Hemorrhagic enteritis virus induced changes in the lymphocyte subpopulations in turkeys and the effect of experimental immunodeficiency on viral pathogenesis.

We examined the changes in the lymphocyte subpopulations in the spleen and peripheral blood of turkeys and the effects of experimental immunodeficiency in the B and T cell compartments on the pathogenesis of hemorrhagic enteritis (HE) in turkeys. Inoculation of turkeys with hemorrhagic enteritis virus (HEV) induced a drop in the relative proportions of IgM bearing cells on Day 2, 3, and 9 post-infection and an elevation in the relative proportions of CD4+ cells on Day 4 and 6 post-infection. Elevated levels of CD8+ cells were observed in the infected turkeys only on Day 16 after infection. Marked depletion of IgM+ cells may play a role in immunodepression caused by HEV. Cyclophosphamide (CY) treatment induced B cell deficiency in turkeys severely impaired HEV replication in the spleen suggesting that B lymphocytes are important for viral replication. Cyclosporin A (CsA) selectively impaired T cell mitogenesis and protected the turkeys against HEV-induced intestinal hemorrhages. CsA did not prevent viral replication in the spleen or the associated splenomegaly. This result suggested that T cell immunity may be important for intestinal hemorrhaging induced by HEV.

Hemorrhagic enteritis of turkeys.

Hemorrhagic enteritis (HE), an economically important disease of turkeys is caused by a type II adenovirus. The virus is ubiquitous and is liable to infect most field turkeys. In unprotected turkey flocks, infection with virulent hemorrhagic enteritis virus (HEV) may result in variable mortality and immunodepression. Turkeys younger than 2-4 weeks of age are resistant to clinical HE. This age-related resistance is expressed in the presence or absence of maternal antibodies against HEV. Clinical disease is characterized by HE and splenomegaly. The virus causes intranuclear inclusions in the reticuloendothelial cells. Bursectomy or splenectomy abrogate clinical HE. Field data and laboratory studies indicate that HEV causes immunodepression in the humoral as well as the cellular immune functions of turkeys. The mechanism of immunodepression is not known.

Enteritis Hemorragica por Adenovirus en Pavos / Hemorrhagic Enteritis by Adenovirus in Turkeys

Se describe por primera vez en Colombia la enteritis hemorragica (EH), en pavos de 4 a 11 semanas de edad, mediante estudios macroscopicos, histologicos y de microscopia electronica. Se demostro una enteritis hemorragica severa, y esplenomegalia con inclusiones intranucleares en la mayoria de las celulas de la pulpa blanca esplenica y en algunos mononucleares en el intestino delegado. Las inclusiones son caracteristicas; consisten de un centro eosinofilico, rodeado de cromatina densa y condensada sobre la membrana nuclear y de una estructura muy basofila y densa sobre un polo nuclear que parece corresponder a un nucleolo. Al microscopio electronico se aprecian fases del desarrollo viral, desde un material filamentoso y amorfo hasta la formacion de grandes acumulos de viriones y capsides de 70-80 nm de diametro con morfologia tipica de adenovirus. Los viriones se demostraron facilmente en macerados de bazo fijado en formol, tenidos negativamente con fosfotungstato de potasio; no se visualizaron en el contenido intestinal hemorragico estudiado con el mismo metodo. El estudio de microscopia de luz de bazo e intestino es suficiente para establecer el diagnostico de esta entidad

Evidence for bursal involvement in the pathogenesis of hemorrhagic enteritis of turkeys.

The pathogenesis of hemorrhagic enteritis in turkey poults infected with hemorrhagic enteritis virus (HEV) at 3 days or at 2 or 5 weeks of age was compared with pathogenesis in poults that had been chemically bursectomized neonatally and exposed to cell-culture-propagated virus at 2 or 5 weeks of age. Conventional poults exposed to HEV at 2 or 5 weeks developed clinical disease, and mortality ranged from 38% to 100%. In addition to the splenic and intestinal lesions usually seen with HEV infection, the pancreas, bursa of Fabricius, and thymus were also affected. In contrast, although they were free from detectable maternal antibody, poults infected with HEV at 3 days of age failed to develop clinical disease or mortality; however, virus was demonstrated by histological and electron microscopic examinations in spleens of these poults. Neonatal chemical bursectomy completely prevented the clinical signs, gross lesions, and mortality induced by HEV in poults at 2 or 5 weeks of age. These findings strongly suggest that an intact bursa is necessary for HEV to induce disease in turkeys.

Immunofluorescence studies on the early pathogenesis of hemorrhagic enteritis virus infection in turkeys and chickens.

Chickens and turkeys not previously exposed to hemorrhagic enteritis virus (HEV) were inoculated orally with the virus. Birds were necropsied each day from the first to the eighth day following inoculation, and specimens from various tissues were collected for examination. Clinical illness was noted only in turkeys, although intestinal hemorrhages and swollen, necrotic spleens were seen in both species. The distribution and localization of viral antigens in various tissues and peripheral blood lymphocytes were studied by the immunofluorescent technique. The patterns of HEV infection in chickens and turkeys were similar, except there was a high level and persistence of viral antigen in the thymus of turkeys but not in chickens.