A person who breeds chickens for eggs and meat on his site should not only study the rules for breeding and keeping them, but also have an idea of ​​the diseases that can affect his feathered pets. And not only to know about them, but also to be able to react in a timely manner and correctly, so as not to miss the conditions that are dangerous for the life of birds, as well as for human health. This article discusses a common disease called egg drop syndrome-76.

There are diseases poultry, transmitted from one species to another without pronounced symptoms until a victim is found that has a sensitivity to the causative agent of the disease.

Did you know? Chickens were first domesticated about three thousand years ago in the territory where modern Ethiopia is located.

Egg Drop Syndrome-76 (EDS-76) was first discovered and described in the Netherlands in 1976. It is believed that the virus is carried by ducks: domestic and wild, they themselves, however, are not susceptible to disease.

The fact that no antibodies to the pathogen were found in serum samples obtained from chicken blood before the specified year is considered evidence that this disease arose during this period.

Subsequently, virus strains identical to the original, strain-127, were isolated in various progressive countries: England, France, Italy, Japan, Hungary. This means that the detected disease began to spread throughout the world.

EDS-76, or adenovirus disease (Egg drop Syndrome-76), is characterized by the fact that laying hens due to damage to the reproductive system decreases egg productivity, the eggs change their shape, their quality deteriorates, the shell is fragmentarily depigmented and softens or is completely absent, protein structure is disrupted.

The causative agent of this pathology is a DNA-containing adenovirus (Adenoviridae), hence the other name of the disease. This microorganism does not belong to the known types of avian adenoviruses and is capable, in contrast to the mentioned ones, of gluing (agglutination) of erythrocytes of many, including domestic, birds.

Did you know? The chicken will not lay in the dark, even if the time is right. She will wait until the day comes or the lights are on.

After the chicken has suffered this disease, it acquires antibodies that it can transmit to offspring through the eggs.

The microorganism is sensitive to formaldehyde, but it cannot be destroyed:

• ether;
• chloroform;
• trypsin;
• phenol solution 2%;
• alcohol solution 50%.

At 50 degrees, it is active for 3 hours, at 56 degrees - one hour, at 80 degrees - half an hour. It is known that the pathogen multiplies in the cells of the epithelium of the oviduct and, at the same time, the formation of eggshells of normal quality is disturbed.

Did you know?The one-day-old chick has a set of reflexes and skills that match that of a three-year-old human child.

A bird that has undergone a disease after recovery may experience:

• swelling of the oviducts and atrophic processes in them - shortening and thinning;
• in some cases - cysts;
• changes in the liver: increase in size, yellowing, flabby structure;
• enlargement and fluid filling of the gallbladder.

Causes of the onset of the disease

A chicken of any breed and any age, starting from a productive one, can get sick, however, the “favorite” age for the manifestation of the virus is the peak of chicken productivity: 25-35 weeks. Chickens of pedigree breeds, as well as laying hens belonging to the meat type, are more susceptible to it.

The manifestations of the disease are the brighter, the higher productivity is expected from an individual in accordance with its breed characteristics.
Adenovirus transmitted transovarially (through an egg laid by an infected laying hen) can remain asymptomatic in the body of a young bird until the time when its body experiences stress, for example, the start of laying. At the right moment for him, it is activated, reducing the egg production of the chicken. This transmission method is called vertical.

It is noteworthy that a chicken hatched from an infected egg or infected with the EDS-76 pathogen in the first days of life will not show vivid manifestations of the syndrome at the peak of productivity, however, one should not expect high egg production from it.

The possibility of horizontal infection also remains:

• contact - by means of clothing and footwear of people, transport, household items and care;
• sexual - through the sperm of a cock;
• fecal-oral - through droppings and discharge from the nasal and oral cavities of infected individuals;
• by vaccinating poultry against other diseases.

The carriers of the EDS-76 causative agent are infected, as well as recovered chickens, ducks and geese, both domestic and wild, as well as other waterfowl. Wild birds can carry disease over great distances through contaminated feces.

Important! In the case when the bird is kept crowded, in close contact, the spread of the virus is significantly accelerated and infection of the entire flock can occur in 1-14 days. On the other hand, layers isolated from each other by partitions are able to remain healthy for a long time, even when they are close to an infected individual.

Economic damage

STYA-76 brings significant economic damage to both private farms and large industrial enterprises. During the illness, culling from one laying hen is 10-30 eggs, and in breeding birds it reaches 50. This means 17-25% damage.
It takes from 4 to 6 weeks to restore the productivity of one individual, if it is contained in the cage. In chickens kept on the floor and in contact with other individuals and their biological material, egg production may never be restored to its original level by 6-12%.

As for the hatching eggs laid by infected individuals, many of them are simply unsuitable for hatching young animals due to their too fragile shell. In addition to the fact that a large percentage is rejected already at the initial stage, hatchability of chicks decreases. The level of their survival in the first days after hatching is also reduced.

Although in our time there is much more information about this disease, and enough experience has been accumulated in the fight in comparison with 1976, some questions are still controversial and do not have an unambiguous answer.

Important! The syndrome is widespread in those countries where highly developed industrial technologies of poultry farming are used, and the greatest damage is caused to breeding farms.

Symptoms

Until the beginning of the productive age, in an infected individual, the pathogen resides in the intestine and does not manifest itself in any way. When the time comes and the hormonal background of the chicken changes to ensure egg production, the virus is activated and the stage of viremia begins, that is, the circulation of the virus in the body through the bloodstream.

Reaching the epithelium of the mucous membrane of the oviduct, the virus contributes to the imbalance of minerals: sodium, potassium, magnesium, calcium and others, as a result of which the chicken lays eggs with a shell that is too thin, deformed, or even completely absent.

Did you know? In addition to its reproductive role, a rooster in a chicken herd performs a number of important social and administrative functions: control over the daily routine, prevention of conflicts, protection from danger, even if the enemy is obviously superior in strength and size.

For all the severity of the infection, chickens rarely show any signs of disease.

Occasionally, more often in an insignificant form, the following can be observed:

• signs of general intoxication - weakness, fatigue and others;
• decreased appetite;
• diarrhea and the presence of a green tint in the droppings;
• anemia;
• weak breathing at the peak of an acute condition;
• bluish shade of scallop and earrings.

The main sign and symptom is a sharp decrease in productivity, the laying of thin, deformed eggs of very poor quality. The protein in such a product is watery and cloudy. Chickens hatched from these eggs have low viability and die in large numbers in the first days of their life.
Symptoms can vary depending on the breed of chicken:

• "Fatty egg" and reduced shell quality are more common in brown crosses and broilers;
• protein change. Its thinning and haze is more typical for white crosses.

Important! Death is not a common symptom of this disease, and its rate is rarely higher than 5%. The cause is mainly yolk peritonitis.

Diagnostics

In order to make a preliminary diagnosis and keep the subsequent records, it is necessary to develop graphs demonstrating the development of egg production, taking into account the fact that, due to adenovirus, a decrease in egg production occurs in layers of 200-240 days of age.

In the event of a drop in productivity in an individual over 300 days of age, the cause is most likely some other factor.
In any case, before diagnosing "egg production syndrome-76", you should exclude:

• bronchitis of infectious etiology;
• poisoning with various substances;
• inadequacy of the diet;
• other factors that can provoke a decrease in egg production.

How and where to go

If a virus is detected at an industrial enterprise, the economy is transferred to the category of dysfunctional and appropriate restrictions are imposed: measures for mechanical cleaning and disinfection, vaccination, culling, and the like.

Finding a chicken with suspected EDS-76 in a private chicken coop is a reason to invite a veterinarian who will examine and vaccinate, and will give recommendations.

What surveys will be carried out

The diagnosis of "adenovirus infection" is made on the basis of research:

• epizootological;
• clinical;
• pathological;
• laboratory.

For analysis, the laboratory examines:

• oviduct;
• ovaries with follicles;
• the rectum and its contents;
• blood;
• washings from the nasopharynx and cloaca.

It is preferable to conduct research in the first days of the disease (3-5 days), and use material from a bird that died or was slaughtered no more than 2 hours ago.

It is advisable to take blood for the isolation and study of its serum from individuals of the following groups (15-20 samples from each):

• 1-200-day-old individuals;
• 160-180-day-old individuals;
• 220-day-old individuals;
• 300-day-old specimens;
• retired elderly individuals;
• specimens with signs of the disease.

Did you know? Chickens have their own "language", capable of transmitting about 30 different signals to other individuals with the help of sound. There is even a "mother" language with which the hen communicates with the offspring. Moreover, a chick that has not yet hatched, a few days before this event, communicates with a hen through the shell, using up to ten different signals for this.

As for eggs, it is desirable to investigate substandard samples with a violation of the structure of the shell and / or contents.

How to treat

As with many other viral diseases, there is no specific treatment. It is recommended to focus on the completeness of the diet, its saturation with essential amino acids, vitamins and minerals. The production of antibodies begins on the 5-7th day of the disease and lasts for 2-3 weeks, after which the individual receives lifelong immunity.

The necessary measures include the mandatory isolation of the first sick layers from the rest of the flock, especially if floor keeping is practiced. In this case, it is necessary to observe the rest of the bird for signs of symptoms.

If the nature of the disease is not isolated, quarantine measures are necessary. An unhappy bird is slaughtered, the biological material taken from it is sent for analysis for laboratory confirmation of the diagnosis.

The chicken coop is treated and disinfected with a 2% formaldehyde solution. Eggs for incubation are used after a 2-month break. At the very beginning of the disease, it is advisable to introduce a vaccine: liquid sorbed or emulsified inactivated.

Important! It is very important to track the onset of the disease and not trigger the situation: this can help avoid many problems associated with the spread of the virus in the chicken herd.

This measure can be effective in skipping the phase of viremia - the spread of the virus through the bloodstream throughout the body. Consequently, the pathogen will cause less harm to the bird, will not be present in the body's secretions, in addition, this measure allows you to improve the quality of eggs and the productivity of the bird.

Prevention and vaccine against the virus

To prevent such an unpleasant disease as egg production syndrome-76, vaccination is used, which prevents the viremia phase, which improves the productivity and quality of the eggshell.

Individuals of 16-20 weeks are vaccinated by injecting the drug subcutaneously or intramuscularly, and after 2 weeks the bird develops immunity lasting one year.

The following vaccines are used for immunization:

• liquid inactivated;
• emulsified inactivated;
• associative inactivated.

Preventive measures are based on the implementation of veterinary and sanitary rules in order to prevent the introduction of the pathogen from the external environment. To hatch chickens, eggs taken from layers over 40 weeks of age are used, and you should first make sure that their analyzes are normal.

The bird, in whose blood the pathogen is found, is slaughtered. The fact that a virus has been detected indicates its presence on the farm. In this case, you need to monitor your chicken coop and take the necessary measures in time.

To reduce the risk of an outbreak in your chicken coop, you need to:

• comply with sanitary standards;
• keep birds in isolation by age groups;
• keep the chicken herd separately from the goose and duck herd;
• from time to time, clean and disinfect the premises, as well as inventory.

Video: what to do when a chicken is sick

Did you know? Chickens are capable of emotions: sympathy, sadness. In addition, they have a sufficient level of intelligence to remember the appearance of about a hundred other creatures, and also use their experience and information about the environment to make decisions. 5 once already
helped

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.

Egg Drop Syndrome 76(Egg drop Syndrome-76, EDS-76, casting of eggs, avian adenovirus disease) is a viral disease of laying hens, characterized by softening, absence or depigmentation of the egg shell and accompanied by a significant decrease in egg production. The disease, dubbed Egg Drop Syndrome-76, was first described by Dutch scientists in 1976.

Information about the pathogen... Egg production in this syndrome correlated with the appearance of precipitins to adenovirus in hens. In these cases, they were also infected with Mycoplasma synoviae. Only in 1976 was a new pathological agent discovered, called "Egg drop syndrome-76" (EDS-76), which is rapidly spreading among many poultry farms in Western Europe. EDS-76 does not belong to any of the 12 avian AB serotypes. differing from them in serological reactions, as well as hemagglutination of chicken, duck and goose erythrocytes. The role of AB in the development of egg production syndrome-76 has been confirmed by numerous researchers. McFerran first isolated the virus in Northern Ireland from the nasal and laryngeal mucosa of chickens that showed a decrease in clutch. the EDS-76 virus is now known as strain 127. In 1978, Baxendale isolated a virus serologically identical to the piece from chicken leukocytes. 127. It was named BC-14. McCacken et al. During experimental infection of chickens on the conjunctiva and per os with strain 127 reproduced the disease and confirmed its etiological role. In subsequent years, during outbreaks of a similar disease in chickens in England, France, Italy, Hungary, Germany and other countries, the leading role of the EDS-76 virus was confirmed. 20 of them found precipitating, neutralizing AT and anti-HA against the BC-14 virus. Subsequently, Baxendale et al. Hypothesized that the EDS-76 virus was initially isolated from ducks without showing pathogenicity to birds of this species. The reason for this assumption was the fact that it was discovered in Holland, a country that is intensively engaged in breeding ducks. According to the authors, the infection of chicken flocks in this country has occurred as a result of the widespread use of the live vaccine against Marecais pc. "Rispens" produced in duck fibroblast cell culture

Since the detailed description of the disease of egg production syndrome (EDS) by Eck et al., And the discovery of the virus itself, there have been numerous reports of outbreaks of this disease in many countries of the world in the Netherlands, Northern Ireland, Japan, England, France, Belgium, Italy, USA , Iraq and our country AT to the EDS-76 virus were detected in 51% of the examined ducks, 66% of geese, 1% of chickens. Japanese researchers reported that from 1978 to 1980. in 14 broiler herds of chickens in the country, a decrease in egg production was noted, and 11 isolates were isolated from the cloacal swabs of sick birds and their etiological role was proved. In laying hens at the age of 8-9 months. egg production within 3-7 weeks. decreased by 6-25%, and the eggs were softened and deformed. The authors believed that the pathogen was brought to Japan from European countries by a imported bird. Virus 127 has also been shown to spread naturally widely among ducks, with chickens in contact with infected ducks not becoming infected. According to McFerran, birds in Northern Ireland have only recently become susceptible to virus 127, since no specific ATs were detected in chicken sera before 1976.

Lohr et al in 1981 conducted a serological survey of herds of chickens, ducks, geese and gulls in England and the Netherlands. In poultry farms in Denmark, this disease and the economic damage it causes were studied by Badstue, in England - by Baxendale. According to the latter, in 80% of chickens with low egg production, AT to EDS-76 was constantly found. Later, the wide spread of the virus in adult ducks and young animals of various breeds was repeatedly confirmed. In ducklings up to 2 weeks of age, passive ATs were detected in 40-90% of cases, but at 3 weeks of age they were no longer detected. A later increase in the AT level indicated the persistence of the virus. In Israel, in 1980, herds of domestic and wild birds (turkeys, chickens, geese, ducks, herons) were examined and found the presence of AT in Peking and muscovy ducks, as well as high levels of antihemagglutinins in Egyptian herons. Serological examination of wild birds showed the presence of anti-HA in the blood of owls, storks, swans and wild geese. Eggs laid by positively reacting wild birds (owls, storks) had poorly formed shells. A similar chicken disease is found in many poultry farms in Hungary. In England, an analysis of the decline in poultry productivity was carried out. In 80% of the examined chickens with low egg production, antibodies to EDS-76 were detected. As a result of a serological examination of 16 herds of White Leghorn and Khaki Kembpel ducks, specific antihemagglutins were injected in 27 and 37.6% of cases, respectively. In the Russian Federation in 1980-1982. in a number of poultry farms antihemagglutins to the EDS-76 virus have been identified.

Back in 1975 in France, it was noted that the average loss from this disease was 15 eggs per hen. Sick poultry produced up to 15% deformed, completely shellless or with very weak shell eggs. In breeding hens, the eggs of which are used for incubation, the culling reached 50 eggs per head (16). This syndrome caused a decrease in egg production by 15-25%, according to other sources - by 15%. Losses in productivity in this disease averaged 12 eggs per hen. In England, the damage of this infection reached 2.4 million pounds per year. In 1979, in 6 states of the United States, the economic damage from declining egg production and egg quality reached $ 5 million. Other scientists have cited similar data. On poultry farms in Japan, the recovery of productivity in recovered poultry lasted 3-7 weeks, with floor keeping, its egg production never recovered to its original level by 6-12%. The number of eggs with shell defects can reach 38-40%. There was also a decrease in hatchability, as well as the viability of chickens in the first days of life.

Virus localization, viremia, carriage of viruses and virus isolation. The virus in the body of an infected bird may be dormant until puberty or the start of oviposition. In organs and tissues of experimentally infected chickens, it persisted for up to 5 weeks. and was excreted in feces for 2 weeks. after infection. IN AND. Burtsev et al. Showed that when chickens were infected into the conjunctiva, cloaca and peros, the pathogen could be realized on the 7th day from the intestines, spleen, trachea, uterus, and rectum.

Experimental infection. There are unambiguous results in the literature for this question. Experimental infection of chickens of different age groups and chickens prior to laying showed that they had no clinical signs of the disease. In their organs and tissues, the virus persisted for up to 5 weeks and was excreted in feces for 2 weeks. after infection. When 1-day-old SPF chicks were infected in the eye or cloaca, after 7 days, the virus was re-isolated from their intestines and Fabritius bursa. Chicks hatched from eggs laid by hens during the acute phase of EDS-76 did not develop AT and the virus was isolated from them. The latter was constantly isolated from eggs laid in the first 8-9 days after infection, when their shells were normal, but the virus was already present in the oviduct of the laying hen. The virus (pcs. VS-14) was also able to be isolated from the blood leukocytes of experimentally infected chickens within 15 days after infection, but unsuccessfully - from field samples at a later date.

In chicks infected at 19 weeks of age, the onset of laying was delayed by 9 days in comparison with control birds. At the beginning of the experiment, it was 15-20% lower than in control birds, while the percentage of discarded eggs increased, reaching a maximum by the 15-16th day after infection. In case of experimental infection of laying hens before oviposition pcs. D-61 there was a delay in her and a decrease in egg productivity by about 20%. As already mentioned, experimental infection of chickens and chickens of different age groups is not accompanied by the appearance of clinical signs of the disease until the time of laying. Symptoms of the disease appear only in adult chickens during the laying period. It was not possible to isolate the virus from the protein and yolk of eggs laid without shells. This suggests that vertical transmission of infection (via the egg) occurs only for a short time, probably in the first 7 days after infection.

EDS-76 pathology manifests itself in the same way in laying hens of different lines and breeds. So, for example, when brown chickens of the lines BC, HC and white Leghorn hens of the WL line were infected with the H-162 strain, already 7 days after infection, the bird showed antibodies, a decrease in egg production, and within 3 days the shell was broken. Eggs, especially those with abnormal shells, that have passed through the affected oviduct can carry the virus. Infected eggs can be important in the spread of the EDS-76 virus to the environment. EDS-76 infection suppressed the formation of group-specific AT to AVI caused by the CELO group AB (FAV). Relatively little data has been published on the sensitivity of other bird species to experimental infection. In experiments 8, 19, 29-day-old goslings, as well as geese during the laying period, are highly susceptible to infection with the EDS-76 virus. In all infected persons, the presence of the virus and anti-HA was found in the feces within 3 weeks after infection. During experimental infection with this virus, siskins showed no visible symptoms of the disease during the entire observation period, but the virus was isolated from feces, and AT was found in all birds in a titer of 1: 64-1: 256. AT have also been identified in sparrows living near poultry farms It is assumed that in natural conditions, cross-infection occurs between wild and domestic poultry, and the isolation of the virus in feces makes it possible to spread it over different distances.

Cultivation. The EDS-76 virus multiplies m vitro in the cells of duck embryos more intensively than in the embryos of birds of other species, therefore, duck embryos and single-layer cell cultures of duck origin are the optimal system for culturing this virus JBFerran adapted strain 127 in the liver cell culture of chicken embryos. it on duck embryos.

Epizootic characteristic The source of infection is an infected bird that secretes the virus with feces or passes it on to offspring with an egg, i.e., vertical or transovarial transmission is observed. To date, opinions on the sources and routes of transmission of this infection are not always unambiguous. The analysis of such messages allows one to form the following idea of ​​the epizootic features of the EDS-76. First, in vivo, the reservoir of the causative agent of the disease is domestic and wild ducks of all breeds. When examining a herd of ducks, PA, BHA and anti-HA were detected in 85% of cases. VS-14, and isolated isolates from the cloaca of 10 clinically healthy white Peking ducklings that did not differ from the VS-14 unit. This indicates a wide spread of the EDS-76 virus among ducks, and in natural conditions it is always transmitted from duck to duck, but there is no direct evidence of its transmission through contact from ducks to chickens, although antihemagglutinins were detected in chicken farms only after they were detected the ducks. In chickens in these cases, AT were found very rarely and in low titers (maximum 1:20). Anti-HA anti-HAs have been found in commercial US duck herds. 127 The question of the natural carriage of this virus by ducks, chickens, geese and other species of birds is confirmed by a large number of essentially unambiguous examples. Under natural conditions, convalescent chickens remain virus carriers for a long time, and the activation of a persistent virus is a consequence of the stress effect on the body caused by the onset of oviposition. Weak horizontal transmission of EDS-76 virus has been shown in both experimental and field conditions. This is confirmed by the fact that sometimes EDS-76 is recorded for a long time in one part of the room, while other parts are free from infection. Therefore, partitions between groups of birds can be an obstacle to the spread of EDS-76 infection. With outdoor maintenance, the disease spreads within 1-15 days. Under these conditions, the pathogen is transmitted by contact through service personnel, care items, vehicles, etc. When feeding infected eggs to healthy birds, the latter fall ill. When EDS-76 is present on the farm and egg casting is observed, most, if not all of the birds on the dysfunctional farm are seropositive, which also proves horizontal transmission of the virus. Poultry can become infected when transported in poorly disinfected trucks, when feed is used from infected areas, and through care items, especially through contaminated egg trays. The main route of transmission of infection is not only horizontal, but also vertical - through eggs laid by infected birds. Cases of the spread of the causative agent of the disease with the semen of roosters have been noted. The vertical transmission of the virus was confirmed by the isolation of pcs. In 61 from the liver of hatched chickens. Vertical transmission of the virus to offspring in the first week after infection has been experimentally proven.

Clinical signs diseases in chickens, as a rule, do not appear. Only a few authors noted isolated cases of prostration, ruffled feathers, anemia, diarrhea, anorexia and depression during oviposition. Cyanosis of catkins and crest was also observed in 10-70% of sick birds. The main characteristic clinical sign of infection in a herd is a decrease in egg production up to 15% or more. According to E Gough, this percentage reached 30, and according to IBrugere-Picoux - 50. The peak of oviposition can be delayed up to 4-5 weeks, recover after 4-6 weeks, but does not reach the initial level. -12 weeks In addition, for chickens of egg breeds, a change in the internal quality of eggs is characteristic, their white becomes watery and cloudy with whitish flakes.

EDS-7 6 symptoms were also observed among young muscovy ducks among the Peking ducks. At the onset of the disease, an increase in the number of colorless eggs with a thin and rough shell or eggs with cracks is noticeable. This was followed by the production of eggs without shells at all ("casting eggs"). This was more common in layers 25-35 weeks of age, although birds of all ages were prone to this syndrome. Disruption of egg production was manifested in two ways: either the inability to reach the expected peak of productivity, or a drop in egg production immediately after reaching the peak. The decline in productivity can range from 3-55%, the most sharp drop occurs if the bird has reached the peak of productivity or infection in the flock spreading rapidly. With a slow spread of the infection, there is usually a slight decrease in egg production, but lasting for a longer time.

A bird infected with EDS-76 usually looks healthy and only in some cases, broken and watery eggs, a temporary decrease in appetite or drowsiness of the bird suggest an EDS-76 infection in the farm.

It is interesting that in the groups of birds where antihemagglutins are detected, there are no signs of the disease characteristic of the EDS-76 syndrome, but in those groups of birds where they are absent or they are detected in low titers, egg production decreases. Signs of the disease usually appear at the 30th week. at the onset of the peak of egg production This indicates that the virus in the latent phase was in the body earlier, but began to manifest itself sharply and actively against the background of physiological stress - an increase in egg production and an increase in hormones.

Pathological changes are characterized by edema and infiltration of the tissues of the uterus and oviduct, minor catarrhal enteritis, however, in a number of cases, when opening corpses, there are no pronounced changes.Histological examination revealed degeneration of calcific glands, their mononuclear infiltration, lymphoid hyperplasia of various degrees in the liver, spleen and other organs uterine glands, infiltration of heterophiles, lymphocytes and plasma cells, accompanied by extensive edema. Infection of chickens 110-135 days of age intramuscularly and intratrachealovirus EDS-76 (pcs. B8 / 78) leads to lesions of various parts of the oviduct and intestines. When the virus was injected intramuscularly, pathological changes were observed in muscle tissue.

As for the mechanism of damage to the eggshell, it is still not clear. Histological examinations of the oviduct did not show profound changes; when examining serum, only a decrease in alkaline phosphatase, an enzyme that is part of the complex of mechanisms of shell formation, was found.

The EDS-76 virus in duck embryos causes an increase in the content of some enzymes (aldelase and cholinesterase), which correlates with the multiplication of the virus. Next, the researchers followed the behavior of some transferases and found an increase in their activity, especially aminotransferase and pyrovate oxidase. For example, the EDS-76 virus was. According to A. Bartha et al., The infection of chicken flocks with the virus occurred as a result of the use of the vaccine against Marek's disease from the piece. "Respens", reproduced in duck fibroblast cell culture

Diagnosis set on the basis of laboratory studies, taking into account epizootological data, clinical signs and pathological changes To find out the cause of the disease, methods of early and retrospective diagnosis are used

Early diagnosis method

Isolation of the virus. From pathological material (cloaca of the liver, spleen, oviduct, leukocytes, blood, feces), the virus is more successfully isolated in the first 10 days of infection using duck embryos or a culture of kidney cells, liver of duck and geese embryos, duck and goose fibroblasts, and cells of hepatocytes TBE. However, FEC and the embryos themselves are not suitable for this purpose. To isolate the virus, at least 3 consecutive passages are required. The material taken from the cloaca, pharynx, oviduct, pieces of the liver and spleen, as well as leukocytes is inoculated with the material taken from the cloaca, pharynx, and leukocytes into a sensitive cell culture. At least 3 consecutive passages are carried out at 7-10 days intervals. The presence of the EDS-76 virus in the medium is established with with the help of the RSA. Usually, antihemagglutinins were detected in the serum of all experimentally infected birds in the RSHA. In experiments where there was one infected bird among a group of healthy contact birds, the latter, as a rule, became seropositive, but it was not possible to isolate the virus from them, and the infection was not further transmitted to the next batch of contact birds.

Indication of the isolated virus. The EDS-76 virus, as a rule, is typed in RGHA and PH on duck embryos or in a cell culture of duck origin. Considering that between the pieces. of the EDS-76 virus isolated in different countries, there is no antigenic difference, as specific sera for typing the newly isolated virus I use tanty sera to strains 127, BC-14, E-7, B8 / 78, 3877 and JPA-1.

Antisera to the strains are prepared on SPF-laying hens and rabbits and used for an indirect immunofluorescence method with labeled rabbit or goat anti-chicken serum conjugated with FITC.

The first changes in the infected cell culture of duck fibroblasts are noted as early as 48 hours after infection, when distinct and frequent seals appear in the border areas, zones of the cell monolayer. 72 hours after infection, many rounded cells and dead cells appear floating in the medium; the monolayer begins to shrink and large holes appear in it. By the 96th hour, a monolayer of infected cells containing coalesced granules forms long strands. Epithelial cells undergo such changes. However, the fibroblasts between the epithelial islets are not affected. Often, a large number of round, free-floating cells are present in the culture medium. This, in fact, is the cytopathic effect induced by the piece. 127.

The staining of the infected monolayer with hematoxylin-eosin allows the detection of intranuclear inclusions.

EM. 24 h after infection of the duck fibroblast cell culture, virions and several types of inclusions are detected in the cell nuclei. The particle size was 70-75 nm in diameter. 2 main types were noted. Some of them had an electron dense core (nucleotide) 50 nm in diameter, separated from the outer capsid by a light space. Other particles had an electron-luminous (bright, transparent) center contained in a membrane connected to the capsid. This inner structure (40 nm) was also separated by a light space from the outer capsid.

Serodiagnostics. In addition to isolating and identifying the virus using RHA-RZGA and IF, sera are examined in birds of a suspicious flock for the presence of specific antibodies. This is done in 3 cases: when the dynamics of AT is studied as a result of experimental infection of poultry: during wide field serological examinations of poultry in order to establish the presence of infection in the herd, using the principle of paired sera; and in cases of establishment of the immunological status of the bird after the application of the vaccine. In all cases, serological tests are used (RZGA, RDP, RN and ELISA), for which the diagnostician needs to have positive sera on hand as a control. HA inhibition test (RZGA) with egg yolk. It was proposed in 1985. It has a number of advantages over the analogous RSHA with the tested blood serum.

RN. It is placed in duck embryos in cultures of liver and kidney cells of duck embryos and duck fibroblasts and is important for typing the virus in doubtful cases. For this, a monolayer culture grown in test tubes on Eagle's medium is inoculated with a virus-serum mixture, which is preliminarily incubated (30 min) at room temperature (22 ° C) and inoculated with 0.2 ml in 5 tubes with cell culture. be used to distinguish between typical avian adenoviruses, as this method is not sensitive enough to detect similar antigens. With the help of RDP, a serological study of a herd of chickens for EDS-76 is carried out, but it is less sensitive than RADA, and a low level of AT cannot be detected in RDP. It is convenient to use RDP with yolk extract.

Based on comparative studies on the detection of AT to the EDS-76 virus in RSHA and ELISA, a higher sensitivity of the latter was established. He detected positive sera by 7% more than RSHA.

Immunity and prevention. Recovered chickens acquire a tense long-term immunity There is no information in the literature on repeated illness of birds. Individual birds can be affected within 3-16 days, then they recover and restore their egg production. A small number of birds never develop the disease at all. Usually, in a dysfunctional flock of birds, the recovery process lasts from 4 to 14 weeks. For the specific prevention of EDS-76 in various flocks, mainly inactivated vaccines have been developed and successfully used. So, back in 1978, the possibility of vaccine prevention of this infection with the help of an inactivated oil vaccine containing the BC-14 virus was shown. In 1980, a bivalent vaccine against EDS-76 and NB was developed and successfully tested, and the first virus was represented by two pieces. E-77 and 127, which were first reproduced in the culture of EC hepatocytes, and then in the culture of fibroblasts of duck embryos. BHE multiplied in CE. The viruses were inactivated (with 3-propylactone, a high level of anti-HA (27-210) to EDS-76 and NB was used as an adjuvant. after vaccination, and at a later date - up to a year, as well as a high level of maternal AT in offspring.According to the authors' recommendation, birds are vaccinated intramuscularly at 16-20 weeks of age, 0.5 ml each. transmission of the virus and limits the spread of infection not only within one farm, but throughout the region, from farm to farm.

In 1982, a combined inactivated emulsified vaccine against NB, EDS-76 and IBD was proposed, which was injected subcutaneously at a dose of 0.75 ml. The vaccinated hens had a high titer of anti-HA and BHA. When challenged, they were immune and retained high egg production. Many authors have obtained similar results from the use of an inactivated vaccine. The maximum level of post-vaccination antibodies was noted by the 30th day.

Veterinary and sanitary examination... It is prohibited to release raw carcasses and products of slaughter from patients and suspected of the disease. In the presence of degenerative or other pathological changes in the muscles, the carcass with internal organs is sent for disposal. In the absence of pathological changes, samples are sent for bacteriological examination for salmonellosis. If Salmonella is detected, the internal organs are disposed of, and the carcass is sent for cooking. In the absence of Salmonella, it is allowed to process it into boiled, boiled-smoked sausages, canned food or cooked.

Egg drop syndrome - 76 (Egg drop syndrome - 76, casting of eggs, avian adenovirus disease) is a viral disease of laying hens, accompanied by a sharp decrease in egg production, a change in shape, softening or absence of shells and a deterioration in the quality of hatching eggs.

Economic damage... Damage from EDS 76 is associated with a shortage of up to 10-30 eggs per hen on average, while up to 50 eggs have to be discarded from breeders, the laying of shellless eggs, eggs with a blood ring, a decrease in hatchability of chickens and their low viability up to two weeks age.

Etiology... The disease is caused by a DNA-containing unclassified virus of the adenoviride family, Adenoviridae.

The virus has an icosahedral shape. The symmetry of the capsid is cubic. The diameter of the virion is 75-80nm. The virus does not belong to any of the known avian adenovirus serotypes and, unlike them, agglutinates the erythrocytes of chickens, ducks and geese. Hemagglutinin is stable for 30 minutes at 70 ° C. Identified by some researchers as duck adenovirus. Virulence loses after 30 minutes at 60 ° C, as well as under the influence of trypsin, urea and pyridine. The virus strains isolated in different countries are antigenically related. The virus multiplies in embryos and cell cultures of duck origin more actively than in embryos and cell cultures of other birds. CPE is expressed by the formation of intranuclear inclusions, rounding of cells, deformation of the cell monolayer.

In a recovered (and experimentally infected) bird, specific antibodies are formed, which are transmitted transovarially.

Epizootological data... Chickens of all breeds are sick, mainly when they reach the highest productivity (25-35 weeks), but the disease may occur at any period of the productive cycle. At the same time, breeding poultry and layers of meat lines are most susceptible to the disease. The EDS-76 virus is widespread among domestic and wild ducks, as well as geese, is apathogenic for them and does not cause clinical manifestations of the disease. The virus is able to persist in the body of chickens that have not reached puberty.

It is activated and provokes a decline in egg production as a result of stress caused by the onset of lay. The main route of transmission of the virus, and therefore the spread of the disease, is transovarian, and horizontal is not excluded. The virus is transmitted by contact through the clothes and shoes of the service personnel, transport, feeders, drinkers, poultry care items, cases of transmission of the pathogen with the semen of roosters and droppings are noted.

Clinical signs... In sick birds, isolated cases of prostration, ruffled feathers, anemia, diarrhea, oppression during oviposition, cyanosis of catkins and ridge, and a decrease in feed intake are observed. The main characteristic feature is a sharp decrease in egg production... The bird lays eggs of a changed shape, the shell is softened, sometimes absent. In chickens of egg breeds, the white of the eggs can be watery and cloudy, the peak of oviposition is delayed by 4-5 weeks. The level of hatchability and viability of chicks decreases in the first days of life. With a disease duration of 4-12 weeks, the productivity of chickens decreases to 30-50%. Of these, productivity decreases within 2-6 weeks, and within 2-4 weeks it is restored, but does not reach the initial level. With the cellular content, the productivity of chickens is restored almost completely or remains 1-3% lower than the norm. In the process of recovering from EDS-76, the bird lays shellless ("cast eggs") or depigmented eggs with a thinned shell, with ring-shaped or banded, rough formations on the surface for 6-8 weeks. There is a significant increase in the number of "marbled" eggs, the percentage of broken and notched eggs increases.

Changes in the quality of the shell and the so-called "fatty egg" are most common in colored hens and broilers. In chickens of white crosses, mainly the protein part of the egg is changed in the form of its local liquefaction.

Pathological changes, as a rule, are absent or weakly expressed, in the form of edema and infiltration of oviduct tissues, signs of catarrhal enteritis. In the acute form, in some cases in the ovary, changes of an atrophic nature, a decrease in the number and size of follicles, hyperemia or hemorrhage in the connective tissue capsule of the follicles, their deformation and degeneration are noted. There are areas of the ovary with completely degenerated follicles and turned into a necrotic mass of yellowish-brown color. In some sick chickens, cysts may appear. The oviduct is generally shorter and thinner than that of healthy birds. The liver is sometimes enlarged, flabby and yellowish in color. At the same time, we note an increase in the gallbladder, its overflow with watery fluid. When conducting a histological examination, it is possible to reveal the degeneration of the calcifying glands and their mononuclear infiltration, lymphoid hyperplasia in the liver, spleen and other organs.

Diagnosis... It is set comprehensively on the basis of epizootological, clinical data, pathological changes in the corpses of dead and forcibly killed birds, the results of laboratory studies (virus isolation on duck embryos, duck embryo fibroblast cell culture or liver tissue culture of duck or chicken embryos with subsequent identification of the pathogen in the RHA, RZHA , MFA, ELISA), bioassay setting on chickens, determination of specific antibodies in blood serum or yolks of laying hens' eggs in RZGA or ELISA, histological examination of the reproductive tract organs.

For virological studies, samples of the ovary with follicles, oviduct, rectum with contents, cloacal washings, blood with an anticoagulant are used. Sampling of pathological material is carried out in the first 3-5 days after the onset of the disease and no later than 2 hours after the clinical death or slaughter of the bird.

For serological research, blood serum is sent from birds aged 1-120, 160-180, 220, 300 days and from birds that have been retired by age, as well as chickens with clinical signs of the disease (20-15 samples from each group) ...

When sending eggs for examination from birds suspected of the disease, it is advisable to select substandard eggs (decalcified, depigmented).

Differential diagnosis... We exclude other infectious diseases and factors of non-infectious etiology.

Immunity and specific prophylaxis... Recovered chickens acquire a tense long-term immunity. Antibodies in chickens are detected on the 5-7th day, reaching a maximum by 2-3 weeks after infection. In literary sources, there is no information about the repeated disease of poultry. Passive antibodies in chicks hatched from infected hens' eggs completely disappear after 2-3 weeks.

Abroad, inactivated vaccines are used for specific prophylaxis of the disease. They are administered once subcutaneously or intramuscularly to a bird at 16-20 weeks of age at a dose of 0.5. Immunity after vaccination is formed after 15 days. The maximum level of post-vaccination antibodies is usually noted by the 30th day.

The duration of immunity is 1 year. The following vaccines are used in Russia:

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

After vaccination of the bird, the viremia phase and the associated excretion of the virus are prevented, egg production and shell quality are improved.

Prophylaxis... In order to prevent EDS-76, it is necessary:

• 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 pathogens of infectious diseases;
• 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;
• place birds of different age groups in geographically separate zones;
• not to allow the joint keeping of chicken, goose and duck herds in poultry farming;
• carry out thorough cleaning and disinfection of meat and egg containers;
• to vaccinate birds against EDS -76 when antibodies are detected in the blood serum of hens in RZGA or ELISA or in contact with a farm that is unfavorable for the disease.

Control measures... When the diagnosis of EDS-76 is established, by the Decree of the Governor of the region, the economy (farm) or settlement is declared unfavorable according to EDS-76 and restrictions are introduced in it.

Under the terms of the restrictions, it is prohibited:

• movement of birds within the holding (farm, branch) during the period of illness;
• removal from a dysfunctional economy (branch, farm) of birds of all age groups and their sale to the population;
• removal of hatching eggs to other farms;
• use for incubation inside the farm eggs obtained from chickens from disadvantaged poultry houses;
• taking semen from males and artificial insemination of hens of the parent flock during the period of clinical manifestation of the disease;
• removal of feed, equipment and inventory from dysfunctional production facilities and from the territory of a dysfunctional economy (farm, branch);
• 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;
• entry and exit from the territory of a dysfunctional economy of vehicles without disinfection.

Under the terms of the restrictions, it is allowed:

• 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;
• 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;
• 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 creating conditions that 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, chlorine turpentine vapor, sodium hypochlorite or a stabilized solution of hydrogen peroxide 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 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 time frame provided for by the current instructions for carrying out veterinary disinfection of animal husbandry 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, branch) 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.

In industrial farming, infectious diseases of poultry are costly. At the same time, sometimes diseases arise and are transmitted from one species of bird to another and spread as much as possible with almost no symptoms until a victim sensitive to a certain pathogen is found.

According to scientists, this is exactly what happened when adenoviral disease or egg production syndrome, was first noted in Holland in 1976 and later spread almost all over the world. -76 or Egg drop Syndrome -76 (EDS -76) is a viral disease of laying hens, which is characterized by a decrease in egg production, a change in the shape of eggs, a deterioration in the quality and lack of pigmentation of the shell, as well as a violation of the structure of the protein.

It is believed that the causative agent chicken adenovirus disease is a duck virus that does not cause disease in ducks themselves. Although in natural conditions it is widespread among domestic and wild ducks, which makes them a dangerous source of infection. Egg Drop Syndrome causes a DNA virus from the Adenoviridae family. This explains the second name of the disease - adenovirus disease.

The causative agent of adenoviral disease, unlike other known stereotypes of avian adenoviruses, is capable of agglutinating the erythrocytes of chickens, ducks, geese, turkeys, and the Mexican virus also erythrocytes of pigeons, peacocks and humans. According to scientists, the infection of chickens in the Netherlands could have occurred as a result of the widespread use of a live vaccine against Marek's disease, grown on a culture of duck fibroblast cells. In addition, it was found that duck embryos and cell cultures prepared from them are better suited for its cultivation than cell cultures of chick embryos. This also confirms the hypothesis of the origin of the virus and is widely used for its isolation and obtaining vaccinated material with high titers for the manufacture of diagnostic kits and vaccines.

Spread of adenoviral disease (egg production syndrome).

Laying hens are susceptible to adenovirus, regardless of breed. At the same time, the disease with its characteristic symptoms is most clearly manifested precisely during the period of the highest egg production at the age of 200-240 days, although chicken lesions are possible at any period of the productive cycle. The disease spreads especially quickly when chickens are kept crowded on the floor. Chickens of modern highly productive egg crosses are more sensitive to the disease. Wherein chicken and broilers less susceptible to adenovirus disease, than chicken egg directions. Because of this, according to individual authors, broilers can be a potential spread of infection. The disease cannot be called highly contagious, but one should not exclude its introduction to poultry farms by pigeons and other wild birds. Even sparrows have been found to have antibodies to this infection near poultry farms. It is believed that in natural conditions there is cross-contamination of wild and poultry, and the excretion of the pathogen in feces allows the disease to spread over long distances.

The main path the spread of the causative agent of adenovirus disease considered a transovarial vertical transfer. The reservoir of the causative agent of the disease in natural conditions is domestic and wild ducks of all breeds. This indicates a wide spread of the virus in nature. However, there is no exact data on the probable transmission of the pathogen from duck to chicken through contact. Egg Drop Syndrome has a weak ability for horizontal transmission, which is confirmed by the fact that the pathogen is recorded for a long time only in a certain part of the room, while in other parts of the infection is not noted. Therefore, it can be concluded that impermeable partitions between groups of laying hens can successfully prevent the spread of the disease. If the chickens are kept on the floor, then the disease covers the entire flock within 1-15 days. In such conditions, the pathogen is transmitted by contact, as well as through service personnel, care items, equipment.

After the first clinical symptoms of adenovirus disease also note its horizontal distribution. Eggs are most intensively infected during the period of viremia (the presence of the virus in the blood), which coincides in time with a decrease in egg production. Then the birds excrete the pathogen with droppings and mucus from the respiratory tract, and the roosters, probably with sperm. The possibility of spreading the virus when vaccinating chicken against other infections is not excluded.

Feature diseases of adenovirus infection is the ability of the virus not to manifest clinically until the hen reaches a certain age of puberty. At the same time, it is believed that the mechanism of development of the disease triggers the stress associated with the onset of the egg-laying period. In addition, the higher the productivity is expected from laying hens, the brighter the clinical manifestation of the disease will be.

After all, the longer the bird has not had contact with the virus and the more pronounced the negative serological reaction it gives, the brighter the disease will manifest itself in it. When laying hens hatch from infected eggs or chicks that become infected in the first days of life, a sharp decline in egg production does not occur at its peak, although such a bird is unlikely to achieve its maximum performance.

Such chickens carry the adenovirus throughout their entire life, but they begin to shed it only from the beginning of laying eggs at the age of 22-26 weeks. So, the duration of the asymptomatic persistence of the virus in the body of a bird depends on the age of infection of the chickens. Moreover, the earlier the infection occurs, the longer it takes before the virus is released into the environment and the first clinical signs appear.

Symptoms and signs of chicken adenovirus disease.

When the infection is latent, the pathogen is in the intestine. Then comes the stage of activation and viremia. In this case, viremia is a common stage in the passage of adenoviral disease. It is believed that the pathogen is activated as a result of hormonal changes in the chicken's body before the start of laying... It is this change in the hormonal profile that is the great stress that awakens the disease. With viremia, the virus is found in the epithelial cells of the oviduct mucosa and other organs.

It is considered that causative agent of adenoviral disease has a direct negative effect on the glandular epithelium of the uterus, as a result of which hens lay eggs with a thin and fragile shell or even without it. It was determined that under its influence the "sodium-potassium pump" in the glandular cells of the uterine mucosa was disrupted. This is confirmed by research data, according to which the concentration of sodium in the uterus of sick chickens is significantly increased, while the level of calcium, potassium and magnesium is significantly lower than in healthy or infected birds, but which produces eggs with normal shells.

An increase in acidity also leads to dissolution of calcium and disturbance of the formation of shells. So, adenovirus disease causes swelling of the glandular tissue of the uterine villi with the subsequent destruction of the mucous epithelium, due to which little calcium is absorbed and acidosis occurs due to a decrease in the pH of the secretion of the uterine mucosa and the oviduct. As a result, calcium carbonate, which is formed by the scale gland, is neutralized and eggs are formed with soft, thin and unpigmented shells or none at all.

Special characteristic symptoms of egg production syndrome does not have, the clinical signs of the disease are not significantly expressed. Sometimes patients notice general depression, diarrhea, impaired appetite and anemia. When the disease reaches its peak, the laying hens will notice weak breathing and greenish droppings within 1 to 2 weeks. Over time, cyanosis of the crest and earrings may be noted in 10-70% of sick chickens.

As the name of the disease implies, the main a symptom is a decrease in egg production and the laying of defective eggs by chickens. On average, during an illness in a herd, a drop in egg production can be expected by 15-30%, sometimes up to 50%. It should be noted that the fall in egg production occurs with a certain course of time: within 4-5 weeks, egg production falls, followed by 2-3 weeks of recovery. So, the full cycle lasts about 6-7 weeks, after which the performance of the herd can be restored almost completely. When kept in cages, productivity is restored better than when chickens are kept outside. After recovery, the backlog from the planned productivity usually does not exceed 10%.

During the active manifestation of the disease, the main changes occur in the testicle. So, a laying hen lays eggs that either do not completely have a shell, or characteristic roughness is noted on its surface. Chickens lay much more "marble" eggs, and eggs often beat and crack. The fertility of such eggs and their incubation properties are significantly impaired. The hatchability of chicks decreases, and those that hatch have a low viability. In the blood serum, a low content of alkaline phosphatase, an enzyme that plays an important role in the mechanism of shell formation, is noted.

In a certain way symptoms of adenovirus disease may differ in different breeds of chickens. So, in meat breeds and brown layers, the so-called "fatty egg" of qualitative changes in the shell is often noted, and in white leghorn breeds, changes in the protein part are more often observed: the protein becomes watery and cloudy. Even at the peak of the disease, mortality from SZN-76 is very insignificant and rarely exceeds 5% among adult laying hens. Its main causes are vitelline peritonitis and often pecking.

Pathological changes in the syndrome of decreased egg production.

The main pathological changes during the autopsy of a sick chicken are found in the reproductive organs. So, almost always there is a small number of ripening and mature follicles in the ovary. Often there is even atrophy of the ovaries, on which hilly, deformed and atrophied follicles filled with a gray-yellow or green mass with clots are visible. Many follicles are reddened with massive hemorrhages. The oviducts in sick chickens are shortened and have a thinned wall, sometimes also reddened and with hemorrhages.

Given the disease symptoms, according to some authors, it is also advisable to call it "adenoviral salpingitis". Often at autopsy, pathological changes in the liver are noticed: it is enlarged, edematous, has a flabby consistency and a yellow-clay color. Next to it, the gallbladder is enlarged, filled with light green watery bile. It is the disturbances in the functioning of the liver and gallbladder that determine digestive disorders. An autopsy also notes intestinal overflow with undigested greenish food with admixtures of foam.

Prevention of egg production syndrome.

The causative agent of the syndrome of lower egg production causes the formation of specific antibodies in the infected bird 7-14 days after infection. Chickens that have been ill acquire a tense long-term immunity to the disease. There are no data on the recurrence of adenovirus infection in chickens in the literature.

The diagnosis is made in a comprehensive manner, taking into account epizootological, clinical, pathological signs and laboratory results. For the preliminary establishment of the diagnosis, the graphs of the development of egg production are developed for accounting. In this case, it is taken into account that SZN -76 leads to a decrease in egg production in hens at the age of 200-240 days. If a drop in egg production is observed at a different age, especially when chickens are older than 300 days, then something else must be the reason for this, and not this disease.

Evaluation of the quality of eggs in terms of shape, color and properties of protein and shell is of great importance in establishing a diagnosis. Of decisive importance in establishing a diagnosis are the results of laboratory studies, among which the main one is the hemagglutination delay reaction (HAG). When carrying out a differential diagnosis, it is necessary to exclude a decrease in egg production as a result of infectious bronchitis, Newcastle disease, the CELO virus, as well as inappropriate housing and feeding conditions. For to prevent egg production syndrome, specific prophylaxis has been developed in the form of monovalent and associated vaccines. The chicken is vaccinated once at the age of about 100-110 days. At the same time, vaccination is designed to prevent both vertical and horizontal routes of infection transmission and spread. When a sick poultry is slaughtered and with suspected SZN-76 disease, the carcasses are carefully checked for degenerative and other pathological changes, as well as salmonellosis. If the inspections did not reveal anything, the meat is used as conditionally fit, but is not released for sale raw.

Accordingly, such a disease like egg drop syndrome-76 can cause large material losses to farms due to lack of eggs and poor chick hatching, is of particular importance when it comes to the mother flock. Therefore, the prevention of its appearance and the implementation of effective veterinary prophylaxis is of great importance and should be taken into account both at breeding and commercial poultry farms.

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