Pathology of spontaneous hemorrhagic enteritis of turkeys.

Thirteen turkeys naturally affected with hemorrhagic enteritis were studied pathologically. The main gross lesions were splenomegaly and hemorrhagic contents in the gut. The main histological lesions were intranuclear inclusion bodies in largemononuclear cells in many visceral organs and in reticular cells around the sheathed arteries of the spleens and varying degrees of lymphocytic hyperplasia in most tissues. The inclusions were frequently present in areas of the lymphocytic hyperplasia. The large mononuclear cells with the inclusions frequently showed a degenerative change.     

Role of splenectomy in prevention of hemorrhagic enteritis and death from hemorrhagic enteritis virus in turkeys

Hemorrhagic diarrhea, gross hemorrhagic enteritis, and death caused by intravenous virus injection of hemorrhagic enteritis virus (HEV) were prevented in otherwise susceptible turkey poults by surgical splenectomy. The splenectomized poults produced anti-HEV antibodies, which indicated that splenectomy did not completely prevent replication of the virus. These results indicate that the spleen is necessary for the development of the intestinal lesions of this disease. The role of a toxic factor in this disease is discussed.     

Protection of turkeys from hemorrhagic enteritis with a recombinant fowl poxvirus expressing the native hexon of hemorrhagic enteritis virus.

Hemorrhagic enteritis (HE) is an economically important disease of turkeys caused by a type II aviadenovirus, hemorrhagic enteritis virus (HEV). The vaccines currently available to the commercial poultry producer are highly effective in preventing disease outbreaks; however, they are immunosuppressive. A recombinant fowl poxvirus (rFPV) expressing the native hexon of HEV has been shown to induce an anti-HEV humoral immune response in turkeys. In this study, the rFPV expressing the native hexon of HEV was compared with a commercial HEV vaccine (vxHEV) for its ability to protect turkeys from virulent HEV challenge. Complete protection from the enteritis of HE was achieved in experimental groups vaccinated with either the rFPV or the vxHEV. Lymphocyte stimulation was measured in turkeys inoculated with rFPV, vxHEV, or a sublethal dose of HEV or not inoculated. No statistically significant immunodepression was observed in turkeys receiving the rFPV.     

Colibacillosis of turkeys exacerbated by hemorrhagic enteritis virus. Laboratory studies

Lesions typical of colibacillosis disease were reproduced in laboratory experiments. Mortality resulting from experimentally produced colibacillosis was significantly increased when Escherichia coli O1:K1 was presented to poults that had been orally inoculated with hemorrhagic enteritis virus (HEV) 1 week earlier. These and previous data suggest that HEV infection can exacerbate colibacillosis of older poults. HEV infection apparently damages the poults' defense system enough to account for the observed increase in susceptibility to E. coli.     

Field outbreaks of colibacillosis of turkeys associated with hemorrhagic enteritis virus

In a study of field material and a survey conducted by the authors, typical signs of colibacillosis of 6-to-12-week-old poults included sudden onset, listlessness, rales, and high mortality. Signs persisted for about 2 weeks and were often followed by a low incidence of lameness caused by Escherichia coli. Gross lesions included enlarged and congested spleens and livers, and dilated discolored black or purple duodenal loops. Microscopic lesions included splenic and hepatic congestion. In some birds (freshly killed and fixed immediately), the epithelium at the tips of the duodenal villi was sloughing, but in other birds the villi were intact and normal in appearance. Splenic enlargement, the presence of intranuclear splenic inclusions similar to those found in hemorrhagic enteritis (HE), and the isolation of HE virus from some of the field spleens all indicated that inapparent HE infection often occurs at approximately the same time as this type of colibacillosis. It is therefore believed that HE infection often exacerbates colibacillosis of older poults.     

Increased numbers of duodenal mucosal mast cells in turkeys inoculated with hemorrhagic enteritis virus.

The relation between average duodenal mast cell count, duodenal mucosal mast cell numbers, duodenal connective tissue mast cell numbers, circulating basophil numbers, heterophil-to-lymphocyte ratio, and lesion score were studied to gain an understanding of the events that may lead to intestinal lesion formation associated with hemorrhagic enteritis virus (HEV) infection. Changes in vascular permeability in the duodenum in birds inoculated with HEV were examined, using colloidal carbon and ferritin as vascular markers. Turkeys inoculated with HEV had significantly (P less than 0.05) higher duodenal mast cell counts than did noninfected controls. Birds inoculated with HEV had significantly (P less than 0.05) more mucosal mast cells than did phosphate-buffered saline solution-inoculated birds. Connective tissue mast cell and basophil numbers were unaffected by viral inoculation. Thermal stress did not have significant effect on lesion severity, but did increase number of birds that developed the characteristic intestinal lesions. The heterophil-to-lymphocyte ratio was significantly (P less than 0.05) higher in HEV-inoculated birds, compared with phosphate-buffered saline solution-inoculated controls. Increase in vascular permeability was only detected in HEV-inoculated birds with intestinal lesions. Results indicate that mast cells, and the vasoactive mediators contained within mast cells, may be important in the early manifestation of HEV infection. They also provide a possible mechanism through which biochemical and physiologic changes characteristic of HEV infection can occur.     

Electron microscopic findings of cells with inclusion bodies in experimental hemorrhagic enteritis of turkeys.

The spleen, liver, bone marrow and intestines of two turkeys in which hemorrhagic enteritis of turkeys was experimentally reproduced were examined electron-microscopically. Intranuclear inclusion bodies as described in a previous report were found in all the tissues examined. These occupied most of the area in affected nuclei and were composed of viral particles with morphological characteristics of an adenovirus. The cells with the inclusions were divided into two types of cells, immature and reticular cells. There was some variety in the stage of differentiation of the former cells. As the viral particles developed the cells degenerated and disintegrated. A few particles had been released into the cytoplasm of the degenerated cells but no particles were present in intercellular spaces.     

Response of turkeys to simultaneous vaccination with hemorrhagic enteritis and Newcastle disease viruses.

The effects of single and combined vaccination of turkeys against hemorrhagic enteritis virus (HEV) and Newcastle disease virus (NDV) were investigated. Dual vaccination of turkeys with NDV-B1 and HEVp30 or marble spleen disease virus (MSDV) enhanced white mottling of the spleens and the apoptosis rate in spleen cells (P < 0.05). In addition, simultaneously vaccinated turkeys had fewer HEV-infected spleen cells at 4 days postvaccination than turkeys given HEVp30 or MSDV alone. The anti-HEV antibody response was significantly reduced at 14 days postvaccination (P < 0.05), whereas the anti-NDV antibody response was enhanced (P < 0.05) in turkeys vaccinated with HEVp30 + NDV-B1. Further, the effect of dual vaccination on macrophage function was studied. Spleen cells from NDV-B1-vaccinated turkeys were primed to produce nitric oxide (NO) after stimulation in vitro with lipopolysaccharide. Spleen cells from HEVp30- or MSDV-vaccinated turkeys did not produce NO after in vitro stimulation. In dual-vaccinated turkeys, the priming effect of NDV-B1 was reduced in comparison with single-inoculated birds.     

Necrotic enteritis in turkeys.

Three flocks of turkey hens (16,000 each) between 7 and 12 weeks of age experienced outbreaks of necrotic enteritis. Necropsy revealed a dilated duodenum and jejunum with mucosal surfaces covered with a diphtheritic membrane. Intestinal scrapings showed very few oocysts of Eimeria sp. Histopathological findings were compatible with necrotic enteritis but with deeper, more severe lesions than in broiler chickens. Clostridium perfringens was isolated by anaerobic culture from the intestinal contents. Mortality returned to normal after ampicillin or tetracycline was added to the drinking water.     

In vitro evaluation of B-lymphocyte function in turkeys infected with hemorrhagic enteritis virus

Studies were conducted on B-lymphocyte function in turkeys infected with hemorrhagic enteritis (HE) virus. Hemolytic plaque-forming technique was used to detect antibody-forming cells in turkeys. The plaque-forming cell responses in HE virus-infected and noninfected controls were compared. Results of this study indicated a decreased capability of HE virus-infected turkeys to produce antibodies to sheep RBC. The greatest inhibition of antibody-forming cell production was seen in the turkeys 19 days after exposure to the virus. However, after this period, the turkeys gradually recovered their immunocompetence to sheep RBC.     

Bovine rotavirus in turkeys with enteritis

Rotaviruses are the main agents responsible for diarrhea in different animal species and for infantile gastroenteritis. These viruses have been isolated from various avian species and have often been associated with poult enteritis and mortality syndrome. Nevertheless, the knowledge of rotavirus infection in turkeys is scarce. Six group A rotavirus strains obtained from pooled enteric contents of diarrheic turkeys were isolated in MA-104 cell culture and typed as G(6)P(1), a typical bovine rotavirus genotype. Additionally, the electropherotypes showed a migration pattern identical to the Nebraska calf diarrhea virus, and the complete NSP4 gene phylogeny showed that all six strains segregated in the genotype E2. Taken together, these results point toward a cattle-to-turkey rotavirus transmission. As a conclusion, bovine-origin rotavirus can be found in turkeys, and this transmission route must now be considered for the improvement of the health status in turkey farms.     

Field trials of an immunization procedure against hemorrhagic enteritis of turkeys

The efficacy of oral vaccination for hemorrhagic enteritis of turkeys was assessed by comparing flocks raised on the same premises, under the same management, with and without vaccination. The immunizing virus, a strain of marble spleen disease virus of pheasants, was administered via the drinking water. Vaccinated and unvaccinated turkeys differed significantly in feed conversion rates and spleen weights after challenge.     

Hemorrhagic enteritis of turkeys in California: serologic study of hemorrhagic enteritis virus antibody with an enzyme-linked immunosorbent assay

The incidence of hemorrhagic enteritis (HE) infection in California turkeys was studied by testing 2220 turkey blood samples from 173 flocks for HE virus (HEV) antibody by the enzyme-linked immunosorbent assay (ELISA). Maternal antibody was detected at 1 day of age in all flocks tested, and it vanished after 3 weeks. Acquired HEV antibody appeared at 8 to 10 weeks, and 100% of the meat and breeder turkey flocks were positive after 11 weeks of age. HEV infection occurred earlier in the meat flocks than in the breeder flocks, and it also occurred earlier during summer than during the fall and winter months.     

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.