Transcript Clinical Signs and Symptoms

Newcastle Disease
Exotic Newcastle Disease, Pseudo-Fowl Pest,
Pseudo-Poultry Plague, Avian Pest, Avian
Distemper, Ranikhet Disease, Tetelo Disease,
Korean Fowl Plague, and Avian
Pneumoencephalitis
Newcastle Disease
• First identified in Newcastle in 1926, (Java)
• ND is contagious and fatal viral disease affecting most
species of birds (chickens, turkeys, pigeons, parrots, ducks,
geese, quails) and human.
• Considered the most serious poultry disease worldwide
• Respiratory tract and multi-organ systemic disease with a
near 100% mortality rate
• So rapidly acting that birds may die without showing any
clinical signs
• Endemic to Asia, the Middle East and Africa – where H5N1
Avian Influenza is also established
• Occurs in Europe, Australia and North America
Taxonomy of the NDV :
 Family: Paramyxoviridae.
 Subfamily: Paramyxovirinae.
 Genus: Avulavirus.
Characteristics:
 The virus is enveloped, roughly spherical, with a diameter
around 100-300 nm.
 Enveloped virus (containing lipid, CHO & protein).
 The genome is segmented & single stranded negative
sense RNA consisting of 15,186 nucleotides.
 Two specific virus proteins (hemagglutininneuraminidase & fusion protein) are the main proteins
found in the outer coat of the virus.
 Replication occurs in the cytoplasm of the host cell.
 Affected species; birds & human.
 Morbidity; Up to100% & Mortality; 90%.
Fig1; Diagrammatic representation of Newcastle disease virus.
Inactivation of the virus:
 Minimum core temperature of 80°C for one minute, 75°C
for 5 minutes or 70°C for 30 minutes - completely destroys
the virus in meat.
 Ether sensitive and inactivated by formalin, phenol & acid
pH.
 Destroyed rapidly by dehydration and ultraviolet rays.
 pH 3 - 3 min
Haemagglutination:
 All strains of NDV agglutinate (Chicken, G.pig,
human group O)RBCs.
 Most strains agglutinate (OX & sheep)RBCs.
 Horse RBCs agglutinated by lentogenic strain.
 NDV cause haemadsorption.
Antigenic properties:
 NDV is immunologically distinct from orthomyxoviruses & from
other members of paramyxoviruses.
 Mumps may develop HI antibodies to NDV.
Cultivation:
 NDV is inoculated into 10-12 days hen
embryonated eggs via chorioallantoic membrane
or allantoic sac.
 It produces haemorrhagic lesions and encephalitis
& embryo dies within 34-72 hours.
 NDV grows well in chicken embryo fibroblast cell
culture.
 Maximum titer is obtained after 24-36 hours.
 Titer of the virus in tissue culture is one log lower
than that in embryonated egg.
Strains of NDV classified according to their pathogenicity
into:
1. Velogenic – highly lethal to all life history stages, cause severe
intestinal and/or neurologicdisease resulting in high mortality
–Neurotropic (Beache's form).
–Viscerotropic (Doyle's form).
2. Mesogenic (Beaudett's form)– deadly to embryos and younger
birds, cause respiratory or nervous signs with moderate mortality.
3. Lentogenic (Hitchner form)– mild or asymptomatic respiratory
infection, cause mild or inapparent respiratory disease.
4. Asymptomatic enteric NDV.
Exotic Newcastle Disease = Velogenic & Mesogenic
To differentiate among the pathotypes
The Mean Death Time (MDT) of embryos, the Intracerebral
Pathogenicity Index (ICPI), Intravenous Pathogenicity Index
(ICPI) and plaque on the tissue culture are used.
Enzootic ND
Lentogenic - mild - kills embryos in > 90 hours
Mesogenic - moderate - kills embryos in 60-90 hours
Velogenic - highly virulent neurotropic or viscerotropic - kills
embryos in < 60 hours
Velogenic strains are now officially designated as Exotic
Newcastle Disease (END)
Lentogenic & mesogenic are used as vaccine strains.
Hitchner: B1 - B1 – milder, La Sota: B1 - La Sota - more
virulent.
Incubation period:
 It varies from (2 to 15) days in poultry depending on
the virulence of the strain.
 In chickens infected with velogenic isolates; (2 to 6)
days.
 In some avian species; 25 days.
Pathogenesis:
 The virus replicates in the mucosa of the upper
respiratory and intestinal tracts.
 Virus spreads via blood to spleen and bone marrow
(viremia) causing infection of other organs: lung,
intestines & C.N.S.
Transmission
• Spread primarily via bodily discharges of birds
• Infected birds droppings
• Secretions from the nose, mouth and eyes
• Dissemination by contaminated animals and
humans to susceptible birds
• Infected carriers (e.g., parrots) capable of
shedding virus for > 1 year
Clinical Signs and Symptoms:
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Signs vary with species and virulence
Greenish, dark watery diarrhea
Respiratory symptoms.
Nervous signs.
Digestive symptoms.
Drop in egg production with thin, rough-shelled eggs.
Swelling of tissues around eyes and in the neck.
Sudden death.
Surviving birds may have neurological or reproductive
damage
 In human;(Mild conjunctivitis, influenza-like symptoms and
laryngitis).
Exotic Newcastle Disease
• Clinically indistinguishable from Highly
Pathogenic H5N1 Avian Influenza
• Birds often destroyed based on visual diagnosis
of Newcastle Disease and without H5N1 testing
• Thus, H5N1 infections may remain undetected
Photos: New South Wales Agriculture, Australia
PM and gross lesions:
 Inflammation with Petechial hemorrhages on mucosal membranes
(proventriculi, isthmus of gizzard, trachea and pharynx).
 Edematous, hemorrhagic, or necrotic foci , and ulcerative areas on
Peyer's patches, caecal tonsils.
 Edematous, hemorrhagic, or degenerated ovaries.
 Diphtheriod inflammation on lymphoid tonsils on pharynx
 Severe inflammation of air sacs.
 Pet bird may have mild non-specific lesions and no gross lesions.
(Can have severe enteric type).
 CNS histopathological lesions are present but must be
differentiated from AE and MD
Diagnosis:
It includes:
1. History, Clinical signs and gross lesions.
2. Lab tests include;
 Virus isolation
– Serological tests: Haemagglutination inhibition test, VN - with
known ND antisera, Enzyme Linked Immunosorbant Assay
(ELISA), (No strain information,Cannot differentiate infected
from vaccinated animals, May be used post-vaccination to
confirm immune response)
 PCR & Sequence technology.
 Pathogenicity assessment:
 Plaque test in chicken embryo fibroblast cultures.
 Mean death time.
 Intracerebral pathogenicity index.
 Intravenous pathogenicity index.
Diagnostic Samples:
 Samples from live birds:
 Tracheal swabs.
 Cloacal swabs.
 Faecal swabs.
 Serum.
 Samples from dead birds:
 Lung, kidneys, intestine, spleen, brain, liver, and heart
tissues.
 In cases of mixed viral respiratory infection, NDV will show up in
the embryos before IBV.
Differential Diagnosis
Infectious bronchitis – respiratory
Laryngotracheitis – respiratory
Avian encephalomyelitis – neurological
Vitamin E & selenium deficiency – neurological
Mycotic encephalitis – neurological
Avian influenza - variable pathogenicity
Immune response against NDV:
 Antibody production is rapid.
 HI antibody can be detected within 4-6 days of
infection.
 The level of HI antibody is a measure of immunity.
 Serum antibodies of the hen are transferred to
chicks through yolk, and protect chicks for 3-4
weeks after hatching.
 Serum IgG does not prevent respiratory infection.
 Locally produced IgA prevent respiratory and the
intestinal infection.
Treatment:
 None
 Broad spectrum antibiotics for secondary bacterial involvement
Prevention:
 Quarantine & isolation of all newly purchased birds.
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Transportation of birds in new or disinfected containers.
Restrict personnel movement between new and old birds.
Disinfection of all surfaces and equipment.
Disposal of any destroyed birds and contaminated products.
Removal of insects and mice (vectors).
Control handling of bird carcasses, litter and manure.
Enzootic ND
Vaccination:
Live Virus; B1,
La Sota
Killed Virus in oil adjuvant, produced with B1 virus.
Maternal antibodies interfere with active immunity buffering the
expected vaccine reaction.
Enzootic
Immature Birds - broilers, leghorn pullets, etc. Vaccinated with live
vaccines usually at 1 to 4 days and at around 14 to 28 days.
This virus doesn’t replicate in the Harderian gland, so lower maternal
antibody is desired to prevent vaccine blockage.
Breeders & Leghorns - give killed vaccine at around 12-18 wks. of
age after being primed with live vaccine.