Infectious Bursal Disease

Infectious Bursal Disease Virus (IBDV)
Order	RNA Viruses
Family	Birnaviridae
Genus	Avibirnavirus

Also Known As – Gumboro disease – Infectious Avian Nephrosis – Infectious Bursitis

Caused By - Infectious Bursal Disease Virus – IBDV

Introduction

Bursa of Fabricius in Acute disease, 5 days after infection and 8 days post infection (left to right). Source - Intervet at [http://www.gumboro.com/

Infectious bursal disease is a highly contagious viral disease of birds caused by an avibirnavirus.

The virus can survive in a wide range of environmental conditions, remains viable from pH 2-12 and is activated only in 70⁰C for 30minutes. It is also resistant to some disinfectants.

IBDV can survive in poultry houses for 122 days after removal of infected birds and in contaminated water or feed for 52 days.

Of the two known serotypes of IBDV, only Serotype I is pathogenic, causing bursal disease in chicks by selectively infecting the cells of the Bursa of Fabricius.

This disease is notifiable to the World Organisation for Animal Health [www.oie.int/ (OIE)]

Signalment

IBDV can infect chickens, ducks, geese and guineafowl but only chickens show clinical signs of disease.

Lethal infection is usually seen in chicks 3-6 weeks old due to IBDV being to restricted to cells at a certain stage of development.

Distribution

Worldwide

The main route of transmission is faecal-oral and the virus is shed for up to 2 weeks post-infection in large amounts.

The role of wild birds as a mechanical vector is poorly understood.

IBDV can also be spread by the nematode parasite, Alphitobius diaperinus.

IBD is not thought to be zoonotic.

Clinical Signs

One of the main effects of IBDV infection is mortality. This can be in chicks at 3-6 weeks old or later on as a result of severe immunosuppression allowing other disease to proliferate, in particular, E. coli and gangrenous dermatitis.

Viral virulence varies massively and thus so can disease severity. Initial outbreaks are usually the most severe and recurrent disease milder with lower mortality.

Diarrhoea, recumbency, dehydration, neurological signs and ruffling of the feathers form a typical presentation of IBDV.

Diagnosis

Acute disease is usually recognised in a flock by rapid onset, high morbidity ( diarrhoea) with a spike in mortality and rapid recovery. Diagnosis is confirmed by post-mortem or laboratory testing.

On post-mortem examination, carcasses are dehydrated, often with darkened pectoral muscles. Many petechiae may be present in the thigh and pectoral muscle masses. Mucus may also be present within the intestines. In advanced disease, renal changes may be evident due to prolonged dehydration. Grey foci may also be present on an enlarged spleen.

The bursa of fabricius will usually initially be enlarged, oedematous and haemorrhagic. Its colour turns from white to cream and a yellow transudate covers its serosa early in infection.

From 7-8 days following infection, the bursa atrophies and becomes approximately 1/3 of its original weight.

IBDV antigen can be detected in cloacal bursa or splenic samples by Agar Gel Precipitation or Immunofluorescence.

Antibody ELISA can be used for serological diagnosis within a flock. A mimimum of 30 samples is required.

Treatment

No treatment is available and recovery is usually rapid in an infected flock.

Control

Hygienic measures with appropriate disinfectants are imperative.

Vaccination is also usually required. Both live and inactivated forms are available. Timing is difficult due to interference of maternal immunity, but oil adjuvanted vaccines can extend maternal immunity to 5 weeks. Vaccination can cause immunosuppression and a degree of bursal damage.

References

Animal Health & Production Compendium, Infectious Bursal Disease datasheet, accessed 05/06/2011 @ http://www.cabi.org/ahpc/

Animal Health & Production Compendium, Infectious Bursal Disease Virus datasheet, accessed 05/06/2011 @ http://www.cabi.org/ahpc/