Experimentalinfection of chickens followed by very virulent infectious bursal disease viral challenge: clinical and pathological effects.

Abstract

Infectious bursal disease (IBD) is an immunosuppressive disease that increases susceptibility to avian coccidiosis, but the contrary is unclear. In a battery trial, this study evaluated whether prior(ET) infection of Egyptian Baladi chickens increased the virulence of the very virulent IBD virus. Birds grouped as follows: G1 (control), G2 (ET, 1.5×10oocysts), G3 (ET, 5×10oocysts), G4 (IBDV), G5 (G2+BDV), and G6 (G3+IBDV). At 21 days of age (d), chickens were sham- (G1 and 4) or ET- (G2, 3, 5, and 6) challenged. Four days later, G4-6 received IBDV by intranasal/ocular route. The birds were evaluated for growth performance and inspected clinically. The phagocytic test, cloacal viral shedding, and immunological organ index were evaluated on days 28 and 32. On day 28, the bursa of Fabricius (BF), spleen, and caecum were histologically analyzed, and caecal lesions were scored macroscopically. Compared to the G1, all challenged groups displayed worse growth performance (≤ 0.01). G5 and 6 outperformed G4 regarding weight gain and FI (P≤0.01), however, they still lagged behind G2 and 3 (≤ 0.01). Interestingly, the BF of G2 and 3 had a higher mean severity index (MSI) than G1 (≤ 0.01), indicating histological evidence of Eimeria stages. Nonetheless, G4's MSI was higher than G2's and G3's (≤ 0.01). Compared to G4, G5 and G6 displayed a substantially lower MSI and a higher BF' index. Mortalities in G4 and G6 were 10% and 5%, respectively. Compared to G4, G5 and 6 displayed increased viral shedding titers (≤ 0.01). Regarding coccidiosis, G5 and G6 exhibited lower phagocytic activity and higher oocyst counts and caecal lesion scores than G2 and G3 (≤ 0.01), suggesting that exposure to IBDV after ET enhanced ET pathogenicity and reproduction. Conclusions: ET interfered with the IBDV pathogenesis (increase in viral shedding, but less severe lesions compared to mono-infected birds); this could be because prior ET infection modulated T cells.