Merck Manual

Please confirm that you are a health care professional

honeypot link
Professional Version

Egg Drop Syndrome ’76


Joan A. Smyth

, MVB, PhD, DECVP, FRCVS, Department of Pathobiology and Veterinary Science, College of Agriculture, Health and Natural Resources, University of Connecticut

Reviewed/Revised Jul 2022 | Modified Oct 2022
Topic Resources

Egg drop syndrome ’76 is a viral disease caused by Duck adenovirus 1 that can produce considerable economic losses in laying hens. Waterfowl are the natural hosts, and the virus is found worldwide.

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

Etiology of Egg Drop Syndrome ’76

Egg drop syndrome ’76 is caused by a double-stranded DNA virus, Duck adenovirus 1 (also known as Egg Drop Syndrome virus, or EDSV), which belongs to the species Duck atadenovirus A, of the the genus Atadenovirus. All strains of Duck adenovirus 1 examined thus far are of the same serotype. The virus commonly infects both wild and domestic ducks and geese; however, evidence of infection has also been found in coots, grebes, herring gulls, owls, storks, swans, and quail. The adenovirus group antigen cannot be detected by conventional means, and EDSV differs from other adenoviruses of birds in that it strongly agglutinates avian erythrocytes; therefore, a hemagglutination-inhibition test can be used to detect antibodies against the virus.

The virus can grow 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 hours at 56°C (132.8°F). Infectivity is lost after treatment with 0.5% formaldehyde or 0.5% glutaraldehyde.

Epidemiology and Pathogenesis of Egg Drop Syndrome ’76

The natural hosts for egg drop syndrome virus are ducks and geese, and EDSV has been found in these species worldwide. The virus is thought to have been introduced to chickens via a vaccine that had been grown in contaminated duck-embryo fibroblasts. The virus became established in chickens, causing substantial problems with eggshell quality and loss of saleable and hatchable eggs. Although the virus had been found in waterfowl in North America, EDS ’76 was not reported in laying flocks in the US until 2019. All ages and breeds of chickens are susceptible to infection. Disease tends to be most severe in heavy broiler breeders and in hens that produce brown eggs. Japanese quail (Coturnix coturnix japonica) also develop disease. Rarely, EDSV has been reported to cause either respiratory tract disease or a decrease in egg production in other species (eg, turkeys, ducks, geese, and quail).

Three patterns of disease are recognized in chickens:

  • Classic EDS ’76, which 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.

  • Endemic EDS ’76, which is the result of horizontal infection of the flock during laying. It usually occurs 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 shared egg-packing station.

  • Sporadic EDS ’76, which has been recognized occasionally in flocks. This form of EDS 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, such introduction of the virus could eventually lead to endemic disease.

The main means of horizontal transmission are via contaminated eggs; equipment such as trays, crates, and trucks; and personnel. Droppings are also infective. The virus can be transmitted by blood or via vaccination needles. Transmission by insect vectors has been suggested but not proven.

After horizontal transmission of EDSV, the virus replicates to low titers in the nasal mucosa. This growth is followed by viremia, virus replication in lymphoid tissue, and then massive replication for ~5 days in the pouch shell gland. The fact that this massive viral replication in the pouch shell gland occurs after seroconversion is useful diagnostically. The virus replicates in the surface epithelium of the shell gland, leading to karyomegaly and the production of basophilic intranuclear inclusions. Infected cells degenerate and slough into the lumen. They are replaced initially by squamous and cuboidal cells; eventually, however, normal pseudostratified ciliated epithelium is restored. There is moderate to severe heterophilic inflammatory infiltration of the mucosa during the stages of viral replication, and small amounts of heterophilic exudate admixed with sloughed epithelial cells may form.

Birds that have recovered from EDS ’76 may have occasional residual oviductal lymphoid aggregates. Changes in the eggshell coincide with viral replication in the shell gland. Virus is present in both the shell and interior of eggs produced between 8 and ~18 days after infection. 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 some aviadenoviruses, EDSV has not been found replicating in the epithelial cells of the intestine.

Chicks that hatch from infected eggs may excrete virus and develop antibodies. More often however, the virus remains latent, and antibodies do not develop until the bird starts to lay, at which time the virus reactivates and grows in the oviduct, repeating the cycle.

Clinical Findings of Egg Drop Syndrome ’76

In seronegative flocks that become infected, the first clinical sign of the disease is the production of pale-shelled eggs, quickly followed by thin-shelled, soft-shelled, or shell-less eggs. The internal quality of the eggs is unaffected in experimentally induced disease. Transient signs of depression in affected birds may be evident several days before shell changes are noticed. The thin-shelled and shell-less eggs are fragile, and the birds tend to eat them; these eggs also may be trampled into litter and may be overlooked unless a careful examination is made. Although experiments have shown that eggs usually continue to be produced at a normal rate (so the disease name may be a misnomer), the number of usable 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 the virus and some of the birds have EDSV antibodies, the condition manifests 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 antibodies slow transmission of the virus.

EDS ’76 has no effect on the fertility or hatchability of eggs that have a shell quality satisfactory for setting.

Diagnosis of Egg Drop Syndrome ’76

  • Production of pale, thin-shelled, soft-shelled, or shell-less eggs by a flock that appears otherwise healthy

  • In unvaccinated chickens, demonstration of seroconversion or virus

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

Clinically, EDS ’76 can be distinguished from Newcastle disease Newcastle Disease in Poultry Newcastle disease is a severe, systemic, and fatal viral disease of poultry due to virulent strains of avian paramyxovirus type 1. Clinical signs in unvaccinated birds include sudden death,... read more Newcastle Disease in Poultry and avian influenza Avian Influenza by the absence of illness, and from infectious bronchitis 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 unvaccinated 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 infection by EDSV, these hens will already have seroconverted.

The serologic tests of choice are a hemagglutination-inhibition test using fowl erythrocytes, and ELISA. In addition, the serum neutralization test can be used for confirmation. The double immunodiffusion test also has been used. PCR assays and antigen capture ELISAs 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 the inoculation of embryonated duck or goose eggs or duck- or chick-embryo liver cell cultures. It is important to select actively infected birds for testing; however, these can be difficult to identify, especially with non-caged birds. 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 assay or antigen capture ELISA, respectively. Alternatively, it might be possible to isolate the virus from the pouch shell gland of these hens.

Control of Egg Drop Syndrome ’76

  • Eradication

  • Prevention of infection

  • Vaccination

There is no treatment for egg drop syndrome ’76. The classic form has been eradicated from primary breeders. Using 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 decrease but do not prevent virus shedding. These vaccines are administered during the growing period, usually when chickens are 14–18 weeks old, and they can be combined with other vaccines, such as those for Newcastle disease Newcastle Disease in Poultry Newcastle disease is a severe, systemic, and fatal viral disease of poultry due to virulent strains of avian paramyxovirus type 1. Clinical signs in unvaccinated birds include sudden death,... read more Newcastle Disease in Poultry . Sentinel chickens may be placed together with vaccinated chickens and periodically checked for antibodies, enabling detection of the virus in the flock.

Key Points

  • Egg drop syndrome ’76 is an economically important disease caused by Duck adenovirus 1 (genus Atadenovirus), that can be transmitted vertically and horizontally.

  • EDS ’76 affects mainly laying hens. The virus replicates in the shell gland and damages its surface epithelium, causing the production of pale, thin-shelled, soft-shelled, or shell-less eggs. Ridged eggs and poor internal quality are not characteristic of the disease.

  • EDS ’76 is well controlled in endemic areas by the administration of inactivated vaccines.

For More Information

  • Smyth JA and McFerran JB. Avian adenoviruses. Revue Scientifique et Technique 2000;19, 589–601.

quiz link

Test your knowledge

Take a Quiz!