Hemorrhagic Enteritis of Turkeys and Marble Spleen Disease of Pheasants: Introduction

Hemorrhagic enteritis is an acute GI disorder affecting young turkeys. In its most severe form, it is characterized by depression, bloody droppings, and substantial mortality. Marble spleen disease is an acute respiratory disease of pheasants characterized by depression, enlarged mottled spleens, pulmonary congestion, and death. Both diseases are caused by similar viruses. Species-specific differences in clinical response are thought to be related to differences in the target organs for anaphylaxis and variation in viral pathotype. Infection with less virulent pathotypes in either host may often go undetected until secondary bacterial infections begin to develop as a result of viral-induced immunosuppression.

Etiology and Epidemiology:

The etiologic agent is a nonenveloped, icosahedral DNA virus, 70-90 nm in diameter. It is a member of the family Adenoviridae and has recently been assigned to the new genus Siadenovirus . Based on differences in clinical presentation within host species, numerous viral pathotypes appear to exist. These differ slightly at the DNA level but are indistinguishable serologically.

Both hemorrhagic enteritis and marble spleen disease are geographically widespread and considered endemic in areas where turkeys and pheasants are raised commercially. The usual route of infection is oral, and virus is often introduced onto previously uninfected premises via personnel or equipment contaminated with infectious feces. Turkey poults and pheasants <4 wk of age are resistant to infection due to age-related resistance or, more commonly, the presence of maternal antibody. The virus may survive under moist conditions (ie, in litter) well beyond the refractory period. As infection begins to cycle through a flock, large quantities of virus are shed in the feces, which facilitates rapid spread through susceptible birds. Morbidity usually approaches 100% for both hemorrhagic enteritis and marble spleen disease.

Clinical Findings:

In commercial operations, hemorrhagic enteritis typically affects turkeys 6-12 wk of age. In outbreaks involving highly virulent pathotypes, clinical signs can include depression, pallor, and bloody droppings. Acute mortality ranges from <1% to 60% with an average of 10-15% over a 2-wk period. Birds that survive the acute phase experience a transient immunosuppression related to the lymphotrophic, lymphocytopathic nature of the virus. This often manifests itself in the form of secondary bacterial infections, eg, colibacillosis, Colisepticemia: Introduction) ~10-14 days after initial exposure to the virus. Thus, a second peak in mortality, potentially overlapping the first, may be seen and, in less virulent outbreaks, may actually dominate the clinical picture. The second wave of mortality often lasts 2-4 wk and is characterized by lesions commonly associated with bacterial respiratory disease or septicemia, eg, fibrinopurulent pneumonia, airsacculitis, pericarditis, peritonitis, perihepatitis, hepatomegaly, and splenomegaly. Concomitant or prior exposure to Newcastle disease virus (Newcastle Disease), Bordetella avium (Bordetellosis: Introduction), or Mycoplasma spp ( Mycoplasmosis: Introduction) is known to exacerbate the problem. Similar multiple agent interactions have been implicated in mortality associated with the use of vaccines for hemorrhagic enteritis.

Marble spleen disease typically affects pheasants 3-8 mo of age. Onset is acute, with dyspnea, asphyxiation, and sudden death occurring as a result of pulmonary congestion and edema. Mortality is commonly 2-3% but can reach 15%. Secondary bacterial infections as a result of immunosuppression have also been noted.

Lesions:

Necropsy of moribund or dead birds infected with hemorrhagic enteritis virus reveals gross congestion and intraluminal hemorrhage in the proximal small intestine. The spleen is usually enlarged, friable, and mottled, except in birds that have hemorrhaged extensively. Histopathologic changes in the duodenum include congestion, hemorrhage, and necrosis of the intestinal epithelium. This lesion in particular is thought to be the result of a virally induced, cytokine-mediated anaphylactic reaction, with the GI tract being considered the target shock organ in the turkey. Basophilic intranuclear inclusions can be found in lymphocytes and macrophages in a variety of tissues but predominantly in the spleen where lymphoreticular hyperplasia and lymphoid necrosis are noted.

Hemorrhagic enteritis, intestinal hemorrhaging, turkey

Hemorrhagic enteritis, enlarged spleen, turkey

On histopathologic evaluation of pheasants with marble spleen disease, flooding of the atria and tertiary bronchi with fibrin and RBC, as well as generalized vascular congestion and focal necrosis, are often seen in the lung. As with hemorrhagic enteritis, this response may be anaphylactic in nature, with the lung being considered the target shock organ in the pheasant. Splenomegaly with lymphoreticular hyperplasia and lymphoid necrosis also occur and are the characteristic lesions for which marble spleen disease is named. Basophilic intranuclear inclusions may be found in a variety of tissues excluding the GI tract with the highest concentration of virus again being found in the spleen.

Diagnosis:

Diagnosis of virulent outbreaks of hemorrhagic enteritis or marble spleen disease can often be made based on clinical signs and gross lesions. Confirmation is by histopathology and the presence of seroprecipitating virus in the spleen as determined by agar gel immunodiffusion. PCR techniques to detect hemorrhagic enteritis viral DNA in tissue have also been described and are in regular use in select laboratories. To determine whether hemorrhagic enteritis or marble spleen disease is a predisposing factor in cases of bacterial respiratory disease or septicemia, or to verify a primary diagnosis, acute and convalescent sera (3 wk apart) can be tested using either agar gel immunodiffusion or ELISA. In turkeys, differential diagnoses include colibacillosis, pasteurellosis, paratyphoid, and erysipelas. Reticuloendotheliosis or lymphoproliferative disease should be considered when lymphoreticular hyperplasia is the predominant lesion. GI lesions without splenic involvement should evoke consideration of other viral, bacterial, parasitic, and toxic enteritides of turkeys. In pheasants with acute respiratory disease, differential diagnoses include Newcastle disease, avian influenza, and in the case of birds reared in confinement, gaseous toxins.

Treatment, Control, and Prevention:

Virulent outbreaks of hemorrhagic enteritis have been successfully treated and controlled by SC injection of exposed birds with 0.5-1.0 mL of antiserum obtained from recovered flocks. It is presumed that a similar approach may be effective for pheasants. In anticipation of secondary bacterial complications, antibiotics may be used, but if possible, an informed choice should be made based on current antibiotic susceptibility profiles for locally obtained Escherichia coli isolates. In addition to good biosecurity, prevention hinges on the use of vaccines administered in the water at ~4-5 wk of age. Commercially available tissue culture products and crude splenic preparations containing avirulent isolates produce lifelong protection. Vaccines intended for use in turkeys should not be used in pheasants, and vice versa, because the avirulent isolates used for vaccinating one species are typically virulent in the other. Due to potential for interaction with other agents, including live vaccines, regular disease monitoring and careful integration of hemorrhagic enteritis and marble spleen disease vaccines into flock vaccination protocols is encouraged. Intuitively, vaccines should not be administered to birds exhibiting signs of illness or within 2 wk of any other vaccination.