Newcastle Disease

Incubation in poultry is 2 to 15 days, commonly 2 to 6 days in chickens with velogenic strains. Early signs are lethargy, poor appetite, ruffled feathers and reddened, swollen conjunctivae, followed by greenish or white watery diarrhoea, gasping and coughing, and swelling of the head and neck. Egg production falls sharply and eggs are misshapen or thin-shelled. Nervous signs (tremors, wing or leg paralysis, twisted neck, circling) usually come later; sudden death with few signs is common. At necropsy, haemorrhage, ulceration or necrosis of the caecal tonsils and intestinal lymphoid tissue is particularly suggestive, with proventricular petechiae and tracheal congestion.

Newcastle disease is caused by virulent strains of avian paramyxovirus type 1 (APMV-1, also called Newcastle disease virus), an enveloped RNA virus of the genus Orthoavulavirus, family Paramyxoviridae. Virulence depends largely on the cleavage site of the viral fusion (F) protein. Virulent strains carry several basic amino acids at that site, so the ubiquitous intracellular protease furin activates them in most cell types and the virus spreads systemically. Low-virulence strains have a single basic residue, need secreted trypsin-like proteases, and stay confined to the respiratory and intestinal tracts. Strains are grouped into viscerotropic velogenic (haemorrhagic intestinal lesions), neurotropic velogenic, mesogenic, lentogenic and subclinical enteric pathotypes, although these overlap.

The virus can infect more than 200 bird species; chickens are the most susceptible, turkeys less so, and ducks and geese are usually infected without signs. Virulent strains remain endemic in parts of Africa, Asia and South America and, per CFSPH, the Middle East, where the disease is reported as an important cause of illness in captive falcons. Birds shed virus in faeces and respiratory secretions; spread is by direct contact and by contaminated feed, water, equipment and clothing, and nearly all birds in a flock can be infected within days. The virus survives for weeks in the environment, longer in cool conditions. Humans can develop a short-lived conjunctivitis. It is a WOAH-listed disease subject to official control in most countries.

High pathogenicity avian influenza produces the same spectrum of sudden high mortality, respiratory, enteric and nervous signs and cannot be separated clinically; both agents should be tested for together, with RT-PCR and fusion-gene sequencing or virus isolation confirming APMV-1 and its virulence. Low-virulence APMV-1 strains made worse by co-infection or poor husbandry can mimic milder forms and are separated by F-gene cleavage-site sequencing or ICPI. Other avian paramyxoviruses (notably APMV-3, -7 and -12) cross-react in haemagglutination inhibition.

Respiratory tract (trachea, lungs, air sacs), intestine (caecal tonsils, Peyer's patches), proventriculus, brain and nervous system, spleen, ovary and oviduct, conjunctiva, head and neck subcutis

Live (lentogenic or mesogenic), inactivated and vectored vaccines; biosecurity keeping poultry away from wild birds, pigeons and pet birds; disinfection, pest control, all-in/all-out; surveillance and stamping out with quarantine in outbreaks.

Velogenic strains cause morbidity and mortality up to 100% in susceptible chickens; mesogenic strains usually kill under 50%, lentogenic strains cause mild or no disease. Survivors may keep nervous deficits or reduced laying.