To determine passive haemagglutination (PHA) antibody titer that would protect chicks against Nigerian isolates of the Infectious Bursa Disease Virus (IBDV), five groups of chicks aged 30 days which had different antibody titers were challenged with a Nigerian isolate of virulent IBDV. Mortality rates of the different groups were plotted against their respective mean PHA antibody titers. A group with zero antibody titer had a mortality rate of 75% while those with PHA antibody titers of 185.6, 243.2, 256 and 307.2 had mortality rates of 40%, zero, zero and zero respectively. Linear equation generated for a line of best fit of the graph of mortality rates of the chicks on their IBD antibody titers gave antibody titer (X) at which mortality (Y) would be zero as 300. A mortality of 75% and the high antibody level needed to protect chicks suggest that the isolate may be a hypervirulent strain.
Infectious Bursa Disease (IBD) is an acute, highly contagious viral disease of young chickens. The virus attacks primarily lymphoid cells, especially B-cells. Lymphoid tissues of the cloacal bursa are most severely affected [
Clinical signs of IBD in chicks include ruffled feathers, trembling, depression, diarrhea, pecking of the vent. Fever starts 48 hours post infection but body temperature drops below normal just before death. The disease runs its full course in about 7 days [2-7].
In fully susceptible flocks, IBD appears suddenly and there is a high morbidity rate. Mortality in IBD may be nil but can be as high as 20% - 30%, usually beginning on the third day of onset of clinical signs and peaking and receding in a period of 5 - 7 days.
Initial outbreaks on a farm are usually the most acute. Recurrent outbreaks in succeeding broods are less severe and frequently go undetected. Many IBDV infections are silent, owing to age of birds (less than 3 weeks old or above 12 weeks), previous infection with virulent field strains of IBDV or infection occurring in the presence of maternal antibody [
The most prominent lesions of IBD are found in the bursa of fabricius, hence the name infectious bursa disease (IBD) which is used presently [8,9]. Gross lesions described by Cosgrove [
Helmboldt and Garner [
Lensing [
These earlier reports of gross lesions of IBD were confirmed by later reports [15-17]. Schobries [
There are two distinct serotypes of IBDV, designated as serotypes 1 and 2. Viruses of serotype I are pathogenic to chickens whereas serotype 2 viruses, mostly isolated from turkeys, do not replicate in chicken cells [
Viruses belonging to one antigenic subtype are commonly known as variants. Variants of IBDV serotype 1 have been reported to breakthrough high level maternal antibodies in commercial flocks, causing up to 60 to 70 percent mortality rate in chicken [
McFerran et al. [
The two serotypes can be differentiated by virus neutralization test, but they are not distinguishable by fluorescent antibody test or Enzyme-linked Immunosorbent Assay. Immunization against serotype 2 does not protect against serotype 1. The reverse situation could not be tested, because there are no virulent serotype 2 IBD viruses for challenge [26,27].
The first isolates of serotype 2 originated from turkeys and it was thought that this serotype was host specific [
So, two serotypes of IBDV are known to exist and within the serotypes. There are variants. Variant strains of IBDV, which have major antigenic differences from the “standard” strains, cause immunosuppression but do not cause disease in older chickens [
Economic importance of IBD stems from heavy morbidity and mortality, reduction in growth rate and immunosuppression, making the birds susceptible to other diseases, such as Newcastle disease [
IBD has been reported from every poultry-producing country in the world. First diagnosed in 1962, the causative virus has changed form and has manifested itself in different forms that make it even a bigger threat to the poultry industry [
Apart from mortality rates, antibody titer which protects chicks against IBDV challenge can be used as a measure of virulence of the IBDV variants in the locality. Lukert and Saif [
Fifty cockerel chicks were used for the experiment. They were randomly allocated to 5 groups of 10 chicks each. Different vaccination methods were adopted for the groups, to achieve different levels of immunity.
Three weeks post vaccination, 5 chicks from each of the groups were bled and the sera used to measure antibody titer of the groups, by the passive haemagglutination method while the remaining 5 chicks were challenged with a virulent Nigerian isolate of the IBDV (NVRI, Vom, Nigeria) to record mortality rates. Mortality rates of the five groups were plotted against their respective antibody titers. Equation for a line of best fit of the graph was generated by the formula reported by Gujarati [
Antibody titers of the vaccinated groups of chicks and their mortality rates following challenge with the virulent Nigerian isolate of IBDV, were as follows: For chicks with Zero antibody titer mortality was 75%. For antibody titers of 185.6, 243.2, 256 and 307 mortality rates were 40%, Zero%. Zero% and Zero% respectively. The mortality rates and the antibody titers are presented on
PHA antibody titer that protects chicks against IBDV
challenge in Europe and America is 64 [
IBDV variants, different from the “standard” strains, cause immunosuppression but not clinical disease in chickens immunized against the standard IBDV [
Effectiveness of vaccinations to control IBD is dependent on variants of the virus in circulation in the area. Variants of IBDV of same serotype 1 have been reported to break through high levels of maternal antibodies in commercial flocks vaccinated with vaccines made from different variants, causing up to 60% to 70% mortality [