Effect of Infectious Bursal Agent on the Response of Chickens to Newcastle Disease and Marek's Disease Vaccination

Giambrone, J. J.; Eidson, C. S.; Page, R. K.; Fletcher, O. J.; Barger, Bruce O.; Kleven, S. H.

doi:10.2307/1589386

Cited by 66 publications

(20 citation statements)

References 6 publications

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“…The dramatic reduction in IgA synthesis by IBDV may provide an explanation as to why prior exposure to IBDV renders birds more susceptible to several common respiratory (Giambrone et al, 1976) and enteric (Wyeth, 1975) pathogens. Since IgA is primarily responsible for production of local immunity, a reduction in synthesis of IgA could increase the susceptibility of chicks to local infection.…”

Section: Discussionmentioning

confidence: 99%

Effect of Infectious Bursal Disease Virus on the Immunological Responsiveness of the Chicken

1977

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The immunological response of chickens infected at 28 days of age with infectious bursal disease virus (IBDV) was examined. Cellular immunity was studied by the graft-versus-host reaction and delayed type hypersensitivity skin reactions to tuberculin. Antibody responses to sheep red blood cells (S-RBC's) were tested by a direct hemagglutination test. Circulating levels of immunoglobulins (Ig's) IgM, IgG and IgA were monitored by the radial immunodiffusion test. The results of the graft-versus-host reaction and delayed type hypersensitivity reactions were similar for both the infected and control chicks. IBDV significantly reduced the primary antibody response to S-RBC's, but had no marked effect on the secondary antibody response. Chicks infected with IBDV had normal levels of serum IgM and IgG, but significantly lower levels of IgA when compared to uninfected control birds.

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Section: Discussionmentioning

confidence: 99%

Effect of Infectious Bursal Disease Virus on the Immunological Responsiveness of the Chicken

1977

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“…However, in one of his trials, the latent period of MD defined as an absence of clinico-pathological manifestations, was much longer in the IBDV-infected group. Giambrone et al (1976) noted markedly enhanced incidence of MD in chickens exposed to an environment contaminated with IBDV. On the other hand, Sharma (1984) showed that pathogenic IBDV reduced the gross MD lesion response.…”

Section: Discussionmentioning

confidence: 90%

Effect of reticuloendotheliosis virus and infectious bursal disease virus on MAREK'S disease herpesvirus latency

1989

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“…Η κένωση αυ τή σε πρώιμα στάδια της ζωής των ορνιθίων οδηγεί σε σο βαρή ανοσοκαταστολή (Lucio and Hitchner 1980). Η επί δραση αυτή έχει επιπτώσεις στις αποδόσεις των ορνι θίων, συμβάλλει στην ανάπτυξη δευτερογενών μολΰνσε-ων, επηρεάζει δυσμενώς την ανοσολογική απάντηση των ορνιθίων σε επακόλουθους εμβολιασμοΰς, που είναι ου σιώδεις σε όλους τους τΰπους ορνίθων εντατικής ζωικής παραγωγής (Giambrone et al 1976). Η πλέον σοβαρή και παρατεταμένη ανοσοκαταστολή συμβαίνει όταν μολΰνο νται από τον IBDV νεοσσοί 1 ημέρας (Sharma et al 1994).…”

Section: παθογενειαunclassified

Gumboro disease (IBD)

Georgopoulou

2017

J Hellenic Vet Med Soc

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Gumboro Disease (IBD) caused by Infectious Bursal Disease Virus is an immunosuppressive condition of chickens, which resulted in severe economical losses. Approximately 47 years after the first appearance of the disease, the changes in the form of presentation and pathogenicity of IBDV in the field has resulted in continual changes and adjustments of the vaccines used to control IBD. The original form of the disease, also known as classic or clinical IBD, was usually observed after the third week of life with high mortality, depending on factors, such as virulence of the strain of virus involved, age of the birds and maternal antibody status. The acute IBD is caused by the very virulent IBDV strains, characterized by high mortality rates in vaccinated chickens and the clinical signs and lesions are similar to those of the classic form. The subclinicalform of the disease is associated with the "variant" strains of IBDV and is characterized by low mortality and severe immunosuppression. Initially, the classic IBD was controlled by the use of mild vaccines produced in the early 1970s and from the late 1980s revealed absence of protection from wIBDV in vaccinated chickens. Another group of vaccinal strains, known as intermediate plus vaccine, has been used to control wIBDV strains. These vaccines multiply in birds, even in the presence of high maternal antibody titers. In the USA and other countries, the disease from the variant strains was controlled by intermediate strains as well as by inactivated vaccines that included variant strains, thus providing maternal antibodies against both the standard and variant strains. Until today, the IBD continues to pose an important threat to commercial poultry industry. The high resistence of IBDV to physical and chemical agents accounts for persistence of the virus in the outside environment, particularly on contaminated farms, despite disinfection. Nevertheless and not quite unexpected for the IBDV mutations in the genome, resulted in the emergence of antigenic variant strains in vaccinated flocks. The IBD requires heightened vigilance and the incidence and prevalence of the clinical and immunosuppressive forms must be evaluated more precisely.

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Effect of Infectious Bursal Agent on the Response of Chickens to Newcastle Disease and Marek's Disease Vaccination

Cited by 66 publications

References 6 publications

Effect of Infectious Bursal Disease Virus on the Immunological Responsiveness of the Chicken

Effect of Infectious Bursal Disease Virus on the Immunological Responsiveness of the Chicken

Effect of reticuloendotheliosis virus and infectious bursal disease virus on MAREK'S disease herpesvirus latency

Gumboro disease (IBD)

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