3. Introduction
• Infectious bursal disease also known as IBD, Gumboro Disease,
Infectious Bursitis and Infectious Avian Nephrosis
• a highly contagious disease of young chickens caused by IBDV .
characterized by immunosuppression and mortality generally at 3 to 6
weeks of age.
• The virus attacks the birds lymphoid organs especially the bursa were it
affects the B-cells causing immunosuppression. Let’s just say the bird’s
immune system is affected and it becomes susceptible to all sorts of
infections.
• Affected chickens have reduced antibody response to vaccinations,
strong post vaccinal reactions, and increased susceptibility to
concurrent or secondary infections.
4. Introduction(cont,(
• Clinical disease is associated to bird age with the greatest bursal mass,
which occurs between 3 and 6 weeks of age. The greatest bursal mass is
mostly a result of a large population of maturing IgM-bearing Blymphocytes
(lymphoblasts), the main target of infection. Young birds at
around two to eight weeks of age that have highly active bursa of Fabricius
are more susceptible to disease. Birds over eight weeks are resistant to
challenge and will not show clinical signs unless infected by highly virulent
strains.
• The bursa of Fabricius, which is the organ responsible for disease
protection in young birds, is the main target for the virus. Normally, the
bursa of Fabricius regresses by early maturity. Hence, infectious bursal
disease is most important in birds up to 4 week of age, and most critical
between 2 and 4 weeks of age.
• Subclinical disease occurs in chickens infected before three weeks of age.
At this age the B-lymphoblast population is smaller and the systemic
effects are insufficient for generating clinical signs.
5. History
• IBD was first described as a specific new disease by Cosgrove in 1962 in
the town of Gumboro, Delaware, USA.
Variant IBDV strains were first reported in the USA in 1986/87.
Hyper or very virulent IBDV strains were first reported in Belgium and
The Netherlands in 1987.
• Currently IBDV has a worldwide distribution, occurring in all major
poultry producing areas.
• The classical and hyper virulent forms of IBD are predominant in all
countries with the exception of North America and Australia.
• In the USA the variant strains of IBDV predominate
6. Pathogenesis
• During embryonic development, and through approximately 10 weeks of
age, immune system cells (lymphocytes) travel to the BF to become
programmed to become antibody-producing cells. If the IBD virus
damages the BF in young chickens, the BF will not be capable of
programming sufficient numbers of lymphocytes. Thus, the chickens will
experience reduced immune system capabilities (immunosuppression).
• After ingestion, the virus destroys the lymphoid follicles in the bursa of
Fabricius as well as the circulating B-cells in the secondary lymphoid
tissues such as GALT (gut-associated lymphoid tissue), CALT (conjuntiva),
BALT (Bronchial) caecal tonsils, Harderian gland, etc. Acute disease and
death is due to the necrotizing effect of these viruses on the host tissues.
Kidney failure is a common cause of mortality. If the bird survives and
recovers from this phase of the disease, it remains immunocompromised
which means it is more susceptible to other diseases.
7. The economic impact
• Morbidity rate very high reaches to 100 %
• Mortality rate in borilers 20 – 30 % and in layers and Baladi 50-70%
• Immunosuppresion which leads to the birds are susceptible to 2ry
infections such as NDV , IB , HVT ,Inclusion Body Hepatitis and
gangrenous dermatitis and increased susceptibility to CRD.
8. The virus
• IBDV is a double stranded RNA virus .
• belongs to the genus Avibirnavirus of family Birnaviridae .
• There are two distinct serotypes of the virus, but only
serotype 1 viruses
cause disease in poultry.
9. Virus structure
• Five viral proteins desighnated : VP1 , VP2 , VP3 , VP4 , VP5 have been
recognized.
• VP1 plays a key role in the encapsidation of the virus particle.
• VP2 encodes the major antigenic determinants of the virus, including
epitopes that are important in virus neutralization.
• VP3 is a group specific antigen that is recognized by non-neutralizing
antibodies. VP3 acts as an intermediary, interacting with both VP1 and
VP2, and the formation of VP1-VP3 complexes is likely to be an
important step in the morphogenesis of IBDV particles.
• VP4 is a minor and non-structural polypeptide.
• VP5 likely has a regulatory function
10.
11. Virus Classification:
• IBDV strains are classified into two distinct serotypes,
differentiated by a virus neutralization test. There is no
crossprotection between these serotypes.
Standard/Classic
Antigenic
Variants
Pathogenicity
• Mild
•
•
Classical
Very virulent
• Vv.Virulent
Immunosuppressant
Serotype 2 a pathogenic infects ducks and turkeys
but does not cause clinical disease or immunosuppression.
Serotype 1
13. Cont,
1.Mild field and vaccine IBDV strains:
cause no mortality or clinical symptoms, but bursal
damage dependant on virulence of the virus may still be
evident.
2.Classical IBDV strains:
cause mortality (<20%) and bursal lesions. Able to break
through a moderate level of maternal derived antibody.
3.Hyper or very virulent IBDV strains:
cause severe mortality (>20%) and bursal lesions. Able to
break through higher levels of antibody than classical strains.
14. • Via Ingestion ( horizontally through contaminated food and water )
• Mechanical transmission via people , animals ,vehicles and equipments
when transferred from diseased flock to healthy one .
• May be via the conjunctiva or respiratory tract, with an incubation
period of 2-3 days.
• It has been demonstrated that the lesser mealworm (Alphitobius
diaperinus) could act as a vector carrying IBDV from one cycle to the
next.
• There is no vertical transmission. (no transmission from parent to day
old chick through the egg)
• The virus remains after previous history of disease for 122 days .
• The infected birds shed virus for 14 days n their feces. Feed, water, and
poultry house litter become contaminated.
15. Stability
• Due to the hardy nature of the virus it persists in the environment of
the poultry house, infections are thus potentially carried over from one
cycle to the next.
• he virus is resistant to many disinfectants such as :
• QACs 1000ppm , also resistant to 0.5 % formalin for 5 hours .
• PH 2
• 60 C for 30 minutes and 56 C for 1 hour in prescense of 0.5 % phenol
16. The virus could be controlled by
• Effective disinfectants
• 0.5 % chloramine
• 0.5 % NaOH
• Iodine 50 ppm
• PH 12
• 80c FOR 10 minutes .
17. Clinical sings :
• Infectious bursal disease follows one of two courses,
depending on the
age at which chickens , breed and virulence of field virus
• 1-clinical form
• 2-subclinical form
18. Clinical form
• The clinical form of IBD usually occurs in chickens from 3 to 6 weeks
of
age .
• appears in : sudden onset of mortality rate and poor performance
1-a rapid drop in feed and water consumption
2- mucoid (slimy) diarrhea with soiling of the vent feathers
3- depression,ruffled feathers and closed eyes
4- Many birds may be reluctant to move with a tendency to sit
5-picking at own vent and sleeping with beak touching the floor
6-poor FCR so variability in body weight .
7-Affected chickens experience a transient immunosuppression.
19. Factors affecting mortality rate
• Age of birds
• presence or absence of passive immunity.
• Mangment ( cleanout and Disinfection )
• Breed
• Virulence of field virus
• concentration of IBD
• Exposure time
20. Subclincal form
• The subclinical form of the disease occurs in chickens less than 3 weeks
of age. Chickens present no clinical signs of disease, but experience
permanent and severe immunosuppression
• Early subclinical infections are the most important form of the disease
because of economic losses. The disease can cause severe, long-lasting
suppression of the immune system. Chickens immunosuppressed by
early IBDV infections do not respond well to vaccination and are
predisposed to infections with normally nonpathogenic viruses and
bacteria.
• Very virulent (vv) strains of the virus that cause high
mortality and morbidity were detected first in Europe.
21. Lesion
• Oedematous bursa (may be slightly enlarged, normal size or reduced in
size depending on the stage), may have haemorrhages, rapidly
proceeds to atrophy. Five days after infection, the BF diminishes in size
rapidly .
• Haemorrhages in skeletal muscle (especially on thighs) and junction of
the proventriculus and gizzard.
• . because the IBD virus interferes with the normal blood clotting
mechanism.
• Swollen kidneys with urates. Such lesions probably result form severe
dehydration, not direct viral damage.
• Dehydration.
• Chickens that have recovered from IBDV infections have small,
atrophied, cloacal bursas due to the destruction and lack of
regeneration of the bursal follicles.
22.
23. Gumboro disease: Summary of expected changes in bursal size, weight
and morphology
Days post infection
2-3
Size
Bursa increases in size
and weight
Morphology
Oedematous with
gelatinous yellow
transudate covering
serosal surface.
Color changes from
normal white to a
cream color.
Petechial to extensive
haemorrhaging may
be present.
4
Bursa double the normal
weight and size
Transudate and edema
disappear. Bursa turns
a grey color.
5
8
Bursa returns to normal
weight
Bursa 1/3 of original
weight
24. • Variant IBDV strains do not cause as severe an inflammatory
response. However severe bursal atrophy
is characteristic and mortality is usually less than 5%.
• Very virulent IBDV strains cause severe lesions in other
lymphoid organs such as the thymus, caecal tonsils and
spleen in addition to bursal lesions. with high mortality.
25. • Bursas from Left to Right:
1) Acute stage. Enlarged edematous bursa
2) 5 days post infection bursa returns to normal
size. May be hemorrhagic as in this specific
bursa
3) 8 days post infection bursa atrophied and up to
1/3 of normal size
26. Bursa from inside with petechial
hemorrhages.
Hemorrhages at the juncture of
proventriculus& gizzard.
petechial hemorrhages present in pectoral
muscles
27. Microscopic Lesions
• Microscopically, lymphocyte necrosis is present in the BF within 36
hours after infection. By 48 hours, few lymphocytes are present.
Edema, hyperemia, and inflammatory cell infiltration are evident.
• By 8 to 12 days after infections, the BF is shrunken to less than
onefourth of its original size. The lymphoid follicles are cystic and
depleted of lymphocytes. The epithelium lining the BF is irregular
and
infolded. Fibroplasia is present in the interfollicular connective
tissue.
28. • in severe cases of IBD, all the follicles are affected simultaneously. In less
severe cases, only scattered follicles are affected, and the lesions spread
to other follicles. Typically, the follicles in the tips of bursal folds are
affected first.
Histopathology slide of healthy bursa Histopathology section of atrophied bursa
29. Diagnosis
• 1-flock history
2-symptoms (Subclinical disease - A history of chicks with very low levels of maternal antibody
(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. )
3-postmortem examination
4-histopathology
5- virus isolation and identification
6- Serology and fluorescent antibody techniques
7- RT-PCR (as mentioned above) was designed for the detection of IBDV
genome
8- Serological tests such as agar gel precipitation and ELISA, for detecting
antibodies
30. D.D
• Differentiate clinical disease from: Infectious
bronchitis (renal); Cryptosporidiosis of the bursa
(rare); Coccidiosis; Haemorrhagic syndrome.
31. IBDV COCCIDIOSIS
1- sudden onset
2-droopy appearance
3-ruffled feather
1-Coccidiosis
4-blood in dropping
Avian Nephritis virus
1- Birds show kidney lesions &nephrosis
2-Cloacal bursal lesion
&atrophy of bursa
2-NO clinical signs until 28
day of infection
4-muscular hemorrhagic
5-enlarged edematous or
hemorrhagic cloacal bursa
2-disease cause nephrosis:
IBDV
32. Treatment
• There is no treatment for Gumboro virus , but support therapies,
such
as vitamin and electrolyte supplements and antibiotics to treat any
secondary bacterial infections, may reduce the impact of the
disease.
• If secondary diseases become a problem, antibiotic therapy may be
required, but this should be kept to a minimum.
• Drug therapy is often inadvisable in the presence of severe kidney
damage.
33. Prevention and control
• Can be achieved by good mangment and suitable
vaccination programme
• An effective IBD prevention and control program
must involve an effective breeder vaccination
program, an effective biosecurity program, and an
effective broiler vaccination program
34. Management
• Good ventilation, warm temperatures and fresh water will help to
reduce mortality.
• All infected litter and carcases of infected birds must be suitably
disposed of away from the site or any other poultry operation.
• A thorough well planned disinfection regimen
• -shift for cleanout
• -followed by GPC 8 as an efficient disinfectant .
• Downtime between successive flocks must be maximised. (A minimum
of 10 days is recommended between successive broiler flocks.)
• Control of the traffic ( people,vehicles and equipments )
35. Vaccinations
• Vaccines need to be selected based on the types of viruses present in
the area.
• The timing of broiler vaccination depends on the level of maternal
antibody present in the chicks. High levels of maternal antibody at the
time of vaccination will neutralize the vaccine virus. Thus, only a
limited active immune response results and chickens will be
susceptible to disease as maternal titers decrease. If low levels of
maternal IBD titers are present in the chicks, vaccination may not be
effective on farms contaminated with virulent field virus. Basically, this
means that vaccinating the chicks too early and too late will produce a
negative effect and will not protect the birds.
36. Vaccines
• Three categories of vaccines, based on their pathogenicity, have
been
described:
1) mild
2) intermediate
3) intermediate plus (hot strain )
• The intermediate type IBD vaccines are most commonly used.
These
vaccines can stimulate the broiler to produce antibodies earlier
than
the mild-type vaccines, without significant damage to the BF as may
occur with the virulent type vaccines.
37. Vaccines cont,
• Breeder flocks should be vaccinated one or more times during the
growing period, first with a live vaccine and again just before egg
production with an oil-adjuvanted, inactivated vaccine. Inactivated
vaccines of chicken embryo. The immune status of breeder flocks
should be monitored periodically with a quantitative serologic test
such as virus neutralization or ELISA. If antibody levels fall, hens
should be revaccinated to maintain adequate immunity in the
progeny.
