10-week old, male, turkey, (Meleagris gallopavo).One of three turkeys found dead without
premonitory signs on one day from a large flock of commercial fattening birds.
Further individual birds also died over the following two weeks.
In good body condition, severe diffuse
hemorrhagic enteritis and splenomegaly. Pale mottling of spleen by multifocal
0.5 to 3mm diameter, white, round to irregularly-shaped lesions.
Spleen: Multifocal to
coalescing areas of necrosis in white pulp area containing eosinophilic
amorphous material together with moderate numbers of admixed heterophils, ma-crophages,
lymphocytes and plasma cells. There is accompanying diffuse severe vascular
congestion. Numerous large cells (approximately 15 mm in
diameter) contain large nuclei (approximately 12 mm in diameter) which in turn
exhibit large basophilic intranuclear inclusions with associated chromatin
Necrotizing splenitis: acute; multifocal to coalescing; severe, with
basophilic in-tranuclear inclusions consistent with a diagnosis of turkey
No significant bacteria
isolated from spleen or small intestine following aerobic and anaerobic culture
on blood agar. PCR on splenic samples detected turkey hemorrhagic enteritis
gross and histopathological findings are consistent with a diagnosis of turkey
hemorrhagic enteritis (THE) disease of turkeys caused by infection with THEV.11
This was confirmed by PCR. HE affects growing turkeys resulting in depression,
bloody diarrhea, splenomegaly, immunosuppression and death.7 The
most consistent postmortem finding is splenomegaly with a multifocal to
coalescing splenitis with individual cell necrosis and large intranuclear
inclusions affecting lymphocytes.1, 11
Intestinal lesions and the scale of the mortality depends at least in part on the virulence of the THEV strain.9,10 THEV is classified as a type II adenovirus, of the family Adenoviridae, and has been further classified as a member of the more recently formed genus Si-adenovirus.1,4,11 It was originally identified in the USA, where it has been widely reported.11 The virus spreads via horizontal transmission including the oral route and rapidly replicates in the spleen of poults.12 A necrotizing splenitis is frequently described in the splenic white pulp13 with targeting of macrophages and particularly IgM-bearing B-lymphocytes.12,13 Infected B-lymphocytes and macrophages undergo both necrosis and apoptosis.9 Although the pathogenesis is incompletely understood infection of turkeys with virulent strains of THEV results in hemorrhage into the lumen of the duodenum and jejunum by erythrocytes diapedesis without obvious attendant vascular injury.9
Splenitis, histiocytic, diffuse, severe with lymphoid depletion and intrahistiocytic,
intranuclear viral inclusion bodies.
Adenoviruses in avian or mammalian species may occur as
asymptomatic infections or as primary pathogens as seen in this case of THEV.
Previously two genera of adenovirus existed, Mastadenovirus and Aviadenovirus,
but the adenoviridae family was revised in 2005 and now includes two
additional genera Sia-denovirus and Atadenovirus, the former of
which includes THEV.6 The Aviadenovirus genera, which was
previously designated as group I avian adenovirus, includes many of the
pathogenic avian adenovirus diseases including inclusion body hepatitis, quail
bronchitis virus and hydropericardium syndrome. Siadenovirus, which was
pr-eviously designated as group II avian adenovirus, in addition to THEV
includes MSD in pheasants and splenomegaly virus of chickens, another disease
very similar to THEV and MSD. This genera is di-stinguished genetically by the
presence of a gene that encodes for sialidase (for which it is named), and also
includes an adenovirus of frogs.5 Atadenovirus, which was pr-eviously
designated as group III avian adenovirus, includes egg drop syndrome, which is
characterized by decreased egg production and thin-shelled eggs; ducks and
geese are the natural hosts. Atadenovirus also includes viruses which
affect mammals and reptiles.5,6
Adenoviruses of the Mastadenovirus genera include the majority of common mammalian adenoviruses and do not cause disease in avian species. The age of affected turkeys is approximately 4 weeks and older, with most infections occurring between 6 11 weeks; the course of clinical disease is approximately 7-10 days. Mortality rates may exceed 60%. Due to immunosuppression and secondary bacterial infections or co-infections, such as with E. coli, the course of disease and severity of losses can be exacerbated. Infection and recovery, as well as va-ccination, provides protection against subsequent challenge.8 It is postulated that persistent infection or latency may occur within macrophages or B-lymphocytes in birds infected with avirluent strains of THEV, which are used in live virus vaccines.2
The differential diagnosis list for the splenic lesions includes lymphoid neoplasia and bacteremia associated with infections such as E. coli, P. multocida and E. rhusiopathiae.8 A similar condition occurs in confinement-raised pheasants of approximately 3-8 months of age due to infection with an indistinguishable virus, and the condition is known as marble spleen disease (MSD). These two viruses are nearly genetically identical, although the pr-esentation of the disease in these respective species has some distinctions. In pheasants, MSD is characterized by diffuse necrotizing splenitis with hemorrhage and loss of architecture, but generally presents as a respiratory condition in naturally infected birds. Gross lesions may include congested lungs in addition to the splenic changes.8 THEV and MSD affect a slightly different age range of fowl but retain many similar features in regards to their effect on the spleen. Macrophages and B lymphocytes are the main target of both THEV and MSD as discussed above and although viral replication chiefly takes place within the spleen, virus may also be found in the intestine, bursa of Fabricius, thymus, liver, kidney and lung.
Conference participants described multifocal areas of pallor characterized by necrosis and loss of B lymphocytes within follicles / white pulp. There is extensive histiocytic infiltration of the spleen, primarily surrounding the vascular tree within the white pulp, and histiocytes frequently contain pale basophilic intranuclear viral inclusion bodies. Inclusion bodies are id-entified also within morphologically re-cognizable lymphocytes, although no IHC was performed to definitively establish the range of cell targets. The moderator com-mented about the histiocytic infiltration around splenic arteries, which is suggestive of the pathogenesis of THEV. The virus has a cytopathic effect on B lymphocytes and also replicates within macrophages, and transient immunosuppression occurs in infection by both virulent and avirulent strains.2,8 In response to infection, there is a large influx of macrophages, as well as T-lymphocytes in an attempt to clear the virus.8 Conference participants discussed the diagnosis of inflammatory splenitis vs. infiltrative and or necrotizing disease of the spleen. The moderator led a discussion around other features of THEV infection including the rapid clinical course and characteristic presence of hemorrhagic feces just prior to death, for which it is appropriately named. The hemorrhage is thought to be secondary to endothelial disruption and not due to viral destruction.2 Grossly, the spleen appears enlarged, friable and mottled.
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