Infectious Bursal Disease

Introduction

Gumboro disease, also known as Infectious bursal disease (IBD), is a highly contagious disease of young chickens caused by the Infectious Bursal Disease Virus (IBDV). The disease is characterized by inflammation followed by atrophy of the Bursa of Fabricius and immunosuppression. Despite the wide use of vaccines and increased biosecurity measures, IBD continues to be a significant concern in the poultry industry.

The disease was first described in Gumboro, Delaware in 1962. After the initial outbreak in the US, clinical IBD was reported in many other countries. Since the 1980s, variant strains and more virulent forms (vvIBD) have emerged. Today, vvIBD is predominant in most countries, and variant strains of IBD are present in several countries, leading to sub-clinical forms of the disease.

 

Worldwide IBD prevalence world map

 

The cost of IBD has been very well documented in different publications in the last decade. It has a direct impact on mortality, from 5% to 30%, depending on the degree of protection of the birds and the form of the disease (Rosenberger et al., 1986; Van den Berg, 1991).

In subclinical cases, it can reduce the income per flock by up to 14%, with an 11% reduction in yield and a 10% reduction in profit due to weight loss and increased FCR (McIlroy, 1992).

Recently, interesting calculations have been performed especially focused on the subclinical variant IBD strains. Researchers have identified a positive correlation between serological IBD titers with increased lesions and condemnations during processing.

Understanding IBD

IBD is caused by a double stranded RNA virus of the genus Avibirnavirus which replicates and damages the bursa of Fabricius. The signs and lesions vary [Infectious Bursal Disease Symptoms], and basically presents 3 different clinical forms: immunosuppressive, clinical, and subclinical.

The variability in clinical signs and lesions could depend on several factors including:

  • Type of IBDV infecting the chickens,
  • Virulence of the virus,
  • Genetic type of the chickens,
  • Passive and active immune status of the chickens,
  • Age at infection,
  • Concomitant infections with other pathogens
  • Environmental and management factors like the season, litter management, feed quality, etc.

The immunosuppressive form is the consequence of the infection in chickens less than 2 weeks old and associated with variant IBD strains. During this time, the B-lymphocytes need to mature to become functional and provide the chickens with effective humoral (antibody) response capabilities. Extensive and persistent depletion of the lymphoid follicles leads to marked bursal atrophy.

The clinical form is associated with the “classic” strains of IBD and observed when birds are infected after 3 weeks of age. The virus replicates very rapidly and at a high level, leading to inflammation and tissue damage in the bursa. Clinical signs include depression and ruffled feathers. Diarrhea and dehydration are also present. Mortality approaching 30% could be observed in cases of vvIBD.

The sub-clinical form of the disease corresponds to infection of chickens after 2-3 weeks of age, but without occurrence of typical clinical signs. Subclinical IBD could lead to:

  1. decreased flock performance
  2. slightly increased mortality rate
  3. losses in feed conversion
  4. decreased weight gain
  5. subpar flock uniformity.

The sub-clinical form is currently the most common form of Gumboro and it has a significant negative economic impact on the poultry industry.

How is IBD Spread?

IBD is highly contagious and capable of surviving in poultry houses even after routine cleaning and disinfection procedures.

The transmission of Infectious Bursal Disease is from bird to birds, primarily via the feco-oral route, but also from water, feed, and fomites in and from an infected premise.

The persistence and survivability of IBDV makes eradication unrealistic and makes IBD an enzootic disease. IBD challenge will occur at some point in time. The use of built-up litter increases virus pressure due to higher loads of virus and increased transmission.

Nevertheless, biosecurity measures, cleaning and disinfection play a role in reducing virus pressure and helping to prevent the emergence of new variant viruses. Successful and relevant immunization is another key intervention.

Control of IBD

Given the enzootic nature of IBD, immunization is the principal method of disease control.

The objectives of an IBD vaccination program are:

  • Protection from infection during rearing until movement to the processing plant or laying house (“viral protection”).
  • Protection from the clinical consequences of infection (“clinical protection”).
  • Reduced virus shedding, hence reducing virus build-up in the house environment cycle after cycle.
  • To slow/stop the evolution of the IBD virus towards a form that could escape the vaccination program.

The last two points are summarized by our phrase “Stop the Gumboro cycle”. To control IBD, the vaccination program should be tailored to the farm and the flock.

Several types of Gumboro Vaccines are available in the market and can be classified into 3 categories:

  • Immune Complex vaccines
  • Vector HVT-IBD vaccines
  • Conventional field vaccines

Other factors that should be observed for optimal short-term and long-term control of Gumboro Disease include biosecurity, cleaning & disinfection, and achieving passive immunity.

Biosecurity, cleaning and disinfection, passive immunity, and an effective vaccination program, such as a live immune complex vaccine will help to displace field strains with a vaccine strain.

Passive Immunity (Maternal Antibodies)

As vaccine doesn’t take effect for the first two weeks, only relevant passive immunity transferred from the hen to the chick can be effective at this stage.

This is why the breeders should also be vaccinated with inactivated IBD vaccines before the laying period, so that maternal antibodies are passed to the progeny. Commercial and/or autogenous inactivated vaccines are used to produce relevant maternal antibodies to help protect against classic and variant IBD.

How Does IBD Impact Bird Performance?

Subclinical IBD may not cause an immediately perceptible negative effect, but it will create the opportunity for the field virus to multiply, naturally produce variants and spread. There are two very important consequences that will impair the future sanitary and/or economic performance:

  • The virus pressure for the next flock(s) will increase.
  • Increased opportunity for a variant virus to colonize the house/farm. The IBDV multiplying could surmount passive immunity from the breeder vaccination program and active immunity from progeny vaccination

In terms of performance and economic impact, it is well established that IBD can lead to morbidity, mortality, secondary infections, decreased weight gain, increased feed conversion, and increased condemnations.

Following is an example of an economic analysis of the cost of infection:

  • In a situation where 10% of the flocks has the subclinical infection, there will be a 10% decrease in feed conversion
  • Increase of general feed conversion, from 1,60 to 1,61, or to 1,63, or to 1,65.
  • Increase of 0,5% of mortality (example from 4% to 4,5%)

IBD Infection

Following are several publications showing the impact on the performance:

Since most IBD is subclinical, it is important to monitor all the links in the production chain, including the processing plant. The following publications demonstrate the cost of the subclinical IBD at the processing plant:

Conclusion

In conclusion, IBD can be immunosuppressive, clinical, or subclinical, but in all cases, it will impact bird performance, and the profits of the poultry producer.

As an enzootic disease, it needs to be controlled through immunization. A successful vaccination program against IBD should ensure the protection against clinical signs, decrease virus shedding and significantly reduce the risk of emergence of variant virus.