Download Egg Drop Syndrome Egg drop syndrome (EDS) is characterized by

Egg Drop Syndrome
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 achieves high titers in embryonating eggs or in cell
cultures of duck or goose origin. It replicates well in chick kidney or chickembryo 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 1serotype but at least 3genotypes: 1associated
with classical EDS, 1with ducks in the UK, and 1with EDS in Australia .
Epidemiology :
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. Classical EDS probably was
due to contamination of a vaccine for Marek’s disease grown in duckembryo 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, 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. 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. Humans 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 ~ 8days 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 ~ 18days 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 .
Clinical Findings :
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 eggshell 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 %01-11mainly 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 %01-11), 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 .
Lesions: 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 .
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 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 (%0-0) of egg yield .
EDS can be distinguished from Newcastle disease (Newcastle Disease)
and influenza virus infections (Avian Influenza: Introduction) by the
absence of illness, and from infectious bronchitis (Infectious Bronchitis:
Introduction) 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 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 the ELISA test are the serologic and
diagnostic tests of choice. In addition, the serum neutralization test can be
used for confirmation. The double immunodiffusion 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 .
Control :
There is no treatment. The classical 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 18-10wk, 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 .