Egg drop syndrome (EDS) is characterized by the production of soft-shelled and shell-less eggs in apparently healthy birds. It has been recognized worldwide, except in the USA.
The causal adenovirus, in the genus Atadenovirus, is widely distributed in both wild and domestic ducks, geese, coots, and grebes. Antibody has also been detected in herring gulls, owls, storks, and swans. The adenovirus group antigen cannot be demonstrated by conventional means, and EDS virus also differs from other avian adenoviruses by strongly agglutinating avian RBC. The virus achieves high titers in embryonating eggs or in cell cultures of duck or goose origin. It replicates well in chick kidney or chick-embryo liver cells and to a lesser degree in chick-embryo fibroblasts. It does not grow in embryonating chicken eggs or in mammalian cells.
The resistant virus has one serotype but at least 3 genotypes: one associated with classical EDS, one with ducks in the UK, and one with EDS in Australia.
The natural hosts for EDS virus are ducks and geese, and the disease has been described in Japanese quail (Coturnix coturnix japonica). Three types of disease are recognized in chickens. Classic EDS probably developed due to contamination of a vaccine for Marek's disease grown in duck-embryo fibroblasts and subsequent adaptation of the virus to chickens. Basic breeding stock was infected, and the virus was transmitted vertically through the egg. The virus often remained latent until the chick reached sexual maturity, when it was excreted in the eggs and droppings to infect susceptible contacts. Because the virus is vertically transmitted and is reactivated around peak egg production, there was an apparent breed and age susceptibility. However, all ages and breeds of chickens are susceptible. Disease tends to be most severe in heavy broiler-breeders or brown egg producers.
Arising from the classic form, endemic EDS has been reported in many areas and is usually seen in commercial egg producers. Flocks become infected at any stage in lay. Contaminated egg collection trays are one of the main forms of horizontal transmission, and outbreaks are often associated with a common egg-packing station.
Rare, sporadic EDS has been recognized in isolated flocks. It appears to be due either to contact with domestic ducks or geese or, more often, to water contaminated with wildfowl droppings. The risk is that these introductions could become endemic.
The main method of horizontal spread is through contaminated eggs; droppings also are infective. People and contaminated fomites such as crates or trucks can spread virus, which also can be transmitted by needles when vaccinating and drawing blood. Insect transmission is possible but not proved.
After horizontal or experimental 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 ∼8 days in the oviduct, especially in the pouch shell gland region. Changes in the egg shell occur coincidentally. Both the exterior and interior of eggs produced between 8 and ∼18 days after infection contain virus. A copious exudate in the lumen of the oviduct is rich in virus, and this contaminates the droppings. Unlike other fowl adenoviruses, there is little, if any, growth in the epithelial cells of the intestine.
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.
In flocks without antibody, the first sign is loss of color in pigmented eggs, quickly followed by soft-shelled and shell-less eggs. Diarrhea and a transient dullness may be seen before the shell changes. Birds tend to eat the shell-less eggs, which therefore may be missed unless a search is made for the membranes. Egg production falls 10–40% mainly because of the shell-less eggs. 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 are experiencing a series of small EDS episodes. Birds with antibody slow the spread of virus.
There is no effect on fertility or hatchability of those eggs suitable for setting.
The major pathologic changes are seen in the pouch shell gland. Surface epithelial cells develop intranuclear inclusion bodies and degenerate; they are replaced by squamous, cuboidal, or undifferentiated columnar cells. There is moderate to severe inflammatory infiltration of the mucosa.
In classic EDS, the combination of poor egg shell quality at peak production in healthy birds is almost diagnostic. With endemic or sporadic EDS, disease can be seen in laying birds of any age. In cage units, spread can be slow, and the clinical signs may be overlooked or perceived as a small depression (2–4%) of egg yield.
EDS 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 egg shell changes that occur at or just before the drop in egg production and by the absence of ridges and malformed eggs sometimes seen in infectious bronchitis.
EDS should be suspected whenever peak egg production parameters are not met; however, the observation of clinical signs alone does not provide enough reliable information for diagnosis. The virus can be isolated by inoculating embryonating duck eggs or duck- or chick-embryo liver cell cultures. It is important to select birds producing abnormal eggs, but this can be difficult, especially if the birds are on litter. An easier method is to feed affected eggs to antibody-free hens. Virus isolation from the pouch shell gland of these hens can be attempted when the first abnormal eggs are produced.
The hemagglutination inhibition test (high levels of hemagglutinins are produced) using fowl RBC or ELISA are the serologic and diagnostic tests of choice. In addition, the serum neutralization test can be used for confirmation. The double immuno-diffusion test also has been used. If one adenovirus has been isolated, restriction endonuclease analysis can be used to classify the virus as EDS. When selecting birds for diagnosis, especially in cage units, it is important to bleed only birds that have produced affected eggs.
There is no treatment. The classic form has been eradicated from primary breeders. Washing and disinfecting plastic egg trays before use can 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 made, control the disease. They reduce but do not prevent virus shedding. These vaccines are given during the growing phase, usually at 14–18 wk, and can be combined with other vaccines such as for Newcastle disease. Sentinel birds are frequently placed along with vaccinated chickens to detect the presence of virus in the flock. Sentinel chickens will become serologically positive on hemagglutination inhibition test.
Last full review/revision March 2012 by Pedro Villegas, DVM, MS, PhD, DACVM, DACPV