PATHOGENESIS OF HEMORRHAGIC ENTERITIS VIRUS-INFECTION IN TURKEYS

The pathogenesis of hemorrhagic enteritis was investigated in 4-week-o ld specific-pathogen-free (SPF) turkeys after oral administration of h emorrhagic enteritis virus. The virus antigen was detected and quantif ied in tissues at various days post-infection (DPI) by an avidin-bioti n-enhanced enzyme immunoassay and was located by a monoclonal antibody -based immunoperoxidase (IF) staining technique. In the intestinal tra ct, 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 p ositive 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 re ached 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 cel ls occurred with time. The maximum number of inclusion bodies in the s pleen were found on day 6 PI. Following splenomegaly, viremia resulted in high levers of the virus appearing in the lamina propria of the sm all intestine. The lamina propria had numerous lymphoreticular cells p ositive 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 conse quent HEV antigen widely distributed in the body. The time course of t he 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.