Adenovirus infections are diseases of birds of various species (chickens, turkeys, guinea fowls, pheasants, musky ducks, pigeons, quails, budgerigars). Caused by 12 types of avian adenoviruses that do not share a common group antigen with other human, simian, porcine, and mouse adenoviruses.
Avian adenoviruses belong to the adenovirus family, as they are united with this family by a number of common properties: particle size, virion structure, genome structure, replication type. In adenoviruses, the virion is devoid of an outer lipoprotein shell, does not contain lipids and glycoproteins, has a spherical capsid shape, and a size of 70-80 nm.
Adenovirus infections in birds include: СELО - infection, EJS-76 - egg drop syndrome, adenovirus respiratory disease, hepatitis with inclusion bodies.
Egg drop syndrome- a disease of laying hens, characterized by softening, absence (casting) or depigmentation of the egg shell. Accompanied by a significant decrease in egg production.
The disease was first described in Holland in 1976 by J. Van Ecke et al. The conducted studies allowed to exclude NB, ILT of birds. Before him, no one in the world paid attention to the characteristic dynamics of the decrease in egg productivity. Antibodies to the EDS-76 virus were also not found in any museum sample of blood serum obtained from chickens before 1976. This is an indisputable confirmation that the onset of the disease is confined to a certain period.
At various times in a number of countries, strains of the ECC-76 virus were isolated: BC-14 in the UK, B / 78 in Hungary, E-77 in Italy, 3877 in France, J RA-1 in Japan. All obtained isolates were serologically completely identical to the first isolated strain -127.
EDS-76 is widespread in countries with highly developed industrial poultry technology and causes very significant economic damage, especially in breeding farms. Losses consist of lost eggs from laying hens during the peak of laying (according to some data - up to 15 eggs per hen, according to others - up to 25%, in the USA - the damage reached 5 million dollars), as well as from a decrease in the commercial quality of commercial eggs and from breeding layers (culling was up to 50 eggs per head). As a rule, in those who have been ill, egg production is not restored to its original level. At present, the disease has been sufficiently studied, however, the issues of etiology, epizootology, and pathogenesis are largely controversial.
Pathogen- DNA-containing virus of the adenovirus family. It was isolated in 1976 in Northern Ireland from nasal cesspools and ovaries of diseased birds and is now known as 127 and identified as the causative agent of EDS 76.
There is an opinion of a number of scientists that the EDS-76 virus is a duck adenovirus that does not cause pathology in natural "hosts". The disease first appeared in Holland, a country of intensive duck breeding. Primary infection of chickens with it was artificially produced by introducing a vaccine against Marek's disease from the Rispens strain, prepared using a culture of duck embryonic fibroblast cells contaminated with adenovirus. The virus quickly adapted to the new "host" - chickens and showed its pathogenic properties.
The characteristic of the causative agent ECC-76 fully corresponds to the characteristics of other avian adenoviruses, with the exception of its ability to agglutinate erythrocytes of chickens, ducks and geese. On this basis, it is even more "avian adenovirus" than other adenoviruses that do not have hemagglutinating ability.
The virus is unstable to heat: temperature +65C completely inactivates the virus in 30 minutes. The EDS virus is 15 times more sensitive to UV radiation than the virus infectious bronchitis. The ECC-76 virus is resistant to changes in the pH of the medium, and is especially resistant in an alkaline environment. Resistant to repeated freeze-thaw, to the effects of other physical factors and also to disinfectants.
Epizootology. Most often, EDS-76 affects laying hens of all breeds with the maximum manifestation of the disease during the period of increased oviposition at 26-35 weeks of age. Particularly susceptible bird meat breeds.
It was noted that birds older than 40 weeks of age do not suffer from EDS-76 and do not excrete the virus, but the blood contains antibodies to this virus.
Adenoviruses are also widespread among domestic and wild ducks, which at the same time do not get sick. Antibodies were detected in 85% of ducks and 65-100% of geese in Hungary. In natural and wild environment they are the reservoir of the pathogen in nature. Despite the low contagiousness of the disease, there is a risk of introducing the pathogen into the territory of the farm. wild birds: pigeons, sparrows.
The main source of the EDS-76 pathogen is sick chickens that excrete the virus with feces or pass it on to their offspring with an egg.
The main route of adenovirus spread is vertical. Of lesser importance is the horizontal and contact path of transmission of the pathogen. The disease spreads more quickly when chickens are kept on the floor.
The epizootological feature of the disease is a strictly defined time of reactivation of the pathogen after the contaminated bird reaches full sexual maturity. The reason for this may be stress, which is the physiological restructuring of the body of laying hens before the start of the active stage of oviposition. Other specific predisposing factors for the onset of the disease, except for age, have not been established.
Pathogenesis. During the period of latent infection, the virus persists in the intestine. Reactivation of the virus occurs due to a change in the hormonal profile at the beginning of oviposition, which is considered as a stress factor. Apparently, the virus has a direct effect on the glandular epithelium of the uterus, which leads to the laying of shellless or thin-shelled eggs.
Clinical signs. There are no characteristic symptoms of ESS-76. The bird has reduced appetite, ruffled plumage, diarrhea. The bird carries depigmented, deformed and defective eggs for 2-3 weeks. Significantly increases the number of "marble" eggs, increases the percentage of the fight and notches. The egg white is watery and cloudy.
Egg productivity decreases on average by 15-30%, in some cases - up to 50%. The decrease in productivity increases gradually over 5-6 weeks, after which the productivity is very slowly restored with the cellular content of chickens, and does not recover with the floor.
The death of a bird during EDS-76, even at the peak of the disease, is insignificant. Mortality among laying hens is up to 3-5%, mainly due to yolk peritonitis, pecking.
When embryos are infected with a virus, their death begins on the 4-6th day after infection and continues until the chicks hatch.
Pathological changes are localized mainly in the organs of the reproductive tract and are expressed in the form of ovarian atrophy, sometimes hemorrhages are found in them. In all cases, a small number of maturing and mature follicles in the ovary are noted. The oviduct, as a rule, is shortened, its wall is thinned, with foci of hyperemia. The liver may be enlarged, edematous, flabby in consistency.
Diagnostics. The preliminary diagnosis is based on integrated assessment epizootological survey data of the poultry industry. At the same time, special attention is paid to the dynamics of egg production of adult chickens, mass death day old chicks. An important diagnostic value is the age of the birds during the decline in egg production.
Histological examination of the affected areas of the oviduct reveals intranuclear bodies - inclusions in epithelial cells.
Laboratory diagnostics is based on the isolation of the virus from pathological material (preferably on duck embryos) and its identification in the RZGA, MFA.
Serological diagnostics (RZGA, RDP, ELISA) is used to detect the dynamics of antibodies to the EDS-76 virus in birds in paired blood sera, as well as to establish the intensity of immunity.
In the differential diagnosis of EDS-76, a decrease in egg production caused by CELO viruses, infectious bronchitis, Newcastle disease, or violation of conditions of detention is excluded.
Prevention and control measures. In a point that is unfavorable in terms of EDS, strict observance of veterinary and sanitary measures is mandatory to exclude the spread of the pathogen from the source of infection. Sanitize the supply and exhaust ventilation system.
A favorable prognosis is possible only with the use of specific prophylaxis. Birds are immunized with a liquid inactivated adsorbed vaccine against ECC-76 once intramuscularly at the age of 100-110 days. Monovalent and associated forms of vaccines based on mineral and oil adjuvants (against infectious bronchitis, IBD, Newcastle disease and EDS-76) have been developed and introduced into the practice of poultry farming.
If you decide to start breeding chickens on your personal plot, you should know not only about the rules for keeping and breeding birds, but also about possible diseases in order to identify and cure them at an early stage in time. After all, everyone knows that the disease of even one chicken is a very dangerous, troublesome and, importantly, costly event. Therefore, it is always better to prevent a disease than to cure it. This article will focus on such a common disease in laying hens as egg drop syndrome.
Egg Drop Syndrome EDS 76 is viral disease, which most often kills laying hens. With this disease, the reproductive system of the chicken is affected, which, in turn, leads to a significant decrease in the level of egg production; the shell of the eggs becomes very soft, and in some cases is completely absent. In general, egg quality deteriorates significantly.
For the first time, egg drop syndrome was described in 1976 by a Dutch scientist.
All laying hens are at risk of contracting this disease, most often this occurs during the most productive period. The most susceptible to this virus are highly productive chickens of egg and meat-and-egg crosses. Also, egg drop syndrome often affects wild and domestic ducks, geese, but at the same time, the disease does not manifest itself clinically in them and is not pathogenic. Interestingly, it is geese that can be considered the source of this disease.
The route of infection is transovarial. Most often, eggs become infected precisely during the period of viremia - when viruses, along with blood, are carried throughout the body; this just coincides with the decline in egg production. It is also impossible to exclude the possibility of transmission of the virus with the sperm of a rooster. The horizontal spread of this syndrome is noticed at the initial stage and is most pronounced in the floor keeping of poultry. At this time, the infection is excreted with feces, mucus, while contaminating food and surrounding equipment in the chicken coop. This is very dangerous, as other birds from the flock can quickly become infected because of this. Also be careful, the disease is often carried by people themselves with clothing that has had contact with an infected bird. But there are times when, living in the same herd, one chicken gets sick, while others retain normal egg production.
Pathological changes after the egg drop syndrome, as a rule, are not observed or are very weakly expressed, often in the form of edema of the oviducts. In a severe form of the disease, deviations of an atrophic nature are observed. In some chickens, the appearance of a cyst can also often be observed, and the oviduct becomes several times shorter and thinner than in healthy birds. Also, this infection affects the change in the size of the liver and its color - it increases significantly and becomes flabby, acquires a yellow tint. Also, the gallbladder increases in size, which overflows with fluid.
The damage from this syndrome is quite tangible. Calculate for yourself - with such a disease, on average, from one laying hen you will receive less from 10 to 30 eggs, and sometimes up to 50.
signs
It is very important to identify the disease at an early stage, then there is a great chance to avoid sad and often irreversible consequences. The following signs of egg drop syndrome can be distinguished: general prostration in the chicken is observed, anemia, feathers are very ruffled, diarrhea, a significant decrease in appetite, cyanosis of the crest and earrings is observed, and chickens look very depressed during the period of egg production.
But certainly the main symptom of the disease is a sharp decrease in the level of egg production. The hen begins to lay irregularly shaped eggs, often without shells. The egg white becomes cloudy and watery. Also, the peak of egg production in young hens is shifted by a month and a half. The level of hatchability from such eggs is greatly reduced, as well as the viability of chickens in the first days of their life. If the disease lasts about 4-12 weeks, then the level of egg production drops by 30-50%. Please note that with cellular content, egg production in chickens is restored almost completely, which cannot be said about chickens that are kept on the floor. During this period, there is an increase in the laying of the so-called "marble" egg.
In laying hens of colored crosses, a change in the shell and the appearance of a “fat egg” are noticed, but in hens of white crosses, the protein part of the egg mainly changes.
The diagnosis is made on the basis of clinical and epidemiological analyses. For research, samples of the oviduct, ovary with follicles, rectum with all its contents, blood with an anticoagulant, as well as cloacal washings are taken. It is best to take material for research in the first days of the onset of the disease, and also no later than 2 hours after the death or slaughter of an infected bird.
For the study of eggs, it is better to send substandard eggs to the laboratory, namely depigmented and decalcified.
Methods of treatment and prevention
Chickens that have contracted this disease must be given an injection of a liquid adsorbed or inactivated emulsified vaccine.
After such vaccination, the viremia phase and, accordingly, the associated infected excretion can be avoided. In other words, the virus will no longer be present in the litter and other secretions of chickens. Egg production and egg quality are also significantly improved.
Remember that it is very important to isolate infected birds in time to avoid infection of the entire flock.
Chickens that have been ill with egg drop syndrome become immune to this disease. Antibodies in a bird begin to be produced on the 5th-7th day after infection and reach a maximum amount on the 2nd-3rd week. Re-infection is virtually impossible.
Below are a few simple rules that will help to significantly reduce the risk of disease:
- adhere to strict sanitary standards;
- birds different ages place in different rooms;
- it is forbidden to keep together goose, duck and chicken flocks;
- be sure to regularly disinfect the premises and all inventory.
Remember that it is better to avoid a disease than to treat it. Therefore, it is recommended to follow the above rules, and then you will never encounter such unpleasant diseases and even less pleasant consequences.
At industrial cultivation infectious diseases poultry lead to big losses. At the same time, sometimes diseases arise and are transmitted from one bird species to another and spread as much as possible almost asymptomatically until a victim sensitive to a particular pathogen is found.
According to scientists, this is exactly what happened when adenovirus disease or egg drop syndrome, was first noted in Holland in 1976 and subsequently spread throughout almost the entire 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, deterioration in quality and lack of shell pigmentation, as well as a violation of protein structure.
It is believed that the causative agent chicken adenovirus disease is a duck virus that does not cause disease in ducks themselves. Although under natural conditions it is widely distributed among domestic and wild ducks, which is why they are a dangerous source of infection. Egg drop syndrome causes a DNA-containing virus from the Adenoviridae family. This explains the second name of the disease - adeno viral disease.
The causative agent of adenovirus disease, unlike other known stereotypes of avian adenoviruses, is able to agglutinate erythrocytes of chickens, ducks, geese, turkeys, and the Mexican virus can also agglutinate erythrocytes of pigeons, peacocks and humans. According to scientists, infection of chickens in the Netherlands could occur 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 has been found that duck embryos and cell cultures prepared from them are better suited for its cultivation than chicken embryo cell cultures. This also confirms the hypothesis about the origin of the virus and is widely used to isolate it and obtain virus-containing material with high titers for the manufacture of diagnosticums and vaccines.
The spread of adenovirus disease (egg drop syndrome).
Laying hens are sensitive 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 meat breeds and broilers less susceptible to adenovirus disease, than chicken egg directions. Because of this, according to some authors, broilers can be a potential spreader of the infection. The disease cannot be called highly contagious, but its introduction to poultry farms by pigeons and other wild birds should not be ruled out. Near poultry farms, antibodies to this infection were found even in sparrows. Cross-infection of wild and domestic birds is believed to occur under natural conditions, and excretion of the pathogen in the faeces allows the disease to spread over long distances.
Main way spread of the causative agent of adenovirus disease transovarially vertical transfer is considered. The reservoir of the causative agent of the disease in natural conditions are domestic and wild ducks of all breeds. This indicates a wide distribution 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 also 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 herd within 1-15 days. Under such conditions, the pathogen is transmitted by contact, as well as through service personnel, care items, and equipment.
After the appearance of 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 of the respiratory tract, and the roosters, probably with sperm. The possibility of spreading the virus when vaccinating chickens against other infections is not ruled out.
feature adenoviral infections is the ability of the virus not to manifest itself clinically until the chicken reaches a certain age of puberty. At the same time, it is believed that the mechanism of the development of the disease triggers the stress associated with the onset of the egg-laying period. In addition, the higher the productivity 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 more pronounced the disease will manifest itself in it. When laying hens are hatched from infected eggs or chicks infected in the first days of life, a sharp drop in egg production does not occur at its peak, although it is unlikely that such a bird will be able to achieve its maximum productivity.
These hens carry the adenovirus throughout their lives, but only begin to shed it from the start of laying eggs at 22-26 weeks of age. Thus, the duration of asymptomatic persistence of the virus in the body of a bird depends on the age of infection of chickens. Moreover, the earlier the infection occurred, the longer it takes before the virus is released into the environment and the first clinical signs appear.
Symptoms and signs of adenovirus disease of chickens.
When the infection is latent, the pathogen is in the intestine. Next comes the stage of activation and viremia. In this case, viremia is a common stage in the passage of adenovirus disease. It is believed that the causative agent activated as a result of hormonal changes in the body of the chicken 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 mucosa of the oviduct and other organs.
It is believed that causative agent of adenovirus disease has a direct negative effect on the glandular epithelium of the uterus, as a result of which laying hens lay eggs with a thin and fragile shell or without it at all. It was determined that under its influence the "sodium-potassium pump" in the glandular cells of the uterine mucosa is disrupted. This is confirmed by research data, according to which the sodium concentration in the uterus of diseased chickens is significantly increased, while the level of calcium, potassium and magnesium is significantly lower than in a healthy bird or an infected one, but which produces eggs with a normal shell.
An increase in acidity also leads to the dissolution of calcium and disruption of shell formation. So, adenovirus disease causes swelling of the glandular tissue of the uterine villi, followed by 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 oviduct. As a result, calcium carbonate, which is formed by the shell gland, is neutralized and eggs are formed with a soft, thin and unpigmented shell or without it at all.
Special characteristic symptoms of egg drop syndrome does not have, clinical signs of the disease are expressed slightly. Sometimes patients notice general depression, diarrhea, loss of appetite and anemia. When the disease reaches the peak of its development, the laying hens notice weak breathing and greenish litter for 1-2 weeks. Over time, cyanosis of the comb 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 a herd illness, one can expect a drop in egg production by 15-30%, sometimes up to 50%. It should be noted that the drop in egg production occurs over time: within 4-5 weeks, egg production drops, 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, the recovery of productivity is better than when keeping chickens on the floor. After restoration, the backlog from the planned performance 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 have a shell at all, or characteristic roughness is noted on its surface. Chickens lay much more "marble", eggs also beat and crack more often. The fertility of such eggs and their incubation properties are significantly deteriorating. The hatchability of chickens is reduced, and those that hatch have low viability. In the blood serum, a reduced content of alkaline phosphatase, an enzyme that plays important role in the mechanism of shell formation.
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 “fat 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, the incidence of SZN-76 is very low and rarely exceeds 5% among adult laying hens. Its main causes are yolk peritonitis and often pecking.
Pathological changes in the syndrome of egg drop.
The main pathological changes at the opening of a sick chicken are found in the reproductive organs. So, almost always note a small number of maturing and mature follicles in the ovary. Often there is even atrophy of the ovaries, which show hilly, deformed and atrophied follicles filled with a gray-yellow or green mass with clots. Many follicles are reddened with massive hemorrhages. The oviducts of sick chickens are shortened and have a thin wall, sometimes also reddened and with hemorrhages.
Considering 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 texture and a yellow-clay color. Next to it, the gallbladder is enlarged, overflowing with light green watery bile. It is violations in the liver and gallbladder that predetermine digestive disorders. At autopsy, overflow of the intestines with undigested greenish food with foam impurities is also noted.
Prevention of egg drop syndrome.
The causative agent of egg drop syndrome causes the formation of specific antibodies in the infected bird on the 7-14th day after infection. Chickens that have been ill acquire intense long-term immunity to the disease. There are no data on the re-infection of chickens with adenovirus infection in the literature.
The diagnosis is made in a complex way, taking into account epizootological, clinical, pathoanatomical signs and results. laboratory research. To pre-set the diagnosis for accounting, graphs for the development of egg productivity are taken. At the same time, it is taken into account that SZN -76 leads to a decrease in egg production in chickens at the age of 200-240 days. If drop in egg production is observed at a different age especially when chickens are older than 300 days, something else must be the cause and not this disease.
Important in establishing the diagnosis is the assessment of the quality of eggs in the form, color and properties of protein and shell. Of decisive importance in establishing the diagnosis are the results of laboratory studies, among which the main one is the hemagglutination delay reaction (RHA). When making 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 prevention of egg drop syndrome, specific prevention has been developed in the form of monovalent and associated vaccines. 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 transmission of the infection and its spread. When slaughtering sick birds and with suspected SZN-76 disease, carcasses are carefully checked for degenerative and other pathological changes, as well as salmonellosis. If nothing was found by the checks, the meat is used as conditionally fit, but is not released for sale in its raw form.
Accordingly, such illness like egg drop syndrome-76 can cause large material losses to farms due to the lack of eggs and poor hatching of chickens, is of particular importance when we are talking about the mother flock. Therefore, the prevention of its occurrence and the implementation of effective veterinary prevention is of great importance and should be taken into account both in breeding and commercial poultry farms.
Chicken egg-laying syndrome, egg casting syndrome, EDS-76, "Syndrome-76", adenovirus disease of chickens(Egg drop syndrome - English) - a viral disease that affects commercial and breeding laying hens, is 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. Currently, it is registered in Holland, England, Northern Ireland, France, Italy, Germany, Spain, Belgium, Yugoslavia, Denmark, Hungary, Sweden, Argentina and the USA.
Economic damage caused by the disease is due to losses associated with a decrease in egg production. According to J. Macpherson, in England the damage amounted to 2.4 million pounds per year. French scientists note that in caged birds, productivity is restored within 4-6 weeks, and when kept on the floor, it is 8-10% lower. The loss of eggs per bird in the affected flocks is 17.7%, which is estimated at 116.9 pence. A sick bird lays up to 15% deformed, with or without a weak shell or depigmented eggs. According to Darbyshire (1980), the number of affected eggs can reach 38-40%. J. McFerran et al. (1978) note that the loss of productivity due to 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 chickens in the first days of life.
Pathogen. Several strains have been isolated by various researchers, the identity of which has been confirmed by serological studies. Strain 127 is isolated in Northern Ireland from the mucous membrane of the nasal cavity and pharynx of birds. The virus (BC 14) was isolated from blood leukocytes, its identity to virus 127 isolated from the oviducts, feces, and nasopharynx of chickens in affected herds was serologically confirmed; 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 infecting laying hens and broilers, and it was found that the 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 was identified as an adenovirus (Todd, McNulty, 1978), but group-specific antigens with the main avian adenoviruses were not established by gel diffusion (W. Ba-xendale, 1977; J. McFerran et al., 1978). However, some degree of cross-reactivity with avian adenoviruses was observed using the method of indirect immunofluorescence (W. Baxendale, 1978).
The egg drop 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 its ability to agglutinate erythrocytes of chickens (J. McFerran et al., 1977), ducks and geese (W. Baxendale, 1977).
The EDS-76 virus multiplies at 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 cultivated in mammalian cells. It replicates in the nuclei of cells according to the method described for the first subgroup of adenoviruses. Electron microscopic examination 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 in 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) studied isolate 127 by electron microscopy. Three 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 hemagglutination 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 hemagglutination activity.
Hemagglutinin of the virus is stable for 30 minutes at 70°C, but more heat causes inhibition of activity. Purified soluble hemagglutinin contains 2 polypeptides with a molecular weight of 65,000 and 67,000, consists of rod-shaped structures 25-30 nm long.
The virus is icosahedral, particle size, capsid structure, number of capsomeres are typical for adenoviruses (V. Kraft et al., 1979).
epidemiological data not studied enough. Egg drop syndrome affects laying hens of all breeds between 25 and 35 weeks of age. The most susceptible are meat breeds that produce brown eggs, as well as breeding birds. Breeds that lay white eggs are less susceptible. The egg-casting syndrome virus is thought to be of duck origin, but is non-pathogenic to ducks. Chickens in Northern Ireland are believed to have become infected after being vaccinated against Marek's disease from a strain of Rispens produced in duck tissue culture in the Netherlands. In Ireland and Germany, the disease with signs of ECD-76 was observed for the first time in chickens imported from the Netherlands.
The disease is reproduced by artificial infection of the bird conjunctivally and orally. The virus spreads vertically through the egg. A number of researchers also recognize the horizontal route of infection transmission, attaching great importance to litter. The spread of the virus with the semen of roosters is expected.
Epizootological feature of egg drop syndrome- the ability of the virus not to manifest itself in the body of birds until they reach puberty. The reason for the activation of the pathogen is a 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 hemorrhages are also observed. In the uterus, acidity increases, which can lead to the dissolution of calcium and disruption of shell formation. During experimental infection of laying hens, defective eggs appear on the 4-7th day, the content of protein and calcium in the blood does not change.
Clinical signs, as a rule, do not appear. However, there may be ruffled feathers, anemia, diarrhea, a state of prostration, decreased activity during lay. In the later stages of the disease, cyanosis of the wattles and comb may appear in 10-70% of the birds. Typical signs of the disease are discoloration of the shell of eggs with a brown color, the appearance of eggs with or without a thin shell, a decrease in egg production. These signs persist from 2-3 to 6-12 weeks and are typical for chickens of meat breeds and brown crosses. For hens of egg breeds, a change in the internal quality of eggs is also characteristic: the protein 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. Diagnosis is based on these clinical signs, pathological changes and serological examination. The most reliable diagnostic method is the hemagglutination inhibition test (HITA). In the study of paired sera after 15 days and 2-3 weeks after infection, an increase in the titer of antihemagglutinins to 1: 1280-1: 2560 is noted.
Egg casting syndrome must be differentiated from Newcastle disease, infectious bronchitis, coccidiosis, helminthiases, poisoning with pesticides, fungicides, mycotoxins, and various factors of non-contagious etiology that cause a decrease in egg production (keeping conditions, feed quality, balanced diet, etc.).
Treatment not developed. In order 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 trace elements.
Immunity and means of specific prophylaxis. A naturally ill bird develops a strong immunity. 7 days after infection, neutralizing, antihemagglutinating and precipitating antibodies associated with IgG immunoglobulin are detected. Chicks hatched from eggs of infected hens retain maternal antibodies, which have a half-life of 3 days. Passive antibodies provide chicken resistance to infection in the first 4 weeks of life.
For specific prophylaxis, an oil-based formol vaccine is used from the BC 14 strain grown in duck embryonic cell culture. The vaccine is administered once intramuscularly or subcutaneously at a dose of 0.5 ml (1000 HAU), starting at 18 weeks of age.
The vaccine against SSJ-76 has been tested in France, the Netherlands, Great Britain, Belgium and Luxembourg, Argentina. After vaccination, the viremia phase and the associated excretion of the virus are not observed, egg production and shell quality are improved. Immunity is formed after 15 days, the maximum antihemagglutinins accumulate after 30 days. The antibody titer begins to decline 12-16 weeks after vaccination. After 40-50 weeks, antibodies are not detected.
Vaccination is seen as a temporary measure due to the risk of the virus spreading and adapting to chickens. In Yugoslavia (M. Krecov et al., 1980), a vaccine inactivated by 13-propiolactone and adsorbed by aluminum hydroxide, made from strain 127 virus, was tested with a positive result.
Prevention and control measures. For incubation, it is recommended to use eggs from hens older than 40 weeks of age, giving negative results in serological tests. In England, Northern Ireland and Germany, the slaughter of a bird that reacts positively in serological reactions is considered a radical measure for the control and prevention of egg drop syndrome in order to prevent the vertical transmission of the pathogen through the egg. It is allowed to use an inactivated vaccine.
