The kidneys are enlarged, light gray to dark brown in color, with a clear pattern of tubules and ureters filled with urate. In addition, catarrhal enteritis and hemorrhages in the mucous membrane of the glandular stomach and in the cecal tonsils are noted.

Histological examination of the Bursa of Fabricius in the initial period notes necrosis of lymphocytes, and then of the reticular stroma with the formation of necrotic detritus in the majority of lymphoid nodules. Atrophied nodules, glandular structures and cysts may be detected. In the thymus at the onset of the disease, delymphotization of the cortical layer, depletion of lymphocytes in the medullary zone with a simultaneous increase in the number and size of Hassal's bodies and hyperplasia are observed. reticular cells. In the red bone marrow, a decrease in the total number of cellular elements and an activation of the macrophage reaction are detected. In the spleen of sick chickens, necrosis of individual lymphocytes in the periarterial couplings (T-lymphocytes) and lymphoid nodules (B-lymphocytes), hyperemia of red pulp vessels, micro- and macrophage reactions are detected. Similar changes are found in the esophageal and cecal tonsils.

1. Serous-hemorrhagic or fibrinous-necrotic inflammation of the bursa of Fabricius.

2. Serous-hemorrhagic inflammation of the spleen.

3. Atrophy of the thymus, bone marrow, esophageal and cecal tonsils.

4. Dotted and spotty hemorrhages in the muscles of the thighs and wings (on the medial side), in the serous integument.

5. Granular dystrophy of the liver and kidneys, overflow of the ureters with urates.

6. Serous-fibrinous pericarditis, aerosacculitis, pleuroperitonitis, perihepatitis (complication).

7. Histo: total necrosis of lymphocytes in the bursa of Fabricius, thymus and spleen, serous-inflammatory edema of interstitial tissue, infiltration with histiocytes and pseudoeosinophils in acute and subacute cases; atrophy and depletion of lymphocytes in the bursa of Fabricius, thymus, spleen, esophageal and cecal tonsils, absence of micro- and macrophage reaction during the latent course of the disease.

Diagnostics

Diagnosis of infectious bursal disease is carried out taking into account epidemiological data, clinical symptoms, pathomorphological changes, as well as a set of laboratory tests. It should be taken into account that this disease It is difficult to detect, is masked by other infections, and only in the case of a typical course is it diagnosed based on clinical signs and postmortem findings. Therefore, at an early stage of the disease and during a latent course, laboratory tests are necessary.

Laboratory diagnostics of IBD includes the isolation of the virus in developing SPF chicken embryos (CE) or in the culture of chicken embryo fibroblasts (FEC), its identification in the neutralization reaction (RN) and the immunodiffusion reaction (IDR), performing a bioassay on sensitive chickens, identifying the viral antigen by reaction immunofluorescence (RIF), indirect hemagglutination inhibition reaction (IHRA), latex agglutination reaction (RAL), electron microscopy, counter immunoelectrophoresis reaction, as well as detection of specific antibodies in PH, RID, VIEF, indirect hemagglutination reaction (IRHA), enzyme-linked immunosorbent assay (ELISA) ) and conducting histological studies.

Selection of pathological material.

From 5-10 corpses of fallen or killed from diagnostic purpose Bursa Fabricius, spleen, liver, and kidneys are taken from sick chickens. Organs are placed in clean, dry, sterile penicillin vials. The material is placed in a thermos with ice and stored until sent to the laboratory.

For serological testing, paired samples (25-30) of blood serum from sick birds are sent, taken at an interval of 21 days. The resulting serums are placed in clean, dry, sterile penicillin vials under rubber stoppers and placed in a thermos with ice.

Material sent to the laboratory is supplied with a covering letter. In the laboratory, the material is stored frozen or filled with a 50% aqueous solution of glycerol.

In the laboratory, pieces of pathological material are homogenized in 0.01 M phosphate-buffered saline (pH = 7.2) or meat-peptone broth in a ratio of 1:10, frozen and thawed three times, followed by centrifugation for 30 minutes at 5000 rpm. 100 U/ml penicillin and 0.1 mg/ml streptomycin are added to the supernatant liquid, incubated for 12 hours at 4°C, and checked for sterility.

Virus isolation in chicken embryos.

To isolate and titrate the pathogen, use SPF embryos of 9 days of age in an amount of at least 10. The prepared homogenate in an amount of 0.2 ml is applied to the chorion-allantoic membrane or into the allantoic cavity of the embryo. 5-10 uninfected embryos are left in the control.

The death of chicken embryos during the first day is considered nonspecific. If there is a virus in the test material, death of TBE occurs within 3-5 days. Dead embryos are dissected to detect specific pathological changes. The chorion-allantoic membrane (CHM) is edematous. Retarded growth and development, the presence of serous-hemorrhagic edema of the skin in the head, neck, limbs and abdominal wall are noted. In the lungs, congestive hyperemia and pulmonary edema, necrotic nephrosis, granular myocardial degeneration, enlarged liver and spleen are detected. The bursa of Fabricius is usually not affected.

From dead embryos with growth retardation and pronounced pathomorphological changes, allantoic fluid and CAO are collected into sterile tubes and checked for sterility by inoculating 0.2 ml of fluid with MPA and MPB. Whether the isolated agent belongs to the Gumboro disease virus is determined by setting the RN and RID.

Infection of cell cultures.

To isolate the virus, 24-48-hour cultures of EC fibroblasts are used. The timing of the onset of CPE depends on the dose of the virus and the number of passages. During its initial isolation, specific changes are observed after 2-3 passages of virus-containing material. CPD manifests itself 48-72 hours after infection of the cell culture and is characterized by vacuolization and rounding of cells, the phenomena of karyopyknosis and karyolysis. The specificity of cytopathic changes is confirmed by staging RN.

Bioassay on chickens.

For infection, 21-day-old SPF chickens or 35-40-day-old birds from a commercial flock with well-developed Fabrician bursae are used. To do this, from the total number of chickens intended for bioassay, 5-10 heads are randomly caught, killed, individual absolute body weights and bursae are determined, and the bursal index (BI) is derived using the formula:

where Ms is the mass of the bursa of Fabricius (g),

BW – body weight of birds

Chickens in the flock of which the bursa index is 4 or higher are used to perform a bioassay. Infection of chickens with an index below 4 does not cause an acute course of the disease. Determination of the bursal index has important diagnostic value, since in infected chickens there is a decrease in this indicator by 3-9 times.

Before infection, blood serum samples are taken from 10-20 birds selected for bioassay for serological testing (RID, RN, RNGA, ELISA) for the presence of antibodies to the Gumboro disease virus. The test material is administered intranasally in a dose of 0.5 ml.

The bioassay is considered positive if the infected chickens develop characteristic clinical signs of the disease after 2-5 days (diarrhea, dehydration, general depression, dirty gray feathers). At autopsy of sick and recovered birds, characteristic pathological changes are noted.

15 days after infection, the surviving chickens undergo a repeat serological test of the blood serum to isolate a diagnostic (4-fold) increase in the titer of specific antibodies and then they are killed in order to establish pathological changes.

Neutralization reaction.

It is used to identify the Gumboro disease virus and to detect specific antiviral antibodies. The reaction is carried out on chicken embryos. It uses normal and specific hyperimmune serum, and the virus isolated on BE is used as an antigen. Before the reaction, the serum is inactivated in a water bath at +56°C (30 min), after which penicillin (1000 U/ml) and streptomycin (1 mg/ml) are added.

Hyperimmune and normal serum are poured into sterile test tubes using dry sterile pipettes of 0.5 ml. Then each of them contains 0.5 ml of the test antigen in dilutions from 10 -1 to 10 -9. After shaking, the tubes are kept at +37°C for 30 minutes. The resulting mixtures in a dose of 0.2 ml are injected into the allantoic cavity of 9-day-old embryos. Ovoscopy is performed twice a day. Dead embryos are dissected. On the 10th day, all embryos are dissected to identify specific changes in organs and tissues. The pH results are expressed by the neutralization index, which is determined according to the generally accepted method. The reaction is considered positive if the difference in titers with normal and hyperimmune sera is 2 lg or more.

Immunofluorescence reaction.

It is a rapid diagnostic method, as it allows a diagnosis to be made within 2-3 hours from the moment of delivery of the pathological material.

Imprint smears (at least 3) are prepared from the bursa of Fabricius of dead birds or killed for diagnostic purposes on thin, dry, fat-free glass slides, fixed for 10-20 minutes in acetone, washed twice in two shifts with 0.01 M phosphate-buffered saline ( pH=7.2-7.4), then dried and painted according to the generally accepted method. Control fingerprint smears are prepared from the bursa of healthy chickens.

The reaction is considered positive if at least 3 lymphocytes with a specific bright green glow of the antigen in the cytoplasm (small granules or a diffuse halo around the nucleus) are detected on all preparations.

Except strokes-prints For RIF, cryosections of the bursa of Fabricius can be examined. To do this, the organ is frozen in petroleum ether, cooled to minus 76°C in a mixture of acetone and dry ice. They are then frozen to the microtome block. Sections are prepared with a thickness of 4-5 microns.

Inhibition reaction of indirect hemagglutination.

This technique can be used to indicate the viral antigen in pathological material, as well as to identify the virus isolated in EC and CC.

From pathological material from sick and dead birds, chorion-allantoic membranes of dead birds after TBE infection, a homogenate is prepared in a sterile 0.85% sodium chloride solution (pH = 7.2-7.4) in a 1:1 ratio. After freezing and thawing three times, the homogenate is centrifuged at 5000 rpm. within 25 minutes. The supernatant liquid is drained for testing in the RTNGA. Allantoic fluid samples are used in their native form after centrifugation for 15-20 minutes at 3000 rpm. Suspensions from control birds and EC are prepared in the same way. In addition, specific immune serum to the Gumboro disease virus and a positive erythrocyte antigen from the BelNIIEV diagnostic kit are used for serological diagnosis of this disease in the RNGA.

RTNHA is performed using the micromethod using a Takachi microtiter. In this case, a twofold dilution of the test material from 1:2 to 1:128 is prepared in the first row of wells of the panel in a volume of 0.025 ml. To do this, add 0.025 ml of 0.85% sodium chloride solution containing 0.5% glycerol to each well. Add 0.025 ml of the test material to the first well and, while mixing, transfer 0.025 ml to another well, etc. (up to a dilution of 1:128. In the second row, a virus-free suspension is prepared in the same way. To each dilution of both rows, add 0.025 ml of immune serum, diluted 1-2 times less than its limiting titer in the RNGA. The panel with the mixtures is shaken and placed in a thermostat for 60 minutes at 37°C. The reaction is taken into account after the erythrocytes have settled.

The reaction is considered positive if, in the first row with the test material, agglutination is inhibited in the first two or three wells, provided that the second row is completely agglutinated.

The latex agglutination test is used to indicate viral antigen. Pathological material is homogenized in 0.01 M phosphate-buffered saline (pH = 7.2) in a 1:1 ratio, frozen and thawed three times. The virus-containing suspension is centrifuged at 3000 rpm. 30 minutes. The supernatant liquid is drained to perform RAL.

Hyperimmune serum to the IBD virus is obtained by immunizing chickens with an inactivated oil-emulsion vaccine. The gamma globulin fraction is isolated from the serum by precipitation with ammonium sulfate.

Latex antibody diagnosticum is prepared by mixing a latex suspension (2% particle concentration) with an equal volume of gamma globulin fraction in an appropriate buffer solution. The mixture is incubated for 16-18 hours at 4°C, then centrifuged for 30 minutes at 3000 rpm. and wash the precipitate three times with a buffer solution. The sensitized latex is resuspended in the same solution to a final particle concentration (0.5-2.0%) and 0.05% sodium azide is added. The finished diagnosticum is stored in the refrigerator at 4°C.

The latex agglutination reaction is performed on a glass slide. Apply 25 µl of antigen diluted from 1:2 to 1:512 with a dispenser, add 25 µl of latex antibody diagnosticum and mix, turning smoothly. The results of the reaction are taken into account after 2-5 minutes using a three-point system: sharply positive reaction (+++) - clear agglutination, large flakes in a clear liquid; positive (++) – agglutination is visible, but the background is not completely cleared; negative (-) – cloudy homogeneous liquid. The control is a mixture of latex with a 0.85% sodium chloride solution (diagnosticum control), with positive and negative antigens (positive and negative control).

Immunodiffusion reaction (IDR).

This technique is widely used both for the purpose of indicating and identifying the Gumboro disease virus and for determining specific antibodies. When diagnosing RID, kits for diagnosing Gumboro disease VNIVIP or ARRIAH are used.

In the laboratory, the pathological material is weighed, an equivalent amount of 0.85% sodium chloride solution or distilled water is added, homogenized, frozen and centrifuged at 3000 rpm. within 10 minutes. The supernatant is drained and used for RID testing.

To set up the reaction, use 1.25% agar with 8% sodium chloride and 0.5% phenol. Petri dishes are filled 24-72 hours before use, pre-dissolving the agar by steaming and pouring 20 ml into the dishes. The agar layer should be at least 3 mm.

To study samples, a linear order of wells is used. Make 3 rows of vertical holes with a diameter of 5 mm, at a distance of 5 mm. Agar plugs are removed with a needle or tweezers.

Each sample of the tested diagnostic serum is diluted with physiological solution (0.85% sodium chloride solution), first 1:2, and then sequentially in twofold steps up to 1:256.

Before use, dry reference antigens are dissolved with distilled water or 0.85% sodium chloride solution to a volume of 0.5 ml. Dry diagnostic sera are first diluted with distilled water in the volume indicated on the label, and then a series of successive two-fold dilutions are prepared.

When examining pathological materials, positive serum is added to the central row of wells in a working dilution of 0.05 ml, and normal, positive (1 well each) and test antigens in a volume of 0.05 ml are added to the peripheral rows. When studying bird blood sera, a positive antigen in a working dilution in a volume of 0.05 ml is added to the central row of wells, and normal, positive (1 well each) and test sera in dilutions of 0.05 ml are added to the peripheral rows.

After filling the wells, the Petri dishes are placed in a thermostat at a temperature of 37°C. The reaction is recorded 24 and 48 hours after the reaction is performed. The cups are viewed against a dark background in a directed beam of light. The reaction is taken into account only if there are precipitation lines between the positive antigen and the positive serum in the control and the absence of precipitation lines between the positive antigen and normal chicken serum, as well as positive serum and normal antigen.

For positive result when examining pathological materials for the detection of viral antigen, the formation of 1-2 lines of precipitation between the wells with the test material and positive serum is taken, and when antiviral antibodies are detected, the presence of precipitation lines between the wells with the test serum and the positive antigen.

Counter immunoelectrophoresis is used both for the purpose of indicating and identifying the Gumboro disease virus and for determining specific antibodies. The essence of the technique is the simultaneous movement of protein molecules with different electrophoretic mobility in agar with the formation of a precipitate from homologous antigens and antibodies. To set up VIEF, use devices PEF-3, EF-2 or similar brands and a set of diagnostic kits for setting up RID. The reaction is carried out on glass plates coated with a 1% agar solution in 0.85 M veronal-medinal buffer (pH = 8.6). Wells with a diameter of 4 mm are cut out in the agar, at a distance of 4 mm from each other.

A positive antigen and test sera are added to the wells at the anode, and a positive antigen and the pathological material to be tested are added to the wells at the cathode. Electrophoresis is carried out for 1.5 hours at a current of 4 mA/cm. Negative antigen and serum serve as controls

The plates are viewed in oblique light against a dark background. The reaction is considered positive if one or two lines of precipitation form between the wells containing the test antigen or serum and the positive serum or antigen.

The indirect hemagglutination reaction is based on the ability of antibodies to agglutinate red blood cells sensitized with a specific antigen. RNGA can be used both for serological diagnosis and for studying the serological epizootology of Gumboro disease.

When staging RNGA, erythrocyte antigen and control (positive and negative) sera from the BelNIIEV diagnostic kit are used to diagnose infectious bursitis (Gumboro disease).

The reaction is carried out using the micromethod in a Takachi microtitrator. In the wells of horizontal rows of plexiglass plates, successive twofold dilutions (from 1:2 to 1:1024) are prepared from the test plates in a 0.85% sodium chloride solution containing 1% glycerol, in a volume of 0.025 ml (1 drop). Add 0.025 ml of test serum to the first wells, mix, and transfer 0.025 ml of the mixture to the next wells, etc. From the last wells, after mixing, 0.025 ml of the contents are removed into the disinfectant solution. Add 0.025 ml of a 1% suspension of virus-sensitized erythrocytes to each well with an appropriate serum dilution and shake.

At the same time prepare: control of erythrocyte antigen for spontaneous agglutination (0.025 ml of negative serum and 0.025 ml of erythrocyte antigen are added to 2-3 wells); positive control (0.025 ml of positive serum and 0.025 ml of erythrocyte antigen are added to 2-3 wells); negative control (0.025 ml of negative serum and 0.025 ml of erythrocyte antigen are added to 2-3 wells).

Plexiglas plates with components are placed in a thermostat for 1-1.5 hours at t=37°C until the red blood cells settle.

The reaction is recorded only in the case when the control of the erythrocyte antigen for spontaneous agglutination and with obviously negative serum is negative, and the control with positive serum is positive.

A positive reaction is characterized by the appearance of a sediment of red blood cells in the form of an umbrella at the bottom of the well. A negative reaction is manifested by the precipitation of red blood cells in the form of a point or ring with smooth edges.

When agglutination of erythrocytes with test sera in a dilution of 1:8 and above, RNGA is considered positive, and 1:4 and below is considered negative.

Enzyme immunoassay is widely used as the most specific test for detecting specific antiviral antibodies in the blood serum of immune birds. To perform this reaction, a set of ARRIAH diagnostic kits is used to determine antibodies to the infectious bursal disease virus (Gumboro disease) by ELISA. The essence of this technique is to detect the antigen-antibody complex on the surface of the wells of a polystyrene plate. The resulting specific complex interacts with the anti-species immunoperoxidase conjugate against chicken Ig G and causes decomposition of the substrate, staining the contents of the wells of the plate.

Before preparing working solutions, the kit and components are kept for 30 minutes. at room temperature (18-20°C).

Solution No. 1. Dissolve 0.97 g of tris (hydroxymethyl) aminomethane (bottle 5.1), 6.61 g of tris (hydroxymethyl) aminomethane hydrochloride (bottle 5.2) and 11.7 g of sodium chloride (bottle 5.3) in 1000 cm 3 of distilled water. After measuring the pH of the resulting solution (which should be between 7.4-7.6), 1.0 ml of Tween-20 liquid detergent (bottle 7) is added to it. This solution is used for diluting control sera, test samples, anti-species conjugate and inter-stage washing.

Solution No. 2. To prepare the substrate buffer, 5.37 g of sodium dihydrogen phosphate (bottle 6.1) is dissolved in 50 ml of distilled water. Bottle contents 6.2 (1.51 g citric acid) is also dissolved in 50 ml of distilled water. Then mix 224.3 ml of sodium dihydrogen phosphate solution with 25.7 ml of citric acid solution, add 50 ml of distilled water. The resulting solution should have pH=4.9-5.0. If necessary, add acidic or alkaline components.

Solution No. 3. 1.0 cm 3 of whole lyophilized positive serum against Gumboro disease (bottle 1) is dissolved in 0.5 ml of solution No. 1. The resulting solution can be stored for 3 days at 4 °C.

Solution No. 4. 1.0 cm 3 of whole lyophilized negative serum against Gumboro disease (bottle 1) is dissolved in 0.5 ml of solution No. 1. The resulting solution can be stored for 3 days at 4 °C.

Solution No. 5 The contents of solution 4 with the anti-species conjugate are dissolved in 0.5 ml of solution No. 1. To obtain a working dilution of 1:200, 0.05 cm 3 per 10.0 ml of solution No. 1 (per 1 tablet) is taken from this bottle. Prepare before use. Cannot be stored.

Solution No. 6. One tablet of hydroperite is dissolved in 20 ml of distilled water. Store in a place protected from light at 4°C for no more than 20 days.

Solution No. 7. Substrate-indicator mixture. A tablet of orthophenylenediamine (substrate) is dissolved in 20 ml of solution No. 2, shaken until completely dissolved and 0.4 ml of solution No. 6 is added for every 20 ml of this solution. Cannot be stored.

A plate is taken from the kit, in the wells of which the purified antigen of the Gumboro disease virus is adsorbed. Samples of the blood serum samples under study are diluted 1:100 with solution No. 1. For this purpose, add 1 ml of solution No. 1 to 0.01 ml of serum.

0.1 ml of solution No. 1 is added to the wells of rows B1-12...H1-12, and 0.2 ml of diluted serum samples is added to wells A2-11 and titration is carried out in vertical rows, 1:100 to 1:12800 . Dilutions of 1:100 control (negative and positive) sera are added to wells A1 and A12 and titration is also carried out in vertical rows. From the last wells H1 and H12, 0.1 ml is removed.

The tablet is carefully shaken, covered with a lid and transferred to a thermostat for 2 hours at a temperature of 37°C. Then the wells of the plate are emptied of the contents by shaking and washed three times with solution No. 1. Add 0.1 ml of solution No. 5 to all wells of the plate, place in a thermostat for 1 hour, and wash three times with solution No. 1. Then 0.1 ml of solution No. 1 is added to all wells. Leave at room temperature for 10 minutes. The reaction is stopped by adding 0.05 ml of a 0.5% sulfuric acid solution to each well.

Detection of specific antibodies in blood sera can be carried out without titration of the test sera. In this case, 1 ml of blood serum at a dilution of 1:400 is added to all wells of the A2-12...H2-12 plate. Positive control sera are added to wells A1 and B1 of the vertical row, and negative control sera at a dilution of 1:400 are added to the next two C1 and D1, and wells E1 and F1 serve as a conjugate control - 1 ml of solution No. 1 is added to them.

The results of the analysis are recorded after stopping the reaction in one of the following ways: visually - by the intensity of coloring of the contents or instrumentally - using a spectrophotometer with a vertical beam at a wavelength of 492 nm. During visual recording, the color of the contents of the wells of the test sample plate is compared with the color of the wells of the control samples. The titer of the test serum is taken to be its last dilution, at which a color visible to the eye is observed, more intense than that of the negative sample. Samples with a dilution of 1:400 and higher are considered positive. When assessing the results without serum titrations, the reaction is assessed according to the principle - “yes” - a positive reaction (specific antibodies are present in the sample) or “no” - negative reaction(there are no specific antibodies in the sample).

Instrumental photometric recording makes it possible to quantify titers of specific antibodies by determining extinction. The final dilution of the test serum is considered to be its last dilution, in which the extinction exceeds the control by 2.0-2.1 times.

Histological examination.

From the corpses of dead or forcedly killed birds, pieces of the bursa of Fabricius, thymus, spleen, liver, kidneys, heart, and skeletal muscles are taken. Organs with labels are placed in a glass container and filled with a 10% formaldehyde solution for fixation. The volume of fixing liquid must exceed the volume of the pieces being fixed by at least 10 times. Fixation is carried out at room temperature (18-20°C) for 24-48 hours. The criteria for completing fixation are: uniform compaction of organs and the same color on the surface and on the section. Fixed pieces with labels are placed in a container with a fixative liquid or in plastic bags with cotton wool soaked in a fixative and sent to the laboratory with a covering letter.

In the laboratory, the material is compacted by freezing with liquid nitrogen or on semiconductor stages, as well as by embedding in paraffin. Histological sections are obtained on freezing or sleigh microtomes and stained with hematoxylin-eosin. Stained sections are examined under a light microscope.

In the bursa of Fabricius, at the onset of the disease, massive necrosis of lymphocytes and then reticular cells is noted with the formation of necrotic detritus in place of the majority of lymphoid nodules. Lymphoid nodules are replaced by glandular structures. At the same time, a local immune reaction is detected, in which, along with necrosis of lymphoid nodules, extensive lymphocytic proliferations are formed with the formation of small lymphoid nodules in them. Edema, infiltration of pseudoeosinophils and histiocytes, and hyperplasia of reticular cells are observed in the interstitium.

It should be taken into account that during the latent course of the disease, atrophy and delymphatization of lymphoid nodules develop due to necrosis of lymphocytes.

In the thymus during the acute course of Gumboro disease, necrosis of lymphocytes is found in the cortical, less often in the medulla, and an increase in the number and size of Hassall's bodies. Inflammatory hyperemia of blood vessels, micro- and macrophage reactions, and hyperplasia of reticular cells are noted. Subacute and latent course is accompanied by early accidental involution of the organ.

In the spleen at the onset of the disease, hyperemia of red pulp vessels, macrophage infiltration, necrosis of lymphocytes in periarterial couplings (T lymphocytes) and lymphoid nodules (B lymphocytes) are detected. At a later date, pronounced plasmatization of the organ is revealed.

In the kidneys during the acute course of Gumboro disease, vascular hyperemia, vacuolar degeneration and necrosis of epithelial cells, and destruction of convoluted tubules are recorded. In some areas, extensive lymphocytic-histiocytic proliferations are detected. The chronic course is characterized by the phenomena of nephrosclerosis, the accumulation of urate crystals in the lumens of the tubules.

In the liver, hyperemia of the central veins of the lobules, focal hemorrhages, granular and fatty degeneration of hepatocytes, as well as accumulations of lymphocytes, macrophages (less often microphages) in the interstitium of the organ are noted.

In skeletal and cardiac muscles, hyperemia of blood vessels and sometimes granular degeneration are detected. At chronic course Between the muscle fibers, weakly expressed lymphocytic-histiocytic proliferations are detected.

Differential diagnosis

At differential diagnosis gumboro disease highest value has an exclusion of tumor diseases of birds, adenovirus infection, reduced egg production syndrome (SSY-76), infectious bronchitis, influenza and Newcastle disease, as well as streptococcosis, pasteurellosis, colibacillosis, eimeriosis, prostagonymosis, hypovitaminosis A, nutritional dystrophy and radiotoxicosis.

Marek's disease affects chickens from 4 to 30 weeks of age, occurring in the form of enzootics, less often epizootics. Chickens get sick more often, and cockerels less often. During life, sick birds exhibit impaired coordination of movement, paresis of the legs and wings. Gray eyes, hyperplasia of feather follicles, weakness, and progressive emaciation are noted. In dead chickens, diffuse or focal sebaceous neoplasms are found in the bursa of Fabricius, spleen, liver, intestinal wall, and thickening of the sciatic nerves is noted. During histological examination, atrophied lymphoid nodules are found in the Bursa of Fabricius, replaced by cysts or glands, and a growth of interfollicular connective tissue. The development of tumors in internal organs, characterized by the proliferation of lymphoblasts, histiocytes and plasma cells, is often noted.

Pathological diagnosis:

1. Growth of sebaceous tumor tissue in the spleen, liver, kidneys, ovary, testes, heart, lungs, wall of the glandular stomach and intestines, thymus, bursa of Fabricius or their atrophy.

2. Hyperplasia of feather follicles.

3. Gray eyes, pupil deformation.

4. Neuritis with sharp thickening in sciatic nerves and in the nerves of the brachial and lumbar plexuses.

5. Histo: proliferation of lymphoblasts, histiocytes, plasma cells and reticulocytes in tumor nodes; atrophy of the lymphoid nodules of the bursa of Fabricius, their replacement with cysts, glands, growth of internodular connective tissue.

Additional laboratory tests are carried out: a bioassay is performed on chickens, blood serum is examined in RID, and histopathological examination of affected organs and tissues is carried out.

Chicken leukosis usually occurs in the form of enzootics. Birds older than 8-12 months of age become ill. Sick chickens experience lethargy, diarrhea, and exhaustion. When autopsying dead birds, diffuse or focal fat-like growths of tumor tissue are found in the bursa of Fabricius, spleen, liver, kidneys, heart and other organs.

Histological examination reveals proliferation of tumor cells in the bursa, forming a tumor focus, the infiltrative growth of which leads to destruction of the organ. In the liver, kidneys, and heart, the growth of immature lymphoid cells is detected.

Pathological diagnosis:

1. Growth (diffuse or in the form of nodes) of sebaceous tumor tissue in the bursa of Fabricius.

2. Tumor-like sebaceous nodes in the spleen, liver, kidneys, wall of the glandular stomach and small intestine, heart, lungs

3. Exhaustion and general anemia.

4. Histo: proliferation of immature lymphoid cells in tumor nodes.

Laboratory diagnosis is based on histological examination of the pathological material, staging of RSK and RNGA.

Rous sarcoma is accompanied by progressive cachexia, decreased egg production, diarrhea, drooping abdomen, anemic skin and visible mucous membranes. At autopsy, numerous tumor nodes are revealed in the skin, skeletal muscles, as well as in the spleen, intestinal mesentery, liver, kidneys, and ovary. In the presence of a large number of tumor metastases in the internal organs, atrophy of the lymphoid nodules of the bursa of Fabricius and delymphatization are observed. There is a 2-3 times thickening of the internodular connective tissue septa, their hyperemia and swelling.

Pathological diagnosis:

1. Tumor nodes in the skin, skeletal muscles, spleen, liver, kidneys, intestinal mesentery, ovary.

2. Exhaustion, general anemia.

3. Histo: proliferation of poorly differentiated polymorphic cells in tumor nodes, atrophy and necrosis of elements of the parenchyma of internal organs; atrophy and delymphotization of lymphoid nodules, hyperemia and serous edema of the interstitium in the bursa of Fabricius.

To confirm the diagnosis, a virological study is performed.

Adenoviral infection mainly affects young animals 2-3 months of age. The pathogen is highly contagious. The disease is accompanied by drowsiness and anemia of the mucous membranes. In dead or forcedly killed chickens, hemorrhages in the muscles, enlargement of the liver with bile overflowing the gallbladder are found. The kidneys are swollen, with hemorrhages.

Histological examination reveals numerous micronecrosis, hemorrhages (under the capsule), interstitial lymphocytic-histiocytic proliferations in the liver, and eosinophilic and basophilic inclusions in the nuclei of hepatocytes. In the Bursa of Fabricius, atrophy of lymphoid nodules, depletion of lymphocytes in the medulla, interstitial edema, and thinning of the folds of the mucous membrane are detected.

Pathological diagnosis:

1. Alterative hepatitis, bile overflow of the gallbladder.

2. Acute catarrhal-hemorrhagic enteritis.

3. Enlarged spleen.

4. Hemorrhages in skeletal muscles, liver, kidneys, and in the wall of the gallbladder.

5. General anemia, exhaustion.

6. Histo: liver - intranuclear basophilic and eosinophilic inclusions, vacuolar degeneration and necrosis of hepatocytes, hemorrhages, interstitial lymphocytic-histiocytic proliferations; pancreas – pancreatitis with the presence of intranuclear polychromatophilic inclusions in the cells of the glandular tissue; bursa of Fabricius - atrophy of lymphoid nodules, depletion of lymphocytes in the medulla, interstitial edema, thinning of the folds of the mucous membrane; spleen – serous splenitis with intranuclear inclusion bodies in reticulocytes.

Additional laboratory tests are carried out: virus isolation on chicken embryos.

Reduced egg production syndrome (RES-76) affects chickens of all breeds during the laying period. The virus is capable of persisting in the body of birds and becoming more active under stress caused by the onset of oviposition. The disease is accompanied by ovarianitis and catarrhal salpingitis. Histological examination of the uterine section of the oviduct in epithelial cells Basophilic intranuclear inclusions are detected. Changes in the bursa of Fabricius are not pathognomonic.

Pathological diagnosis:

1. Ovariitis, hemorrhages in the ovary.

2. Catarrhal, catarrhal-hemorrhagic salpingitis.

3. Reduction in shell thickness (by 30-60%) and its depigmentation (in eggs of colored breeds) to a faint yellow or white color.

4. Gangrenous dermatitis (complication).

The decrease in egg production in chickens is taken into account, and early and retrospective diagnostics are used using RZGA.

Infectious bronchitis is characterized by damage respiratory tract(respiratory form) in chickens and oviduct in adult birds with decreased egg production (reproductive form). At autopsy, dead and forcedly killed chickens show acute catarrh upper respiratory tract, serous-fibrinous aerosacculitis, in chickens - atrophy of the ovary and oviduct, deformation of the egg follicles. Histological examination also reveals granular degeneration of the epithelium of the convoluted tubules of the kidneys.

The nephroso-nephritis form of infectious bronchitis is recorded in chickens 3-9 weeks of age. In a sick bird, watery diarrhea, depression, and prostration are observed. Presenters pathological processes, detected at autopsy and histological examination: granular and fatty degeneration kidneys and accumulation of urates in the renal tubules and ureters, fatty degeneration (small-droplet) of the liver, pseudoeosinophilic reaction in the interstitium of these organs.

Pathological diagnosis:

respiratory form

1. Serous-catarrhal rhinitis, conjunctivitis.

2. Serous-catarrhal fibrinous tracheitis and bronchitis.

3. Focal catarrhal or catarrhal-fibrinous pneumonia.

4. Serous-fibrinous aerosacculitis.

5. Exhaustion.

nephroso-nephritis form

1. Nephroso-nephritis, accumulation of urates in the ureters.

2. Overflow of the rectum and cloaca with whitish feces mixed with urates.

3. Visceral uric acid diathesis.

reproductive form

1. Atrophy of the ovary and oviduct.

2. Cyst of the ovary with the presence of a caseous-fibrinous mass in its lumen.

3. Yolk peritonitis.

Additional research is carried out: isolating the virus on EC and CC, placing a bioassay on 9-day-old embryos (in which, already on the 5-6th day after infection of the embryos with the virus, a “dwarfism effect” is noted - a growth retardation of 3-4 times compared with control), as well as serological reactions - RN, RID, RNGA.

Bird flu affects chickens of all ages and is acute. Morbidity and mortality rates can reach 100%. The disease is characterized by nervous phenomena, swelling of the head, cessation of egg production, diarrhea, cyanosis of the comb and earrings followed by their necrosis. At autopsy, numerous pinpoint and spotty hemorrhages are found on the mucous membranes and serous tissues, a hemorrhagic ring in the mucous membrane of the glandular stomach at its border with the muscular stomach, and acute catarrhal enteritis. Histological examination reveals micronecrosis in the brain, and depletion of lymphocytes in the bursa of Fabricius, thymus, spleen, esophageal and cecal tonsils.

Pathoanatomical diagnosis:

1. Hemorrhagic diathesis.

3. Cyanosis of the comb and catkins.

4. Serous-fibrinous pericarditis and pleuroperitonitis.

5. Catarrhal, catarrhal-hemorrhagic enteritis.

6. Serous edema subcutaneous tissue.

7. Unchanged spleen.

Histo: micronecrosis in the brain; delymphatization of the bursa of Fabricius, thymus, spleen, esophageal and cecal tonsils.

Laboratory diagnosis is based on the isolation of the virus in chicken embryos, the production of RGA and RZGA with specific hyperimmune sera, and histological examination of the pathological material.

Newcastle disease affects birds of all ages and occurs acutely, subacutely and chronically. The acute course is characterized by fever, depression, drowsiness, diarrhea (watery feces, greenish-yellow in color). When breathing, you can hear wheezing and bubbling in the throat. Cyanosis of the comb and catkins is observed.

In subacute and chronic cases, it is observed nervous symptoms, shortness of breath, cough, wheezing.

The main pathological changes are characterized by the phenomena of hemorrhagic diathesis, the appearance of a hemorrhagic ring in the mucous membrane of the glandular stomach at its border with the muscular stomach. Fibrinous-necrotic, erosive-ulcerative enteritis with the formation of scab-buds, granular degeneration of parenchymal organs, venous hyperemia and pulmonary edema are also detected. Histopathological examination reveals non-purulent lymphocytic encephalitis in the brain; in the organs of the immune system - massive necrosis of lymphocytes, processes of destruction of lymphoid nodules.

Pathological diagnosis:

1. Hemorrhagic diathesis.

2. Hemorrhagic ring in the mucous membrane of the glandular stomach at its border with the muscular stomach.

3. Cyanosis of the comb and catkins.

4. Fibrinous-necrotic, erosive-ulcerative enteritis with the formation of scab-buds.

5. Serous edema of the subcutaneous tissue.

6. Slight enlargement of the spleen.

7. Histo: non-purulent lymphocytic encephalitis; death of lymphocytes and destruction of lymphoid nodules in the bursa of Fabricius and spleen.

To make a final diagnosis, additional laboratory tests are carried out: isolation of the virus on chicken embryos and its identification using RTGA, RN, RSK, RIF, ELISA. Data from histological examination of the brain are taken into account.

Streptococcosis occurs at lightning speed or acutely. In a sick bird, drowsiness, ruffled feathers, depression, diarrhea, anemic comb and earrings, and sometimes paralysis of the limbs are observed. Pathological changes are characterized by serous-hemorrhagic edema of the subcutaneous tissue, serous-fibrinous inflammation of the serous integument, and splenic hyperplasia. The liver is in a state of granular degeneration with miliary foci of necrosis.

Pathological diagnosis:

1. Cyanosis of visible mucous membranes and skin.

2. Serous-hemorrhagic edema of the subcutaneous and intermuscular tissue.

3. Venous hyperemia, granular and fatty degeneration of the liver, foci of necrosis in it.

4. Enlarged spleen.

5. Acute venous hyperemia and pulmonary edema.

6. Acute venous hyperemia, granular degeneration and serous glomerulonephritis of the kidneys.

7. Acute catarrhal enteritis.

8. Serous-fibrinous peritonitis, pericarditis, perisplenitis, ovariosalpingitis (with subacute and chronic course).

9. Ovarian hyperemia, deformation of egg follicles and hemorrhages in them.

Laboratory tests are carried out: microscopy of organ smears, isolation of a pure culture of the pathogen, determination of its virulent properties.

With chicken pasteurellosis, sick birds experience lethargy, thirst, fever, depression, diarrhea, cyanosis of the comb and earrings, and in a chronic course, diphtheritic inflammation of the wattles. When opening dead and forcedly killed chickens, signs of septicemia are found, lobar pneumonia. During histological examination, pronounced atrophy and delymphotization of lymphoid nodules with simultaneous thickening of interfollicular connective tissue septa are recorded in the bursa of Fabricius.

Pathological diagnosis:

acute course

1. Cyanosis of the comb and earrings.

2. Croupous pleuropneumonia.

3. Serous-fibrinous pericarditis.

4. Hemorrhagic diathesis.

5. Granular dystrophy and miliary necrosis in the liver and myocardium.

6. Acute catarrhal, catarrhal-hemorrhagic duodenitis.

7. Enlarged spleen (not always).

chronic course

1. Fibrinous-necrotic inflammation of the barbs, sometimes their falling off.

2. Croupous, necrotizing pneumonia.

4. Fibrinous-purulent arthritis.

5. Exhaustion.

Histo: atrophy of the lymphoid nodules of the bursa of Fabricius, thickening of the interstitium. To clarify the diagnosis, carry out bacteriological examination and perform a biological test on chickens.

Colibacillosis is characterized by fever, depression, diarrhea, and increasing exhaustion. At autopsy they find: catarrhal inflammation of the small intestine, serous-fibrinous inflammation of the serous covers, air sacs. Microscopy of sections of the bursa of Fabricius reveals focal hemorrhages, hyperemia and edema of the interstitium, and atrophy of lymphoid nodules. A depletion of lymphoid elements in the cortical and medullary zones of the nodules and swelling of the cytoplasm of reticular cells are noted.

Pathological diagnosis:

1. Serous-fibrinous perihepatitis, perisplenitis, pericarditis, peritonitis, aerosacculitis.

2. Dotted and spotty hemorrhages in parenchymal organs, mucous and serous membranes.

3. Acute catarrhal enteritis.

4. Enlarged spleen.

5. Granular dystrophy and miliary foci of necrosis in the liver.

6. Serous-fibrinous polyarthritis (with chronic course).

7. Histo: hemorrhages in the bursa of Fabricius, atrophy of lymphoid nodules, hyperemia and edema of the interstitium.

Additional research is carried out: isolating a culture of the pathogen, determining its virulence.

Pathological diagnosis:

1. Catarrhal-hemorrhagic erosive-ulcerative typhlitis and proctitis.

3. Granular dystrophy of the liver, kidneys and myocardium.

4. Exhaustion.

5. Histo: atrophy of the lymphoid nodules of the bursa of Fabricius, swelling of the interfollicular connective tissue, accumulation of histiocytes, pseudoeosinophils and eosinophils in it.

To make a final diagnosis, microscopy of feces or scrapings of the intestinal mucosa is performed to identify eimeria oocysts.

Prostagonymosis occurs in the form of enzootic outbreaks, most often on farms located near water bodies. In sick birds, depression, drowsiness, diarrhea (white or greenish feces), decreased egg production, and an enlarged abdomen are observed. When opening dead or forcedly killed birds, ovarianitis, purulent-fibrinous salpingitis and peritonitis, hyperemia and edema of the bursa of Fabricius are discovered. Microscopy of bursa sections reveals serous-inflammatory edema of the interstitium, infiltration of pseudoeosinophils and eosinophils.

Pathological diagnosis:

1. Ovariitis, deformation and rupture of follicles.

2. Purulent-fibrinous peritonitis.

3. Purulent-fibrinous salpingitis, egg stones in the lumen of the oviduct.

4. Acute catarrhal enteritis.

5. Granular dystrophy of the liver, kidneys, myocardium.

6. Hyperemia and swelling of the bursa of Fabricius.

7. Exhaustion, exicosis.

8. Histo: Serous-inflammatory edema and microphage infiltration of internodular connective tissue in the bursa of Fabricius.

Additional laboratory tests are carried out - microscopy of the droppings of sick birds to detect helminth eggs.

Hypovitaminosis A is recorded in chickens, as well as productive birds. Symptoms: immobility, stunted growth, conjunctivitis, laryngitis, general anemia. Upon opening, miliary gray-yellow nodules (hyperplasia and keratinization of the epithelium of the mucous glands) are found on the mucous membrane of the pharynx and esophagus, and granular degeneration and urate deposition are found in the kidneys.

Pathological diagnosis:

1. Hyperkeratosis of the skin, dullness and brittleness of feathers.

2. Fibrinous conjunctivitis, xerophthalmia, keratomalacia, panophthalmitis.

3. Catarrhal rhinitis, laryngitis, tracheitis.

4. Millet-like nodules in the mucous membrane of the pharynx and esophagus.

5. Visceral uric acid diathesis and gout.

6. Exhaustion and general anemia.

To establish a final diagnosis, a biochemical study of the liver, blood, egg yolks, and feed is carried out for the content of vitamin A and carotene.

Nutritional dystrophy, most often observed in chickens 15-20 days of age, is characterized by depression, diarrhea, and exhaustion of the bird. At autopsy, the absence of fat in the fat depot, atrophy of skeletal muscles and internal organs are recorded. Histological examination of sections of the thymus and bursa of Fabricius reveals early involution of the organ, accompanied by atrophy and devastation of lymphoid nodules.

Pathological diagnosis:

1. Lack of fat in the fat depot.

2. Atrophy of skeletal muscles and internal organs.

3. Serous edema in the subcutaneous and intermuscular tissue.

4. General anemia, exicosis.

5. Histo: accidental involution of the bursa of Fabricius and thymus.

A chemical and toxicological study of feed is carried out. An increase in acid and peracid numbers is detected.

Radiotoxicosis is recorded in birds of all ages. Sick chickens and chickens experience anorexia, thirst, and swelling in the head area. An autopsy reveals hemorrhagic diathesis, serous infiltration of subcutaneous tissue, and histopathology reveals atrophy and necrosis of lymphoid tissue in the central and peripheral organs of the immune system.

Pathological diagnosis:

1. Hemorrhagic diathesis.

2. Serous swelling of the subcutaneous tissue in the head area.

3. Subacute or chronic catarrhal, erosive and ulcerative enteritis.

4. Atrophy of the bursa of Fabricius, thymus, spleen, Harder gland.

5. General anemia, exhaustion, exicosis.

6. Histo: focal necrosis or atrophy of lymphoid tissue in the thymus, bursa of Fabricius, Harder's gland, spleen, esophageal and cecal tonsils.

Radiological examination of feed is carried out.

Prevention and control measures

In order to protect poultry farms from the introduction of the pathogen, veterinary specialists are obliged to: use eggs for incubation from poultry farms that are free from infectious bursal disease; equip poultry houses with birds of the same age; observe inter-cycle technological breaks with thorough cleaning, disinfection, disinfestation and deratization; carry out disinfection of eggs and containers being carried out; provide the necessary veterinary requirements for keeping and feeding birds.

When a diagnosis of IBD is established, restrictions are imposed on the farm, under the terms of which it is prohibited: the export of eggs for incubation, young and adult birds, feed, tools and equipment to farms free from IBD and for sale to the public; stocking flocks with recovered poultry.

It is allowed to sell eggs for food purposes after disinfecting them with formaldehyde vapor.

After a clinical examination, all sick and suspected chickens are slaughtered and disposed of. The remaining healthy chickens are vaccinated, followed by the slaughter of all birds that have reached slaughter conditions from the premises where the disease was recorded. Stop incubating eggs and accepting young animals for rearing. The incubator is disinfected. Laying eggs for incubation is resumed no earlier than 10 days after the hatching of the last batch of incubated eggs.

Separate maintenance personnel are assigned to each poultry house. Overalls are disinfected daily in a steam-formalin chamber.

Poultry slaughter is carried out with complete gutting of the carcasses. If there are no pathological changes in the carcasses, they are used after boiling at t=100°C (for 90 minutes). Carcasses with intramuscular hemorrhages, edema, deposits of uric acid salts are sent along with internal organs for technical disposal.

For wet disinfection, use a 4% solution of sodium hydroxide, a clarified solution of bleach (containing at least 3% active chlorine), and a 2% aqueous solution of formaldehyde with an exposure of at least 6 hours.

Litter and deep litter are disinfected biothermally.

Restrictions are lifted after final veterinary and sanitary measures and in the absence of clinical and pathological changes in at least 3 batches of young animals reared up to 60 days of age after a preventive break.

Specific prevention

According to the observation of a number of researchers, general veterinary and sanitary measures do not ensure complete recovery of farms from infectious bursal disease. Therefore, in the complex of measures to prevent and eliminate this infection, the main place is given to specific prevention using live and inactivated vaccines.

Protection of chickens from infection with the IBD virus is achieved by creating a high level of passive antibodies in young animals by immunizing replacement chickens with inactivated vaccines and using live virus vaccines as transovarial immunity decreases.

Live virus vaccines are used to immunize chickens. Birds are vaccinated orally at 7-14 days of age (depending on the level of passive immunity and the epizootic situation), and revaccinated 14 days later. 6 hours before immunization, the supply of water and feed in poultry houses is stopped. The vaccine is dissolved in warm water and feed the chickens in such a way that there is one dose of vaccine (10-15 ml) per head. The supply of water and food is resumed no earlier than 2 hours after drinking the vaccine. Establish clinical observation of the condition of the bird.

The disadvantage of most live virus vaccines against infectious bursal disease is that the vaccine strains of the virus, along with immunogenicity, have pronounced immunosuppressive properties. Therefore, live vaccines, depending on the degree of reactogenicity, are divided into moderate-, weak- and apathogenic with high immunogenic activity. The effectiveness of reactogenic strains has been established when vaccinating chickens with high levels of maternal antibodies; they are unacceptable for susceptible chickens.

One of the indicators of the reactogenicity of vaccine strains for Gumboro disease is a decrease in the level of antihemagglutinins in birds vaccinated against Newcastle disease. A correlative relationship has been established between the immunogenic activity of vaccine strains of the virus, its damaging effect on the morphological structure of the bursa and a decrease in the bursal index. The most immunogenic strains cause more pronounced lesions of the bursa of Fabricius. A decrease in the bursal index was established when reactogenic vaccines were administered to weakly immune birds early age. Therefore, before vaccinating chickens against IBD, we recommend determining their immune status and background levels of specific antibodies. To do this, send blood serum and immune organs from 10-20 chickens to the laboratory of diseases of birds and bees of the BelNIIEV or to the department of diseases of small animals of the VGAVM for research.

It has been shown that even weakly pathogenic vaccines against IBD are capable of causing pathomorphological changes in the organs of the immune system, thereby causing the development of an immunodeficiency state in birds. For example, a single immunization of chickens with the dry live virus vaccine “Bursin-2” leads to a sharp decrease in the size of lymphoid nodules due to the processes of delymphotization of their cortical layer. In the medulla, phagocytosis of destroyed cells is recorded with the formation of many round cavities like a honeycomb. In chickens vaccinated twice with this vaccine, the lesions of the bursa of Fabricius intensify. There is an almost complete disappearance of lymphocytes, atrophy and destruction of lymphoid nodules, fibroplasia and transformation of the organ into a glandular structure. Cortical atrophy is observed in the thymus.

Double vaccination of chickens with attenuated vaccines “Gambovac” and “Gumboral-ST” (made in France) causes almost complete atrophy bursa of Fabricius with loss of its functional part.

The results of our studies showed that when administered orally, a dry live virus vaccine from pcs. “D 78” (produced in Holland) in immune chickens, processes of atrophy and delymphatization develop in the thymus, bursa of Fabricius and cecal tonsils, leading to immunosuppression.

We have also established that oral immunization of birds against Gumboro disease with a dry live virus vaccine from pcs. “Winterfield 2512” (produced by the All-Russian Research Institute of Animal Health, Vladimir) is accompanied by active immunomorphological changes in the organs of the immune system and does not cause an immunodeficiency state. In the bone marrow of chickens immunized with this vaccine, we recorded an increase in the number of myeloblastic cells, an increase in the leukoerythroblastic index, as well as the bone marrow index of eosinophil and pseudoeosinophil maturation. In the thymus of immune chickens, an increase in the specific volume of lymphoid tissue was noted, and in the bursa of Fabricius, hyperplasia of lymphoid nodules was observed. In the spleen and cecal tonsils of chickens immunized with this vaccine, we detected an increase in the density of nodular lymphoid tissue, an increase in the size of lymphoid nodules, as well as active accumulation of plasma cells. In this regard, the use of dry live virus vaccine from pcs. “Winterfield 2512” (manufactured by ARRIAH) is most preferable for immunizing chickens against Gumboro disease, given the high immunogenicity and low reactogenicity of this biological product.

BelNIIEV has developed a live embryonic virus vaccine against Gumboro disease from the KMIEV-15 strain. It is currently undergoing extensive production testing. Studying the effectiveness of this biological product is of particular interest, given the antigenic relationship of the vaccine and epizootic strains of the virus circulating in the Republic of Belarus.

At the age of 110-120 days, inactivated vaccines are used for replacement young animals. They are administered once, intramuscularly, into the area pectoral muscle in a dose of 0.5 ml. The vaccine injection site is treated with 70% ethanol. It has been established that the introduction of inactivated vaccines increases the antibody titer in birds previously immunized with live vaccines. The immunizing effect is more pronounced the later the inactivated vaccine was used. Immunization of replacement chickens with inactivated vaccines creates more intense and long-lasting immunity than when using live vaccines.

Despite the immunization of replacement chickens, there is often significant variability in passive antibodies in a chicken flock, which creates conditions for disease in birds with a weak level of transovarial immunity. This necessitates the need to stimulate the post-vaccination immune response through the use of immunotropic agents.

We have conducted studies to study the influence of a number of immunostimulants (sodium thiosulfate, thymalin, ASD-2, levamisole) on the immunogenic properties of the liquid sorbed inactivated vaccine of the ARRIAH against infectious bursal disease (manufactured in Vladimir, Russia). It has been established that immunization of replacement chickens together with sodium thiosulfate and thymalin helps to create a more intense antiviral immunity than when using a single vaccine. The drugs ASD-2 and levamisole did not significantly affect the immunogenicity of this vaccine.

Method of immunization of replacement young chickens against IBD with liquid sorbed inactivated vaccine ARRIAH together with sodium thiosulfate:

The bird is vaccinated at 110-120 days of age. First prepare a fresh 35% sodium thiosulfate solution. The resulting solution is sterilized by boiling for 30 minutes, and, after cooling, 50 ml of 35% aqueous solution sodium thiosulfate is mixed with 200 ml (bottle - 400 doses) of the vaccine. The resulting mixture (containing 7% sodium thiosulfate) is administered once, intramuscularly, into the pectoral muscle area, in a dose of 0.6 ml (thus, the volume of the administered vaccine increases by 0.1 ml). The injection site is treated with 70% ethanol.

We have established that immunization of replacement young animals against Gumboro disease with a liquid sorbed inactivated vaccine (produced by the All-Russian Research Institute of Animal Health, Vladimir) together with the immunostimulant sodium thiosulfate (in a 7% aqueous concentration) activates the processes of immunomorphological restructuring in the central (red bone marrow, thymus, bursa Fabricius) and peripheral (spleen, blood) organs of the immune system of birds, which helps to increase the level of specific antibodies by 20-50%., creating more intense post-vaccination immunity in breeding stock, and thereby enhancing immune protection in chickens due to a high level of transovarial immunity. .

Method of immunization of replacement young chickens against IBD with liquid sorbed inactivated vaccine ARRIAH together with thymalin:

The bird is immunized at 110-120 days of age. On the day of vaccination, 10-20 heads of replacement chickens are selectively weighed to determine the average weight of the birds. Timalin is administered together with the vaccine at a dose of 1 mg/kg body of birds. The drug is available in powder form in 10 mg bottles.

Example. The average weight of birds is 2 kg. Therefore, 1 dose of the vaccine should contain 2 mg of thymalin. 800 mg (80 bottles) of thymalin are dissolved in a vaccine bottle (200 ml - 400 doses). The resulting mixture is administered once, intramuscularly, into the pectoral muscle area, in a dose of 0.5 ml. The injection site is treated with 70% ethanol.

Our studies have shown that immunization of birds together with thymalin promotes an increase in specific antibodies in the blood by 1.5-4.4 times compared to the use of a vaccine without an immunostimulant.

At the same time, sodium thiosulfate is a cheaper and more accessible drug. Therefore, its use during the period of immunization of replacement chickens is preferable.

Assessment of the intensity of post-vaccination immunity.

To assess the intensity of immunity in Gumboro disease, serological methods are used: RID, VIEF, RN, RNGA and ELISA. In all chickens vaccinated with live virus vaccines, antibodies are detected in the blood serum starting from 20-30 days of age. Specific antiviral antibodies in replacement chickens vaccinated at the age of 110-120 days are detected in chickens up to 46 weeks of age. Maternal antibodies are detected in chickens up to 17-20 days of age.



G.V. Beginin, chief veterinarian of the Gayskaya PF

The epizootic and economic well-being of poultry enterprises largely depends on timely diagnosis and implementation of measures specific prevention against infectious diseases, which include Gumboro disease.

Gumboro disease at the Gayskaya poultry farm in the Orenburg region was first registered in November 1995 among 45-day-old chickens of the Zarya-17 cross. Clinically, the chickens were observed to be lethargic, lack of appetite and watery diarrhea. Characterized by ruffled plumage and at times muscle tremors.

During the epizootic period, the disease manifested itself in 6 workshops of the poultry farm. The disease was observed simultaneously in different poultry houses and the number of sick chickens in some poultry houses reached 50%, and in others – 10–20%. Chicken mortality in some workshops was more than 30% within 7–10 days. The maximum death of birds was noted on the 3rd–5th day of illness and decreased in the next 4–5 days.

At autopsy, dry subcutaneous tissue, pinpoint or diffuse hemorrhages in the pectoral and femoral muscles were noted, the bursa of Fabrice was enlarged 2–3 times, hyperemic or with hemorrhages (in 30–40% of cases), sometimes there were fibrin deposits in its cavity. Kidney lesions were noted in 40% of the examined corpses.

They were enlarged, with hemorrhages, and there was an accumulation of urates in the ureters. The diagnosis was made on the basis of epizootic data, clinical signs, pathological changes and the results of laboratory tests conducted at VNIVIP.

Since the outbreak of Gumboro disease, different vaccines have been tested at the poultry farm, varying in their effectiveness due to the presence of maternal antibodies and changes in poultry crosses.

Initially, against the background of low passive immunity, the double use of the vaccine from the “VNIVIP” strain made it possible to ensure high safety and productivity of poultry in unfavorable conditions. After a long period of successful prevention, clinical signs and lesions in the bursa of Fabricius during autopsy of dead birds appeared in the vaccinated flock after reaching 35–37 days. Then the disease spread to other buildings where birds of an age susceptible to the IBD virus were kept.

An analysis of the reasons for the failure of vaccine prophylaxis showed that by that time the young animals accepted for rearing had high levels of maternal immunity, since they were obtained from hyperimmunized laying hens, and in the batch of chickens where a specific death was observed, there were violations of the vaccine application technique, in some In some cases, the poultry house housed chickens of different ages with different immune backgrounds.

It was possible to stabilize the epizootic situation on the farm with the help of a vaccine from the BG strain. With the transition to the new vaccine, the clinical manifestation of the disease was not observed, but we were faced with such problems as atrophy of the bursae of Fabricius, retardation of poultry in growth and development, a high percentage of their rejection, a low percentage of commercial pullets and kidney pathology in replacement young stock caused by an increased content of uric acid salts in the ureters.

After changing the poultry population to the Rhodonit cross, in which the parent flock was not vaccinated with the inactivated Gumboro vaccine and the level of maternal antibodies in the RDP of day-old young animals did not exceed 30%, they began to use a vaccine from the KBK strain produced by Biovet LLC (St. Petersburg ). The vaccine was administered once into the upper third of the neck of day-old chickens subcutaneously in a volume of 0.2 ml. To dilute the vaccine, we used a Marek's disease vaccine diluent produced by the Kursk biofactory.

The effectiveness of the vaccine from the KBK strain was assessed by the level of specific antibodies in the RDP, bursal index and titers to the Newcastle disease virus.

In the blood serum of vaccinated chickens 25–30 days of age, a positive reaction in the RDP was noted in 80–100% of cases. The bursal index at the age of 30 and 40 days was at least 3.5. The bag had a natural color and without visible signs defeats. Group immunity against Newcastle disease 15 days after revaccination was 6.42 log2, which indicates a pronounced immunological reaction of the bird to the vaccine. Observations have shown that the vaccine from the KBK strain does not cause immunosuppression; the growth and development of poultry complied with zootechnical standards. Safety among young animals during the period of use of this vaccine increased by 5%, the yield of commercial pullets was 97% with high uniformity of the herd.

Some batches of chickens were vaccinated against Marek's disease and Gumboro disease simultaneously. Performance indicators for separate and joint immunization against Marek's and Gumboro's diseases did not differ significantly.

In 1998, another change of livestock was carried out to the “Loman White” cross, where the prevention of Gumboro disease was carried out according to the program of the “Loman” company (Germany) and passive immunity in the first days of life, according to ELISA data, was 1: 5000 and higher. In the current situation, it was necessary to change the vaccine and adjust the existing disease prevention program.

Taking into account previous experience in preventing the disease and positive feedback from colleagues on the prevention of Gumboro disease using an inactivated vaccine on young birds, it was decided to vaccinate with this vaccine from the “52/70 M” strain (produced by Biovet LLC). At the same time, a comparison was made with a live vaccine from the BG strain and a scheme for using the killed vaccine was worked out to develop tactics for preventing the disease in the future.

To do this, one group of chickens was vaccinated with an inactivated vaccine at 10 days according to the instructions for using the drug; the second group was vaccinated at 16 days with an inactivated vaccine; the third and fourth groups of chickens were simultaneously vaccinated with inactivated and vaccine from the “KBK” strain at 10 and 16 days, respectively; chickens of the fifth group were vaccinated with a vaccine from the “BG” strain at 7 and 17 days.

The effectiveness of vaccines and their application schemes was judged by the well-being of the farm against Gumboro disease, general safety, productivity, business output of replacement young stock and by the results of blood serum studies for the presence of specific antibodies in the RDP of 30-, 40-, 50- and 60-day-old chickens. At the same time, we studied the level of post-vaccination immunity against Newcastle disease, and also determined the bursal index in different terms poultry rearing.

Comparative production indicators for raising poultry according to the specified vaccination schemes are given in Table No. 1.

Table 1
Performance indicators of chickens vaccinated with different vaccines against IBD

Indicators	Group numbers
Number of goals
Average daily weight gain, g
weight 1 head. when transferred to 112 days, g
% business pullet
Safety, %
Uniformity, %
% of egg laying in 150 days.
Culling, %

From the presented data it is clear that the vaccines used against Gumboro disease according to the indicated schemes provide complete protection of chickens from the field virus. Administration of inactivated vaccine to chickens does not cause adverse reactions of local and general. Chickens vaccinated with an inactivated vaccine at different times separately and in association with a live vaccine have the highest rates of safety (up to 99.4%), average daily weight gain that meet regulatory requirements, a high percentage of commercial pullet yield (97.4%), and a low percentage of rejection (0.49%) and high uniformity of the herd (88.3%).

The dynamics of serological indicators of the reaction to the introduction of vaccines indicates that the most active group immunity was established in the IV group of chickens simultaneously vaccinated with live and inactivated vaccines at 16 days. The arithmetic mean titer of serum in the RDP was 3.8 log2. High performance bursal index (more than 5.2) were noted in groups I-IV, while in group V, low bursal index values ​​were observed starting from 30 days of age.

CONCLUSION
The effectiveness of preventing Gumboro disease is closely related to the type of vaccine, compliance with the rules for its use, and the presence of maternal antibodies, which negatively affect the development of post-vaccination immunity, both when administered live and inactivated vaccines.

The vaccine from the KBK strain is effective against a low immune background of passive antibodies. The use of a vaccine from the “BG” strain helps to stop the infection, but causes damage to the bursa and kidneys, which leads to a decrease in the overall safety and productivity of the bird.

High safety and productivity in our farm conditions was achieved with joint vaccination with inactivated and live vaccines against IBD at 16–18 days.

Prepared based on the materials of the “Vth International Veterinary Congress on Poultry Farming” for the website

19.04.2018

Vaccines for the prevention of chicken infectious bronchitis (IB) and Gumboro disease are live and inactivated preparations of imported and domestic production. These drugs are produced in the form of monovalent as well as polyvalent vaccines that protect poultry from 2-4 different infectious diseases. A huge role here is played by live vaccines that provide a rapid immune response, including drugs of modern technologies.

Vaccination of birds against IBV is carried out intraocularly, intranasally, orally and by spray method (coarse and fine spray), against Gumboro disease - orally and in ovo.

Infectious bronchitis of chickens

Infectious bronchitis of chickens (IB) is a highly contagious viral disease, manifested by damage mainly to the respiratory and reproductive organs and kidneys. The disease affects birds of all ages and is especially dangerous for chickens.

The causative agent of IB

Caused by an RNA virus with high genetic variability. Mutations of the pathogen are facilitated by a number of factors, including the reproduction of the virus in poultry of different ages, mixed infections, and the co-circulation of vaccine and field viruses in the same flock.

There are many strains of chicken infectious bronchitis virus circulating around the world, which makes the diagnosis and prevention of this disease difficult. Currently, the greatest danger to the Russian poultry industry is posed by viral strains of the Massachusetts serotype, viruses of serotype 793B, as well as highly contagious QX strains and some other pathogens. Several strains circulate simultaneously in poultry farms, but 1–2 major serotypes usually predominate.

Certain serotypes of infectious bronchitis virus can multiply in various tissues of the bird's body.

IBV serotype Massachusetts (Mass) primarily affects the respiratory system, causing severe respiratory disease. Immunization against Massachusetts serotype viruses can be carried out from the first days of life.

Respiratory strains of IBV viruses lead to death (mortality rate 15–35%) and create a favorable background for the development of bacterial infections.

The Massachusetts serotype has become widespread throughout the world and was identified in the 40s of the twentieth century in Europe and the USA.

Later it turned out that a number of strains of IBV viruses also infect the excretory organs, while respiratory symptoms can be expressed to varying degrees.

The nephroso-nephritis form of IB is characterized by weak and short-term respiratory signs followed by depression, the mortality rate of young animals ranges from 25–30% to 70%. Nephropathogenic properties are most pronounced in the QX strain, which came to Europe from Asia and has been circulating in Russia since the early 2000s.

The highly contagious and pathogenic strain QX actively reproduces in the tissues of the respiratory tract, kidneys, ovaries and lymphoid tissues of the cecum and colon.

In the 90s of the last century, scientists identified the nephropathogenic serotype 793B, which causes high mortality in broilers. Immunization of chickens against this pathogen is usually carried out during the second vaccination. But there are vaccines that can be used from one day of age.

Serotypes close to Massachusetts, as well as 793B, are the most common strains of IBV viruses in poultry farms in Russia and Europe; the largest number of immunobiological drugs have been developed to protect against these strains. When used together, sufficient cross-protection against the QX strain is formed.

Some strains of the IBV virus (including M41) can long period reduce the egg production of poultry (causing a drop in productivity parameters from 30 to 89%), deteriorate the quality of egg shells and change their color.

As a result, laying hens are found on farms with normally expressed secondary sexual characteristics, but unable to lay eggs due to adhesions of the oviducts as a result of salpingo-oophoritis, provoked by the multiplication of the IBV virus in chickens at an early age.

Among the new virulent strains that have appeared over the past few years, it is necessary to highlight VAR 2 (Variant 2), circulating in Asia and the Middle East, and recently in Central Europe. This virus mainly affects the kidneys, respiratory and reproductive organs.

Considering the rapidly increasing infectious pressure of IBV types QX and 793B and new variant strains of type 2 in Europe, the Middle East and Russia, Phibro Animal Health Corporation (USA) has developed a live attenuated vaccine TABIC IB VAR 206. It was created on the basis of a field strain Option 2 (IS/1494/06).

The TABIK IB VAR 206 vaccine is produced using the TAbic technology, patented and owned by Phibro (production of live vaccines in the form of sterile water-soluble tablets). This promising development has been appreciated by other major vaccine manufacturers.

Boehringer Ingelheim, based on scientific developments in the production of effervescent forms by Sanofi under license from Phibro Animal Health, began producing vaccines in the form of effervescent tablets (NEO line). This dosage form significantly reduces storage space and facilitates the work of veterinarians.

During the study of strains of infectious bronchitis pathogens in chickens, interesting facts were revealed. For example, a combination of some strains of IBV pathogens can cause cross-protection from other strains. For example, immunization with strains Ma5 of serotype Massachusetts and serotype 793B protect birds from the highly pathogenic strain QX (vaccination occurs with one strain, revaccination with another strain). The phenomenon of such a synergistic effect of vaccines is called protectotype. It was discovered by Jane Cook, and today it is the main concept in IB immunity.

IBC protection programs

The infectious bronchitis virus is constantly changing. PCR studies on sequencing the IBV genome, carried out in the early 2000s in Russia, showed that about a third of the viruses were previously unstudied and constituted a group of local strains.

Programs to protect chickens from infectious bronchitis include live and inactivated vaccines. The main purpose of vaccination is to develop immunity in birds against wide range viral agents. Immunization against IBV is carried out once or twice (depending on the recommendations of the drug manufacturer and the epizootic situation on the farm). Chicks are vaccinated from the first day of life, regardless of the level of maternal bodies. A third (additional) revaccination against IBV should be carried out in both parent and commercial flocks before the start of laying (on days 98–120).

Live vaccines are the main tool for protecting chickens from parent flocks, broilers and laying hens from IBV. They create an early specific protection, developing in a chicken within 2 weeks. The main disadvantage of live vaccines is the potential ability of the vaccine strain to revert to the wild type and restore virulence due to mutations. Viruses respiratory diseases are able to compete for the same receptor sites in the mucous membrane of the upper respiratory tract. Therefore, when using two live vaccines with a different set of strains in an IBV immunization regimen, it is necessary to maintain a time interval of at least 14 days.

Inactivated vaccines used for young laying hens and parent flocks (re-vaccination), they cause the production of maternal antibodies. For vaccination with inactivated vaccines to be effective, a live vaccine must first be used to prime the antigen, at least four to five weeks before the inactivated vaccine is administered. The content of several heterologous strains in an inactivated vaccine causes the formation of high levels of antibodies to more strains of the IBV virus. Primary vaccination with a live vaccine and revaccination with an inactivated one provide protection on average in 95% of cases, while the combination of two inactivated immunobiological drugs provides approximately 90% protection.

Identification of the type of virus circulating in the herd using PCR and other methods in specialized laboratories will help you choose the right drug for immunization.

From the moment they are born, chickens are at risk not only of IBV, but also of Newcastle disease. A fairly large number of drugs have been created for comprehensive protection against these diseases.

The company Ceva Sante Animale proposed a vaccine for vaccinating day-old chicks against Newcastle disease and infectious bronchitis (strain H-120) VITABORN L.

A high-quality vaccine against infectious bronchitis of chickens BRONIPRA-1 (strain H-120) for use on the first day of life is offered by the Spanish company Laboratorios HIPRA, S.A. For areas unaffected by Newcastle disease, the company also has bivalent vaccines HIPRAVIAR-B1/H120 and HIPRAVIAR-CLONE/H120, which are successfully used from the first day of life using the large-droplet spray method.

Monovaccines for the prevention of infectious bronchitis in chickens

Vaccine	Description	Strain and serotype of the pathogen	Manufacturer
AVIVAC-IBC	live dry	A/91 serotype 793/B	NPP "AVIVAC", Russia
AVIVAC-IBC	live dry	H-120 serotype Massachusetts	NPP "AVIVAC", Russia
Bioral H120 NEO	live tablet	H120 serotype Massachusetts	Boehringer Ingelheim, France
BRONIPRA-1	live dry	H-120 serotype Massachusetts
Vaccine against infectious bronchitis of chickens from the variant strain RV-07 live dry	live dry	strain RV-07
	live dry	H-120 serotype Massachusetts	FSBI "ARRIAH", Russia
Vaccine against infectious bronchitis of chickens from strain N-120 live dry	live dry	H-120 serotype Massachusetts	OJSC "Pokrovsky Plant of Biological Preparations"
Vaccine against infectious bronchitis of chickens, multi-strain inactivated emulsified	inactivated emulsified	Taganrog serotype 793/B + Kaluga strain + H-52 serotype Massachusetts	FSBI "ARRIAH", Russia
Live dry virus vaccine against chicken infectious bronchitis (IBV) from strains N-120, RV-07	live dry	H-120 serotype Massachusetts, variant strains RV-07	Kronvet, Russia
Volvac IB Mass MLV	live dry	modified Massachusetts serotype virus	Boehringer Ingelheim, Germany
Galliwack IB 88	live lyophilized	CR88121 serotype 793B	Boehringer Ingelheim, France
Galliwack IB 88 NEO	live tablet	CR88121 serotype 793B	Boehringer Ingelheim, France
Gallimun 793B	dry inactivated	variant strains of serotype 793B	Boehringer Ingelheim, France
	live dry	H-120 serotype Massachusetts	FKP “Shchelkovo Biocombine”, Russia
Nobilis IB 4/91	live dry	4/91 serotype 793B	Intervet/MSD, Netherlands
Nobilis IB Ma5	live dry	Ma5 serotype Massachusetts	Intervet International/MSD, Netherlands
Pulvak IB H120	live dry	H-120 serotype Massachusetts	Zoetis Inc., USA
Pulvak IB QX	live dry	serotype QX (L1148)	Zoetis Inc., USA
Pulvak IB Primer	live dry	H-120 serotype Massachusetts + variant strains D274	Zoetis Inc., USA
Sevak iBird	live dry	1/96 serotype 793B	Ceva Sante Animale, France
Sevak MASS L	live dry	B-48 serotype Massachusetts	Ceva Sante Animale, France
Sevak BRON 120 L	live dry	H-120 serotype Massachusetts	Ceva Sante Animale, France
TABIK H-120	live dry tablet	H-120 serotype Massachusetts	Phibro Animal Health, Israel
TABIK IB Var	live dry tablet	233A serotype 793B	Phibro Animal Health, Israel
TABIK IBVAR2-06	live tablet		Phibro Animal Health, Israel
HatchPack IB H120	live frozen	H-120 serotype Massachusetts	Boehringer Ingelheim, France

Immunization of chickens against IBV can also be carried out polyvalent drugs:

– produced by Ceva Sante Animale: Sevak Megamun ND-IB-EDS-SHS K, Sevak NB L, Sevak VITABRON L;

– produced by Intervet/MSD: Nobilis Ma5 + Clone 30, Nobilis IBmulti + ND + EDS, Nobilis IBm + ND + EDS, Nobilis RT + IBmulti + G + ND;

– produced by Laboratorios HIPRA, S.A: HIPRAVIAR-TRT4, HIPRAVIAR-CLONE/H120, HIPRAVIAR-B1/H120, AVISAN MULTI;

– produced by Boehringer Ingelheim: Volvac ND + IB + EDS KV, Gallimun 303, Gallimun 407;

– produced by Abic Biological Laboratories Ltd (a division of Phibro Animal Health): VH + H120, Quadractin VP 2, SSY + NB + IBK;

– produced by Zoetis: Provak 4, Pulvak Aero;

– produced by AVIVAC: AVIVAC-IBK + NB, AVIVAC NB + IBK + IBB + SSYA + REO

and some other vaccines.

Gumboro disease

Gumboro disease, or infectious bursal disease (GD, IBD) is highly contagious viral disease chickens 2–20 weeks of age, accompanied by damage to the bursa of Fabricius, to a lesser extent to other lymphoid organs and kidneys, the presence of hemorrhages in the muscles of the thigh, chest, wing and in the mucous membrane of the glandular stomach. Along with Marek's disease, IBD is the main immunosuppressive disease in poultry.

IBB - a blow to poultry farming

The Gumboro virus was first discovered in the 50s of the twentieth century in the USA. Today it circulates in all countries of the world with developed poultry farming and causes great economic damage. From time to time, outbreaks of highly virulent strains of IBD are recorded in Europe, leading to mortality of 10 to 30% of young poultry.

The pathogen is resistant to external environment. In droppings, water, and feed, it does not lose its infectious properties for 56 days; on poultry farm equipment - up to 122 days or more.

Infectious bursal disease can occur in both acute and subclinical forms, accompanied by retardation in the growth and development of chickens, suppression of their immunity, susceptibility to viral, bacterial and other diseases.

The subclinical form of the disease, no less than its acute course, causes significant damage to farms. According to Intervet/MSD, the profit from raising broiler flocks free of Gumboro disease is on average a third higher than that obtained from raising birds with subclinical disease.

It is possible to detect the IBD virus by ELISA, PCR, diffuse precipitation reaction on agar gel and some other methods.

Modern methods of protection

Live vaccines IBB is used for vaccination of healthy broiler chickens and replacement young animals of meat and egg breeds. They provide rapid formation of immunity. The frequency of vaccination is double or single, depending on the recommendation of the manufacturer of a particular drug. Live Gumboro disease vaccines are given 6 to 8 weeks before the inactivated vaccine. The disadvantages of live IBD vaccines include immunosuppression, which provokes an insufficient response to vaccination and increases the likelihood of developing other infectious and invasive diseases.

The range of industrial strains is quite extensive. For example, vaccines containing a moderately attenuated strain of the Gumboro disease virus are produced, such as AviPro Presize (Elanco) - LC-75, Nobilis Gumboro 228E (Intervet/MSD) - strain 228E, HIPRAGAMBORO-GM97 (Laboratorios HIPRA, S.A.). To protect poultry, the intermediate vaccine strain Winterfield 2512 is used, which is part of the imported and domestic immunobiological preparations Sevak TRANSMUN (Ceva Sante Animale), HIPRAGAMBORO-CH/80 (Laboratorios HIPRA, S.A.), AVIVAC-IBB ​​(NPP AVIVAC). There are vaccines containing weakly attenuated (hot) strains, for example TABIC MV (Phibro Animal Health) - strain MV, etc.

Prevention of Gumboro disease is complicated by the presence of maternal heterogeneous antibodies in chickens. With a high level of maternal antibodies, the vaccine virus is quickly recognized and neutralized by the cells of the chicken's immune system.

Thanks to special innovative technology specialists of the company Ceva Sante Animale was created immune complex vaccine Sevak TRANSMUN, which allows solving the problem of preventing Gumboro disease in chickens with a heterogeneous level of maternal antibodies. The vaccine is administered once to chicken embryos at the age of 18.5 days using the in ovo or day-old broiler chickens subcutaneously. Once the vaccine virus has replicated, the immune response culminates in the production of protective antibodies against Gumboro disease.

At the origins of the creation of immunocomplex vaccines was the company Embrex, owned by Zoetis, a manufacturer of equipment for in ovo vaccinations.

There are other similar drugs. The Zoetis company has developed the drug Bursaplex based on strain 2512 of the Gumboro virus and antibodies from the hyperimmune blood serum of SPF chickens.

Cloned live vaccine KHIPRAGAMBORO-CH/80 has a minimal immunosuppressive effect on the bird's body and has high antigenic activity and immunogenicity. Intended for use in safe, unfavorable and threatened breeding and commercial poultry farms. Contains a culture of fibroblasts of SPF embryos of chickens infected with the cloned virus CH/80 of the Gumboro disease strain Winterfield 2512. Chickens are vaccinated twice starting from the age of 7 days.

Along with immune complex preparations, recombinant vaccines do not require monitoring the level of maternal antibodies.

Recombinant live vaccine Vaxitek HVT+ IBD is manufactured by leading health protection expert Boehringer Ingelheim. The vaccine contains the V2 gene, cloned from the Faragher 52/70 strain, using the turkey herpes virus as a vector. The drug is prescribed to chickens of meat and egg breeds once at one day of age or in ovo and provides protection against both classical and variant and highly virulent strains.

Thanks to ongoing developments in the field of recombinant and immunocomplex vaccines, it is possible to take a step towards eradicating a number of animal viruses.

But it is too early to write off classical drugs. A properly selected traditional live vaccine based on an intermediate strain provides the necessary level of protection. This is evidenced by a number of studies, including those from Phibro Animal Health specialists.

Domestic manufacturers offer vaccines with a wide range of current vaccine strains. The drugs are produced using modern equipment and meet international standards. A great contribution to the protection of poultry health and ensuring food security in Russia is made by the vaccines of NPP AVIVAC, FKP Shchelkovo Bioplant and FSBI ARRIAH.

In 2018, a new drug was registered by the Federal Center for Animal Health (ARRIAH). The basis of the live dry vaccine Gamboromix is ​​a combination of Gumboro disease strains Winterfield 2512 and GD, positioned as “intermediate” and “hot” variants of the virus.

Monovalent vaccines against Gumboro disease

Vaccine	Dosage form	Strain	Manufacturer
AviPro Presize	live dry		Elanco, Germany
AVIVAC-IBB	live dry		NPP "AVIVAC", Russia
AVIVAC-IBB	live dry		NPP "AVIVAC", Russia
AVIVAC-IBB	live dry	Winterfield 2512	NPP "AVIVAC", Russia
AVIVAC-IBB	liquid inactivated		NPP "AVIVAC", Russia
Bursaplex	live dry	2512 + antibodies of hyperimmune blood serum of SPF chickens	Zoetis Inc., USA
Bursin Plus	live dry	Lukert, protein stabilizer H	Zoetis Inc., USA
Vaccine against infectious bursal disease from the “VNIVIP” strain, live, dry	live dry		FKP “Shchelkovo Biocombine”, Russia
Virus vaccine against infectious bursal disease from the BG strain	live dry		FSBI "ARRIAH", Russia
Virus vaccine against infectious bursal disease from the Winterfield 2512 strain	live dry	Winterfield 2512	FSBI "ARRIAH", Russia
Gamboromix	virus vaccine against infectious bursal disease live dry	Winterfield and BG	FSBI "ARRIAH", Russia
Nobilis Gumboro D78	live dry		Intervet/MSD, Netherlands
Nobilis Gumboro 228E	live dry		Intervet/MSD, Netherlands
Pulwak Bursa F	live dry		Zoetis Inc., USA
	dry live		Phibro Animal Health, Israel
SEVAK IBD L	live dry	Winterfield 2515, G-61	Ceva Sante Animale, France
SEVAK GUMBO L	live dry		Ceva Sante Animale, France
HIPRAGAMBORO-SN/80	live dry	Winterfield 2512, clone CH/80	Laboratorios HIPRA, S.A., Spain
HIPRAGAMBORO-GM97	live dry		Laboratorios HIPRA, S.A., Spain
Transmoon IBD	dry live	Winterfield 2515 + immunoglobulin complex from hyperimmune blood serum of SPF chickens	Ceva Sante Animale, France

Inactivated vaccines against IBD are used as part of polyvalent drugs for parent stock. They ensure the creation of the proper level of maternal antibodies in chickens.

Polyvalent vaccines against Gumboro disease are presented:

– Nobilis RT + IBmulti + G + ND (Intervet/MSD);

– HIPRAVIAR-TRT4 (Laboratorios HIPRA, S.A.);

– Sevak ND-IB-IBD-EDS K (Ceva Sante Animale);

– Provac 4 (Zoetis Inc.);

– Vaxitek HVT + IBD, Bursa Guard REO (Boehringer Ingelheim);

– Quadractin VP 2 (Abic Biological Laboratories Ltd, a division of Phibro Animal Health)

and some other vaccines, including those manufactured in Russia.

Number of impressions: 2243
Author: V. Lavrenova, marketer at the publishing house "Agricultural Technologies"

Mass breeding of chickens on farms requires compliance with many rules and regulations. Highly productive and healthy birds are the result of daily care for their health, because today there are many diseases with a rapid pace of development and a high mortality rate. One of them is Gumboro disease: let’s look at its features and the main methods of control.

What kind of disease is this

Gumboro disease, or infectious bursitis, is an acute viral disease of chickens, the appearance of which first became known in 1962 in the city of Gumboro (United States of America). Today it affects livestock not only in America, but also in other countries of Europe and Asia.

Economic damage

For poultry farmers, the losses are significant and are calculated not only in the number of dead livestock, but this is 10–20% of the total flock. Sometimes deaths are observed in 50% of the total number of sick chickens: it all depends on the age, breed and conditions of their keeping.

A large percentage of culled carcasses, which lose their attractiveness due to multiple hemorrhages and exhaustion, also bring losses.

The disease also has many indirect negative factors. Firstly, it greatly weakens the herd, making it susceptible to many other infections, and secondly, it significantly reduces the effect preventive vaccinations, thirdly, it negatively affects the productivity of the livestock.

Important!There is still no way to cure infectious bursitis. Most effective method combating the disease - timely vaccination.

The causative agent of the disease

The causative agent of the disease enters the bird's body through the mucous membranes. It is able to withstand temperatures up to +70°C for half an hour, and is resistant to alkalis (pH from 2 to 12) and acids, as well as lipid solvents. The causative agent of Gumboro disease can survive in chicken droppings for up to four months.

Only disinfectants can quickly destroy virus cells:

• formalin;
• iodine derivatives;
• chloramine

This virus does not have antigens and is classified as a reovirus. For a long time, the bursitis virus was classified as an adenovirus. For some time after the disease was identified, it was believed that infectious bursitis and infectious bronchitis were caused by the same pathogen.

Only chickens are susceptible to the infectious bursitis virus, although it is believed that the disease also affects sparrows and quails.

Epizootological data

The main risk group is reproductive farms that house individuals of different ages. The main source of bursitis is chickens infected with the virus. Most often, the disease has an acute and subacute course; less often, bursitis passes without symptoms.
The virus quickly affects the entire herd. It is noteworthy that Gumboro disease is not observed in young birds up to two weeks of age and in adult birds. Even if they are artificially infected, they will remain immune to the virus. Chicks suffer from bursitis between the ages of 2 and 15 weeks. Chickens aged 3 to 5 weeks are most susceptible to it.

Did you know? - chickenoriginally from South America,which lays blue and green eggs. The reason for this phenomenon is the increased content in the chicken’s body of a special bile pigment that colors the shell.

Keeping sick and healthy birds together, contaminated food and water, droppings, and bedding are all factors in the spread of the virus. It can also be transmitted mechanically - it is carried by people, other species of birds, and insects.

Clinical signs

Gumboro disease has a hyperacute course. The chicken dies within a week, sometimes even faster. The incubation period for bursitis ranges from three to fourteen days.

Clinical manifestations are similar to coccidiosis:

• diarrhea;
• severe apathy;
• trembling;
• disheveled;
• refusal of food;

A pathological autopsy of a bird infected with the bursitis virus reveals characteristic signs indicating the cause of death - inflammation and hyperplasia of the bursa of Fabricius, excessive hemorrhages in muscle tissue, skin and nephritis.
Such signs allow a clear diagnosis.

Important! Chickens that die from Gumboro disease die in a characteristic position - with their legs and neck outstretched.

Pathogenesis

The disease is characterized by rapid spread: its pathogen, which enters the body orally, reaches the intestinal lymphoid cells within five hours. Rapid dissemination of the disease is achieved by the penetration of these cells into all circulating systems.

After 11 hours, the virus infects the bursa of the plant. Thus, after two days, infectious bursitis affects all organs. The main place of concentration of the virus is the bursa of Fabricius: it can remain there for up to two weeks.

Damage to lymphoid tissue leads to a pronounced immunosuppressive effect. The number of lymphocytes sharply decreases, and almost complete suppression of immunity is observed.
In general, immunity weakened by the Gumboro disease virus leads to an increased incidence of poultry with viral hepatitis, salmonellosis, gangrenous dermatitis and coccidiosis.

Diagnostics

Clinical and pathological features make it possible to accurately diagnose the typical form of the disease. Identify an atypical course of the disease or establish it early stages allows laboratory test, based on the isolation and identification of the virus.

To exclude bursitis in differential diagnosis, you need to make sure that the chickens are not sick:

• lymphoid leukemia;
• sulfonamide poisoning;
• fat toxicosis.

Treatment

Due to the fact that the body of recovered chickens develops immunity to Gumboro disease, a large number of live vaccines with a high degree of immunogenicity have been created. The most common vaccines: Gumbo-Vax (Italy), LZD-228 (France), Nobilis (Holland).

Did you know?A chicken can be put into a state of hypnosis by gently pressing its head to the ground and drawing a straight line from the bird's beak with chalk.

Day-old chicks are vaccinated by drinking or intraocularly, young animals over three months of age are vaccinated intramuscularly. Antibodies from vaccinated individuals at high levels are transferred to chickens and protect them during the first month of life.

Prevention

To avoid the disease, you must:

• provide the bird complete diet nutrition;
• carry out cleaning and disinfection in a timely manner;
• keep birds of different ages separately;
• equip the poultry house with individuals of the same age;
• carry out incubation of own-produced and imported eggs separately;
• place day-old young stock brought from other farms separately from the main herd;
• comply with the timing of preventive vaccination;
• ensure the protection of the herd from the introduction of infection: purchase eggs and day-old young animals only from farms that are free from infectious bursitis;
• strictly comply with zootechnical and veterinary requirements for keeping and feeding birds.

Compliance preventive measures and careful attention to the products and young stock purchased for incubation can significantly reduce the risk of birds becoming infected with infectious bursitis. In the event that this does happen, the sick individuals must be destroyed.