NEWCASTLE DISEASE(RANIKHET)

1. Newcastle disease
SUBMITTED BY: M. MUTAHIR REHMAN
SUBMITTED TO: DR QAISER AKRAM

2. Outline
 Definition
 Virus overview
 Hosts
 Route of transmission
 Pathogenesis
 Epidemiology
 Clinical findings
 Post mortem lesions
 Diagnosis
 Treatment
 Vaccination
 Control & prevention

3. Definition
Virulent Newcastle disease (VND), formerly exotic Newcastle
disease is a contagious viral avian disease affecting many
domestic and wild bird species caused by APMV-1 and is
characterized by respiratory, intestinal and nervous signs with
high mortality
First described in 1926 when severe outbreaks were reported in
Newcastle, England & in Java
Other major outbreaks occurred in the Middle East during the
late 1960s and in the 1970s when pigeons were the species
primarily affected

4. Virus overview
• Formerly grouped in Myxoviridae together with orthomyxovirus because of their
affinity with mucus membrane
• Pleomorphic
• 150nm diameter
• Enveloped 2 types of paplomers
• SS RNA (-ve sense)
• Cytoplasmic replication
• Sensitive to heat , disinfectants, detergents & lipid solvents
Fusion protein(F)
Attachment protein(HN or G)

5. Hosts

6. Hosts

7. Route of transmission
• NDV is spread primarily through direct contact between healthy
birds and the bodily discharges of infected birds
• The disease is transmitted through infected birds' droppings
and secretions from the nose, mouth, and eyes
• High concentrations of the NDV are found in birds' bodily
discharges; therefore, the disease can be spread easily by
mechanical means
• Virus-bearing material can be picked up on shoes and clothing
and carried from an infected flock to a healthy one

8. • NDV can survive for several weeks in a warm and humid
environment on birds' feathers, manure, and other materials
• It can survive indefinitely in frozen material
• However, the virus is destroyed rapidly by dehydration and by the
ultraviolet rays in sunlight
 Smuggled pet birds, especially Amazon parrots from Latin
America, pose a great risk of introducing NDV into the US
 Amazon parrots are carriers of the disease, but do not show
symptoms, and are capable of shedding NDV for more than 400
days
Contin….

9. Epidemiology
• Infection with NDV is probably endemic in wild birds
especially waterfowl
• Strains of NDV differ in their virulence
• It appears that virulent strains may arise from progenitor
viruses of low virulence following passage in chickens
• Humans may become infected; manifested by unilateral or
bilateral reddening, excessive, lachrymation, edema of the
eyelids, conjunctivitis and sub-conjunctival hemorrhage

10. Pathotypes
 On the basis of virulence and tissue tropism isolates are categorized in to 5 groups
or pathotypes:
1. Viscerotropic velogenic Doyle’s form mortality 100%
2. Neurotropic velogenic Beach’s form mortality 100%
3. Mesogenic Beaudette’s form mortality <10%
4. Lentogenic Hitchner’s form negligible mortality
5. Asymptomatic enteric by lentogenic strains

11. Pathogenesis
Entry
Replication in epithelia
of respiratory tract & intestine
Viremia
Spread to spleen & bone marrow
Secondary viremia
infection to other organs

12. • During replication, NDV particles are produced with a precursor
glycoprotein, F0, which has to be cleaved to F1 and F2 for the virus
particles to be infectious
• This post translation cleavage is mediated by host cell proteases
• Trypsin is capable of cleaving F0 for all NDV strains
• The cleavability of the F0 molecule was shown to be related directly to
the virulence of viruses
• This allows these viruses to spread throughout the host, damaging vital
organs

13. Clinical findings
• Numerous deaths within 24 to 48 hours
 Deaths continue for 7 to 10 days
• Restlessness, weakness and drop in egg production
• Surviving birds may have neurological damage
• Edema of head, especially around eyes
• Greenish, dark watery diarrhea
• Neurological signs include wing paralysis, leg paralysis,
torticollis and muscle spasms
• Respiratory signs include gasping, rales

16. Postmortem lesions
• Hemorrhagic internal lesions
1. Tracheal mucosa
2. Proventriculus
3. Intestinal mucosa
• Edema, hemorrhage, necrosis or ulceration of lymphoid
tissue

18. Diagnosis
• On the basis of clinical signs & symptoms
• Tracheal & oral swabs
• Feces, intestinal contents and portion of trachea
• Haemagglutination – inhibition test
• Intracerebral pathogenicity test

19. Control
• Disinfection of premises
• Delay re-introduction of new birds for 30 days
• Control insects and mice
• Limit human traffic
• Combination of vaccination and slaughter policies

20. Vaccination
• Vaccination routine worldwide
• Reduces clinical signs
• Does not prevent virus replication or shedding
• Not an alternative to good management, biosecurity or good hygiene in rearing
practices
• Lentogenic & mesogenic strains propagated in eggs or tissue culture are used in
live vaccines
• Vaccines are administered as a spray, drinking water or by intranasal or
intraconjuctival instillation