67. Infectious bursal disease (Gumboro-disease). Flashcards
Virus info?
Birnaviridae
- dsDNA, two genome segments
- 4 structural proteins, 60nm, icosahedral capsid, no envelope
- 4 genera
- Avibirnavirus genus: infectious bursal disease virus
- Aquabirnavirus genus: infectious pancreatic necrotic virus (+ 2 species)
- Blosnavirus genus: fish
- Entomobirnavirus: Drosophila X virus
History, Occurrence( Ethiology) ?
Etiology
- A highly contagious disease of young chickens characterised by immunosuppression and morality generally at 3-6 weeks of age
- History, occurrence
- Gumboro, Delaware (USA), 1962: first description (Cosgrove)
- Name by Hitchner in 1970
- Immunosuppressive effect by Allan, 1972
- Present worldwide
- 1960-1980s classical strains: USA, Europe, SU, Japan, India
- End of 1980s
‣ Emergence of very virulent strains (Europe, Asia, Africa, South America)
‣ Emergence of USA variant strains (Europe, South America, recently South Africa and Western Europe)
- Present practically in every large chicken farm
Causative agent?
Causative agent:
Causative agent: infectious burial disease virus (IBDV)
- 2 serotypes
‣ Serotype 1: pathogen
‣ Serotype 2: non-pathogen, isolated from turkey but infects chickens too
‣ Serological cross-reactions but no cross-protection
- High resistance
‣ 56℃, 30 minutes: pH 3-9, in litter for 1-4 months
‣ Disinfection: halogens (chlorine), aldehyde, 0.05% NaOH + detergents at 40℃
- Propagation: embryonate egg CAM, cell cultures
- Hosts: mainly chicken, but also pheasants (IBD), turkey (immunosuppression), ostrich (immunosuppression)
- Virulence variants
‣ Classical virulence strains (cvIBDV)
‣ Very virulent strains (vvIBDV)
‣ Attenuated vaccine strains: hot, intermediate plus, intermediate, mild
- Antigenic variants of serotype 1
‣ Viral protein 2 (VP2): VN antigen, at least 6 subtypes
‣ Viral protein 3 (VP3): sero-specific and group-specific, cross-reacting antigens
Epizootiology?
Epizootiology
- Highly contagious
- Virus shedding within one day after infection, for 2 weeks, via faeces
- Contaminated environment is the main source of infection ➝ feed, drinking water
- Mechanical transmission between farms and stables ➝ vehicles, people, insects, rodents
- Germinative route is not significant, but faeces-contaminated egg shell
- Infection routes
- Per os (most frequent)
- Conjunctival, air-borne
Pathogenesis?
Pathogenesis
• Infection PO ➝ multiplication in the gut-associated macrophages and lymphatic tissue
- Primary viraemia in liver, bursa of Fabricius
- Main target cells: premature B lymphocytes and other bursal cells
- The virus also destroys B lymphocytes in the gut (GALT) conjunctiva (CALT) and bronchi (BALT), caecal tonsils, Harderian gland
- The highest activity of the bursa of Fabricius in-between the age of 2 and 8 weeks ➝ the effect of the infection is influenced by age
‣ 0-3 weeks of age: 0-30% mortality, permanent immunosuppression
‣ 2-8 weeks of age: 5-100% mortality, but immunocompetence after recovery
‣ Over 8 weeks of age: no clinical signs
- Young age infection: damage of the B-cell receptor expression ➝ weak immune responses against mild antigens ➝ inefficient
vaccinations
- Immunocomplex deposition, and necrotising agents cause the signs of acute disease
Pathogenesis: Factors influencing the severity of the disease?
• Factors influencing the severity of the disease
- Age of the chicken (up to 2 weeks, 2-8 weeks, over 8 weeks)
- Immunity ➝ level of maternal antibodies
- Breed of chicken ➝ layers are more sensitive than meat hybrids
- Virulence of virus strain
‣ cvIBDV: 5-6% (15-20%) mortality
‣ vvIBDV: 30-50 (90-100%) mortality
- Antigenicity of virus
‣ Wild type virus ➝ vaccine virus ➝ specificity of yolk immunity
- Immunosuppression ➝ concomitant infections
‣ Reoviruses, CAV, E. coli, Ornithobacterium rhinotracheale
‣ Mycotoxins
Clinical signs?
Clinical signs
- In 3-6 week old chickens, 2-3 days incubation time
- Fever, trembling, depression, debilitation, dehydration ➝ exsiccosis
- Watery diarrhoea, swollen, blood-stained vent, crate crystals on the feathers around the vent
- Recumbence, ruffling of the feathers
- Anaemia ➝ pale combs ➝ cyanosis later
- Subclinical: immunosuppression
- Retarded growth
- Weaker feed utilisation
- Ineffective vaccinations
- Changed appearance of other infectious diseases
Pathology, Histopathology?
Pathology, histopathology
Pathology, Histopathology
• Acute phase
- Bursa of Fabricius: oedema, inflammation, haemorrhage, caseous exudate
- Haemorrhages
‣ Connective tissue under skin
‣ Muscles
‣ Proventriculus and gizzard mucosa
- Nephritis: pale, yellow, mottled kidneys
- Enlarged spleen, sometimes haemorrhages
- Liver oedema, dystrophy, necrotic foci
- Bursa lymphatic depletion, reticular cell karyorhexis, follicular necrosis, inter follicular tissue proliferation, mononuclear cell
infiltration
- Necrotic processes in the bone marrow
- Lymphoid depletion in the thymus cortex and medulla too
• Chronic phase
- Bursa atrophy, early involution
- Complications, signs of co-infections
Diagnosis?
Diagnosis
- Age, clinical signs, pathology ➝ lesions in the bursa of Fabricius
- Histopathology ➝ early infections, lymphatic depletion and necrosis
- Virus isolation ➝ embryonate egg CAM, cell cultures
- RT-PCR, IF, IHC
- Determination of the virulence
- Experimental infection
- RT-PCR + RFLP (less accurate), RT-PCR + sequencing
- Monoclonal antibodies
- Differentiation between wild type and vaccine strains: RT-PCR + sequencing
- Serology
- VN ➝ very specific, less sensitive
- ELISA ➝ very sensitive, less specific
Differential diagnosis?
Differential diagnosis
- Newcastle disease ➝ any age, respiratory and CNS signs
- Bacterial septicaemia ➝ any age, cultivation of bacteria
- Reticuloendotheliosis ➝ usually older, tumors
- Chicken anaemia ➝ no inflammation in the bursa (only atrophy)
- Malabsorption syndrome ➝ no bursa inflammation
Treatment, Prevention Control?
Treatment, prevention, control
- Treatment ➝ hyperimmune yolk sac SC, increased Vitamin E
- Hygiene measures ➝ prevention of infection in the first 2 months
- Disinfection of egg shell
- Decontamination of fomites
- Cleaning and disinfection of stables
- All in all out technology
Immunisation?
Immunisation
• Immunisation
- Attenuated live vaccines
‣ Mild - no bursa damage but no effect even in low maternal Antibody level
‣ Intermediate - mild bursa damage, efficient in lower maternal Antibody level
‣ Hot - pathogen for seronegative chicken, efficient in higher maternal Antibody level
- Immunocomplex vaccines
‣ Live vaccine strain + specific antibodies (Virus Protecting Factor)
‣ Regulates virus multiplication + protects from maternal antibodies
‣ Captured by the spleen follicular dendritic cells
- Recombinant, vector-vaccines
‣ VP2 gene cloned into turkey herpes vector
‣ Efficient in high maternal antibody level too, continuous stimuli, harmless
- Inactivates vaccines
‣ Usually for booster vaccination
‣ High, homogenous, long-lasting immunity
‣ Complete virus
‣ Subunit vaccines ➝ recombinant VP2 (produced in yeast or in plants)
- Timing of immunisation
‣ Inhibitory effect of maternal antibodies ➝ sensitive period
‣ Homogenous maternal antibody level is necessary for the efficient vaccination
‣ The vvIBDV easier breaks through the maternal antibody protection
‣ Determination according to the maternal antibody level in the flock
‣ Usually starting at Day 16-18 but vaccination of day-old chicken with inactivated vaccine is possible too
‣ In ovo vaccination also applicable
Application of the vaccine?
• Application of the vaccine
- Live virus ➝ drinking water, aerosol, conjunctival SC
- Immunisation of layers in drinking water may result in non-homogenous maternal antibody levels in the chicken
- Identification of the virulence of the present wild-type virus is necessary
- Identification of the antigenic subtype of the present wild-type virus is necessary
- Usually repeated immunisations
- Combined vaccines are also available (NDV, IBV, EDSV)
- Vaccination programs for different viruses may interfere in young age
