Veterinary Immunology and lmmunopathology, 30 ( 1991 ) 67-71

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Elsevier Science Publishers B.V., Amsterdam

Hemorrhagic enteritis of turkeys J.M. Sharma Department of Veterinary PathoBiology, College of Veterinary Medicine, University of Minnesota, St. Paul, MN55108, USA

ABSTRACT Sharma, J.M., 1991. Hemorrhagic enteritis of turkeys. Vet. Immunol. Immunopathol., 30:67-71. 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 agerelated 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. ABBREVIATIONS AASV, avian adenosplenomegaly virus; HE, hemorrhagic enteritis; HEV, hemorrhagic enteritis virus; MSDV, marble spleen disease virus.

INTRODUCTION

Hemorrhagic enteritis (HE) is an economically important disease of turkeys and pheasants. Antibodies to HE virus (HEV) have also been reported in commercial chicken flocks (Domermuth et al., 1979; Yamaguchi et al., 1982) although the significance of the disease in chickens is not known. In turkey flocks, HE outbreaks usually occur when the birds are 7-9 weeks of age (Domermuth and Gross, 1984). The HEV is ubiquitous and commercially raised turkeys acquire virus infection from the environment. The mortality caused by HEV is usually low but highly variable and may reach 60%. Economic loss occurs because HEVinfected turkeys perform poorly because of immunodepression. A turkey flock undergoing HEV-induced immunodepression may experience an increased incidence of opportunistic infections such as colibacillosis (Sponenberg et al., 1985; Larsen et al., 1986). 0165-2427/91/$03.50

© 1991 Elsevier Science Publishers B.V. All rights reserved.

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Most turkey flocks are protected against the pathogenic and immunodepressive effects of HEV by vaccination. Conventional vaccines consist of spleen extracts prepared from turkeys infected with nonpathogenic HEV (Domermuth and Larsen, 1984 ). In recent years, cell culture-propagated vaccines have also become available (Fadly et al., 1985; van den Hurk, 1990). My objective here is to present a brief overview of HE in turkeys and discuss the current status of our understanding of the immunodepressive capabilities of HEV. ETIOLOGY

Hemorrhagic enteritis of turkeys is caused by a type II adenovirus. The type II avian adenoviruses include HEV of turkeys, marble spleen disease virus (MSDV) of pheasants and the avian adenosplenomegaly virus (AASV) of chickens. These three type II adenoviruses are morphologically and serologically closely related but show no cross-reaction with any of the type I avian adenoviruses (Domermuth and Gross, 1984). The HEV is a nonenveloped, DNA virus with a diameter of 70-90 nm and an icosahedral symmetry. The virus replicates in the cell nucleus and may cause intranuclear inclusions in infected cells (Domermuth and Gross, 1984). Restriction endonuclease analysis of HEV, MSDV and AASV revealed that the viruses have different cleavage patterns (Zhang and Nagaraja, 1989). Upon infecting the host, HEV replicates and induces viral antigen in a number of different tissues (Fasina and Fabricant, 1982 ). PATHOGENESIS

Experimental or natural exposure to HEV in turkeys often leads to HE and splenomegaly (Itakura and Carlson, 1975 ). The intestinal lesion, appearing within 5-6 days of oral exposure to virulent HEV, is often characterized by grossly visible accumulation of blood in the duodenum and jejunum. Along with the intestinal lesion, the spleen may become grossly enlarged and mottled. Histologically, severe intestinal hemorrhages may be associated with necrosis of the tips of villi and a varying degree of lymphoid cell hyperplasia in the lamina propria. The spleen lesion is characterized by lymphoid cell necrosis, reticular cell hyperplasia and the appearance of intranuclear inclusion bodies. Histopathological changes may also be present in a number of other organs including liver, lungs, pancreas, bursa of Fabricius and thymus (Itakura and Carlson, 1975; Gross and Domermuth, 1976; Fadly and Nazerian, 1982 ). Susceptibility of turkeys to HE is influenced by their age at the time of exposure to HEV. Generally, poults younger than 2 weeks of age are refractory to clinical HE (Fadly and Nazerian, 1982, 1989; Domermuth and Gross, 1984). The early age resistance lasts longer in pours that hatch with maternal

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antibodies to HEV than in those without such passively acquired antibodies. For instance, in one experiment (Fadly and Nazerian, 1989), poults from maternal antibody positive and maternal antibody negative groups were compared for susceptibility to virulent HEV at 2, 6 and 8 weeks of age. Although the maternal antibody levels reached undetectable levels by about 6 weeks of age, the incidence of HE was lower in the poults from the maternal antibody positive groups than in the poults from maternal antibody negative groups at all age levels tested. The mechanism of continued resistance beyond the time when all passively acquired antibody has disappeared is not known. The target cells of HEV replication have not been clearly identified. The virus-induced inclusions have been detected in reticuloendothelial cells thus indicating that HEV replicates in these cells. The role of lymphoid cells in the pathogenesis of HE is not clear, although circumstantial evidence indicates that lymphoid cells may be involved. HEV replicates in vitro in Marek's disease virus transformed lymphoblastoid cells and causes extensive in vivo lymphoid cell necrosis in the bursa, spleen and other lymphoid organs. B cell deficiency induced by neonatal treatment with cyclophosphamide abrogated clinical HE in turkeys (Fadly and Nazerian, 1982 ). This result indicates that B lymphocytes may play a role in the pathogenesis of HE. The spleen appears to be a critical target organ for the clinical expression of HE because splenectomy prior to exposure to virulent HEV prevented detectable enteritis (Ossa et al., 1984). How the spleen mediates development of enteritis remains to be elucidated. EFFECT ON IMMUNE COMPETENCE

Laboratory studies have revealed that infection of turkeys with virulent HEV may compromise T cell functions. In one study (Nagaraja et al., 1982a) cultures of whole blood cells from turkeys infected with HEV responded poorly to the T cell mitogens, concanavalin A and phytohemagglutinin. The mitogen responses were lower in HEV-infected turkeys than in virus-free turkeys for up to 7 weeks following infection with virulent HEV. In another study (Nagaraja et al., 1985 ), infection with HEV caused a transient inhibition of the mitogenic response of whole blood cells to PHA. The inhibition of mitogenic response was evident at 1 week following HEV but not at 2 weeks or later, Infection with HEV may also inhibit humoral immune responses. Antibody response against sheep erythrocytes was lower in HEV-infected turkeys than in virus-free turkeys (Nagaraja et al., 1982b). HEV infection also inhibited primary and secondary antibody levels against Newcastle disease virus vaccine (Nagaraja et al., 1985). A field observation that HEV could be isolated from a flock of turkeys undergoing an outbreak of colibacillosis indicated that the immunodepression caused by HEV may have exacerbated colibacillosis (Sponenberg et al.,

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1985 ). In s u b s e q u e n t l a b o r a t o r y studies, i n f e c t i o n o f t u r k e y s w i t h H E V sign i f i c a n t l y i n c r e a s e d the s e v e r i t y o f d i s e a s e c a u s e d b y e x p e r i m e n t a l e x p o s u r e to Escherichia coli (Domermuth a n d L a r s e n , 1984). T h u s , b o t h l a b o r a t o r y a n d field d a t a suggest t h a t H E V is i m m u n o d e p r e s sive for t u r k e y s . Little h a s b e e n r e p o r t e d o n t h e m e c h a n i s m ( s ) b y w h i c h H E V mediates immunodepression.

REFERENCES Domermuth, C.H. and Gross, W.B., 1984. Hemorrhagic enteritis and related infections. In: M.S. Hofstad, H.J. Barnes, B.W. Calnek, W.B. Reid and H.W. Yoder, Jr. (Editors), Diseases of Poultry. Iowa State University Press, Ames, IA, 8th edn., pp. 511-516. Domermuth, C.H. and Larsen, C.T., 1984. Vaccination against hemorrhagic enteritis of turkeys: an update. J. Am. Vet. Med. Assoc., 185" 336. Domermuth, C.H., Harris, J.R., Gross, W.B. and DuBose, R.T., 1979. A naturally occurring infection of chickens with a hemorrhagic enteritis/marble spleen disease type of virus. Avian Dis., 23: 479-484. Fadly, A.M. and Nazerian, K., 1982. Evidence for bursal involvement in the pathogenesis of hemorrhagic enteritis of turkeys. Avian Dis., 26: 525-533. Fadly, A.M. and Nazerian, K., 1989. Hemorrhagic enteritis of turkeys. Influence of maternal antibody and age at exposure. Avian Dis., 33" 778-786. Fadly, A.M., Nazerian, K., Nagaraja, K. and Below, G., 1985. Field vaccination against hemorrhagic enteritis of turkeys by a cell-culture live-virus vaccine. Avian Dis., 29: 768-777. Fasina, S.O. and Fabricant, J., 1982. Immunofluorescence studies on the early pathogenesis of hemorrhagic enteritis virus infection in turkeys and chickens. Avian Dis., 26:158-163. Gross, W.B. and Domermuth, C.H., 1976. Spleen lesions of hemorrhagic enteritis of turkeys. Avian Dis., 20" 455-466. Itakura, C. and Carlson, H.C., 1975. Pathology of spontaneous hemorrhagic enteritis of turkeys. Can. J. Comp. Med., 39: 310-315. Larsen, C.T., Domermuth, C.H., Sponenberg, D.P. and Gross, W.B., 1986.Colibacillosis of turkeys exacerbated by hemorrhagic enteritis virus. Laboratory Studies. Avian Dis., 29: 729732. Nagaraja, K.V., Patel, B.L., Emery, D.A., Pomeroy, B.S. and Newman, J.A., 1982a. In vitro depression of the mitogenic response of lymphocytes from turkeys infected with hemorrhagic enteritis virus. Am. J. Vet. Res., 43:134-136. Nagaraja, K.V., Emery, D.A., Patel, B.S., Pomeroy, B.S. and Newman, J.A., 1982b. In vitro evaluation of B-lymphocyte function in turkeys infected with hemorrhagic enteritis virus. Am. J. Vet. Res., 43: 502-504. Nagaraja, K.V., Kang, S.Y. and Newman, J.A., 1985. Immunosuppressive effect of virulent strain of hemorrhagic enteritis virus in turkeys vaccinated against Newcastle disease. Poult. Sci., 64: 588-590. Ossa, J.E.,'Alexander, J. and Schurig, G.G., 1984. Role of splenectomy in prevention of hemorrhagic enteritis and death from hemorrhagic enteritis virus in turkeys. Avian Dis., 27:1106Ill1. Sponenberg, D.P., Domermuth, C.H. and Larsen, C.T., 1985. Field outbreaks of colibacillosis of turkeys associated with hemorrhagic enteritis virus. Avian Dis., 29" 838-842. van den Hurk, J.V., 1990. Efficacy of a virulent hemorrhagic enteritis virus propagated in tur-

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key leukocyte cultures for vaccination against hemorrhagic enteritis in turkeys. Avian Dis., 34: 26-35. Yamaguchi, S., Imada, T. and Kawamura, H., 1982. Survey on antibody against hemorrhagic enteritis virus among chicken flocks in Japan. Natl. Inst. Anim. Health Q., 22:180-181. Zhang, C. and Nagaraja, K.V., 1989. Differentiation of avian adenovirus type-II strains by restriction endonuclease fingerprinting. Am. J. Vet. Res., 50: 1466-1470.

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 i...
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