PATHOGENESIS OF HEMORRHAGIC ENTERITIS VIRUS-INFECTION IN TURKEYS

The pathogenesis of hemorrhagic enteritis was investigated in 4-week-old specific-pathogen-free (SPF) turkeys after oral administration of hemorrhagic enteritis virus. The virus antigen was detected and quantified in tissues at various days post-infection (DPI) by an avidin-biotin-enhanced enzyme immunoassay and was located by a monoclonal antibody-based immunoperoxidase (IF) staining technique. In the intestinal tract, low levels of viral antigen were detected from 1 to 3 and 9 to 15 DPI, whereas high antigen levels were found from 4 to 7 DPI. The bursa had viral antigen from 2 to 7 DPI. The plasma fraction of blood was positive for the antigen at day 1 PI and the cellular fraction of blood on day 3 PI. Antigen was first detected in the spleen at 2 DPI and reached a peak on day 6 PI. Initially, the viral antigen was present in a few reticular cells of the spleen and an increase in IP positive cells occurred with time. The maximum number of inclusion bodies in the spleen were found on day 6 PI. Following splenomegaly, viremia resulted in high levers of the virus appearing in the lamina propria of the small intestine. The lamina propria had numerous lymphoreticular cells positive for intranuclear viral inclusions from 5-7 DPI. It was at this time that intestinal congestion and hemorrhage were seen. The results suggest that HEV replicates first in the lymphoid cells of intestinal tract including the bursa, and then in those of the spleen with consequent HEV antigen widely distributed in the body. The time course of the high levels of HEV (mainly 4-7 DTI) in the lymphoid organs (cells), and occurrence of hemorrhagic enteritis (congestion, hyperemia) from 5 to 7 DPI and intestinal hemorrhage (5-8 DPI) appear to suggest that the intestinal lesion may be an immune-mediated response.