AI Summary & Key Takeaways
AI InsightThese findings suggest that immune dysfunction could be a contributing factor in the increased mortality of birds affected by IBH-HPS, which renders the birds immunosuppressed for the rest of their lives.
📌 3 Key Takeaways
Abstract
Inclusion body hepatitis-hydropericardium syndrome (IBH-HPS) in broilers is caused by an adenovirus, here referred to as inclusion body hepatitis-hydropericardium syndrome virus (IBH-HPSV). This study describes the immune status of broiler chickens experimentally inoculated with an isolate of fowl adenovirus-4 serotype-1, involved in IBH-HPS in various trials. When compared with the unchallenged controls, IBH-HPSV-inoculated broilers had significantly higher atrophy of the bursa of Fabricius (BF) by up to 2-fold, as well as of the thymus (up to 9-fold) and spleen (up to 1.5-fold) (P < 0.05), with up to 60% mortality. Upon challenge with sheep red blood cells (SRBCs), IBH-HPSV-inoculated birds had from 2- to 3-log lower anti-SRBC antibody titers than the control. Response to phytohemagglutinin-P (PHA-P) was significantly reduced in IBH-HPSV-inoculated birds (P < 0.05) as compared to the control. Results of the studies revealed that the immune status of broilers is compromised significantly during IBH-HPSV infection in terms of lymphoid organ integrity, humoral, and cell-mediated immune responses, respectively. These findings suggest that immune dysfunction could be a contributing factor in the increased mortality of birds affected by IBH-HPS, which renders the birds immunosuppressed for the rest of their lives.
Özet
Inclusion body hepatitis-hydropericardium syndrome (IBH-HPS) in broilers is caused by an adenovirus, here referred to as inclusion body hepatitis-hydropericardium syndrome virus (IBH-HPSV). This study describes the immune status of broiler chickens experimentally inoculated with an isolate of fowl adenovirus-4 serotype-1, involved in IBH-HPS in various trials. When compared with the unchallenged controls, IBH-HPSV-inoculated broilers had significantly higher atrophy of the bursa of Fabricius (BF) by up to 2-fold, as well as of the thymus (up to 9-fold) and spleen (up to 1.5-fold) (P < 0.05), with up to 60% mortality. Upon challenge with sheep red blood cells (SRBCs), IBH-HPSV-inoculated birds had from 2- to 3-log lower anti-SRBC antibody titers than the control. Response to phytohemagglutinin-P (PHA-P) was significantly reduced in IBH-HPSV-inoculated birds (P < 0.05) as compared to the control. Results of the studies revealed that the immune status of broilers is compromised significantly during IBH-HPSV infection in terms of lymphoid organ integrity, humoral, and cell-mediated immune responses, respectively. These findings suggest that immune dysfunction could be a contributing factor in the increased mortality of birds affected by IBH-HPS, which renders the birds immunosuppressed for the rest of their lives.