Clinical Traits and Pathology of Newcastle Disease ... Visit and Differential Diagnosis Dr. Ilaria CAPUA,

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  • Issue No.36 / May 2011

    Clinical Traits and Pathology of Newcastle

    Disease Infection and Guidelines for Farm

    Visit and Differential Diagnosis Dr. Ilaria CAPUA, Director

    and Dr. Calogero TERREGINO, head of the Diagnostic Virology Laboratory

    OIE/FAO Reference Laboratory for Avian Influenza and Newcastle Disease OIE Collaborating Center for Diseases at the Human-Animal interface

    IZVe - Istituto Zooprofilattico Sperimentale delle Venezie


    The main body of evidence regarding the clinical aspects of avian paramyxovirus type 1 (APMV-1) infection has been collected from poultry, mainly chickens. Based on the occurrence and severity of clinical manifestations, Beard and Hanson (1984) identified five viral pathotypes (Table 9.1). The clinical manifestations of this disease are highly variable and there are no lesions or signs that can be considered pathognomonic (McFerran and McCracken 1988).

    Clinical signs produced by the same virus are influenced by numerous factors, including the species infected, the age and the production status or health of the host, especially in the presence of co-infections with other viruses, bacteria or parasites. In addition, vaccination against Newcastle disease (ND) virus infection is carried out globally. Consequently, clinical signs may also vary depending on the level of immunity to the virus, which may be passively derived from maternal antibodies or actively induced by vaccination. Several factors influence the immune status to ND following vaccination, including underlying immunosuppressive diseases, quality and type of vaccine, and number of administrations. The clinical manifestations of infection, even with highly virulent viruses, may therefore not be as overt as described and illustrated in this chapter.

    Velogenic Mesogenic Lentogenic Asymptomatic

    Enteric Viscerotropic Neurotropic

    Diarrhea +++ - - - -

    Respiratory distress - +++ ++ (+) -

    Central nervous system signs (++) +++ (++) - -

    Drop in egg production +++ +++ ++ (+) -

    Morbidity +++ +++ ++ (+) -

    Mortality +++ ++ + (+) -

    Severity of signs observed : +++ severe, ++ intermediate, + mild, ( ) clinical signs only in compromised or young birds

    Table 9.1 Clinical course of avian paramyxovirus type 1 (APMV-1) infection in chickens (Gallus gallus var. dom.)

    (Modified from Beard and Hanson. 1984)


    Velogenic ND is an acute condition that affects birds of all ages and categories. In naïve birds, ND is often characterized by a sudden onset of clinical manifestations. Some birds die peracutely, prior to the onset of clinical signs, whereas others show more general signs of disease such as anorexia, ruffled feathers and dropped wings. In laying birds the most pronounced sign is a marked drop in egg production or a complete cessation of egg laying. Eggs are often misshapen, with thin shells and watery albumen. Depending on the tropism of the strain involved, clinical manifestations may occur predominantly in the gastrointestinal tract (velogenic viscerotropic, VVND) leading to a severe enteritis mainly characterized by diarrhea, which is often green in colour. In contrast, velogenic neurotopic forms are dominated by respiratory distress, which is followed by central nervous system disorders (Figs. 9.1-9.6) For both velogenic forms, flock morality levels in fully susceptible birds may be as high as 90-100%. Some velogenic viruses cause a less severe disease in turkey than in chickens.

    In contrast, clinical manifestations of infection with mesogenic viruses are strongly dependent on the age of the infected animals. In young birds morbidity within a flock can be as high as 100%, while in adult healthy chicken it ranges between 5% and, exceptionally, 50%. The main clinical signs of infection with a mesogenic virus are a drop in egg production, poor egg quality (shell-less or soft-shelled eggs, off-coloured eggs; (Figs. 9.7, 9.8) and decreased feed consumption. However, most of the so-call mesogenic viruses are not naturally occurring; rather, they are velogenic viruses that have been attenuated by a variety of methods in the laboratory. There is evidence that some of these viruses may revert to the virulent phenotype after passage in chickens.

    Fig.9.1 Layer hens, naturally infected with Newcastle

    disease (ND) virus, velogenic neurotropic pathotype, exhibiting nervous signs

    Fig.9.2 Layer hen, naturally infected with ND virus, velogenic neurotropic pathotype, exhibing serious nervous signs with

    torticollis and paresis

    Fig.9.3 Layer hen, naturally infected with ND virus, velogenic

    neurotropic pathotype, exhibiting torticollis

    Fig.9.4 Caged layer hens, naturally infected with ND virus,

    velogenic neurotropic pathotype, exhibiting nervous signs with


  • Fig.9.5 Layer hen, naturally infected with ND virus, velogenic

    neurotropic pathotpe, exhibiting serious nervous signs with

    incoordination of muscular movement

    Fig.9.6 Chicken experimentally infected with ND virus,

    velogenic neurotropic pathotype, exhibiting torticollis and toe

    paralysis. (Courtesy of Dr. Zenon Minta)

    Fig.9.7 Soft-shelled, irregular-shaped and off-coloured eggs

    produced by hens affected by ND

    Fig.9.8 Discoloured eggs produced by hens affected by ND


    Lentogenic pathotypes such B1 and La Sota are usually apathogenic in adult birds and are used as live vaccines. The same viruses, if administered to 1- to 7-day-old chicks, can cause reduced food intake and respiratory distress, the latter characterized by sneezing and snicking (Alexander 2003).

    In addition to the age of the infected animals, variability in the clinical course of ND may arise due to co-infections with other microorganisms, including Mycoplasma, Escherichia coli or other APMV viral pathogens will lead to more pronounced clinical signs (Gross 1961; Kim et al. 1978, Nakamura et al. 1994). The animal’s immune status also greatly influences the outcome of ND virus infection. In immunocompromised animals, for example, as a result of infection with viruses such as infectious bursal disease virus (which produces Gumboro disease), chicken anemia virus, hemorrhagic enteritis virus or Marek’s disease virus, infection with ND strains of low virulence can lead to overt clinical disease with subsequent economic losses in terms of reduced performance and mortality.


    Ostriches (Struthio camelus) are considered to be moderately susceptible to ND and outbreaks have been reported in zoo and farmed ostriches (Alexander 2000). Clinical signs of disease include inappetence, apathy, ataxia and torticollis. The duration of ND in adult animals is estimated to be 3-16 days (Kauker and Siegert 1957; Verwoerd 1995). Clinical manifestations are predominant in younger birds between 5 and 9 months of age. Clinical signs include those involving the nervous system, such as atonic paralysis of the neck, torticollis, rhythmic twitches of the muscles of the back, oedema of the head and total paralysis, leading to death in approximately 330% of infected animals (Samberg et al. 1989). Different aclnical manifestations, such as respiratory distress due to haemorrhagic tracheitis, have been reported in ostrich chicks reared indoors (Huchzermeyer 1996).


    Reports on clinical manifestations following natural infection of game birds are few, although partridges and pheasants are highly susceptible to ND (Aldous and Alexander 2008). In pheasants, clinical signs reported in natural outbreaks are highly variable and resemble those seen in chickens. The disease can appear in an acute form, with sudden onset, nervous signs (incoordination, head shaking) and high mortality, or as a mild disease with respiratory distress, blindness and ataxia as the only detectable clinical signs. There is a subclinical (asymptomatic) form of ND as well as many intermediate forms. The clinical signs include dropping wings and depression, lack of appetite, respiratory distress with beak gaping, coughing, sneezing, gurgling and rattling and yellowish-green diarrhea. In laying flocks, a sudden drop in egg production and a high proportion of eggs laid with abnormal (soft) shells is often an early sign of disease. Young birds are particularly susceptible and mortality can be extremely high, with survivors often exhibiting permanent nervous signs.


    Some waterfowl are known to be highly resistant to the clinical manifestations of ND, although they are susceptible to infection. On rare occasions, infection has been associated with a mild to severe clinical condition. Outbreaks in geese flocks have been characterized by signs ranging from ruffled feathers or mild depression to severe systemic infection with anorexia, white diarrhea, ocular and nasal discharges and in some birds red and oedematous eyelids. The disease spreads very rapidly, with high fatality. Some birds die overnight, others shortly after the appearance of signs and others after a relatively prolonged course (between 3 and 12 days post-infection).

    Natural infections of domestic ducks resulting in clinical manifestations are exceptional findings that have been associated with mortality and acute nervous signs (Kingston et al. 1978). Natural infections leading to clinical disease in wild Anatidae have been documented only rarely. Bozorgmehri-Fard and Keyvanfar (1979) reported rapid deaths in captured teals (Anas crecca) from which APMV-1 was isolated. Estudillo (