A160 - NEWCASTLE DISEASE

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A160 - NEWCASTLE DISEASE

Nature of the disease
Newcastle disease (ND) is a highly contagious, generalised virus disease of domestic poultry and wild birds characterised by gastro-intestinal, respiratory and nervous signs.
Classification
OIE List A disease.

Remark on the classification by OIE

The ND is defined by the OIE as an infection of birds by a virus of avian Paramyxovirus serotype 1 that meets one of the following criteria of virulence:

  1. The virus has an intracerebral pathogenicity index (CPI) in day-old chicks (Gallus gallus) of 0.7 or greater
  2. Multiple basic amino acids have been demonstrated in the virus (eitheir directly or by deduction) at the C-terminus of the F2 protein and phenylalanine at residue 117, which is the N terminus of the F1 protein. The term 'multiple basic amino acids' refers to at least three arginine, or lysine residues between residues 113 and 116. Failure to demonstrate the characteristic pattern of amino acid residues as described above would require characterisation of the isolated virus by an ICPI test.

Therefore serological evidences of Newcastle disease should be completed by molecular characterisation or ICPI test.

Susceptible species
ND occurs in domestic fowl, turkeys, pheasants, pigeons, quail and guinea fowl. Ducks and geese are susceptible but severe disease is rare. Many species of wild birds are also susceptible. Psittacines (parrots) are highly susceptible and can excrete virus for long periods. Human infections, with ’flu-like symptoms and conjunctivitis, have been reported.
Distribution
Strains of ND are present in most countries. In many countries there is a wide spectrum of strains from non-pathogenic to highly virulent. New Zealand, Papua New Guinea, Fiji and a number of Pacific island countries have non-pathogenic strains of virus, but are free of pathogenic strains. In 2002 outbreaks occurred in Australia and later in Japan.
Clinical signs 
ND strains are classified as lentogenic (lowly virulent), mesogenic (moderately virulent) or velogenic (highly virulent) depending on the speed with which they kill chickens or embryonated eggs. They are also classified according to the predilection sites for virus infection as pneumotropic (respiratory), viscerotropic (gastro-intestinal), or neurotropic (nervous) strains. However the current tendency is to refer directly to the ICPI index.

Clinical signs are very variable depending on strain of virus, species and age of bird, concurrent disease and pre-existing immunity. Four broad clinical syndromes are recognised.

Viscerotropic velogenic
  • Sudden appearance
  • Spreads rapidly
  • Marked depression and loss of appetite
  • Sharp drop in egg production
  • Increased respiratory
  • Profuse bright green diarrhoea
  • Oedematous swellings of the head and cyanosis of the combs and conjonctivitis
  • Prostration with many birds dying within a few days
  • Nervous signs in those that survive initial phase
  • High mortality (>90%) in susceptible flocks
Neurotropic velogenic
  • Acute respiratory and nervous signs predominate
  • Sudden depression
  • Loss of appetite
  • Drop in egg production
  • Respiratory distress — severe coughing
  • Gasping nervous signs — head tremors, wing and leg paralysis, torticollis
  • Mortality rate in adults 10–20%. May be much higher in young chickens
Mesogenic
  • Depression
  • Weight loss
  • Drop in egg production and quality (lasting 1–3 weeks)
  • Acute respiratory disease with coughing
  • Gasping nervous signs may develop late in the clinical course
  • Mortality rate about 10%
Lentogenic
Commonly subclinical may be
  • Mild respiratory signs
  • Temporary loss of appetite
  • Drop in egg production
  • No nervous signs
  • Negligible mortality unless concurrent disease is present
Post-mortem findings 
Gross lesions are variable. Young chickens and those dying peracutely may have no lesions.

In the viscerotropic velogenic form:

  • Oedema of the interstitial tissues of the neck
  • Haemorrhages and necrosis in the proventriculus, gizzard and small intestinal wall. Small haemorrhages are often present in other internal organs.

In the neurotropic velogenic and mesogenic forms:

  • Acute laryngitis and tracheitis congestion and catarrhal exudates air sacs thickened and cloudy
  • Sometimes haemorrhages in the proventriculus, but rarely elsewhere

Gross lesions may not be present in birds that only show nervous signs

Differential diagnosis
  • Avian influenza
  • Infectious laryngotracheitis
  • Infectious bronchitis
  • Fowl cholera
  • Salmonellosis
  • Other avian paramyxovirus infections
Specimens required for diagnosis
Samples should be taken from:
  • live clinically affected birds:
    • serum or cloated blood for serology
    • cloacal and tracheal swabs and/or fresh faeces for pathogenicity assessment and virus characterisation
  • recently dead birds:
    • alimentary tissues ( proventriculus, intestine, caecal tonsil) and respiratory tissues (trachea, lung) for pathogenicity assessment and virus characterisation

Fresh samples and swabs in transport medium should be forwarded chilled.

Once serological evidences have been found, a pathogenicity assessment be done as soon as possible. Different techniques are available including plaque test in chicken embryo fibroblast cultures, mean death time of embryonated chicken eggs, intracerebral, pathogenicity index in 1-day-old chickens (ICPI).

Transmission
ND virus is relatively heat stable and survives well in protected environments. Within a flock main method of transmission is inhalation of virus in the air, or by ingestion of water or feed contaminated with nasal secretions or faeces containing virus (NB coughing is not required to produce infective aerosols).

Spread of ND between flocks has been attributed to: movement of clinically normal but virus-shedding birds (including vaccinated birds) insufficiently treated infected poultry products (meat, eggs and egg pulp) and by-products people wearing virus contaminated clothing/footwear contaminated equipment, litter and manure feed containing uncooked poultry offal.

Wild birds (e.g. pigeons) can be a source of infection for domestic poultry either directly or by contaminating poultry feed. Wind-borne spread of virus may occur under favourable conditions.

Risk of introduction
ND has a proven ability to spread internationally and cause major outbreaks. It undoubtedly is a threat to the Pacific region that quarantine authorities should be aware of.

Potential methods of introducing the disease include infected day old chicks, frozen carcasses and contaminated feed or equipment. Wild and caged birds have played a major role in international spread on ND.

Psittacines and other birds can be reservoirs of infection and can continue to excrete virus for up to 12 months after recovering from clinical disease. Imports of these birds should be carefully regulated.

Control / vaccines
Vaccination or a stamping out policy (based on slaughter of infected and potentially infected birds, quarantine procedures, cleaning and disinfection) or a combination may be used to control ND, depending on circumstances.

In an emergency situation in a previously free country eradication by stamping out should be the preferred option. Vaccination in the face of an outbreak can be considered, using an aerosol spray vaccine. Where the disease is well established, a systematic vaccination program should be initiated. Both attenuated and inactivated vaccines have been developed. Vaccine-induced immunity is short-lived (8–10 weeks) and repeated vaccinations are needed to maintain adequate protection.

References
  • GEERING WA, FORMAN AJ, NUNN MJ, Exotic Diseases of Animals, Aust Gov Publishing Service, Canberra, 1995, p.173-181
  • MORGAN-CAPNER P, BRYDEN AS (1998), New Castle Disease In Zoonoses, ed by SR PALMER, Lord SOULSEY and D.I.H. SIMPSON, Oxford University Press, Bath Press, Avon, 1998, p.323-326
  • Newcastle Disease, In Merck Veterinary Manual, National Publishing Inc. Eight ed, 1998, Philadelphia, p 1941-1942
  • Office International des Epizooties, 2003