Disease caused by Picornavirus

• L. pico = small; rna = ribonucleic acid

• Disease caused by Picorna Virus:
• Enterovirus: Avian encephalomyelitis
• Avian nephritis, Duck hepatitis
• Turkey viral hepatitis
• non-enveloped, +ve sense SS RNA
• serologically different, but similar in
morphology and physical and chemical
properties.
• only physical difference between genera is pH
stability.
 Avian Encephalomyelitis
• Also known as Epidemic Tremor
• It is an infectious viral disease of young chickens,
• turkeys, pheasants, and quail characterized by
ataxia and rapid tremors, especially of head & neck
• All strains appear to be antigenically uniform, but
there are variations in neurotropism and virulence.
• Field strains are mainly enterotropic, whereas egg-
adapted strains are mainly neurotropic
Spread:
Ingestion is the usual route of entry
Transmitted horizontally by fomites and mechanical
carriers
Vertical transmission is a very important means of
virus dissemination
Virus shed in faeces & quite resistant
Infected birds are enteric carriers & excrete virus
Pathogenesis:
• Significant differences between egg-adapted and field
strains in pathogenesis
• young chicks exposed orally to field strains, primary
infection of alimentary tract, especially duodenum, is
rapidly followed by viraemia, & subsequently in other
visceral organs, skeletal muscle & finally CNS
• Purkinje cells & molecular layer of the cerebellum are
favoured sites of virus replication
• Persistence of infection is common in CNS, pancreas
and alimentary tract.
• CNS and pancreas are the only sites uniformly infected
by egg-adapted strains
• Age at exposure is important in pathogenesis
• Birds infected at 1 day of age generally die,
whereas 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
(ended) the age resistance
• This indicated that humoral immunity was the basis
of age resistance
• recovered birds develop circulating antibodies
capable of neutralizing the virus
Signs:
• seen in chicks of 1-2 week age
• Dull expression of eyes, progressive ataxia from
incoordination of the muscles
• chicks show an tendency to sit on hocks, Finally
come to rest, or fall on their sides
• Tremors of head & neck followed by inanition,
Prostration and finally death
• Some chicks may survive and grow to maturity
• Survivors may later develop blindness from an
opacity giving a bluish discoloration to the lens
Lesions:
• Only gross lesions in chicks are whitish areas in
muscles of ventriculus, which are due to masses of
infiltrating lymphocytes
• No gross lesion in adult birds, except lens opacities
• Microscopically, main changes CNS & some viscera,
PNS not involved
• In CNS, lesions are those of a disseminated, non-
purulent encephalomyelitis & ganglionitis of the
dorsal root ganglia
• Most common finding is striking peri vascular
infiltration in all portions of the brain & spinal cord
except cerebellum
• Microgliosis occurs as diffuse and nodular
aggregates
• Another lesion of pathognomonic importance is
central chromatolysis of the neurons in the nuclei
of the brain stem, particularly the medulla
oblongata
• Dense Iymphocytic foci (aggregates) in
provetriculus is the pathognomonic lesion
(unfortunately also occur in MD)
• Diagnosis:
• History, clinical sign, absence of gross lesion
• microscopic lesion in brain, SP & visceral organs
• VN, ELISA test at beginning
• Differentiated from nutritional encephalomalacia,
RD, MD
Treatment and Control
• No specific treatment
• Control by vaccination in the parents
• Live and attenuated vaccine are available
• Live vaccine widely used
• Given to the parents between 10-16 weeks of age
through drinking water
• Also available in combination of fowl pox vaccine
and given by wing web prick method
 Avian Nephritis
• Caused by an enterovirus, is an acute, highly
contagious, typically subclinical disease of young
chickens that produces lesions in the kidneys. The
virus, called" avian nephritis virus (ANV)“
• First described in Japan in 1979
• morphology being 30 nm small round particles
• ANV is distinct from avian encephalomyelitis virus
and duck hepatitis viruses.
• Spread: occurs by direct or indirect contact
• most common method is ingestion of faecal
contaminated material
• vertical transmission has been suggested on the
basis of field observations
• Pathogenesis: Only young chickens are known to
develop clinical disease and distinct kidney lesions
• Virus is first detected in faeces within 2 days, with
maximum virus shedding at 4-5 days.
• Virus is widely distributed, with maximum titres in
the kidney and jejunum and lower titres in bursa of
Fabricius, spleen, and Iiver.
• Virus is consistently isolated from kidney, jejunum,
and rectum, but not from brain and trachea
• Signs: in day-old chicks is only transient diarrhoea,
but not all chicks show the signs
• Weight gain is depressed
• Broiler chickens, symptoms vary from none
(subclinical) to outbreaks of the so-called "runting
syndrome“ and "baby chick nephropathy"
• Lesions: Gross lesions in dead chicks are mild to
severe discoloration and swelling in kidneys, and
visceral urate deposits
• Chalk-like urate crystals are seen on the surface of
the peritoneum, heart and liver
• Microscopically, necrosis & deg. of epithelial cells
of PCT with infiltration of granulocytes.
• The degenerating epithelial cells show acidophilic
granules of various sizes in the cytoplasm
• Also, there is interstitial lymphocytic infiltration
and moderate fibrosis
• In the later stages, lymphoid follicles develop
• Virus particles and viral antigens can be
demonstrated in the degenerating epithelium by
electron microscopy, and also by
immunofluorescence.
 Duck Hepatitis
• It is a highly fatal, rapidly spreading viral infection
of young ducklings characterized primarily by
hepatitis
• It can be caused by any of three different viruses,
namely, duck hepatitis virus (DHV) types 1, 2 and 3
• Spread: Natural infection reported only in ducks
• Virus remains viable for many weeks in faeces
• Infection occurs by ingestion
• Egg transmission is not thought to occur
• Pathogenesis: In natural outbreaks, DH type 1
occurs only in young ducklings
• Adults apparently do not become ill and continue
in full production
• Chickens and turkeys are resistant
• Ducklings after oral exposure, have mottled livers,
and enlarged gallbladders and spleens
• Duck hepatitis virus type 1 can be isolated from
livers up to 17 days
• Signs: are peracute, and death usually follows
within an hour of their onset
• Affected birds are often in good condition
• Head is usually stretched upwards and backwards
• Morbidity is 100% and mortality rate 90%
• Highest losses occur in duckling below 7 days
• Lesions: Main lesions are in the liver, which is
enlarged and has a number of petechial and
ecchymotic haemorrhages
• In addition, fatty kidneys described as "duck fatty
kidney syndrome“
• Microscopically, primary changes in the acute
disease consist of necrosis of hepatic cells
• Survivors with more chronic lesions show
widespread bile duct hyperplasia
• Inclusion bodies are not found
 Turkey Viral Hepatitis
• It is a highly contagious usually subclinical disease
of turkeys, characterized by multifocal hepatic
necrosis, with or without pancreatic necrosis
• Outbreaks usually seen in turkeys under six weeks
• Transmission of infection occurs by both direct and
indirect contact.
• Faeces from infected turkeys is believed to be the
main source of virus transmission.
• Vertical transmission probably occurs.
• The disease is usually diagnosed only at PM
examination, when lesions are seen in liver and
sometimes in pancreas
• Liver lesions are macroscopic pale foci 1-2 mm in
diameter, occurring on the surface & in
parenchyma
• Focal necrosis of hepatocytes and infiltration with
mononuclear cells
• liver is usually enlarged