The Role of the Infectious Bursal Agent and Several Avian Adenoviruses in the Hemorrhagic-Aplastic-Anemia Syndrome and Gangrenous Dermatitis

Jk, Rosenberger; Klopp, Spangler; Rj, Eckroade; Wc, Krauss

doi:10.2307/1589185

Cited by 103 publications

(29 citation statements)

References 7 publications

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“…Thus examination of livers from natural cases of IBH have revealed either very few or no virus particles in the inclusions (Bickford et al, 1973;Howell et al, 1970;McCracken and McFerran, unpublished observations;Pettit and Carlson, 1972), whereas examination of livers from adenovirus induced hepatitis has shown cells with numerous adenovirus-like particles (Bickford et al, 1973;McCracken and McFerran, unpublished observations;Nakamatsu et al, 1968) similar to those described for chicken kidney cells infected with the eight prototype Japanese serotypes (Maeda et al, 1967). Rosenberger et al (1975) demonstrated that lack of immunity to infectious bursal disease in breeder flocks was related to an increased susceptibility of their progeny to anaemia and dermatitis. They postulated that chicks devoid of maternally derived antibody would be susceptible to infectious bursal disease virus infection in the first weeks of life, and the resulting immuno-suppression would allow the adenoviruses to produce the haemorrhagic-aplastic-anaemia syndrome.…”

Section: Inclusion Body Hepatitis In Fowlmentioning

confidence: 99%

Avian adenoviruses ‐ a review

1977

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Section: Inclusion Body Hepatitis In Fowlmentioning

confidence: 99%

Avian adenoviruses ‐ a review

1977

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“…IBDV infects young chickens through the digestive tract and massively destroys B cells in the bursa of Fabricius, a primary lymphoid organ, causing immunosuppression and death. Surviving birds are severely immunocompromised and more susceptible to other avian pathogens (38). IBDV is therefore of major concern in the poultry industry.…”

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confidence: 99%

Abilityof Lactococcus lactis To Export Viral CapsidAntigens: a Crucial Step for Development of LiveVaccines

Dièye

Hoekman²,

Clier

et al. 2003

Appl Environ Microbiol

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The food grade bacterium Lactococcus lactis is a potential vehicle for protein delivery in the gastrointestinal tract. As a model, we constructed lactococcal strains producing antigens of infectious bursal disease virus (IBDV). IBDV infects chickens and causes depletion of B-lymphoid cells in the bursa of Fabricius and subsequent immunosuppression, morbidity, or acute mortality. The two major IBDV antigens, i.e., VP2 and VP3, that form the viral capsid were expressed and targeted to the cytoplasm, the cell wall, or the extracellular compartment of L. lactis. Whereas VP3 was successfully targeted to the three compartments by the use of relevant expression and export vectors, VP2 was recalcitrant to export, thus confirming the difficulty of translocating naturally nonsecreted proteins across the bacterial membrane. This defect could be partly overcome by fusing VP2 to a naturally secreted protein (the staphylococcal nuclease Nuc) that carried VP2 through the membrane. Lactococcal strains producing Nuc-VP2 and VP3 in various bacterial compartments were administered orally to chickens. The chickens did not develop any detectable immune response against VP2 and VP3 but did exhibit an immune response against Nuc when Nuc-VP2 was anchored to the cell wall of lactococci.

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“…Clostridia may also contribute to other conditions in poultry under certain circumstances. Thus, Clostridium perfringens has been reported to cause necrotic enteritis (Parish, 1961) and has been isolated along with some aerobic bacteria from gangrenous dermatitis (Rosenberger et al, 1975;Cullen & Pattison, 1980;Milakovic-Novak et ah, 1984). Other reports of clostridial involvement in poultry diseases include C: perfringens type A (Al-Sheikhly & Truscott, 1977;Nillo, 1976), Clostridium novyi (Peterson, 1964), Clostridium sporogenes (Peterson, 1967), Clostridium septicum (Fowler & Hussaini, 1975) and Clostridium fallax (Ellwood & Halliwell, 1973).…”

Section: Discussionmentioning

confidence: 99%