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1-First recorded as a specific disease in 1962 by Albert Cosgrove in
the town of Gumboro, Delaware-USA and so known as Gumboro
2-IBD was recorded for the first time in Egypt in 1974 by El-sergany
et al. depending on the clinical and pathological investigation of the
3-The very virulent strains of IBDV were first recorded in Egypt in
1989 by Khafagy et al. depending on the isolation and identification
of the isolated strains.
4-The variant strains of IBDV are first recorded in Egypt in 2003 by
El.Khayat depending on the direct isolation, serological
identification and the application of Antigen-Capture ELISA
“Monoclonal antibody” technique.
Definition: IBD is an acute, highly infectious and contagious disease
of only young chickens (mostly 3-6 wk in age) and is characterized:
-Profuse watery yellowish white diarrhea.
-Tremor of the whole body.
-Characteristic spiking curve of mortalities.
-inflammatory enlargement of BF followed by atrophy.
-edematous to hemorrhagic BF.
-Ecchymotic hemorrhage on the lateral aspect of the thigh.
-Peripheral yellow infarction.
It is economically important to the poultry industry worldwide due
to increased susceptibility to other diseases and negative
interference with effective vaccination.
The economic importance of the disease is manifested in two
1-The mortality, up to 20%, in chickens in the age of three
weeks and older.
2-the severe, prolonged immunosupression of chickens
infected at an early age.
3-the financial losses due to reduced production parameters
as a result of sub-clinical infections.
Cause: Birnavirus → belonging to Birnaviridae
-55-60 nm in diameter.
-The genome is “bisegmented dsRNA genome”. IBDV has 2 segments
of RNA “segment A and B”.
-Birnaviruses have 4 structural proteins. VP1 (90,000), VP2 (41,000),
VP3 (35,000) and VP4 (28,000). All of these viral proteins are
immunogenic but VP2 is the only protectogenic one.
-Has a predilection for lymphoid tissue, esp. Bursa of Fabricius “BF”
and replicates in the immature bursal-derived lymphocytes (B-
lymphocytes) causing immunosuppression that may be “either severe,
prolonged if the chicks are infected earlier than 3 wks of age or
moderate and transient if the chicks are infected post three wks of age.
-Non-enveloped = naked → “highly resistant” to the physical &
chemical disinfectants. IBDV is only sensitive to iodine, formalin and
nascent oxygen compounds.
-It persists for a long period "more than 4 months” in poultry house and the
-Has two serotypes (Pathogenic serotype-1 & Non-pathogenic serotype-2).
-Serotype-1 has 3 different subtypes or pathotypes of variable pathogenicity
and global distribution:
-Classic or virulent strains (e.g. strain 52/70) cause up to 50% mortality in
SPF birds but only 1-2% in conventional commercial broiler chicks.
-Very virulent strains, cause up to 100% mortality in SPF birds, 20-25% in
commercial broiler chicks and 50-60% in commercial layers. They do not grow
in cell culture unless propagated in cells such as chicken embryo fibroblasts
for a number of passages to allow adaptation.
-Variant strains causing less than 5% mortality without bursal lesions.
Sometimes, a pathotype of viruses is identified with antigenic relation to both
classic and variant viruses.
Virulent serotype 1 strains induce both mortality & bursal lesions but their
vaccines cause no mortality but possess residual pathogenicity with bursal
lesions varying from mild to moderate or even severe.
Serotype 2 strains cause neither mortality nor bursal lesions in SPF birds.
Chicken are the only susceptible host for IBD . The main age of
susceptibility is 3-6 wks of age with extremely rare clinical
cases of IBD are recorded in an older ages.
Baby chicks' future-layers are more susceptible than the
commercial broiler chicks and the baby chicks' future-breeders.
White baby chicks' future-layers are more susceptible than
brown baby chicks' future-layers.
Source of Infection:
-Infected birds… excrete the virus up to 2-3 wks.
-The darkling beetles or "Lesser meal worm” = Alphatobious diapernus → → carry
IBDV up to 8 wks.
-Litter mites → → carry IBDV up to 8 wks.
-Dogs…if eat infected birds.
Mode of Infection: oral via ingestion of contaminated materials. Infection can take
place via the respiration tract, and the eyes and by experiment via infection in the
blood and via the cloaca.
Mode of Transmission:
-Direct contact between healthy and infected birds.
-Indirect contact between healthy susceptible birds & the fomites of the infected
-Mechanical transmission via the contaminated feed, water and contact persons.
-Mosquitoes are possible mode of transmission.
-There is neither carrier state nor egg-transmission in IBD.
-No air borne infections.
Incubation period: Short I.P “2-3 day”.
-After oral infection of the intestinal lymphoid tissues, virus reach
the liver in 8-12 hrs post-infection.
-From the liver, IBDV enters the blood stream and then infects the
cloacal bursa (initial low-level viremia).
-IBDV multiplies in the bursal and splenic macrophages after 24 hrs.
It does not replicates in the peripheral lymphocytes.
-It reaches the highest concentration in 4-5 days.
-As the BF undergoes infection, the second, massive viremia occurs.
-Antibodies against IBDV are detected as early as 3 days post-
Forms of IBD
There are 2 forms of IBD:
Sub-clinical IBD: It occurs either due to infection of young birds
with a variant IBDV strain at any time of age or infection of young birds
with a classic strain of IBDV in age less than 3 wks.
This occurs due to IBDV breaks through MDA. The degree of
immunosuppression varies depending on the virulence of the virus
strain and age of infection. It is greater the closer the infection occurs to
hatch and because the birds are a young age, it is permanent hence;
infected chickens with IBDV at 1-day old are completely devoid of IgG
and produce only monomeric IgM. It has no clinical signs, no
inflammatory bursal lesions although a rapid silent strong persistent
Clinical IBD: here, infection of young birds with a classic strain of
IBDV in age from 3-6 wks. It has obvious clinical signs and the morbidity
may reach 100% of the flock and mortality can range from 0% to over
50% with very virulent IBDV (vvIBDV) strains. Immunosuppression is
transient in the clinical form.
-Sudden onset of self-vent picking with vent inflammation.
-Depression & severe prostration due to serum calcium depletion.
-Ruffled feathers with soiled vent feathers due to the copious watery
yellowish white diarrhea leading to dehydration.
-Anorexia, in-coordination, wobbly gait and trembling.
The signs, morbidity & mortality are most evident in birds older than
3 wks of age.
Mortality varies from 1-10% in commercial broilers & baby-chicks
future breeders while in commercial layers & balady breeds it may
Mortality occurs in a characteristic spiking curve hence the mortality
gradually increases through the 1st three to four days of the disease
course then suddenly decline.
The disease usually runs its course in 4-7 days, but outbreaks of 2-3
days are also possible.
Some factors which can influence the severity of a field infection:
a) infection pressure.
b) virus characteristics.
c) level of immunity.
d) genetic constitution.
e) other immune-suppressive agents
2.3.a infection pressure: The IBDV is very stable and can survive
for months on a farm even without birds. It's very resistant to
several disinfectants. Consequently, once a farm is infected
only extremely thorough cleaning and disinfection can reduce
virus pressure, elimination of the virus will be extremely
But with sound sanitary measurements and good vaccinations,
the disease can be controlled.
2.3.b virus characteristics: Most of the Gumboro isolates belong to the
same serotype (serotype I) but there is a wide variety within this
serotype. Both the pathogenic type and most of the weak types used for
vaccination belong to this group. The serotype II isolates were first
found in turkeys. This type can also infect chickens.
2.3.c genetic constitution: The genetic constitution of the bird
influences the ability to respond to vaccines and to pathogenic field
exposure. There appears to be a relation between the bursa size and the
susceptibility to IBD. In general susceptibility occurs in the following
order from greatest too lowest: white layers, brown layers and meat
2.3.d other immune-suppressive agents: Various agents, besides IBD
viruses are known to give an immune-suppressive effect. The best
known examples are Chicken Anemia Virus (CAV), Reticulo
Endotheliosis Virus (REV) and Mycotoxines, which can effect the
response to Gumboro challenge or vaccination.
2.3.d level of immunity
There are 2 forms of immunity; active and passive. Passive immunity
consists of the maternal antibodies derived from the mother. Active
immunity is a result of developed antibodies after challenge with field
virus or after challenge with vaccine virus. The level of maternal
immunity depends on the immune status of the parents; the
vaccinations and the disease history influence this. These two together
will greatly influence the optimal moment for vaccination. A vaccination
for Gumboro can only be effective if the vaccine virus can break through
the level of immunity of the chicken. Vaccine virus can be neutralized
by maternal antibodies if they are at a high level, in this situation
vaccination is done too early. When field virus will break through the
maternal immunity it will lead to an immune-suppression. Birds, which
have suffered from IBD, have a definitely lower response to
Days of Course
Spiking Curve Of Mortality
Chicks may be infected when only a few days old “sub-clinical IBD”.
Although no clinical signs nor inflammatory bursal lesions are seen,
permanent damage to the bird’s immune system occurs in birds up to
3 wks of age.
1-This predisposes the birds to other diseases known as “Gumboro-
-Gangrenous dermatitis & Ulcerative enteritis.
2-It also reduces their response to the routine vaccination against
other diseases e.g. ND, IB, coccidiosis and ILT.
IBDV attacks the rapidly proliferating “immature” lymphocytes in
BF leading to severe lymhocytic apoptosis → severe suppression of
humoral immunity whose persistence is dependent on the age of
•less severe & transient suppression of cell mediated immunity.
incidence of other diseases, e.g. Marek’s, UE & GD, Coccidiosis.
antibody response to standard vaccination program e.g. ND, IB.
Chickens infected with IBDV at one day of age are completely
devoid of serum immunoglobulin G (IgG) and produce only
non-specific morbidity and mortality.
Determining Percentage Bursa Weight
It is the weighing of cleaned bursa in correlation to the whole body. If both the
whole bird and the bursa are weighed, the bursa weight can be calculated as a
percent of body weight: % Bursa Weight = (Bursa weight /Body Weight) x 100%.
A 2000 g bird with a 4 g bursa, for example, would have 0.2% bursa weight. The
bursa should be measured with a scale accurate to 0.1 g and the whole bird with
one accurate to 20 g.
Table-Rating % Bursa Weight in Broiler Flocks
-Excellent = 0.30% and Over
-Average = 0.18% to 0.20%
-Questionable = 0.15% to 0.18%
-Poor = Under 0.15%
Diagnosis Sub-clinical IBD
A history of chicks with very low levels of MDA (Fewer than 80% positive
in the immunodifusion test at day old, Elisa vaccination date prediction <
7 days), subsequent diagnosis of 'immunosuppression diseases' (especially
inclusion body hepatitis and gangrenous dermatitis) is highly suggestive.
This may be confirmed by demonstrating severe atrophy of the bursa,
especially if present prior to 20 days of age.
The normal weight of the bursa in broilers is about 0.3% of bodyweight,
weights below 0.1% are highly suggestive.
Other possible causes of early immunosuppression are severe
mycotoxicosis and management problems leading to severe stress.
-Direct Virus Isolation.
-Indirect Serological Identification.
Direct Viral Examination
-Bursa in the acute stage is the best source for virus isolation due to
the high viral concentration.
-The virus is isolated by inoculation of CAM of chicken embryo (9-
11 days old).
-The embryos die in 3-5 days post-inoculation showing mottled
liver, kidneys and congested lung.
-IBDV is also isolated in tissue culture of chick embryo fibroblast,
embryo bursal cells and/or mammalian cell lines by serial
passages. The inoculated virus may produce plaques in the
inoculated tissue culture.
The liver appears pale, bile stained and with wide necrotic foci.
2-Electron Microscopic Examination:
Negative Shadow techniques of IBDV shows the virus particles with
its characteristic viral morphology.
Indirect Serological Identification
1-Immunofluorescence: This is dependent on the examination of
smears of cryostat sections of infected bursal tissues or inoculated
embryo or cell culture stained with convalescent IBD infected birds or
hyper-immunized rabbits serum conjugated with immunofluorescence
reagent shows brilliant fluorescence in the bursal follicles on
examination by fluorescence microscope.
2-Agar gel precipitation test:
*The collected bursal tissues from suspected clinical cases are taken
and homogenized into 50% w/v suspension in PBS. The homogenate
is centrifuged at 3000 rpm for 20 minutes & the supernatant is used
*The suspected antigen is placed into the central well of the AGP
plate while the known sera are placed into the peripheral wells.
*Incubate the plate into a bacteriological incubator at 37 C for 24 hrs
in a humid atmosphere.
*Positive test is obtained by the appearance of a precipitation line
between the central well and the peripheral well containing a specific
3-Enzyme linked immunosorbant assay (ELISA)
Purified virus is coated on microtitre plates or commercial test kits
are used. Usually a single serum dilution is used.
The results of ELISA can be read on ELISA reader.
In positive cases reddish brown color is seen.
It is a good method for testing large number of samples.
4-Specific diagnostic tests:
-Antigen-capture ELISA: specific test depending on the monoclonal
-Virus neutralization test: The test of choice for diagnosis and
measuring IBDV antibodies.
-Polymerase chain reaction “PCR”: specific test depending on the
detection and proliferation of IBDV using the thermocycler.
Immunity of IBD
• MDA is the basic protective immunity during the critical first 2 wks
• Humeral antibody is the basic protective immunity, after the start
of the vaccination program.
• Cell-mediated immunity has a limited role.
Prevention of IBD
Effective biosecurity program: Proper sanitary precautions are
required to break the cycle of infection.
Effective breeder IBD vaccination program: to attain a very
good level of MDA passively transferred from the breeder
hens to their progeny. MDA protects chicks from infection
during the critical first 2 wks of life when IBDV may cause
Effective broiler IBD vaccination program: Vaccination is the
principal means of control according to the proper
Effective biosecurity program
Proper sanitary precautions are required to break the cycle of
Proposal biosecurity program
1-Dry cleaning “proper removal and disposal of poultry litter as
quickly as possible”.
2-Wet cleaning with liquid soap and water “20 liter liquid soap + 500
liter water” for cleaning of 1500 cubic meters.
3-Disinfection “20 liter of formalin + 3 liter of malathion + 500 liter of
water” to disinfect of 1500 cubic meters - - - or - - - “2 kg Virkon S +
3 liter of malathion + 500 liter of water” to disinfect of 1500 cubic
4-Trafic control of workers, visitors and veterinarians.
5-Rodent and dog control.
Key factors in the epidemiology of IBDV:
• The disease is highly contagious, spreading through the movement of poultry
products, equipment, feed bags, vehicles and people, and, to a lesser extent, through
aerosols of dust.
• Clinical signs of the disease are age related, with birds 3–6 weeks most susceptible to
• The antibody status of the exposed birds will influence the clinical expression of the
• The genotype of the birds affects clinical expression, with layer breeds being more
• The virus is highly resistant to heat and chemicals, and can persist in the shed
environment for at least 4 months.
• Normal shed cleaning practices may be inadequate to eliminate the virus.
• Processed and frozen poultry meat may contain infectious virus.
• The virus is not egg transmitted but can survive on the eggshell surface.
• Natural infection is usually via the oral route, but the upper respiratory tract and
conjunctiva (eye) probably also play a role.
• The role of wild birds & rodents is uncertain, but they may act as mechanical carriers.
• Mealworms (Alphitobius diaperinus) have been implicated as reservoirs, and
Aedes vexans mosquitoes as vectors, of IBD virus. Mealworms are extremely difficult to
eliminate from earthen-floored sheds.
• Infected chickens continue to excrete the virus in their faeces for up to 2 weeks after
1.6.4 Factors influencing transmission
The extent to which vvIBD or eavIBD may spread in Australia will largely dependon
• location of the initial outbreak;
• immune status of the flock;
• time before detection;
• efficiency of diagnosis of early cases;
• number of contacts with the infected farm;
• movement of poultry;
• level of biosecurity being practised on farms in the region;
• poultry density of the farm and region; and
• (possible) wild bird and rodent movement from the infected farm.
Effective breeder IBD vaccination program
This is to attain a very good level of MDA passively transferred from
the breeder hens to their progeny. MDA protects chicks from
infection during the critical first 2 wks of life when IBDV may cause
Proposal breeder IBD vaccination program
An example of a comprehensive breeder vaccination program have a
vaccine schedule such as this:
-At 12 days of age -- live intermediate IBD vaccine.
-At 20 days of age -- live intermediate IBD vaccine.
-At 30 days of age -- live intermediate IBD vaccine.
-At 85 days of age -- live intermediate IBD vaccine or inactivated.
-At 120 days of age --IBD inactivated.
-Revaccinate at 38-42 wks of age with an inactivated IBD vaccine if
breeder titers are low or of poor uniformity.
Routinely monitor breeder IBD antibody titers to ensure vaccines are
administered properly and that the chickens respond appropriately.
Effective broiler vaccination program
Vaccination is the principal means of control according to the proper
parameters for designing a vaccination program.
Parameters for Designing IBD Vaccination program
1-Estimation of the quantity of MDA passively transferred from the breeder hens to
their progeny depending on the “ELISA”.
2-Estimation of the uniformity of MDA passively transferred from the breeder hens
to their progeny depending on the estimation of the “Coefficient of Variation =
3-Breed of birds to estimate the “Half life time of MDA”.
4-Epidemiological status of the geographic area to determine the “degree of IBD
5-Aim of vaccination.
6-The used vaccine Strains →
Cloned or non-cloned
Mild, Intermediate or Intermediate plus
Value of Mab of break through of each
1-Quantity of MDA
2-Uniformity of MDA
Coefficient of variation = CV.
CV = SD/N x 100
-30% or less → strongly uniformed →1 vaccination.
-30-50% → moderately uniformed → 2 vaccination.
-50% or more → weakly or non-uniformed → 3-4 vaccination times.
First vaccination timing depends upon various factors including status of
MDA, type of bird, disease pressure and housing conditions.
Vaccination frequency depends upon the degree of MDA uniformity.
Initial vaccination at 1 to 7
days followed by Booster
or Unknown MDA
Effect of Quantity & Uniformity of MDA
High and Uniform
Single vaccination at
10-14 days of age.
1-In commercial broilers → 4 days.
2-In commercial layers & breeders → 5 days.
3-In Balady breeds & house holding birds → 6 days.
3-Breed of birds (Half life time of MDA).
Epidemiological status of the geographic area.-4
Classic = virulent VariantVery virulent
5-Aim of vaccination
Ring = MetaphylaxisRoutine = Prophylaxis
Value of Mab of break through
of each Vaccine type
Proposal routine broiler IBD vaccination program
An example of a comprehensive broiler routine vaccination program
have a vaccine schedule such as this:
-At 8 days of age -- live intermediate IBD vaccine.
-At 13 days of age -- live intermediate IBD vaccine.
-At 19 days of age -- live intermediate IBD vaccine.
Ring “Metaphylaxis” broiler vaccination program
Ring “Metaphylaxis” vaccination program
If there is a production unit of multi-houses is stocked by chickens and
one house is infected by IBD. Ring “Metaphylaxis” vaccination
means the immediate vaccination of the other non-infected houses
as soon as possible using one the cloned vaccines especially strain
D-78 or Bursa vac-3.
6.2.1. Live vaccines
The objective of a live vaccination of broilers is to induce a
protective level of immunity before a field virus can infect the
bird. This is a difficult thing to accomplish because one needs to
find the optimum date for vaccination. The average level and the
variation (spreading) of the maternal immunity influence this.
Another important factor is the strength of the vaccine used.
There are mild, intermediate and hot vaccine strains. Vaccination
is possible at the moment when the ELISA titers are 1:128 for
intermediate vaccines and 1:512 for “hot” vaccines. The half-life
time of maternal antibodies in broilers is 3- 3,5 days and for meat
type breeders 4 days. The half-life time of maternal antibodies in
layers is 4-5,5 days. Blood sampling must be done as soon as
possible, but you must take into account that the half life time
counting starts after 3 days. The first 3 days the yolk is used.
Sometimes a double vaccination is needed when there is a relative
big variation in the titers. Hot strains are used when very virulent
IBDV is present.
6.2.2 Inactivated vaccines
Inactivated vaccines can be given to breeders in order to
increase the level of maternal immunity in the offspring.
Priming with a live vaccine should always precede it. World-
wide there are 2 systems practiced for IBD priming. The
cheapest method is only the priming used as first vaccination
at +/- 21-24 days of age. Some producers use a second priming
(live vaccine) at 6-14 weeks of age in order to try to get a higher
and a more uniform titer at (Grand) Parent stock level. The
killed vaccine can be given as a combination with other
Some producers do not use inactivated IBD vaccines; this will
lead to a higher variation in titers, especially when Parent stock
is challenged with field virus.
Advises for vaccinating chickens against IBD.
-Try to prevent mixing chickens derived from different parent stock flocks,
with different levels of maternal immunity against IBD.
-When given in the drinking water → a good quality cool drinking water
and properly cleaned drinkers (no traces of disinfectants) is essential to
avoid neutralization of the virus. Add 1% skimmed milk powder to the
water to protect the virus (before opening the vaccine vials). Thirsten the
birds for 2 hrs (summer) and 3 hrs (winter), then provide enough drinking
water with vaccine for 1.5–2 hrs. To check the drinking water vaccination
technique one can use water-soluble dyes.
Other vaccination techniques can be used as eye drop vaccination method.
Another vaccination method is in-ovo “inovation” technique. The vaccine
is injected into the hatching eggs, at the transfer time “the 18th days of
incubation”. Maternal antibody levels have no influence on this technique.
Control of IBD
The specific treatment is not available up till now but from our
practical experience we can try the followings:
1-Reduction of crude protein% of feed i.e. formulate a final feed with
relatively high corn% and low soya bean% → to reduce the
metabolic uric acid load on the kidney tissues.
2-Use of a multivitamin + immunostimulant “Immunair”
supplement and facilitating access to water.
3-Use of diuretics “Renyl or Diurel” → 1 gm/liter/8hrs/3 days.
4-Spraying of Verkon-S solution in the atmosphere of the farm → 20
gm/10 liter water daily for 3 days.
5-Antibiotic medication may be indicated if secondary bacterial
infection occurs .