Viral Diseases:
Also called ECG DROP SYNDROME or EDS. It is an infectious viral disease caused by an adenovirus and characterized by alterations that lead to a decline in the production and quality of eggs.
EDS is only diagnosed once the bird has entered the laying phase. It is a disease of relatively minor significance in this type of operation.
This disease is also called “syndrome of the flap of the egg” and EDS/76. It is known in English as Egg Drop Syndrome.
Egg-drop syndrome 76 is an infectious, contagious disease that is transmitted both vertically and horizontally. It tends to become chronic and is characterized by a sudden drop in egg production, accompanied by noticeable abnormalities in the eggs, and is caused by an adenovirus.
There are a number of well-known factors that cause a decrease in egg production, such as viral and bacterial infections, management and nutritional factors.
In light of current research, it has become clear that, in addition to these already known factors, there were previously unknown factors responsible for the decline in egg production.
Since 1975, many Western European countries have had to contend with serious outbreaks that they considered to be among the most significant problems facing the poultry industry.
It was established that the contagion, although atypical, it was real.
The primary cause of economic losses is believed to be the decline in egg production resulting from a drop in production during the peak laying period, accompanied by a decrease in egg quality and, in the case of brown eggs, a change in their color.
It is common to find eggs in clusters, with thin shells and depigmented yolks; the white of these eggs may be watery, and the yolk is sometimes cloudy.
This drop in production can reach up to 40%, and it takes 4 to 8 weeks to return to normal production levels; generally, production levels remain permanently below normal.
In addition to these production losses, we must also factor in expenses for medication and labor.
It was in 1975 when the farmers from Europe began to see a production not usual eggs with shells fine white or accompanied by severe falls after sunset.
The syndrome was first recognized in the Netherlands in 1975; later, in 1976, the causative agent was identified as the EDS/76 virus in Northern Ireland. The disease has gradually spread, and its contagious nature is evident.
Once this observation was made, research centers were alerted; they readily ruled out general diseases, such as Newcastle disease and encephalomyelitis, as causes of this syndrome.
For some time, infectious bronchitis was suspected to play a role, but Van Eck et al. (1976) and many others since then have refuted this hypothesis.
The problem needed to be framed in clear terms—symptoms, lesions, transmission—to guide the researchers.
This new entity was named the “Syndrome of the fall of the start-76” by the researchers.
It was agreed to refer to it as a syndrome, since a syndrome is a cluster of symptoms that occur simultaneously in a number of different diseases; and, given that many aspects of this condition remain unknown, it is prudent to speak of a syndrome rather than a disease.
The number 76 to catalog this set nosológico described by several authors without ambiguities on the observed data.
This syndrome has been reported in Great Britain, Belgium, Spain, Central and South America, possibly Mexico, and Japan.
The virus producer of the syndrome of the fall of the setting (EDS) is considered by ms. baxendale (1977) morphologically similar to the adenovirus.
The EDS is caused by adenoviruses of the duck. The infection is spread in chickens by means of vaccines grown in cells of ducks or in embryos infected with the virus, EDS.
This virus exhibits icosahedral symmetry, consisting of 252 capsomeres (composed of proteins) arranged in 20 faces or equilateral triangles and 12 fibers or spicules; the spicules are often destroyed during viral preparation. The virus’s diameter appears rounder, unlike that of adenoviruses.
The drop-off virus contains a deoxyribonucleic acid (DNA) strand in its genome; this was demonstrated using a specific inhibitor of DNA synthesis, iododeoxyuridine. This is a feature it shares with adenoviruses and a distinguishing characteristic compared to infectious bronchitis viruses, for example.
The test into the ether (chloroform) was performed to determine the presence or absence of a sheath.
The ether dissolves this nature primarily lipid and the virion lost the ability to multiply.
For verification, equal volumes of ether and virus are mixed and allowed to come into contact for 7 hours at 40 °C; a sample of this mixture is then applied to a cell culture.
In the essay, does not demonstrate the reduction of the cytopathic effect after the action of the ether, but allows confirming the absence of wrap for the virus; this case is equal to the adenovirus.
Density and sedimentation coefficient (s) are determined by ultracentrifugation in a cesium chloride gradient.
Regarding the effect of ultracentrifugation, the different particles migrate to a zone where they are in density equilibrium; these zones appear as whitish bands. The density of the virus in these bands was 1.34 in cesium chloride, a finding confirmed by electron microscopy.
The sedimentation constant (s) for the virus corresponds to the rate at which the virus moves under the influence of centrifugation in a linear sucrose gradient; this rate depends on the shape and size of the virus. The values obtained for this virus are 950 s.
The egg-drop syndrome virus has shown high stability across a pH range of 3–10. The virus is equally resistant to temperature; these characteristics are also common to adenoviruses.
Antigenic analysis of the virus was performed using agarose gel; this qualitative technique was applied to the antigenic properties of virus 127 using various antisera. The results of this test showed positive reactions with antibodies 127, BC 14, and 3877, and negative reactions with antisera BI and adenovirus (CELO type).
Below is Melnik’s (1982) viral classification, which outlines its main characteristics.
Other characteristics of the virus that causes drop-egg syndrome include its agglutinating ability; it is capable of agglutinating red blood cells from chickens and ducks, but not those from rabbits, sheep, or horses.
This power hemagglutinating is an important property because it allows to put in evidence the virus in a cell culture by performing a hemagglutination directly with the supernatant fluid of the culture.
We can summarize some characteristics of the virus producer of this syndrome:
It causes hemagglutination of red blood cells from chickens, ducks, and turkeys.
—According to the AGP test, it does not share any major antigens with other avian adenoviruses.
There is no neutralization against other avian adenoviruses in hemagglutination, inhibition, and plaque reduction assays.
Immunofluorescence reveals a certain antigenic relationship with other adenoviruses.
The virus replicates well in chicken embryos, although SPF chicken embryo liver cells (chicken embryo hepatocytes) or duck cells are preferred for culture.
—When culturing in chicken embryo fibroblasts, the cells must be harvested at 9 and 14 days of age.
For the cultivation of kidney cells, the cells must be harvested from the kidneys of 1- to 3-week-old SPF chickens.
—It appears that duck cells are more susceptible than fibroblasts. The virus hardly replicates in kidney cells. The BC-14 virus was isolated by Baxendale from white blood cells, and McFerran was able to isolate virus 127 from the nasal and pharyngeal mucosa of a hen.
Virus 3877 has been isolated from the liver of a laying chicken.
Birds can become infected at any stage of their lives. Hens between 26 and 35 weeks of age are most susceptible, with egg production losses of up to 30%; birds recover after 3–4 weeks, but egg production will remain below normal in most flocks.
Exceptionally, birds between 50-55 weeks may show clinical signs.
It is believed that the birds most susceptible to this syndrome are those that lay brown eggs, while those that lay white eggs are less susceptible.
The disease is transmitted horizontally and vertically.
Vertical transmission:
Several authors have suggested that the virus is transmitted through eggs; the virus can remain dormant in laying hens, waiting for a stressor that triggers physiological changes in both the virus and the animal, thereby facilitating viral replication and spread.
The transmission through the egg is the most important, and the virus can be localized in the liver of infected embryos. The percentage of transmission can be as high as 10 %, but in breeding birds of more than 45 weeks of age, there is little likelihood of transmission.
If the rate of virus transmission is very low, infected chickens will not be able to develop antibodies to the infection until later, when they enter the production phase.
This is called tolerance of immunity. The transmission of the virus can occur in the presence of antibodies, HI high or low, to EDS-76.
Horizontal transmission:
One of the characteristics of the disease is how it spreads within a chicken coop, and this varies depending on the type of housing; transmission occurs slowly in caged flocks and more rapidly in free-range flocks, although it is generally believed that transmission is slow and intermittent in the wild.
It has been hypothesized in terms of epizootiology and transmission that there may be birds that show no symptoms of the disease.
When you start the implementation, these hens carriers infect other susceptible appears and the low position.
Viruses that spread slowly not to damage as visible as in a mass infection, so it has been considered that the percentage of the fall of sunset depends on the amount of carriers and of the circumstances of the environment.
The infection is slow, caused by a few carriers of the virus at the beginning of the set, produces the kind of poor where they do not reach to the peak and the curve of production is much longer than the normal.
The infection more massive, on the other hand, causes decreased more sharply from 20% to 40 % within a very short time. The virus can also be transmitted to the use of vaccines made in the embryo of a duck infected with adenovirus.
The feces of infected birds may become a source of infection for more than 10 weeks post-infection.
The legs play an important role in transmission; transmission from chicken to chicken is poor.
Clinical manifestations:
Usually, the birds look healthy, but it can be observed an incidence of morbidity passing, a slight diarrhea for a few days and sometimes the ridges pale and a decrease in the consumption of food.
The disease can occur in two ways.
The first:
Egg production has declined by 6–50%, though more typically by 15–30%.
This decline in production occurs 13–16 days after infection and can last 6 to 12 weeks; otherwise, the birds would never return to normal production.
There are also problems with the shells, such as soft shells or shell-less eggs (shell-less eggs). In addition, there is a lack of pigmentation and a reduction in egg size; the albumen in these eggs may be watery, and the yolk is sometimes cloudy.
The passage of the egg through the oviduct is significantly shortened. Normally, the regular interval for egg passage through the oviduct is approximately 24–25 hours in a healthy hen, but in hens infected with EDS–76, this interval between the production of consecutive eggs is shorter, which is why many authors attribute the lack of shell calcification to this phenomenon.
These changes in the eggs are most pronounced at the onset of infection and diminish over time. In very few cases does fertility decrease.
The second:
This form of the disease occurs when birds become infected early in the laying period; they never reach the peak of the production curve and remain below normal production levels.
In summary, symptoms appear before the hens reach peak egg production or after peak egg production, usually before 40 weeks of age. The time required for egg production to return to normal ranges from 4 to 8 weeks, and in many cases, the production curve remains permanently below normal.
The autopsy of the hens is not very revealing.
There is some swelling of the intestines and genital tract; the oviduct generally shows no visible lesions.
When lesions are observed, they are more likely to be caused by secondary bacterial infections—such as E. coli salpingitis—rather than by the virus responsible for the disease.
The only place in the pathway of breeding, where it may occur any change, is the uterus. Generally, we observed an increase of exudate albuminous.
Serum protein levels, albumin, and globulins remain virtually unchanged, as do serum calcium levels.
As for phosphatases, these are enzymes capable of hydrolyzing phosphoric acid esters and more complex organic compounds, such as glucose phosphate, phosphoproteins, and phospholipids.
The alkaline phosphatase found in bird serum has three sources: the intestine, the liver, and bone.
Alkaline phosphatase activity is reduced in the hen; it releases calcium into the bloodstream from the bones to form the shell; however, this is not the case here, since these are shell-less eggs.
Consequently, serum calcium levels should be higher than normal; in fact, they show little change, suggesting that some of the calcium is being absorbed or that its absorption is reduced, although it should be noted that this issue is still under investigation.
The disease, lead to a certain reduction in the consumption of food, you can modify a little the activity of serum alkaline phosphatase, hauling in fact a reduction of these enzymes, and their activity in the bowel.
For the diagnosis of this syndrome has been taking into account as a starting point the clinical symptoms of this disease.
The sharp fall in the production of eggs at the time that the production is at the top of the curve of posture and the appearance of soft eggs or in fárfara are signs highly suggestive for the presumptive diagnosis of field of the EDS/76.
The diagnostic lesion does not reveal any information of interest, although this aspect must also be taken into account in the diagnosis.
Another element important diagnostic is the appearance in the serum of the animals of antibody-precipitating, for which you must develop the serological test and agar gel precipitation (A. G. P.) using an antigen-specific and observed in the sera positive lines of precipitation in agar.
The virus's hemagglutinating ability makes it possible to perform a serological diagnosis based on the hemagglutination (HA) reaction.
This test is performed using a microplate assay, employing, as in the Newcastle disease test, four hemagglutination units of antigen in 1:2 and 1:4 dilutions of serum.
The antigen used in this test is an inactivated antigen derived from the V-12 strain.
Hemagglutination-inhibiting (HAI) antibodies have been detected in the sera of affected animals; these antibodies reach peak levels in serum 15 days after infection and persist for a long period of time. A high titer of 1:60 may persist for 3 months, and HAI antibodies may still be present even after 10 months.
These antibodies have also been investigated in the yolk sac of embryos and their titer is equal or approximately half those obtained with hen serum.
Seroneutralization in primary tissues is another technique that has been developed, although it is purely qualitative in nature.
Virological diagnosis requires isolation of the virus, which must be performed in tissue culture using chickens from adenovirus-free flocks.
The cultivation of the virus in fibroblast embryo is sensitive, but the cultivation of liver cells displayed a higher sensitivity. It is not recommended for the isolation and cultivation of this virus in chick embryos.
Once the isolate has been obtained, a neutralization test is performed to confirm the diagnosis.
There are a number of avian diseases that share similar characteristics with EDS/76 in terms of egg production and egg quality, such as Newcastle disease, infectious bronchitis, encephalomyelitis, and mycoplasmosis, from which we must distinguish EDS/76.
Has been recommended by many researchers, the use of a vaccine against the EDS-76.
Many laboratories, including Intervet, have developed inactivated vaccines based on the BC-14 virus (Nov-Vac–EDS-76). En esta vacuna, el virus fue inactivado con formol y puesto en suspensión en la fase acuosa de una emulsión adyuvante.
It is recommended that this vaccine be administered before weaning, preferably between 14 and 18 weeks of age, by subcutaneous or intramuscular injection.
Vaccination is required for breeding stock and laying hens, with a booster shot administered at a later date.
The inactivated BC-14 vaccine provides good protection for birds against the effects of infection with the virulent virus and stimulates the production of antibodies, which appear 15 days after vaccination and reach peak levels at 30 days.
Maternal antibodies are present in chicks; they have a half-life of 3 days and disappear by the fourth week.
Trials have been conducted on the production of a combined NC-EDS–76 vaccine; no significant data have been obtained to date.
In countries where the disease has been diagnosed, measures should focus on maintaining biosecurity and management practices, improving the diet, and culling severely affected birds; generally, birds tend to recover, so a vaccination program should be established, targeting primarily breeding stock and their replacements.
Yes, after several years of successful vaccination, you can leave 5–10% of your flock unvaccinated to detect the presence of the disease.
If that group shows no problems, you should skip vaccinating 20% of the flock, and so on, until you stop vaccinating altogether.
Other aspects to consider are movement of animals and the control of the staff.
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LOHMANN ANIMAL HEALTH (2012)
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