Effect of fowl adenovirus on replication of vaccine strain of Marek’s disease virus in chickens

Abstract

The aim of the study was to determine the effect of field strain, serotype 7 (FAdV-7 JN-5/10), of fowl adenovirus infection on the replication of Rispens/CVI988 strain of Marek's disease virus. Ninety one-day-old SPF chickens were divided into six groups. The chickens from group I were vaccinated against Marek's disease (MD) and 24 h later infected with the adenovirus; chickens from group II were vaccinated and infected simultaneously; chickens from group III were infected with the adenovirus and 24 h after the infection vaccinated against MD. The chickens from groups IV-VI were: control of infection (IV), control of vaccination (V), and neither vaccinated nor infected (VI). After 3, 7, 14, 21, and 28 d post infection, the number of copies of pp38 gene of Rispens strain and hexon gene of FAdV strain was determined in the bursa of Fabricius and liver using real-time PCR. The results indicated that in all cases the replication of Rispens strain was reduced to about 1.0 log 10 -3.5 log 10 in chickens infected with the adenovirus and vaccinated against MD compared with the chickens only vaccinated. Sixty-three one-day-old SPF chickens infected with adenovirus and vaccinated against MD were challenged with vv MD virus field strain. The protection index in this experiment was 55.6%-77.8%.

Research Note: Molecular and pathologic characterization of avian adenovirus isolated from the oviducts of laying hens in eastern Japan

“…The difference in the time of onset could be due to concurrent infection with CAV. Chicken anemia virus may have influenced the course of the disease as a contributing pathogen, affecting the immune response ( Markowski-Grimsrud and Schat, 2003 ), or via secondary effects due to anemia ( Toro et al., 2000 , Niczyporuk et al., 2013 ). The additive effect of CAV with FAdV-4 has been investigated, and their synergism was implicated in severe disease ( Toro et al., 2000 ).…”

“…Although implicated, the pathogenicity of most AAV, particularly FAdVs, is not well defined ( Niczyporuk et al., 2012 ). Some strains may act as primary or secondary pathogens ( Toro et al., 2000 , Niczyporuk et al., 2012 , Niczyporuk et al., 2013 ). However, under certain conditions, such as inclusion body hepatitis ( IBH ) and hydropericardium hepatitis syndrome ( HPS ), FAdVs have been directly involved, wherein disease has been replicated using field isolates ( Okuda et al., 2006 , Mase et al., 2010 ).…”

Whole genome sequencing of Fowl aviadenovirus A - a causative agent of gizzard erosion and ulceration, in adult laying hens

“…Particular serotypes of FAdV are responsible for a number of different clinical signs, including; inclusion body hepatitis (IBH) gizzard erosion and ulceration (GEU) and hydropericardium hepatitis syndrome (HHS) (Fitzgerald, 2013). Moreover, fowl aviadenoviruses may induce immunodeficiency or influence the failure of chicken vaccinations (Saifuddin &Wilks, 1992 andNiczyporuk et al, 2013b). …”

Identification of Fowl Adenovirus as a causative agent of inclusion body hepatitis (IBH) in commercial broilers

“…Immunosuppressors such as IBDV, chicken infectious anemia virus (CIAV), and Marek's disease virus (MDV) are factors that facilitate IBH outbreaks propagation or worsen clinical manifestations of FAdV infections (Morshed, Hosseini, Langeroudi, Fard, & Charkhkar, 2017;Niczyporuk, Woźniakowski, Samorek-Salamonowicz, & Czekaj, 2013). However, several studies showed that IBH might occur as a primary disease (Gomis et al, 2006;Ojkic et al, 2008).…”