Frequently asked questions

Frequently asked questions

01. What is Gumboro disease PROTECTION?

A chicken is protected against IBD when it is made more resistant to the infection and to the disease.

  • The consequences are to avoid the negative impact of the disease on production performance, on clinical signs, and on mortality due to Gumboro disease virus.

Ultimately, a perfect protection would block the infection of the bursa by the field virus.

02. Is there any difference among existing vaccines in protecting against infection?

Yes.

All live IBD vaccines (except some mild strains) are likely to protect against the disease but not all can protect against field infection.

  • Has been demonstrated experimentally that Int. plus vaccines are the fastest to block the infection, which does occur much more slowly by using either intermediate, or vector vaccines.

Field vaccination never covers the whole population of a flock; only hatchery vaccination using an Immune-Complex IBD vaccine (Transmune) is the way to satisfactorily solve this issue.

03. What is IBD PREVENTION?

It’s the reduction of the likelihood of contact between susceptible chickens and field virus > to reduce the risk of challenge. It means:

  • To decrease the amount of field virus (“to reduce virus pressure”)
  • To prevent the likelihood of emergence of new IBDV strains.

This can be done by two ways:

  • Implementation of sound biosecurity procedures and proper management system
  • Use of an immune-complex IBD vaccine (Transmune): the vaccine strain is shed and replaces the field virus.

04. What does IBD CONTROL concept means?

Control means achieving both protection and prevention of IBD.

05. Can IBD be controlled by vaccination?

Yes, if the vaccine is able to:

  • Protect against infection of the bursa.
  • Stop replication and selection of new strains in the flock.
  • Stop the shedding of field virus into the environment.

06. Which vaccines can control IBD?

rHVT-VP2 vaccines do not stop neither the infection of the bursa nor the shedding of field virus which will build up over time.The risk of this partial protection is the selection of new strains that may escape from the narrow VP2 protection.

Intermediate plus IBD vaccines can protect the bursa against infection and block the shedding, but because of the limitations of farm vaccination, will always be a percentage of birds left susceptible to the field infection.

TRANSMUNE combines the strong protection properties of the Int. plus vaccines plus the highest coverage of the hatchery vaccination. The field IBDV will have no opportunity to replicate in the chickens and be shed into the environment. Then, the virus pressure will go down cycle after cycle, with no possibility to mutate.

07. Does Transmune protect against IBDV infection?

Yes.

It was demonstrated that after replication of Winterfield 2512 strain in the bursa, chickens become highly resistant to infection by any other IBDV strain.

08. Does Transmune prevent IBDV challenge?

Yes.

The Winterfield 2512 IBDV strain blocks the field virus from replicating in the bursa and consequently being shed into the environment.

The reduction of the virus load / pressure will decrease the infection risk for the coming flocks.

09. Does Transmune protect against new IBDVs strains?

Yes.

This is the consequence of the mechanism of protection triggered by Transmune. The vaccine virus replicates in the bursa which becomes resistant to the infection.

Several trials have demonstrated that this is true whatever the challenging IBDV.

10. Does Transmune prevent the emergence of new IBDV strains?

Yes.

Transmune makes the vaccinated birds highly resistant to infection by any type of IBDV and consequently stops its shedding into the environment.

No opportunity is left to farm IBDV to infect, multiply or mutate into an antigenically different IBDV.

Since the mechanism of protection is independent from the type of IBDV challenge, no selection pressure for strains escaping the vaccine protection is exerted.

11. Do rHVT-VP2 vaccines protect against IBD?

Yes, partially.

rHVT-VP2 vaccines make the chickens more resistant to the disease (clinical signs), but don’t protect against infection.

The resistance varies according to:

  • Time after injection. Onset of immunity in these types of vaccines is slow, it takes several weeks for reaching a strong immunity (giving more room to the field virus to infect the chickens early).
  • Type of IBDV challenge. Protection depends on the homology between the VP2 of the vaccine and the VP2 of the challenging strain: High homology > strong protection / Low homology > weak protection.

12.Do rHVT-VP2 vaccines prevent IBDV challenge?

No.

rHVT-VP2 vaccines poorly protect against the infection and replication of the field virus in the bursa, which is left “open” for any kind of field IBDV to invade it and consequently to be shed in the environment.

This will help the building up of the prevailing IBDV field strain or increase the likelihood of the emergence of a new strain.

13. Do rHVT-VP2 vaccines prevent the emergence of new IBDV strains?

No.

rHVT-VP2 vaccines are not whole live virus and consequently do not replicate in the bursa and do not make follicles fully resistant to infection. The field IBDV can infect the chickens, invade the bursa and be shed into the environment.

As the protection induced by rHVT-VP2 vaccines is stronger against IBDVs having homologous VP2, new strains are likely to better escape the vaccine protection and replicate in higher amount than homologous IBDVs. This way, a selection pressure is exerted helping the emergence of new strains.

14. Why is Transmune a better choice than rHVT-VP2 vaccines?

15. How can IBDV field pressure increase in the field?

The IBDV field pressure can increase if it is able to find non-protected or partially protected chickens in a flock.

Those chickens will get infected, will replicate the field viruses in the bursa and then, will shed them into the environment.

16. Does Transmune vaccine virus spread into the environment?

Yes.

The vaccine virus of Transmune spreads within a flock from vaccinated to unvaccinated chickens; this is a key property that helps to increase the vaccine coverage in case of a few missed eggs or chicks.

On the contrary, rHVT-VP2 vaccines do not spread, hence any missed bird will remain fully susceptible.

17. Why there are small bursas in Transmune and not in rHVT-VP2 vaccinated flocks?

Transmune vaccine virus replicates in the bursa inducing an inflammatory process. As consequence, the bursa gets partially atrophied before recovery. It has been demonstrated that this atrophy has no consequence on the immune status of the birds.

The mechanism of action of rHVT-VP2 vaccines is related to HVT replication. Therefore it leaves the bursa intact. This is why, in experimental conditions, the bursa in these vaccinated chickens are homogeneously large. However, in field conditions because the bursa is left “open to infection”, it is common to notice small or heterogeneous bursas evidencing the replication of the field virus.

18. Is bursa size important?

No.

There are no bursa size standards.

The relative importance of bursa integrity diminishes beyond 2 to 3 weeks of age as it has been demonstrated by bursectomy, and immunodepression assessment studies.

19. Since Transmune replicates in the bursa, is there any consequence on the immunocompetence of the chickens?

No.

It has been demonstrated several times:

  • Full immunocompetence in several ND vaccination-challenge studies (EU registration file).
  • Transmune and Vectormune ND compatibility study: full immunocompetence after ND challenge.
  • Full immunocompetence (ND antibody response) after bursectomy at 21 and 28 days.
  • Full immunocompetence in IB vaccination-challenge study.

20. Is there any difference between the onset of immunity (OOI) in birds vaccinated with Transmune versus rHVT-VP2 vaccines?

Yes.

The OOI in Transmune vaccinated birds occurs very shortly (1-2 days) after the take (replication of vaccine virus in the bursa), while in the rHVT-VP2 vaccines the OOI takes longer time and depends on several vector’s replication cycles.

21. What does immunity gap mean?

Immunity gap term was introduced to highlight the transition window between the disappearance of MDA and the detection of the active humoral immunity that is elicited by live vaccines where the chickens would not be protected.

Immunologically, it is not a proper term because it only refers to a part of the immune response.

22. Can we rely on ELISA to assess if there is an immunity gap or not?

No.

Commercial IBD ELISAs are useful indicators to detect and quantify the amount of circulating IgY antibodies only. Moreover, several ELISA kits are commercially available and they do not correlate between each other.

Therefore, the only valid criteria to evaluate immunity, including the presence or not of an immunity gap is by implementing challenge tests.