ABSTRACT
BACKGROUND: Fowl adenoviruses (FAdVs) associated with certain clinical diseases including inclusion body hepatitis (IBH) have become of considerable importance in the poultry industry. Currently, an increasing number of IBH outbreaks in different parts of Iranian poultry industries is a growing concern. Infectious bursal disease virus (IBDV) or chicken infectious anemia virus (CIAV) have historically been incriminated as predisposing factors for FAdVs to cause IBH. Furthermore, some have speculated whether IBDV vaccine strains impact on IBH clinical manifestation. The present report assesses the potential predisposing role of IBDV, CIAV, and infectious bursal disease) IBD( vaccine strains for FAdVs in the course of an IBH occurrence in the field. CASE DESCRIPTION: 90000 day-old broiler chickens with the same parent source were housed, at 4 day-interval, in two commercial farms in Shiraz, Iran. Increased mortality with lesions of hepatitis, suggestive of IBH, started in the primitive farm right after blind prescription of IBD vaccine at the age of 12-days-old. Consequently, IBD vaccination was postponed for the apparently healthy chickens of the other farm in which chickens were monitored for the occurrence of IBH afterwards. Laboratory examination was followed by histopathology and polymerase chain reaction (PCR) on liver, cloacal bursa, and thymus samples to determine the involvement of FAdV, IBDV, and CIAV in the occurrence of the disease. FINDINGS/TREATMENT AND OUTCOME: No evidence was found to support the predisposing role of neither IBD vaccination nor IBDV/CIAV infection in this IBH occurrence. The results also demonstrated a primary role of the FAdV-11 as a causal agent of the IBH occurrence. CONCLUSION: The findings suggest that certain FAdVs are pathogenic enough to primarily induce IBH in young broilers.
ABSTRACT
Sudden death syndrome (SDS) is a stress-related disease in broilers with no diagnostic clinical or necropsy findings. SDS is associated with ventricular tachycardia (VT) and ventricular fibrillation (VF); however, its pathogenesis is not precisely described at the molecular level. Dysfunction of ryanodine receptor 2 (RYR2), that controls rapid release of Ca2+ from the sarcoplasmic reticulum (SR) into the cytosol during muscle contraction, has been associated with VT and sudden cardiac death (SCD) in human patients with structurally normal heart, but there is no report describing abnormalities in RYR2 in diseased broilers. In order to advance our knowledge on the molecular mechanisms predisposing broilers to fatal arrhythmia, the present study was conducted to determine the occurrence of possible mutations and changes in the expression level of the chicken RYR2 gene (chRYR2) in broilers that died from SDS. An increase in mRNA expression level and nine novel point mutations in chRYR2 were found in relation to SDS. In conclusion, susceptibility to lethal cardiac arrhythmia in SDS may be associated with specific changes in intracellular Ca2+ cycling components such as RYR2 due to mutation and dysregulation. Finding the probable association of SDS with gene defects can be applied to select for chickens with lower susceptibility to SDS and decrease the poultry industry losses due to SDS mortality. RESEARCH HIGHLIGHTS Investigation of the occurrence of possible mutations and changes in the expression level of chicken RYR2 gene (chRYR2) in broilers that died from SDS. Increase in the mRNA expression level of chRYR2 in relation to SDS. Nine novel point mutations in chRYR2 of broilers that died from SDS. Possible connection between susceptibility to lethal cardiac arrhythmia in SDS and changes in intracellular Ca2+ cycling machinery, such as RYR2, due to mutation and dysregulation.
