Syndrome of decreased egg production of chickens, egg casting syndrome, EDS-76, "Syndrome-76", adeno viral disease chickens(Egg drop syndrome - eng.) - a viral disease that affects commercial and breeder laying hens, characterized by a decrease in egg production, softening or disappearance of the egg shell, loss of shell color in breeds of hens that lay brown eggs.

Prevalence... The disease was first described by Van Eck in 1976. It is currently reported in Holland, England, Northern Ireland, France, Italy, Germany, Spain, Belgium, Yugoslavia, Denmark, Hungary, Sweden, Argentina and the United States.

Economic damage caused by the disease is due to losses associated with a decrease in egg production. According to J. Macpherson, the loss in England was £ 2.4 million a year. French scientists note that in birds in cages, productivity is restored within 4-6 weeks, and when kept on the floor, it is 8-10% lower. Egg loss per poultry in disadvantaged flocks is 17.7%, estimated at 116.9p. A sick bird carries up to 15% of deformed, with a weak or no shell or depigmented eggs. According to Darbyshire (1980), the number of eggs with damaged shells can reach 38-40%. J. McFerran et al. (1978) note that the loss of productivity in this disease is on average 12 eggs per hen.

Economic damage is also associated with a decrease in the quality of hatching eggs. More than 50 eggs from a laying hen are not suitable for incubation due to the fragility of the shell. In addition to high culling, there was also a decrease in hatchability and viability of chicks in the first days of life.

Causative agent... Various researchers have identified several strains, the identity of which has been confirmed by serological studies. Strain 127 was isolated in Northern Ireland from the mucous membrane of the nasal cavity and pharynx of birds. The virus (ВС 14) was isolated from blood leukocytes, its identity was serologically confirmed to the virus 127 isolated from oviducts, feces, nasopharynx of chickens in affected herds; antibodies to this agent were also found (W. Baxendale, 1977, 1978; J. McFerran et al. , 1977, 1978). Under experimental conditions, the disease was reproduced by infection of laying hens and broilers, and it was established that an isolated virus is an etiological agent (W. Baxendale, 1977; W. Baxendale et al., 1978; McCraken, J. McFerran, 1978).

Strain D61 was isolated from the cloaca of a laying hen in England. In Hungary, strain B 8/78, identical to strain 127, was obtained; in France, 3 strains were isolated. The virus has been identified as an adenovirus (Todd, McNulty, 1978), but group-specific antigens with the main avian adenoviruses by gel diffusion have not been established (W. Ba-xendale, 1977; J. McFerran et al., 1978). However, some degree of cross-reactions with avian adenoviruses was observed using the method of indirect immunofluorescence (W. Baxendale, 1978).

The egg-laying virus is not associated with any of the 11 serotypes of avian adenoviruses (J. McFerran et al., 1978) and differs from other avian adenoviruses in the ability to agglutinate erythrocytes of chickens (J. McFerran et al., 1977), ducks and geese (W. Baxendale, 1977).

The EDS-76 virus multiplies in high titers in duck kidneys, duck embryo liver and duck embryo fibroblasts, worse - in chicken liver cells and extremely low in chicken embryo fibroblasts. The virus is not cultured in mammalian cells. It replicates in the nucleus of cells in the manner described for the first subgroup of adenoviruses. An electron microscopic study of thin sections of infected cells revealed viral particles and associated inclusion bodies in both human-type adenoviruses and avian adenoviruses.

The pathogen is resistant to ether and pH over a wide range. Its infectious properties are lost within 30 minutes at 60 ° C, it is also inactivated by trypsin, urea and pyridine. This is a DNA-containing virus that does not have an outer shell, the density in cesium chloride is 1.34; the sedimentation constant in sucrose is 940; the diameter of the virion is 75-80 nm, the symmetry of the capsid is cubic.

V. Kraft et al. (1979) electron microscopic examination of isolate 127. 3 lines were observed in the CsCl gradient. Two lines had a density of 1.32 g / ml, which were not separated by fractionation and were responsible for high hemagglutinating activity and infectivity. These lines contained particles morphologically typical of adenoviruses. The third line (density 1.30 g / ml) consisted mainly of broken particles and showed a noticeable peak in hemagglutinating activity.
Hemagglutinin of the virus is stable for 30 min at 70 ° C, but higher temperatures cause inhibition of activity. Purified soluble hemagglutinin contains 2 polypeptides with molecular weights of 65,000 and 67,000, consists of rod-shaped structures 25-30 nm in length.

The virus is icosahedral, particle size, capsid structure, and the number of capsomeres are typical for adenoviruses (V. Kraft et al., 1979).

Epizootological data insufficiently studied. Egg loss syndrome affects laying hens of all breeds between 25 and 35 weeks of age. The most susceptible beef breeds that give brown eggs, as well as breeding birds. Breeds that lay white eggs are less susceptible. The duck-casting syndrome virus is suspected to be of duck origin, but it is non-pathogenic to them. In Northern Ireland, chickens are believed to have become infected following the use of the Marek's disease vaccine from the Rispen strain obtained from duck tissue culture in the Netherlands. In Ireland and the Federal Republic of Germany, a disease with signs of EDS-76 was observed for the first time in chickens imported from the Netherlands.

The disease is reproduced by artificial infection of poultry conjunctivally and orally. The virus spreads vertically through the egg. A number of researchers also recognize the horizontal route of transmission, attaching great importance to droppings. The spread of the virus is suspected with the semen of the roosters.

Epizootological feature of the egg production syndrome- the ability of the virus not to manifest itself in the body of birds until they reach sexual maturity. The reason for the activation of the pathogen is the stressful effect on the body, due to the onset of oviposition.

Pathogenesis insufficiently studied. It is only known that there is a violation of the formation mechanism eggshell... Ovarian atrophy and hemorrhage are also observed. Acidity increases in the uterus, which can lead to calcium dissolution and impaired shell formation. In case of experimental infection of laying hens, defective eggs appear on the 4th-7th day, the content of protein and calcium in the blood does not change.

Clinical signs are usually not present. However, ruffled feathers, anemia, diarrhea, a state of prostration, and decreased activity during oviposition can be observed. In the later stages of the disease, cyanosis of catkins and scallops may appear in 10-70% of birds. Typical signs of the disease: discoloration of the shell in eggs with a brown color, the appearance of eggs with a thin shell or without it, a decrease in egg production. These signs persist from 2-3 to 6-12 weeks and are typical for chickens. meat breeds and brown crosses. For chickens of egg breeds, a change in the internal quality of eggs is also characteristic: the white becomes watery and cloudy.

Pathological changes or absent, or there is a weak catarrhal enteritis, atrophy, edema and mononuclear infiltration of cells of the glandular tissue of the uterus and oviducts.

Diagnosis and differential diagnosis... The diagnosis is based on data of clinical signs, pathological changes and serological examination. The most reliable diagnostic method is the hemagglutination inhibition reaction (RTGA). In the study of paired sera 15 days and 2-3 weeks after infection, an increase in the titer of antihemagglutinins to 1: 1280-1: 2560 is noted.

The egg casting syndrome must be differentiated from Newcastle disease, infectious bronchitis, coccidiosis, helminthiasis, poisoning with pesticides, fungicides, mycotoxins and various factors of non-infectious etiology that cause a decrease in egg production (housing conditions, feed quality, diet balance, etc.).

Treatment not developed. To maintain the optimal level of hatchability and viability of the offspring, it is recommended to use complete diets, especially in relation to essential amino acids, vitamins and microelements.

Immunity and specific prophylaxis... A naturally recovered bird develops a tense immunity. 7 days after infection, virus neutralizing, antihemagglutinating and precipitating antibodies associated with IgG immunoglobulin are found. Chicks hatched from infected chickens retain their maternal antibodies, which have a half-life of 3 days. Passive antibodies ensure the resistance of chickens to infection in the first 4 weeks of life.

For specific prophylaxis, an oil formol vaccine is used from the BC 14 strain grown on a duck embryo cell culture. The vaccine is administered once intramuscularly or subcutaneously at a dose of 0.5 ml (1000 HAU), starting from 18 weeks of age.

The EDS-76 vaccine was tested in France, the Netherlands, Great Britain, Belgium and Luxembourg, Argentina. After vaccination, the viremia phase and associated virus excretion are not observed, egg production and shell quality are improved. Immunity is formed after 15 days, maximum antihemagglutinins accumulate after 30 days. The antibody titer begins to decline 12-16 weeks after vaccination. Antibodies are not detected after 40-50 weeks.

Vaccination is considered as a temporary measure due to the danger of the spread of the virus and its adaptation to chickens. In Yugoslavia (M. Krecov et al., 1980), a vaccine inactivated with 13-propiolactone and adsorbed with aluminum hydroxide, made from the virus of strain 127, was tested with a positive result.

Prevention and control measures... For incubation, it is recommended to use eggs from hens over 40 weeks of age, giving negative results in serological tests. In England, Northern Ireland and the Federal Republic of Germany, the slaughter of poultry that reacts positively in serological reactions in order to prevent the vertical transmission of the pathogen through the egg is considered a radical measure to combat and prevent egg production syndrome. An inactivated vaccine is allowed.

Egg Drop Syndrome(Edd drapsyndrome-76, EDS-76, egg casting syndrome) is a viral disease of laying hens, characterized by a sharp decrease in the carrier, softening or absence of egg shells, and a decrease in their incubation quality.

History reference. The disease belongs to the poorly understood adenovirus infections of poultry, accompanied by the EDS-76 syndrome (egg production syndrome-76). In 1976, it was found that the duck adenovirus EDS-76 (strain 127) is pathogenic for chickens, causing them to "lay unripe eggs" without hard shells. The disease is reported in many countries around the world.

In poultry farms that are not successful according to EDS-76, there is a decrease in the productivity of laying hens in the ZO - 60%, a deterioration in the quality of eggs, a decrease in fertility in hens and the viability of chickens.

Causative agent of the disease- duck DNA genomic virus EDS-76 (strain 127), belonging to the Adenoviridae family. Virions are spherical, 75 - 80 nm in diameter. The virus agglutinates the erythrocytes of chickens, ducks and geese. In sick chickens, it appears in the oviducts, upper respiratory tract, nasal and pharyngeal mucus and liver within 15 days after the first clinical signs of the disease appear. It multiplies in duck and chicken embryos when infected in the alantoic cavity, causing their death on the 7th - 10th day. It is reproduced in primary cultures of kidney and liver cells of duck embryos, fibroblasts of duck embryos, more difficult - in cultures of liver cells of chickens and kidneys of chickens. Forms intranuclear acidophilic inclusions in the epithelial cells of the muscular stomach, causes degeneration of hepatocytes and vacuolization of the cell cytoplasm. The EDS-76 virus is resistant to chloroform, ether, trypsin, 2% phenol solution, 50% alcohol solution, but is sensitive to formaldehyde. Remains active at 50 ° C for 3 hours, at 56 ° C for 1 hour, at 80 ° C for 30 minutes.

Epizootology of the disease. Laying hens 25 - 35 weeks of age are ill with the syndrome of decreased egg production. The disease mainly affects breeding poultry and meat breeds, laying eggs Brown. The source of the causative agent of the disease is sick and ill chickens, which are carriers of the virus for a long time. Domestic and wild ducks, geese and other waterfowl can be potential sources of the EDS-76 virus. From the body of sick chickens, the virus is excreted in feces, outflows from the oral cavity and nasal openings, eggs. The EDS-76 virus is transmitted vertically through infected eggs, although it is possible for the pathogen to spread horizontally through infected droppings and male semen.

Virus transmission factors can be poultry houses, egg shells, feed, drinkers, poultry care items, clothing and footwear of service personnel contaminated with the secretions of infected chickens. The virus can enter the body of healthy chickens transovarially, alimentary, aerogenic, contact. Disease in infected chickens occurs during the egg-laying period, until that time no clinical signs of infection have been observed.

The pathogenesis has not been studied. It was found that the EDS-76 virus multiplies in the epithelial cells of the oviduct, disrupting their function of forming a high-quality shell.

Clinical signs and course of the disease. The main clinical sign of the disease is a sharp (by 30% - 60%) decrease in hens' egg production within 6 - 7 weeks. At the same time, in the first 4 - 5 weeks, productivity decreases, and in the next 2 - 3 weeks, its gradual recovery is observed. During the first 2 - 3 weeks of illness, hens lay eggs with weak, deformed and depigmented shells, with rings and stripes along the equator, or without shells at all. The quality of eggs also significantly deteriorates, their white becomes watery and cloudy. The incubation qualities of eggs are sharply reduced, chickens that hatch are unviable, frail, most of them die within the first day. Sick chickens become frail and inactive, lose their appetite, lose weight, their ovarian function is disturbed, and sometimes diarrhea appears. After 2 - 3 weeks, the chickens begin to recover, gradually gain weight and restore egg production, but they never reach the initial level.

Pathological changes. Mostly absent or weakly expressed. Sometimes there are signs of catarrhal enteritis, edema and infiltration of the oviducts.

Diagnosis are established on the basis of epizootological data, clinical symptoms of the disease and, mainly, according to the results of laboratory tests.

Laboratory diagnostics. Provides for the isolation of the virus on 12 - 13-day-old duck embryos by infecting them in the alantoic cavity, as well as in primary cultures of fibroblast cells of duck embryos, indication and identification of the isolated virus for RIF (specific luminescence of fibroblast cell cultures is observed already 14 hours after their infection) , for PH (on duck embryos and primary cell cultures of duck fibroblasts), for RGHA, which is considered the most sensitive in comparison with other diagnostic tests. Retrospective diagnosis is carried out with the blood serum of sick chickens of 160 - 180 days of age on the 5th - 7th day of illness and again after 15 - 21 days. An increase in anti-hemagglutinin titers in the second sample indicates the circulation of the virus among the birds. RSHA is recommended for mass serological examinations. At the same time, the carriers of the EDS-76 virus are considered to be the trigger, in the blood of which antibodies are found in titers 1: 4 - 1: 32.

The following are sent to the laboratory in a thermos with ice: from clinically sick chickens (from the 1st to the 7th day of illness) nasopharyngeal washings, scrapings from the conjunctiva, feces (up to the 10th day of illness); from dead chickens - the nasal septum, lungs, trachea, liver, intestines, lymph nodes. For retrospective diagnostics, paired blood serums are sent, which are taken on the 5-7th day of the disease, and then after 15-21 days.

Differential diagnostics. Provides for the need to exclude Newcastle disease, coccidiosis and poisoning. For this purpose, appropriate virological, helminthological and toxicological studies are carried out.

Immunity. Long-term immunity is formed in chickens who have recovered from the egg production syndrome. For specific prophylaxis of the disease, inactivated and live vaccines based on the EDS-76 adenovirus from strains 127 and BC-14 have been proposed.

No treatment has been developed.

Prevention and control measures. They are based on strict observance of veterinary and sanitary rules in order to prevent the introduction of the causative agent of the disease from the outside. For incubation, eggs are used only from chickens older than 40 weeks, which are preliminarily checked for RZGA. Re-examination is carried out in 2 - 3 weeks. Serologically positive chickens with increasing hemagglutinin titers are sacrificed. Their presence indicates the circulation of the virus in the farm.

In the event of an illness, quarantine restrictions are immediately imposed. The entire dysfunctional group of birds is slaughtered. Mechanical cleaning and double disinfection of the premises and places of stay of the infected bird, a preventive break in the incubation of eggs for a period of 2 months is carried out. Carry out clinical and serological examination of all poultry available on the farm. Positively reacting chickens are slaughtered for meat. Adult chickens are vaccinated with the inactivated vaccine before laying.

For disinfection, a 2% formaldehyde solution, a 3% sodium hydroxide solution is used with an exposure of 1.5 hours.

A viral disease of chickens, accompanied by a sharp decrease in egg production, softening and depigmentation of the shell, a deterioration in the incubation qualities of eggs. When eggs are incubated from sick chickens, the number of unfertilized eggs increases due to false infertility, the death of embryos in the early stages of development.

The causative agent is a DNA virus of the Adenoviridae family. There are more than 12 serotypes of the virus that share a common group antigen. The most susceptible to the EDS-76 virus are chickens of high-yielding crosses laying eggs with brown shells (Hisex Brown, Lohmann Brown). This disease is characterized by a wide range of antibody titers even within the same farm, which is associated with the peculiarities of the epizootic situation, the conditions of feeding and keeping poultry, and age-related natural resistance. The virus spreads by aerogenic and alimentary routes, contact and transovarial.

Clinical picture

The incubation period is 1-15 days. The egg production syndrome is often associated with infectious bronchitis of chickens. Clinically, there is a sharp drop in egg production by 20-28%, laying eggs with a rough or softened shell, with white spots. After the manifestation of EDS in the flock, a decrease in egg-laying is observed within 3-5 weeks. Lay recovery is slow and never reaches the target breed standard. In beef breeds, only shell depigmentation and a slight decrease in egg production are observed.

Hemorrhagic ovarianitis with EDS-76

Pathomorphology

The kidneys are enlarged, in the liver there are multiple hemorrhages under the capsule. The bursa and spleen are atrophied. The accumulation of exudate in the cardiac shirt and intermuscular space is noted. EDS is characterized by ovarian atrophy with hemorrhages, hemorrhagic inflammation of the oviduct.

Rough build-up on the shell at STYA-76

Diagnostics

Based on clinical signs (very typical for EDS-76) and serological studies (RIF, RN, RTGA and ELISA).

Differential diagnosis is carried out from infectious bronchitis of chickens, Newcastle disease, infectious laryngotracheitis as well as violations mineral metabolism substances associated with the formation of the shell.

Treatment and prevention

Specific prophylaxis is based on the use of inactivated vaccines:

• Liquid inactivated sorbed vaccine against EDS-76.
• Inactivated emulsified vaccine against EDS-76 (FGU ARRIAH, Vladimir).
• Inactivated liquid vaccine against EDS-76 (OOO VNIVIP-drugs).
• Associated inactivated vaccine "Avivak" against NB, IBV, IBD, EDS-76 and REO (NPP Avivak).

1. Definition of disease

Egg Drop Syndrome-76 (English - Egg drop Syndrome-76; casting eggs, adenovirus infection of chickens, EDS-76) - a viral disease of laying hens, characterized by softening, absence or depigmentation of the egg shell, violation of the protein structure, a sharp but short-term decrease in egg productivity ...

2. Historical background, distribution, hazard and damage

This disease first appeared in 1976 in Holland, hence the name EDS-76. The hypothesis of the occurrence of this disease, proposed by McFerren, is that the causative agent of EDS-76 is a duck adenovirus, which does not cause pathology in its natural hosts. Before the first registration of an outbreak in chickens, a vaccine against Marek's disease was widely used, prepared in cell cultures of developing duck embryos. Probably, duck cells were contaminated with adenovirus, which quickly adapted to a new host for it and showed its pathogenic properties.

STYA-76 quickly spread in the countries of Western Europe with developed industrial poultry farming. Currently, the disease is recorded in most European countries, in the USA, Argentina, India, Iran, Japan, Australia. STYA-76 was noted in different regions of the Russian Federation (Moscow, Nizhny Novgorod, Sverdlovsk, Chelyabinsk, Kaluga and other regions).

The economic damage from the disease is caused by losses associated with a decrease in egg production (the egg production of breeders is reduced by 15%). Disease productivity loss averages 12 eggs per hen. In England, the cost of Egg Drop-76 Syndrome is as high as £ 2.4 million per year. The proportion of eggs with shell defects can be 38 ... 40%, the hatchability level and viability of chickens in the first days of life are sharply reduced.

3. The causative agent of the disease

The Adenoviridae family is divided into two genera: mammalian adenoviruses (Mastadenovirus) and birds (Aviadenovirus).

The causative agent of EDS-76 is attributed to the genus Aviadenovirus. It is a DNA-containing virus with no outer envelope. The diameter of the virion is 75 ... 80nm. Electron microscopic examination of sections of infected cells

showed that viral particles and associated inclusion bodies are characteristic of adenoviruses.

The virulence of the pathogen is lost when heated for 30 minutes at 60 "C. Hemagglutinin is relatively thermostable and can withstand heating for 30 minutes at 70" C. Avian adenoviruses are easily susceptible to the inactivating effect of ultraviolet radiation and photodynamic inactivation. Compared to the BN virus, they are 15 times more sensitive to ultraviolet irradiation and 10 times more sensitive to photodynamic effects. At the same time, they are resistant to 0.25% trypsin solution, 2% phenol solution, 50% ethyl alcohol solution, tolerate multiple repetitions of freeze-thaw cycles well, remain at pH 6.0 ... 9 , 0. The most effective disinfectant is a 1% formaldehyde solution.

4. Epizootology

V In natural conditions, the source of the causative agent of the disease is domestic and wild ducks of all breeds, among which the virus is widespread. In addition, various types of domestic and wild birds can be carriers without clinical manifestations of the disease.

Studies have shown that the main route of transmission of the pathogen and the spread of the disease is transovarian. A number of researchers confirm the horizontal transmission route of EDS-76 and attach great importance to it in the spread of the disease. Cases of the spread of the causative agent of the disease with the semen of roosters during artificial insemination of chickens have been reported.

Under natural conditions, after recovering from the disease, chickens remain virus carriers for a rather long time. When poultry is kept on the floor, the disease spreads within 10 ... 15 days. Under these conditions, the pathogen is transmitted by contact, through service personnel, care items, vehicles, etc.

An epizootological feature of EDS-76 is the presence of a virus carrier, which determines the development of the disease upon reaching puberty. The reason for the activation of the virus is the stressful effect on the body associated with the onset of oviposition.

EDS-76 affects chickens mainly at the very beginning of the period of intensive egg-laying, that is, at the age of 27 ... 32 weeks. It was found that in about 42% of infected birds the first signs of the disease appear at the age of 27 weeks, in 28% - at the age of 30 weeks. It was noted that birds over 40 weeks of age do not suffer from EDS-76 and do not contain antibodies to this virus in their blood.

Another unusual feature of the disease is the well-defined reactivation time of the pathogen after the contaminated bird reaches full puberty. In birds of many parental flocks, it was not possible to detect antibodies to the EDS-76 virus in the blood at the age of 20 weeks, while at the age of 30 weeks, not only antibodies were recorded, but also typical signs of EDS-76 disease.

5. Pathogenesis

The pathogenesis of EDS-76 is not well understood. It is assumed that after infection of the bird, the stage of viremia begins. The pathogen migrates with the blood, reaching the sensitive epithelial cells of the intestinal mucosa and, possibly, the epithelium of the oviduct. Further development of the infectious process largely depends on the age of the infected bird. If the infection occurred in the period preceding the stage of intensive egg-laying, then the virus is actively reproduced in sensitive cells and is excreted in feces and eggs. In the event that the transmission of the virus was carried out transovarially, that is, from parents to offspring, then in the first days of life the chickens serve as a source of the causative agent of infection, infecting intact livestock. In infected birds, infection is latent until the start of oviposition. During this period, it is usually not possible to isolate the virus from any pathological material. In chickens aged 150 ... 180 days, the pathogen is activated, beginning to actively multiply in the epithelial tissue and be released into the external environment.

6. Course and clinical manifestation

Clinical signs of the disease in chickens are not always characteristic. Isolated cases of prostration, ruffled feathers, anemia, diarrhea, and oppression during oviposition have been reported. In addition, in 10 ... 70% of sick birds, cyanosis of the earrings and comb is noted. Appetite does not change or increases slightly; decreased physical activity.

The main characteristic signs of the disease are a decrease in egg production by 15 ... 30%, as well as the presence of eggs with a thin shell or without shell, deformation of eggs and discoloration of the shell, as well as lime deposits on it. After the onset of these symptoms in a herd of chickens, a sharp decrease in egg production is observed. Egg shell depigmentation can also begin after a decrease in egg production. As already noted, egg production begins to decline in birds at the age of 28 ... 30 weeks (the period of peak egg-laying) and lasts 6 ... 12 weeks. The degree of decrease in egg production in the process of re-illing in different herds depends, obviously, on the completeness of feeding the birds, adherence to keeping technology and breed characteristics.

For chickens of egg breeds, a change in the structure of the protein is characteristic: it becomes watery and cloudy.

7. Pathological signs

Pathological changes are characterized by edema and infiltration of the tissues of the uterus and oviduct, minor catarrhal enteritis. In some cases, there are no changes during autopsy. Histological examination revealed degeneration of the calcifying glands and their mononuclear infiltration, lymphoid hyperplasia of varying degrees in the liver, spleen and other organs, as well as atrophy of the uterine glands, infiltration of heterophiles, lymphocytes and plasma cells, accompanied by extensive edema.

8. Diagnostics and differential diagnostics

The diagnosis for EDS-76 is established on the basis of epizootological data, clinical signs, pathological changes and laboratory results.

Pathological material from fallen or forcedly killed birds is taken no later than 2 hours after clinical death or slaughter. To isolate the virus, segments of the intestines of sick birds, cloacal washings and blood leukocytes are used.

The EDS-76 virus is isolated from pathological material on duck embryos or duck fibroblast cell culture. To isolate the virus, it is necessary to carry out at least three consecutive passages. To identify the virus, RDP and RN are performed on the same cell cultures. RIF and ELISA are used as an express diagnostic method.

To find out the cause of the disease, methods of early and retrospective diagnosis have also been used. RSHA is a highly specific and sensitive method for determining the content of antibodies to the EDS-76 virus. Paired blood sera taken from birds suspected of the disease at different ages are examined with an interval of 2 weeks.

EDS-76 should be differentiated from chicken infectious bronchitis (IBC), poisoning with pesticides, fungicides, mycotoxins and various disorders of non-infectious etiology that cause a decrease in egg production.

9. Immunity, specific prevention

Recovered chickens acquire tense long-term immunity and do not fall ill again.

When studying passive immunity, it was found that one-day-old chickens hatched from eggs laid by hens from the 7th to the 11th day after infection with the EDS-76 virus develop specific antibodies that disappear by 2 ... 3 weeks. "

Vaccination provides complete protection against disease and improved egg quality. Immunity occurs 10 days after vaccination and lasts up to 1 year.

The firm "Intervet" (Holland) produces an inactivated bivaccine against Newcastle disease and EDS-76 and a trivalent vaccine against EDS-76, Newcastle's disease and Gumboro disease. These vaccines are effective and widely used in various countries of the world, including Russia. In Russia, the inactivated vaccine against EDS-76 is produced by ARRIAH.

To assess vaccine prophylaxis, immunological control of the vaccinated poultry is necessary.

10. Prevention

In order to prevent EDS-76, it is necessary to: 1) strictly observe the current veterinary and sanitary rules for poultry farms and the requirements for their design, including taking measures to protect the farm from the introduction of infectious pathogens; 2) to equip parental and industrial flocks of birds with hatching eggs and day-old chicks from poultry farms that are safe according to EDS-76; 3) place birds of different age groups in geographically separate zones; 4) not to allow the joint keeping of chicken, duck and goose herds in the poultry farm; 5) carry out thorough cleaning and disinfection of meat and egg containers; 6) to vaccinate birds against EDS-76 when antibodies are detected in the blood serum of hens in RZGA or ELISA or in contact with an unfavorable farm for the disease.

11. Control measures

When confirming the diagnosis of egg production syndrome-76, a decision is made to declare the economy (farm) or settlement as unfavorable and restrictions are introduced.

According to the restrictions, the following are prohibited: 1) movement of birds within the holding (farm, branch) during the period of illness; 2) removal of birds of all age groups from a dysfunctional economy (branch, farm) and their sale to the population; 3) removal of hatching eggs to other farms; 4) use for incubation within the farm of eggs obtained from hens from disadvantaged poultry houses; 5) taking semen from males and artificial insemination of hens of the parent flock during the period of clinical manifestation of the disease; 6) removal of feed, equipment and inventory from dysfunctional production facilities and from the territory of a dysfunctional economy (farm, branch); 7) the entrance to the territory of a dysfunctional economy and the exit from it of the service personnel without complete sanitization, change of clothes and shoes; 8) entry and exit from the territory of a dysfunctional economy of vehicles without disinfection.

Under the terms of the restriction, it is allowed:

1) use eggs from disease-free flocks of birds (poultry houses), in which antibodies to the EDS-76 virus were not detected in the blood serum in the RZGA or ELISA, for incubation for on-farm purposes;

2) to take out eggs from dysfunctional poultry houses after disinfection in a disinfected container for sale in a retail network and a public catering network in cities;

3) in the absence of slaughter points on the farm, take the birds to the poultry processing enterprises within the time frame agreed with the veterinary authorities of the region (region, republic within the Russian Federation), and when conditions are created to exclude the spread of the disease.

For aerosol disinfection of air, surfaces of industrial premises and equipment in the presence of birds in dysfunctional poultry houses, iodotriethylene glycol, lactic acid, chloro-turpentine vapor, sodium hypochlorite or stabilized hydrogen peroxide solution are used, guided by the current instructions for aerosol disinfection of poultry buildings in the presence of birds.

During the period of trouble of the economy (farms, departments) according to EDS-76, they carry out a thorough mechanical cleaning, current and final disinfection of dysfunctional poultry houses, hatcheries, ancillary premises, inventory and equipment, production territory, means of transport and other objects in the manner and within the terms provided for by the current instructions for conducting veterinary disinfection of livestock facilities, as well as disinsection and deratization. For wet disinfection of premises free from birds, a hot solution of sodium hydroxide, a solution of formaldehyde, a clarified solution of bleach, a slurry of freshly slaked lime (calcium hydroxide) by double whitewashing or a hot solution of soda ash is used.

Restrictions on EDS-76 on the farm (farm, department) are removed 2 months after the last case of detection of sick birds (decreased egg production, casting eggs, the presence of deformed and depigmented eggs).

In the former farm, which is not successful in terms of EDS-76, all susceptible livestock are vaccinated for at least 3 years. The question of stopping the immunization of birds is decided by a commission with the participation of representatives of higher veterinary authorities.

Bibliography

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