Disease caused by DS RNA

Virus - BIRNAVIRIDAE
• Birnavirus (L. birna = two)
genomes consisting two segments
of dsRNA
• Non-enveloped
• Only one imp. disease, IBD
 Infectious Bursal Disease

• Also k/a "infectious bursitis", Gumboro

disease is an acute, highly contagious infection
of young chickens (3 to 6 weeks of age at risk)
Since first outbreak occurred in area of
Gumbora district of Delaware state in U.S.A.
called Gumboro disease
In 1962 first recognized by Cosgrove in USA and
referred to as “avian nephrosis”
1970, Hitchner proposed term IBD
1972, Allan and his associates – IBDV-
Immunosuppressive at early age
In India first outbreaks in 1977-78
• Cause:
• two main serotypes (serotype 1 and 2)
• serotype 1 IBDV worldwide in distribution
• Within serotype 1 group, antigenic variants
exist variation in virulence, from
apathogenic to highly virulent strains
• Serotype 2 IBDV also widespread
• No serotype 2 isolates have been
demonstrated to be either pathogenic or
immunosuppressive
• Serotype 1 and 2 viruses infect turkeys &
ducks but cause no disease in these species
• Spread:
• Infection is mainly by oral, and also conjunctival
and respiratory routes
• Affected birds excrete virus in faeces for 10-14
days.
• Infected houses remain infected for 122 days
• Water, feed & dropping from infected pen remain
infected for 52 days.
• Litter mites & meal worms are infected upto 8
weeks
• Mechanical vector such as wild birds, humans &
vermin also transmit disease.
• Litter used as manure spread disease in
particular area. No evidence about transmitted
 Pathogenesis
• Infection through Oral rout mainly, Conjuctival
and respiratory rout
• Virus present in macrophages & lymphoid cells in
caeca, duodenum, jejunum, kuffer cells of liver
• Virus enter in blood stream then viremia occurs
after that bursa is affected
• Bursal infection is followed by 2 nd massive
viraemia
• Virus affects lymphoid tissue, causing destruction
of lymphoid cells within the bursa of fabricius,
spleen & caecal tonsils.
• B lympho. & their precursors are main target cells
Field viruses exhibit different degrees of
pathogenicity.

White Leghorn exhibit the most sever reaction

and has the highest mortality. Less in meat
type
Period of greatest susceptibility is between 3
to 6 weeks in broilers & 7-12 weeks in layer
chicks.
Susceptible chicken younger than 3 weeks do
not exhibit clinical sign but have sub clinical
infection that are economical important
because the result can be severe
Immunosuppression of the chicken.
• No clinical disease in chemical
(cyclophosphamide) or surgically
bursectomized birds
• Microscopic lesion in bursa resemble an
Arthus rection characterized by necrosis,
haemorrhage and large number of
polymorphonuclear leukocytes.
• This reaction (Type-III hypersensitivity) is a
localized immunological injury caused by
antigen-antibody-complement complex
 Clinical signs/ symptoms
• Severe / Clinical form: Birds above 3 weeks of
age Temporary Immunosuppression High
Mortality
• Depression, White watery diarrhoea, Soiled
vent, self vent packling, lying down
• Loss of appetite, Ruffled feathers, Unwilling to
move, Closed eyes, fatigue, Death
• Mild / Subclinical form: Birds below 3 weeks
of age- Permanent Immunosuppression, No
mortality due to IBD
• Poor growth, Decrease response to vaccines
• Immunosuppression
 MORTALITY PATTERN
In broiler
Mortality between 3-6 weeks.
2- 5% mortality rarely goes beyond 10%.
Peak on 2 nd and 3 rd day.
No mortality on 5th day.
In layer
Mortality between 7-12 weeks of age.
30- 70 % mortality
Mortality runs from 7 to 14 days.
Two peak. AT 3 rd and 4 th day
AT 7 th and 8 th day.
In unvaccinated flock 90% mortality.
In cage layer high mortality.
 Postmortem Findings
• Carcass dehydrated
• Pasty vent with white faecal material.
• Hemorrhages on thigh & breast muscles.
• Diffuse haemorrhages on proventriculus-
gizzard junction.
• Kidneys are swollen with white appearance
due to dilation of tubules filled with urates.
• Liver may be swollen & show areas of
necrosis.
• Bursa is the primary organ to be affected
• Birds which die immediately shows peribursal
edema and severe enlargement. Cloaca is dilated
and is filled with white urine material. Bursal
mucosa is severely necrosed and haemorrhagic
• Birds which die after 3-4 days illness shows
reduction in the size of bursa. Bursal wall
becomes thinner and the lumen is filled with
turbid purulent material. The mucosal surface is
necrotic. Often Caseous mass is found in the
lumen
• In recovered bird the bursa becomes totally
atrophied.
• Spleen is slightly enlarged with small grey foci on
its surface.
Chicken with IBD exhibiting depression
and severe prostration.
Normal bursa and atrophied bursa post IBDV
infection
Bursa of Fabricius - enlarged and haemorrhagic
 Bursas from Left to Right:
1. Acute stage. Enlarged oedematous bursa
2. 5 days post infection bursa returns to
normal size. May be haemorrhagic as in this
specific bursa
3. 8 days post infection bursa atrophied up to
1/8 of normal size
Bursa of Fabricius - Edema &
Enlargement
Swollen Haemorrhagic Bursa of
Fabricius
 .

An enlarged haemorrhagic Bursa of

Fabricius.
.
Infectious bursal disease,
chicken
Bursa of Fabricius - (section)
haemorrhages
Muscular Haemorrhages- Breast
Muscular Haemorrhages - Leg
Leg & Breast Haemorrhages
 .

Haemorrhages in the thigh

muscles
Haemorrhages in the pectoral muscles
Haemorrhagic in the proventriculus-gizzard
junction
 Infectious Bursal Disease (3)

Necrosis at the upper-left edge of the liver

right lobe.
Haemorrhagic bursa
Necrosed bursal
surface
Lymphoid necrosis in the bursa of a chicken
infected with Infectious Bursal Disease
(Gumboro's disease) (40X, HE, 107K)
Bursa of Fabricius - There is acute necrosis of
the lymphoid follicles with an intact surface
epithelium and heterophil exudate in the
lumen (10X)
 Diagnosis
1) History
2) Symptoms
3) Postmortem findings
4) Differential diagnosis from
Coccidiosis, Ranikhet, Vitamin A
deficiency, fatty liver , Kidney
syndrome & hemorrhagic syndrome
of muscles.
5) Confirmatory diagnosis- a) ELISA
b) Isolation &
identification of the causal agent.
 Treatment
1) No specific treatment.
2) Supportive treatment is given to reduce
dehydration & improve immunity like
electrolytes, Vitamin E, & selenium.
 Control
1) Thorough cleaning & disinfection of the
houses between the flocks & the
practice “all in, all out” management. It
delays infection & also provide time for
vaccines to produce immunity.
2) Hygienic & sanitary precautions.
3) Formaldehyde & Iodophores are found
to be effective disinfectants.
4) Removal of vectors like mealworms &
rats.
5) Proper vaccination of birds & flocks.
 Vaccines
Two types of IBD vaccines-
1) IBD live vaccine
2) IBD killed vaccine

1) IBD live vaccine- there are 4 types

i) Mild vaccine
ii) Standard intermediate vaccine
iii) Intermediate plus vaccine
iv) Hot vaccine
Strains of different types-
1)Mild – Leukert’s strain
2)Intermediate – Georgea strain,
Gaivellelae strain, Bursin- S-2, 79-B
3)Intermediate plus – MB strain, B-2K,
4)Hot strain- 228-E
 Vaccination Schedule
1) Commercial broilers- 13 day Intermediate plus in
drinking water.
2) Commercial layers- 14 & 28 day Standard
intermediate plus in drinking water & on 21 day
Intermediate plus in drinking water.
3) For breeder hen- Traditionally at prelay stage & midlay
stage IBD inactivated vaccine is given to get high
antibody titer.
 Resistance
• Birds with maternal antibody are
resistant due to high antibody titer.
• When antibody titer drops birds
become susceptible.
• Very virulent strain can break the
antibody barrier at young age.
• Older birds in which bursa is reduced
in size & disappears are more resistant.
 Immunity
1) Active immunity
a) Natural infection
b) Vaccination with either live or killed vaccines.
2) Passive immunity
a) Antibody transmitted through yolk of the egg.
b) Passive immunity protects chicks against
early infection.
c) Half life of maternal antibody is between 3 &
5 days thus, if the antibody titer of the progeny
is known, the time when chicks will become
susceptible can be said.