| Egg drop syndrome (EDS) is characterized by production of soft-shelled and shell-less eggs in apparently healthy birds. It has been recognized worldwide, except in the USA. Etiology:The causal adenovirus 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 grows to 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 chick eggs or in mammalian cells. The resistant virus has at least three genotypes, one of which is associated with classical EDS, one with ducks in the UK, and one with EDS in Australia. Epidemiology:The natural hosts for EDS virus are ducks and geese, and the disease has been described in quail ( Coturnix coturnix japonica ). Three types of disease are recognized in chickens. Classical EDS probably was due to contamination of a vaccine for Marek’s disease grown in duck-embryo fibroblasts and subsequent adaptation of the virus to the chicken. 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, although the disease tends to be most severe in heavy broiler-breeders or brown-egg producers. Arising from the classical 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. The virus is spread mainly horizontally by contaminated egg collection (Keyes) trays, 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. Man 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. Pathogenesis: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 eggshell 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 is reactivated, grows in the oviduct, and the cycle repeats. Clinical Findings and Lesions:In flocks without antibody, the first sign is loss of color in pigmented eggs, quickly followed by soft-shelled and shell-less eggs. 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. Diarrhea and a transient dullness may be seen before the eggshell changes. The major pathological changes occur in the pouch shell gland. Surface epithelial cells develop intranuclear inclusion bodies and degenerate, and are replaced by squamous, cuboidal, or undifferentiated columnar cells. There is moderate to severe inflammatory infiltration of the mucosa. Diagnosis:In classical EDS, the combination of poor eggshell quality at peak production in healthy birds is almost diagnostic. With endemic or sporadic EDS, disease can occur in any age of bird in lay. In cage units especially, spread can be slow and the clinical signs may be overlooked, the problem being perceived as a small depression (2-4%) of egg yield. EDS can be distinguished from Newcastle disease ( Newcastle Disease , Viscerotropic Velogenic Newcastle Dieases (VVND) and influenza virus infections (Influenza, Avian Influenza Viruses )by the absence of illness, and from infectious bronchitis(Infectious Bronchitis) by the eggshell changes that occur at or just before the fall in egg production and absence of ridges and malformed eggs sometimes seen in infectious bronchitis. 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 is attempted when the first abnormal eggs are produced. The hemagglutination inhibition test (high levels of hemagglutinins are produced) using fowl RBC or the ELISA test are the serological tests of choice; the serum neutralization test can be used for confirmation. The double immunodiffusion test also has been used. When selecting birds for diagnosis, especially in cage units, it is important to bleed only birds that have produced affected eggs. Control:There is no treatment. The classical form has been eradicated from primary breeders. The endemic form can be controlled by washing and disinfecting plastic Keyes trays before reuse. 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 old, and can be combined with other vaccines such as for Newcastle disease. |
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