New Castle Disease/

Ranikhet Disease
• A viral disease of poultry, turkeys, wild and cage
birds
• Characterised by marked variation in morbidity,
mortality, signs and lesions
• Humans who come in close contact with New
Castle disease virus for the first time may
develop eye infection conjunctivitis
• Severity depends on the virulence of the virus
and host susceptibility
• IIn wild and caged birds, New Castle disease is
often is inapparent
Signs, when apparent are variable- gasping
respiration, diarrhoea and later CNS
involvement
• Sudden death are often first indication of
disease
 Etiology
• It is caused by Avian Paramyxovirus
serotype(PMV1)of Paramyxoviridae in the
genus Avulavirus
• It is a RNA virus
• Low virulent-lentogenic strain with few or no
signs or no mortality
• lo NDV are widely used as live vaccines
• Moderately virulent-mesogenic strains-
chicks:characterised by respiratory signs, with
concurrent CNS involvement and high mortality
layers: sudden drop in egg production with few or no
signs and little or no mortality
• High virulent(Velogenic) form of New Castle disease –
characterised by a short course, marked respiratory
signs, diarrhoea and paralysis followed by death
• Velogenic and mesogenic are classified as
virulent(vNDV)
 Pathotypes(5)
• Viscerotropic velogenic
• Neurotropic velogenic
• Mesogenic
• Lentogenic or respiratory
• asymptomatic
• Most enzootic strains are lentogenic or mesogenic
• Vaccines prepared from lentogenic strains tend to
produce immunity that is weak and of short duration
• So frequent vaccination is required to maintain
immunity
• More pathogenic mesogenic trains used for vaccine
tend to produce longer and stronger immunity but may
produce mortality
• New castle disease virus agglutinates erythrocytes of
many species including birds
 Epizootiology
• Virus containing excretions from infected birds,
including aerosals and faeces can contaminate
feed, water, footwear, clothing, tools, equipments
and environment(inhalation and ingestion)
• Exposure to any these sources of virus can transmit
• Infected poultry may spread the virus
• Eggs from infected hen may contain virus
• Sparrows, pigeons, doves, crows, owls, waterfowl –
virus isolated
• Chickens are highly susceptible to disease, turkeys not
developing severe signs
• Game birds: pheasants, patridges, quails and guinea fowl
and parrots vary in susceptibility
• Wild birds and waterfowl may harbour virus subclinically
• Ostriches and pigeons are susceptible
• Reported in crows, penguins
• Direct contact with secretions of infected birds
• Fomites feeder waterer farm equipments clothings egg
trays etc
 Clinical signs
Onset is rapid and signs appear 2-12 days
Adult chickens
Lentogenic New Castle
• May not produce any clinical signs or may produce mild
respiratory signs and decreased egg production in layers
• Eggs may be thin shelled, roughened or deformed
Mesogenic strain
• Sudden onset with mild depresion and anorexia
• Respiratory signs usually occur
• Mortality low or absent
Velogenic strain
• Signs vary according to tropism of virus
• Dyspnoea is marked
• Greenish /white watery diarrhoea,
conjunctivitis
• Nervous signs with paralysis, torticollis and
death in 2-3 days
• Sticky occular and nasal discharge
• Sharp drop in egg production, watery albumin,
misshapen, colour change, rough and thin
shelled
• Signs of CNS involvement-tremors, twisting of
headand neck, circling, paralysis, terminal
clonic spasms
• Mortality and morbidity high upto 100%
Young chicks
Lentogenic New Castle
• Broilers may show sudden onset on respiratory signs-
gasping, sneezing coughing, rales and nasal and lacrimal
discharge
• Some birds may have swollen heads
Mesogenic New Castle
• Sudden onset with marked depression and prostration
• Marked respiratory signs: gasping, coughing, hoarse
chirping, and nasal discharge
• Signs of CNS: star gazers, paralysis, prostration
• Trampling by pen mates and deathmortality
can vary upto 50%
Velogenic New Castle
• Signs are similar to those induced with
mesogenic strains in young birds
• Mortality very high 50-100%
• Course is acute
 Lesions
• Lentogenic and mesogenic Newcastle: usually
gross lesions are minimal in young or old birds
• There may be mild air sacculitis, conjunctivitis and
tracheitis
Velogenic strains: severe inflammation of trachea
and air sacs
• Haemorrhages or necrotic foci in the mucosa of
intestines involving lymphoid tissue
• Caecal tonsils often are necrotic and haemorrhagic
• Swelling of periorbital area or entire head
• Oedema of the interstitial/ peritracheal tissue
of neck specially at thoracic inlet
• Congestion and haemorrhage in the caudal
pharynx and tracheal mucosa
• Diptheretic membrane in te oropharynx,
trachea and oesophagus
• Haemorrhages(petichiae and ecchymotic)
occur in the mucosal surface of proventriculus
or in gizzard, serous membranes and mucosa
of oesophagus
• Oedema, haemorrhages or ulceration of
respiratory/ digestive lymphid tissue including
caecal tonsils and Peyer’s patches
• Spllen enlarged, friable and dark red
• Cage birds and wild birds often reveal no
lesions or mild lesions
• Turkeys also mild lesions
• Microscopically in CNS: CNS degeneration,
perivascular cuffing with lymphocytes and
endothelial hypertrophy
New Castle disease(Ranikhet disease)
New Castle Disease (contd)
 Diagnosis
• Clinical diagnosis based on history, signs, and
lesions
• Isolation of virus in chicken embryos
• HA and HI test
• VN
• Tissue culture
• Inoculatin of virus into known immune and known
susceptible virus
• FAT
 Avian Influenza
• A viral disease characterised by mass
mortality,respiratory signs, depression and
reduced feed and water intake
• Wild water fowl and shore birds are
asymptomatic carriers
• Two patho types of AI: the most common low
pathogenic (LPAI) and highly pathogenic AI(HPAI)
• HPAI- Fowl Plague- Highly virulent avian influenza
virus infection
 Occurence
• Throughout the world
• LPAI is common
• Outbreaks are sporadic
• HPAI Out breaks occurred in back yard poultry,
ducks, breeders and commercial chickens in
Nepal
 Etiology
• Type A influenza virus belonging to Orthomyxoviridae
family
• Influenza viruses have two surface antigens:
Haemagglutinin and neuraminidase
• Thse anigens give rise to subtypes eg H1N1
• There are 16 haemaglutinins(1-16) and 9
neuraminidases(1-9)
• Cross protection does not occur between subtypes
• Pathotypes:LPAI and HPAI
• H5 or H7 : major outbreaks
 Epizootiology
• Waterfowl and shore birds are the major natural
reservoir of influenza viruses
• Wild water fowls are asymptomatic may excrete
virus in faeces for long periods
• May be infected with more than one subtypes and
donot develop a detectable antibody response
• Live birds markets serve as a focal point for
gathering and many species of birds and sold to
other cities
• The continuous supply of susceptible poultry in
such markets enhances opportunity for viral
replication and mutation
• This inturn enhances the opportunity for viruses
to be carried back to susceptible poultry flocks
• Imported exotic birds
• Influenza virus shedding in poultry stops after
seroconversion
• AI virus is releases in respiratory secretions and
droppings of infeced birds
• The virus is labile in warm condition but can
survive for months in cold environment
• AI viruses can be transmitted from farm to farm
by direct and indirect contact
• Shoes, clothing, crates and other equipments by
movement of birds
• Poor Biosecurity enhaces the disease
 Clinical signs
• Most outbreaks are caused by LPAI viruses
• Signs vary with age species infected, virulence of virus
and concurrent infections
• Respiratory Signs: coughing, sneezing, rales,
lacrimation, sinusitis, nasal discharges and depression
• In layers decreased egg production and quality
• In young growing turkeys: subclinical or severe when
secondary infection with Pasteurella, E. coli or
bordetella occurs
• Morbidity and mortality are variable
• HPAI is a severe form seen in chickens
• Onset is sudden, the course is short, affected
birds quite ill, mortality can reach 100%
• Signs of respiratory, enteric or nervous
systems
• Diarrhoea oedema of head and face and
nervous disorders
 Lesions
• LPAI: mild to moderate inflammation of trachea,
sinuses, air sacs and conjunctiva
• In layers ovarian atresia and involution of oviduct
• Various degrees of congestive, haemorrhagic,
transudative and necrotic lesions
• HPAI: gross lesions in poultry most extensive and
severe
• Fibrinous exudate in air sacs, oviduct, pericardial
sac or on the peritoneum
• Small foci of necrosis in skin, comb and wattles, liver, kidney,
spleen and lungs
• Vascular damage: congestion, oedema, and haemorrhages at
many sites/ visceral organs
• Classical lesions: cyanosis and oedema of head, vesicles and
ulceration on the combs, oedema of feet,
• Blotchy red discoloration of shanks, petechiae in abdominal
fat and mucosal and serosal surfaces
• Necrosis and haemorrhages in ventriculus and proventriculus
• Sub cutaneous ecchymotic and petechial haemorrhages
Avian influenza
 Diagnosis
• History and signs and lesions suggestive of
LPAI and HPAI
• Screening test- Rapid test kit
• Pathotyping of virus
• HA test
• AGPT
• RT PCR