Egg drop syndrome (EDS) is caused by a viral infection in laying hens. It is characterised by production of soft-shelled and shell-less eggs in apparently healthy birds, leading to a sudden drop in recorded egg production or a failure to achieve a normal peak in production. 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. Transient diarrhoea and dullness and a loss in egg yolk pigment may be seen before the eggshell changes. Mortality is usually negligible. The natural hosts for the EDS virus are ducks and geese, which are asymptomatic (do not show symptoms) carriers. Chickens of all ages and breeds are susceptible but the disease is most severe in broiler breeders and brown-egg layer strains. EDS was first introduced into chickens through contaminated vaccine and spread through breeder flocks. EDS is a notifiable disease in most sates of Australia.
EDS can be distinguished from Newcastle disease and influenza virus infections by the absence of illness, and from infectious bronchitis by the eggshell 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 is caused by infection with the EDS virus. The incubation period is three to five days and the disease course is four to 10 weeks. The virus is transmitted through any of the conventional means of viral disease spread and is also transmitted on and in the egg. The main method of horizontal spread is through contaminated egg trays; droppings are also infective. Contact with wild ducks or geese, or water or ranges frequented by these birds, may be a source of infection. Humans and contaminated fomites (such as crates or trucks) can spread virus, which can also be transmitted by needles when vaccinating and drawing blood. Insect transmission is possible but not proven. Chicks hatched from infected eggs may excrete virus and develop antibody. More often, the virus remains latent (alive but inactive), 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. Birds with antibody slow the spread of virus. There is no effect on fertility or hatchability of those eggs suitable for setting.
There is no successful treatment of EDS. The classical form has been eradicated from primary breeders and the maintenance of EDS-free breeding stock is the main control measure. In layers, induced moulting will restore egg production. The prevention of horizontal spread relies on good biosecurity. 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, prevent clinical 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 (unvaccinated susceptible 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.
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