Ranikhet Disease of Poultry

RANIKHET DISEASE IN POULTRY
Dr. SANJIV KUMAR

ASSTT. PROFESSOR,
DEPTT. OF PATHOLOGY, BVC, PATNA
INTRODUCTION
• Newcastle disease is an acute highly contagious rapidly spreading viral

disease of domestic poultry and many other bird species.
• It is a worldwide problem that presents primarily as a respiratory disease,

but depression, nervous manifestations, or diarrhoea may be the
predominant clinical form with variable mortality.
• Attenuated strain of the Newcastle virus can be used as an anticancer agent.
• Zoonotic importance as causes transitory conjunctivitis in humans.

HISTORY
• The first outbreak of the disease was recorded in 1926, in

Java, Indonesia and in 1927 by Doyle in Newcastle -upon-
Tyne , England .
• In India , the disease was first recorded at Ranikhet in Kumoan
hills (Nainital District, Uttaranchal) by Edward in 1927. Hence
the name Ranikhet disease.
ETIOLOGY
Paramyxovirus type1 (PMV-1 belongs to the genus

Avulavirus, family Paramyxoviridae).
It is a negative-sense, single-stranded RNA virus.

PATHOTYPES
Based on the disease produced in chickens, NDVs have been classified into five
pathotypes:
o Viscerotropic velogenic: The NDVs cause a highly virulent form of the
disease. Haemorrhagic lesions are characteristically present in the intestinal tract.
o Neurotropic velogenic: These NDVs cause high mortality following
respiratory and nervous signs.
o Mesogenic: These NDVs cause low mortality following respiratory and some
times nervous signs.
o Lentogenic: These respiratory NDVs cause mild or inapparent respiratory
infection.
o Asymptamatic: The enteric NDVs cause inapparent enteric infection.

HOST
• ND occurs in almost all avian species.
• Chickens are the most susceptible.
• Waterfowl the least susceptible.
• Have zoonotic importance.

EPIDEMIOLOGY
• Virulent NDV strains are endemic in poultry in most of Asia,

Africa, and some countries of North, Central, and South
America.
• USA and Canada are free of those strains.
Transmission
• Infected birds shed virus in exhaled air, respiratory discharges

and feces.
• Virus may also be present in eggs laid during clinical disease
and in all parts of the carcass during acute virulent infections.
• Chickens are readily infected by aerosols and by ingesting
contaminated water or food.
• In infective faeces, the virus are present in high titre,
• Transfer of virus, especially by the movement of people and

contaminated equipment is the main method of spread between
poultry flocks.
PATHOGENESIS
• The NDV genome encodes nucleus capsid protein (NP), fusion

proteins (F), phosphoprotein (P), matrix protein (M),
hemagglutinin neuraminidase (HN), and large RNA
dependent polymerase protein (L).
• The matrix proteins are part of a layer below the viral
membrane and participate in viral assembly. The hemagglutinin
neuraminidase (HN) and fusion (F) glycoproteins form part of
the viral external envelope and participate in viral infection.
• The cleavage site of the F protein determines the virulence.
• In replication, a precursor glycoprotein (F0) is produced, this must be cleaved
into F1 and F2 to exhibit virulence and become infectious.
• This cleavage which is a part of post-translational modification is facilitated by
host cell proteases.
• The cleavability of the F0 molecule is linked with the virulence.
• It has been studied that the F0 molecules of viruses if virulent and cleaved by
host proteases it would damage vital organs of host.
• In contrast, F0 molecules in viruses of less virulence leads to restriction in
growth of as it has less sensitivity towards host proteases thus it would grow
only in particular host types.
• At the cleavage site in virulent viruses the multiple basic amino acids are
present.
CLINICAL FINDINGS
• Clinical manifestations vary from high morbidity and
mortality to asymptomatic infections.
• The severity of an infection is dependent on the nature of the
infecting virus, its virulence and the age, immune status, and
susceptibility of the host species.
• Onset is rapid, the incubation period for the disease ranges
from 4 to 6 days. .
• Spread is slower if the fecal-oral route is the primary means of
transmission, particularly for caged birds.
• Young birds are the most susceptible.
Observed signs depend on whether the infecting virus has a
predilection for respiratory, digestive, or nervous systems.
Velogenic viruses
Mesogenic viruses
(High virulent)
(Moderately virulent)
• Sudden death • Severe respiratory signs
• Depression • Decreased nervous signs
• Prostration • Increased drop in egg
• Diarrhoea production
• Facial edema • Mortality - 10%
• Cyanosis of comb
• Mortality - 100%
Lentogenic or low virulent viruses
 Mild respiratory sign for short
period
LESIONS
Macroscopic lesions (Velogenic form)

• Young chickens and those dying peracutely may have no lesions
especially in birds that only show nervous signs.
• Remarkable lesions are usually observed only with VVND and
they include
• Haemorrhage in intestine
• Petechial haemorrhage in proventiculus
• Enlarged and necrotic caecal tonsils
• Necrosis and haemorrhage in lymphoid aggregates in intestine
• Splenic necrosis on capsular surface
• Nervous system lesions are not seen regardless of pathotypes
The lesions in birds infected with lower virulence NDV strains may be
limited to respiratory tract.
MICROSCOPIC LESIONS
• Is variable, they are, therefore, of no value in the diagnosis.
• Lesions in the central nervous system are those of non-
purulent encephalomyelitis with neural degeneration, foci
of glial cells, perivascular infiltration of lymphocytes, and
proliferation of endothelial cells.
• Regressive changes in the lymphopoietic system consist of
disappearance of lymphoid tissue.

• Necrotic lesions are found through out the spleen.
• Marked degeneration of the medullary region of bursa.
• The haemorrhagic necrotic lesions in the intestinal tract
develop in lymphoid aggregates.
• Lesions in the upper respiratory tract may be severe and
related to the degree of respiratory distress.
• Lesions may extend through out the length of the trachea.
Cilia may be lost within 2 days of infection.
• Edema, cell infiltration, and increased thickness and density of
the air sacs may occur.
DIAGNOSIS
• None of the clinical signs or lesions can be regarded as specific or

pathognomonic.
• Confirmation test by Haemagglutination-inhibition test, Single radial

immunodiffusion, Agar gel precipition, Virus neutralization (VN) in chick
embryo, ElLISA and plaque neutralization.
Samples
o Live birds - Both cloacal/ faeces or tracheal swabs,

regardless of clinical signs.
o Dead birds - Intestines, intestinal contents and trachea

should be collected together with affected organs and tissues.
DIFFERENTIAL DIAGNOSIS
Avian influenza,
Infectious laryngotracheitis,
Infectious bronchitis,
EDS-76,
Infectious coryza,
Fowl cholera,
Salmonellosis
Some of their lesions resembles those of ND.
PREVENTION
• Live lentogenic vaccines, chiefly B1 and LaSota strains, are
widely used and applied in drinking water or by spray, or, via
the nares or conjunctival sac.
• Healthy chicks are vaccinated as early as day 1-4 of life.

However, delaying vaccination until the second or third week
avoids maternal antibody interference with an active immune
response.
• Oil-adjuvanted inactivated vaccines are also used following

live vaccine in breeders and layers and may be used alone in
situations where use of live virus may be contraindicated.

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RANIKHET DISEASE IN POULTRY

Dr. SANJIV KUMAR

• Newcastle disease is an acute highly contagious rapidly spreading viral

• It is a worldwide problem that presents primarily as a respiratory disease,

• Attenuated strain of the Newcastle virus can be used as an anticancer agent.

• Zoonotic importance as causes transitory conjunctivitis in humans.

• The first outbreak of the disease was recorded in 1926, in

Paramyxovirus type1 (PMV-1 belongs to the genus

It is a negative-sense, single-stranded RNA virus.

o Viscerotropic velogenic: The NDVs cause a highly virulent form of the

disease. Haemorrhagic lesions are characteristically present in the intestinal tract.

o Neurotropic velogenic: These NDVs cause high mortality following

respiratory and nervous signs.

times nervous signs.

o Lentogenic: These respiratory NDVs cause mild or inapparent respiratory

o Asymptamatic: The enteric NDVs cause inapparent enteric infection.

• ND occurs in almost all avian species.

• Chickens are the most susceptible.

• Waterfowl the least susceptible.

• Have zoonotic importance.

• Virulent NDV strains are endemic in poultry in most of Asia,

• Infected birds shed virus in exhaled air, respiratory discharges

• Transfer of virus, especially by the movement of people and

• The NDV genome encodes nucleus capsid protein (NP), fusion

into F1 and F2 to exhibit virulence and become infectious.

• This cleavage which is a part of post-translational modification is facilitated by

host cell proteases.

• The cleavability of the F0 molecule is linked with the virulence.

host proteases it would damage vital organs of host.

• In contrast, F0 molecules in viruses of less virulence leads to restriction in

only in particular host types.

Macroscopic lesions (Velogenic form)

• Is variable, they are, therefore, of no value in the diagnosis.

• Lesions in the central nervous system are those of non-

purulent encephalomyelitis with neural degeneration, foci

of glial cells, perivascular infiltration of lymphocytes, and

proliferation of endothelial cells.

• Regressive changes in the lymphopoietic system consist of

disappearance of lymphoid tissue.

• None of the clinical signs or lesions can be regarded as specific or

• Confirmation test by Haemagglutination-inhibition test, Single radial

o Live birds - Both cloacal/ faeces or tracheal swabs,

o Dead birds - Intestines, intestinal contents and trachea

• Healthy chicks are vaccinated as early as day 1-4 of life.

• Oil-adjuvanted inactivated vaccines are also used following

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