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Newcastle disease
Newcastle disease is a contagious viral disease of birds caused by avian paramyxovirus-1. It is transmitted through contact with infected birds or their feces/secretions. Clinical signs include respiratory, neurological and intestinal symptoms with high mortality in some strains. Diagnosis involves virus isolation from samples and serological tests. Control relies on vaccination, biosecurity, and culling infected flocks.
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Newcastle disease
- 1. Newcastle disease SUBMITTED BY:M. MUTAHIR REHMAN SUBMITTED TO: DR QAISER AKRAM
- 2. Outline Definition Virusoverview 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 • Formerlygrouped 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)
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- 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 cansurvive 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 withNDV 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 thebasis 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 ofrespiratory 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 • Numerousdeaths 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 • Hemorrhagicinternal lesions 1. Tracheal mucosa 2. Proventriculus 3. Intestinal mucosa • Edema, hemorrhage, necrosis or ulceration of lymphoid tissue
- 18. Diagnosis • On thebasis of clinical signs & symptoms • Tracheal & oral swabs • Feces, intestinal contents and portion of trachea • Haemagglutination – inhibition test • Intracerebral pathogenicity test
- 19. Control • Disinfection ofpremises • 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 routineworldwide • 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