EGG DROP SYNDROME

MICROBIOLOGY & IMMUNOLOGY

VETERINARY MEDICINE-UB
EDS ‘76
• A viral disease of birds, chickens, ducks, geese & swans
• In the autumn 1976 ----- a distinct egg drop syndrome was
first identified in Northern Ireland ----- has been identified as
Adenovirus BC14, 127
• EDS’76 to distinguish it from recently recognized flavivirus
disease of ducks : egg drop syndrome in ducks, duck egg
drop syndrome
• It was similar with the disease had been seen over a 4-years
period in broiler parents in Holland.
EDS
• Sudden drop in egg production or failure to achieve a normal
peak in production
• Cause by a viral infection in laying hens
• Chicken in all ages & breeds are susceptible
• Most severe in broiler breeders & brown-egg layer strains
• Ducks & geese are the natural hosts ---- asymptomatic
carrier
• Characterized by: production of soft-shelled & shell-less egg
in apparently healthy animals ----- lead sudden drop or
failure to achieve a normal peak in egg production
Etiologic agent
• The aetiological agent is an adenovirus of group III.
Ducks Adenovirus 1 (DAdV—1)/ Duck adenovirus A (EDSV)/
EDS-76 virus/ adenovirus 127
dsDNA
• Genus Atadenovirus
• Commonly infects both wild & domestic ducks and geese
• EDSV differs from other avian adenovirus ---- strongly
agglutinating avian RBC ----- HA-HI test to detect the virus &
antibody titer
• Grows to high titers:
– in embryonated duck & goose eggs
– In cell cultures of duck or goose origin
• Replicates well in chick-embryo liver cells, less well in chick
kidney cells, and poorly in chick-embryo fibroblast
• It does not grow in embryonated chicken eggs or in
mammalian cells
• Virus resistance:
– Relative tolerant to pH & heat. Resistant to pH 3-10,
heating for 3 hr. at 560C
– Resistant to many common disinfectants.
– Iodophor and aldehyde can be effective. Infectivity is
lost after treatment with 0,5% formaldehyde or 0,5%
glutaraldehyde
– Potentially contaminated water: chlorinated before use
• 20 days carcasses ---- the virus completely inactive
Transmission
• Contaminated vaccine
• On and in the egg (horizontal & vertical transmission),
mainly vertical transmission
• Chicks hatched from infected eggs (develop antibody) --
- excrete the virus immediately ---- often remain latent
until the chickens become sexually mature ---
reactivates ---- growsin the oviduct ---- excrete virus in
both eggs & dropping
• Transmitted horizontally through any of the
conventional means of viral disease spread: oral route,
equipment, droppings, water, fomites
• Iatrogenic transmission: needles
• Contact with wild ducks or geese
• Insects biting
• Spread through breeder flocks
Pathogenesis
Three pattern of disease are recognized in chicken:
1. Classical EDS’76 occurs when primary breeding stock are
infected and the virus is transmitted vertically through the egg
The virus remain latent until the chick reaches sexual maturity --
-- excrete the virus via egg & dropping --- infecting susceptible
contact
2. Endemic is the result of horizontal infection (the main method
of transmission) of flock during lay (usually in commercial flock)
---- contaminated egg collection trays ---- egg-packing station
May via dropping, blood/ vaccination needle
3. Sporadic EDS’76 ---- direct contact
Infection ---- the virus grows to low titer in the nasal mucosa
---- viremia ----- limphoid tissue ---- replication ------
massive replication for ~ 5 days in the pouch shell gland.

Change in the egg shell coinside with viral replication in the

shell gland

Both exterior and interior of eggs produced between 8 & 18

days after infection --- contain virus.

Exudate and secretion from the oviduct are rich in virus ---
pass into the droppings ---- mildly & moderately watery for
2-3 days

Chicks hatched from infected eggs ---- excrete virus &

develop antibody ---- may virus remain latent ---- antibody
does not develop until the animal start to lay ---- virus
reactivates & grows in the oviduct ---- repeating the cycle
Signs:
In flock without antibody
 Incubation period highly variable, usually : 3-5 days
 Egg drop at peak
 Drops may be 5-50% and last 3-4 weeks
 Loss of shell pigment rough, thin or soft-shelled
eggs and shell-less eggs
 Poor internal quality
 Difficult to identify the early stages of the disease --
-- the hens will eat the shell-less eggs & remain
only the egg membrane ---- easy to miss
 The eggs remain fertile & hatch as usual
 Diarrhoea
 The infected animal generally remain healthy (Lack
of signs)
 Mortality is usually negligible (5-7%)
In flock in which there has been some spreads & some
of the chickens have antibody:
• Failure to achieve predicted production targets
• The virus spread slowly

Eggs production by the flock usually returns to normal

There is no effect on fertility or hatchability of those

eggs
Histopathology
 No specific lesion
Only a slight atrophy of ovary and oviduct
 Degenerative changes in the epithelial cells of
oviduct
 Edema & exudates in the uterus (shell gland)
 Severe degeneration & desquamation of oviduct
and uterus
 Infiltration of heterophils, lymphocytes,
plasmacytes
 Intranuclear inclusion body: in the epithelial cells
of the uterus, vaginal glands
Diagnosis
• The virus very contagious by either direct or indirect contact
• Before collecting or sending any samples from animals with
suspected animal disease ---- the proper authorities should
be contacted.
• Samples should only be sent under secure conditions and to
authorized laboratories to prevent the spread of the disease.
• Samples: reproductive tissues including the uterus ,
abnormal eggs, paired serum
Diagnosis
Production of pale, thin-shelled & shell-less eggs ---- even
appears healthy ---- should strong suspicion of EDS ‘76
Transient mild depression
Mild watery dropping
Shrink eggs & poor internal quality
 Serology: HI, ELISA
 It is important to rule out other possible reason for egg
drop
 Management problems
 Nutritional deficiency : Vit E, B12, calcium,
phosporus, selenium
 Other infectious diseases: IB, ILT, Avia
Encephalomyelitis, ND, Marek’s disease, CRD, Coryza,
fowl cholera, parasites, diphtheritic fowl pox
 Metabolic disease: fatty live syndrome, intoxication
Prevention:
 Biosecurity, include disinfecting all
equipment & egg trays; isolation the
infected animals
 Vaccination with inactivated vaccine with
oil adjuvant prior to lay --- prevent clinical
disease, but will not prevent virus
shedding
 The vaccine : during growing period (14-
18 weeks)

Treatment:
 None
 Soluble multivitamin
Public health
• There are no reports of human infections or disease
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