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Overview of Egg Drop Syndrome '76 in Poultry

By Joan A. Smyth, PhD, Department of Pathobiology and Veterinary Science, University of Connecticut

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Egg drop syndrome ’76 (EDS ‘76) is an atadenovirus-induced disease characterized by the production of pale, soft-shelled, and shell-less eggs by apparently healthy laying hens. The disease in laying hens has commonly been called "egg drop syndrome," but the full name (egg drop syndrome ’76 [EDS ’76]) should be used to distinguish it from the recently recognized flaviviral disease of ducks, which has been called "egg drop syndrome in ducks," and "duck egg drop syndrome," creating potential for confusion.

Etiology:

EDS ‘76 is caused by a double-stranded DNA virus, duck adenovirus 1 (also known as EDSV), which belongs to the genus Atadenovirus. The virus commonly infects both wild and domestic ducks and geese, but evidence of infection has also been found in coots, grebes, herring gulls, owls, storks, swans, and quail. The adenovirus group antigen cannot be demonstrated by conventional means, and EDSV differs from other avian adenoviruses by strongly agglutinating avian RBCs, a fact that allows use of a hemagglutination-inhibition test for detection of antibodies to the virus. The virus grows to high titers in embryonated duck and goose eggs and in cell cultures of duck or goose origin. It replicates well in chick-embryo liver cells, less well in chick kidney cells, and comparatively poorly in chick-embryo fibroblasts. It does not grow in embryonated chicken eggs or in mammalian cells. The virus is resistant to pH range 3–10 and to heating for 3 hr at 56°C (132.8°F). Infectivity is lost after treatment with 0.5% formaldehyde or 0.5% glutaraldehyde.

Only one serotype of EDSV has been recognized to date.

Epidemiology and Pathogenesis:

The natural hosts for EDSV are ducks and geese. It is thought that the virus was introduced to chickens through a vaccine that had been grown in contaminated duck-embryo fibroblasts. The virus became established in chickens, causing substantial problems with egg shell quality and loss of eggs. All ages and breeds of chickens are susceptible to infection. Disease tends to be most severe in heavy broiler-breeders and hens producing brown eggs. Japanese quail (Coturnix coturnix japonica) also develop disease. There are rare reports that the egg drop syndrome virus (EDSV) has caused either a drop in egg production or respiratory tract disease in other species, eg, turkeys, ducks, geese, and quail.

Three patterns of disease are recognized in chickens: 1) Classical EDS ‘76 occurs when primary breeding stock are infected and the virus is transmitted vertically through the egg. The virus often remains latent until the progeny chick reaches sexual maturity, at which time the virus is excreted in the eggs and droppings, infecting susceptible contacts. 2) Endemic EDS is the result of horizontal infection of the flock during lay. It is usually seen in commercial egg layers. Contaminated egg collection trays are one of the main vehicles of horizontal transmission between flocks, and outbreaks are often associated with a common egg-packing station. 3) Sporadic EDS ’76 has been recognized occasionally in flocks. This is due either to direct contact with domestic ducks or geese or, more often, to use of a water supply contaminated with wildfowl droppings. Although infection by this route is uncommon, there is always a risk that these introductions of the virus could form a starting point for endemic disease.

The main method of horizontal spread is through contaminated eggs or equipment such as trays, crates, trucks, or personnel. Droppings are also infective. The virus can be transmitted by bleeding or vaccination needles. Insect transmission may be possible but has not been proved.

After horizontal infection, the virus grows to low titers in the nasal mucosa. This is followed by viremia, virus replication in lymphoid tissue, and then massive replication for ~5 days in the pouch shell gland. Changes in the egg shell coincide with viral replication in the shell gland. Both the exterior and interior of eggs produced between 8 and ~18 days after infection contain virus. Exudate and secretions from the oviduct are rich in virus and pass into the droppings, which may become mildly to moderately watery for 2–3 days. Unlike other fowl adenoviruses, there is little, if any, virus growth in the epithelial cells of the intestine. Interestingly, the massive viral replication in the pouch shell gland occurs after seroconversion, a fact that is useful diagnostically.

Chicks hatched from infected eggs may excrete virus and develop antibody. More often, the virus remains latent, and antibody does not develop until the bird starts to lay, at which time the virus reactivates and grows in the oviduct, repeating the cycle.

Clinical Findings:

In flocks without antibody, the first sign of the disease is the production of pale-shelled eggs, quickly followed by production of soft-shelled and shell-less eggs. Internal quality of eggs is unaffected in experimentally induced disease. Transient dullness may be seen in the days before the shell changes are noticed. The thin-shelled and shell-less eggs are fragile, and the birds tend to eat them; these eggs also may get trampled into litter and may be overlooked unless a careful examination is made. Although it has been shown experimentally that eggs usually continue to be produced at a normal rate (so the disease name may be a misnomer), the number of useable eggs produced falls by 10%–40%. Egg production by the flock usually returns to normal. In flocks in which there has been some spread of virus and some of the birds have antibody (usually 10%–20%), the condition is seen as a failure to achieve predicted production targets; careful examination shows that these flocks experience a series of small group episodes of infection and disease. Birds with antibody slow the spread of virus.

There is no effect on fertility or hatchability of those eggs with a shell quality that is satisfactory for setting.

Diagnosis:

Production of pale, thin-shelled and shell-less eggs by a flock that appears otherwise healthy should raise strong suspicion of EDS ‘76. Transient mild depression and/or mild watery droppings may be noted. Ridged eggs and poor internal quality are not features of EDS ’76. Poor egg shell quality at peak production in healthy hens should also raise strong suspicion of classical EDS ’76. With endemic or sporadic EDS ‘76, disease can develop in laying hens of any age. In cage units, spread can be slow, and the signs may be overlooked or perceived as a small depression (2%–4%) of egg yield.

Clinically, EDS ’76 can be distinguished from Newcastle disease (see Newcastle Disease in Poultry) and influenza virus infections (see Avian Influenza) by the absence of illness, and from infectious bronchitis (see Infectious Bronchitis) by the absence of respiratory signs, the absence of ridged and malformed eggs, and the absence of poor internal egg quality. Confirmatory laboratory testing is needed for definitive diagnosis. Searching for evidence of seroconversion is the easiest diagnostic approach for nonvaccinated flocks. When selecting birds for diagnosis, especially in cage units, it is important to target hens that have produced affected eggs, because if the problem is due to EDSV infection, these hens will already have seroconverted. A hemagglutination-inhibition test using fowl RBCs, and ELISA, are the serologic tests of choice. In addition, the serum neutralization test can be used for confirmation. The double immunodiffusion test also has been used. PCR-based tests and antigen capture ELISA tests have been used to detect EDSV DNA and antigen, respectively. Again, appropriate selection of the hens to be examined is very important. EDSV can be isolated by inoculating embryonated duck or goose eggs or duck- or chick-embryo liver cell cultures. It is important to select recently infected birds for testing, but these can be difficult to identify, especially if the birds are on litter. An easier method is to feed affected eggs to antibody-free hens. These hens can then be tested for seroconversion after the first abnormal eggs are produced, or tested for evidence of EDSV DNA or antigen by PCR or antigen capture ELISA, respectively, or virus isolation can be attempted from the pouch shell gland of these hens.

Control:

There is no treatment for EDS ’76. The classic form has been eradicated from primary breeders. Use of dedicated equipment and egg trays for each farm, and/or washing and disinfecting plastic egg trays before use, can help to control the endemic form. The sporadic form can be prevented by separating chickens from other birds, especially waterfowl. General sanitary precautions are indicated, and potentially contaminated water should be chlorinated before use.

Inactivated vaccines with oil adjuvant are available and, if properly administered, successfully prevent the disease. They reduce but do not prevent virus shedding. These vaccines are given during the growing period, usually at 14–18 wk of age, and can be combined with other vaccines, such as those for Newcastle disease. Sentinel chickens may be placed along with vaccinated chickens and periodically checked for antibodies, which would allow detection of the presence of virus in the flock.

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