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Learning objectives

 To know the etiological factors and to understand the pathogenesis of Avian encephalomyelitis,
inclusion body hepatitis andhydropericardium syndrome
 To recognize the clinical signs manifested by the affected birds
 To become familiar with the macroscopic and microscopic lesions of the disease
 To learn the diagnostic methods to confirm the disease
 To know the basic mechanism of fluid accumulation (Heart) in Leechi disease.


 Avian encephalomyelitis (AE) is an infectious viral disease of young chickens, turkeys, pheasants,
and quail.
 It is characterised by ataxia and rapid tremors, especially of the head and neck. AE occurs
 The causative picornavirus is a single-stranded RNA (ss RNA). All strains appear to be antigenically
uniform, but there are variations in neurotropism and virulence.
 Field strains are mainly enterotropic, whereas egg-adated strains are mainly neurotropic.
 The immune status of the affected bird appears to be the main factor influencing the outcome of
 Antobodies are transferred to progeny from the dam through the egg, and can be demonstrated in egg
 Maternal antibodies can protect young birds against systemic infection.


 Ingestion is the usual route of entry. Virus is shed in the faeces for a period of several days and it is
quite resistant to environmental conditions.
 It appears that some birds are enteric carriers and excrete virus in their droppings. Infected litter is a
source of the virus which is easily transmitted horizontally by fomites and mechanical carriers. Vertical
transmission is a very important means of virus dissemination.
 Transmission of the virus occurs through the egg, from infected to susceptible stock.
 Egg transmission occurs during the period from the infection of susceptible laying hens to the
development of immunity, a period of 3-4 weeks.


 In young chicks exposed to field strains, primary infection of the alimentary tract, especially
duodenum, is rapidly followed by a viraemia, and subsequent infection of the pancreas and other
visceral organs (liver, heart, kidney, spleen) and skeletal muscle, and finally central nervous system.
 Viral antigen is abundant in the CNS, where Purkinje cells and molecular layer of the cerebellum are
the favoured sites of virus replication.
 Persistence of the viral infection is common in the CNS, alimentary tract and pancreas. CNS and the
pancreas are the only sites uniformly infected by egg-adapted strains.
 Age at exposure is especially important in the pathogenesis. Birds infected at one day of age
generally die, where as those infected at 8 days develop paresis (partial paralysis) but usually recover.
 Infection at 28 days causes no clinical signs. Bursectomy but not thymectomy abolished the age
resistance. This indicated that humoral immunity was the basis of age resistance.
 It is found that young age correlates with prolonged viraemia, persistence of virus in the brain, and
development of clinical disease


 AE usually makes it appearance when chicks are 1-2 week of age. Affected chicks first show a
slightly dull expression of the eyes.
 This is followed by a progressive ataxia from incoordination of the muscles, which may be detected
readily by exercising the chicks.
 As the ataxia becomes more pronounced, chicks show an inclination to sit on their hocks and finally,
they come to rest, or fall on their sides.
 : The lens of this bird's eye contains a large, roughly circular, well-demarcated pale blue area of
opacity .
 AE affected chicks ataxia, showing inclination to sit on their hocks and falling on their side
 Fine tremors of the head and neck may become noticeable.
 Ataxia usually progresses until the chick is incapable of moving about, and this stage is followed by
inanition (loss of vitality from lack of food and water), prostration, and finally death.
 Some chicks may survive and grow to maturity. Survivors may later develop blindness from an
opacity giving a bluish discolouration to the lens


 The only gross lesions in chicks are whitish areas in the muscles of ventriculus, which are due to
masses of infiltrating lymphocytes.
 In adult birds, no changes have been described except the lens opacities.
 Microscopically, the main changes are in the CNS and some viscera. The peripheral nervous system
is not involved.
 In the CNS, the lesions are those of a disseminated non-purulent encephalomyelitis, and a
ganglionitis of the dorsal root ganglia.
 The most finding is a striking perivascular infiltration in all portions of the brain and spinal cord,
except cerebellum. Microgliosis occurs as diffuse and nodular aggregates. The glial lesion is seen
chiefly in the cerebellar molecular layer.
 In the mid-brain, two nuclei- nucleus rotundus and nucleus ovoidalis – are always affected with a
loose microgliosis which is considered Pathognomonic. Another lesion of Pathognomonic importance
is central chromatolysis (axonal reaction) of the neurons in the nuclei of thebrain stem, particularly
those of the medulla oblongata.
 The dying neuron is surrounded by satellite oligodendroglia.Later, microglia phagocytize the
remains. The central chromatolysis is never seen without an accompanying cellular reaction.
 Visceral lesions appear to be hyperplasia of thelymphocytic aggregates. In the proventriculus, there
only a few small lymphocytes in the muscular wall.
 In AE, theses become dense lymphocytic foci (aggregates). This lesion is Pathognomonic.
Similar lesions occur in the ventriculusmuscle, but unfortunately they also occur in mArek’s disease.
 In the pancreas, circumscribed lymphocytic follicles are normal, but in AE thenumber increases
several times.
 In the myocardium, particularly in the atrium, there are aggregates of lymphocytes. These are
considered to be the result of AE.


 The clinical signs, absence of gross lesions, and microscopic findings in the brain, spinal cord and
visceral organs together with the absence of other virus infections and nutritional deficiencies affecting
the nervous system, are strongly suggestive of avian encephalomyelitis and are frequently used for
presumptive diagnosis.
 A definitive diagnosis requires demonstration of the virus by isolation and identification or by other
 Examination of smears from the brain, or cryostat sections stained by direct immunofluorescence
may also be used to demonstrate virus; positive results are confirmatory and often unreliable.
 A number of serological tests are available for determining the infection. These include virus
neutralization (VN) test, an indirect immunofluorescence test, immunodiffusion and an ELISA test.
Because of its specificity and sensitivity, rapidity of performance and amenability to large-scale
screening, the ELISA has replaced other tests for antibody, including the assessment of efficacy of


 It is necessary to consider other causes of neurological disorders such as nutritional encephalmalacia

and virus infections Ranikhet disease, and Marek’s disease.

Inclusion body hepatitis


 This disease is usually seen in meat-producing chickens aged 3-7 weeks. However it has also been
recorded in birds as young as 7 days old, and as old as 20 weeks.
 It is a rare disease in turkeys. It is characterised by a sudden increase in mortality. This is normally

between 2 and 10% of the flock but upto 30% has been described.
 Significant mortality persists for only a few days.

 The etiology of the disease has not been properly established. There is no separate
inclusion body hepatitis virus.
 Virtually every serotype of fowl Aviadenovirus group I have been isolated from the naturally
occurring cases of IBH.
 Furthermore, all the adenovirus serotypes produce hepatitis when young SPF chicks are inoculated
 Most experimental adenovirus infections produce basophilic inclusion bodies in the hepatocytes
whereas most natural cases produce eosinophilic intranuclear inclusion bodies. If adenoviruses are
involved in producing IBH, they appear to acta with some other factor.
 It has been suggested that immunosuppression produced by infectious bursal disease (IBD) helps
adenovirus to produce IBH. However many flocks undergoing combined infections with these
viruses remain healthy. Furthermore, outbreaks of IBH occurred in both Northern Ireland and
Newzealand before IBD virus was into those countries. Some outbreaks of disease described as IBH
closely resemble haemorrhagic syndrome/ infectious anaemia caused by Chicken anaemia virus.
 Outbreaks of IBH which occurred in Australia in the early 1990s differ significantly from the
above. They occurred in much younger chicks (i.e. under 3 weeks of the age), have caused higher
mortality and predominantly basophilic inclusion bodies were present in hepatocytes.
 Adenoviruses have been isolated from field cases and have reproduced the disease experimentally
in chickens. In India, the disease has appeared as seasonal, especially after monsoon, in the cold
season. The mycotoxin stress seems to be another predisposing factor besides IBD.


 The disease is characterised by sudden onset of mortality, reaching highest after 3-4 days, and
dropping on the 5th day, but some times continuing for 2-3 weeks.
 Morbidity is low. Sick birds adopt a crouching position with ruffled feathers and die within 48 hours,
or recover.
 Mortality may reach 10%, and sometimes as high as 30%. Overall feed conversion and weight gain
are usually decreased.
 Anaemia, jaundice of the skin and subcutaneous fat, haemorrhages in various organs, especially the
muscles, and bone marrow degeneration are usually present, but vary in severity.
 In some outbreaks the bone marrow lesions are most prominent, and it has been suggested that the
disease should be called, “Hepato-myeloporetic disease”.


 The liver in diseased birds is pale, friable and swollen, and frequently has haemorrhages. Petechial or
ecchymotic haemorrhagesmay be present in the liver and skeletal muscles.
 Microscopically, there is a diffuse and generalized hepatitis, with intranuclear inclusion bodies in the
hepatocytes, which are often eosinophilic.
 In the Australian outbreaks, basophilic inclusions predominated. Virus particles were detected only in
cells with basophilic inclusions.
 Eosinophilic inclusions were composed of fibrillar granular material. IN the New zealand outbreaks,
inclusions were eosinophilic.

 This depends on isolation and identification of the virus, and on serological tests. Specimens of
choice are faeces, pharynx, kidney, and affected organs, e.g. livers.
 Virus isolation is best achieved by inoculating both a 10% suspension of the affected organ and a a
faeces suspension into cell cultures. Chicken embryo liver or lung cells, or chick kidney cells, are all
sensitive but chick embryo fibroblatss are relatively insensitive.
 Antibody to the conventional adenovirus group antigen can be detected using the double
immunodiffusion (DID) test. The indirect immunofluorescent test is much more sensitive and rapid,
and is inexpensive. ELISA has been used to detect group antibodies, and it is expensive and
 Demonstration of eosinophilic intranuclear inclusion body in Haematoxylin and eosin staining in
the hepatocytes of chickens in naturally occurring inclusion body hepatitis is diagnostic.

2.Hydropericardium syndrome

 A viral disease, which was reported from Pakistan, affecting particularly broilers and the losses
varies from 10-20%.

 An incomplete virus which requires another adenovirus for its multiplication and growth is
the cause of this disease and certain viral diseases such as adenovirus, IBH, aflatoxicosis are said to be
responsible for the outbreak of this disease.


 The affected chicks died suddenly.

On postmortem examination

 The pericardial sac is filled with straw color fluid,

 Swollen and discolored liver,
 Swollen kidneys with distended ureters
 Due to malfunctioning of liver and kidneys, there is reduction in osmotic pressure resulting in
seepage of fluid in pericardial sac.
 The pericardial sac becomes distended due to excessive accumulation of fluid giving rise the
appearance of LICHI.

 No specific treatment of the disease.

 An auto vaccine, prepared form the liver of affected broiler chicks given at 2 or 3 week of age, is
found to be satisfactory in immunizing the chicks against this disease.
 Proper care should be taken for the control of contributing factors.