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Newcastle Disease Virus | 67

transmission. Once introduced into poultry, backyard birds, or Pathology
other captive bird populations, the virus spreads rapidly between The ability of NDV strains to cause neurological disease depends
premises by the movement of apparently healthy but infected on several factors such as efficiency of replication in peripheral
birds, movement of people and contaminated equipment, move- tissue, ability to cross the blood–brain barrier and efficiency of
ment of contaminated poultry products, contaminated food and replication in neuronal tissue. It was found that differences in the
water, and by airborne spread from one premise to another. rate of NDV replication in nervous tissue differentiate velogenic
strains from mesogenic strains (Moura et al., 2016). The rate of
replication of virulent viruses also determines the tropism (our
Clinical signs unpublished results). The viscerotropic strains replicate at higher
Clinical signs in birds infected with NDV vary widely and are rate than the neurotropic strains, which makes it possible for these
dependent on factors such as: the strain of virus, host species, viruses to spread and replicate efficiently in most host tissues and
age of host, route of exposure, immune status and environmental cause lesions.
conditions. In chickens, NDV strains show a broad range of viru- VVND viruses can produce a wide range of gross lesions.
lence. The disease is more severe in younger birds. The incubation Although no pathognomonic lesions are found in any form of
period for ND after natural exposure varies from 2–15 days (aver- the disease, presence of haemorrhagic lesions in the intestine
age 5–6 days). The clinical signs may include depression, loss of of infected chickens has been used to distinguish viscerotropic
appetite, respiratory signs, torticollis, circling, dehydration, and viruses from neurotropic viruses (Hanson et al., 1973). These
paralysis. Infection with velogenic strains may result in sudden haemorrhagic lesions are often prominent in the mucosa of
high mortality with few clinical signs. The velogenic viscerotropic proventriculus and caecal tonsils and other lymphoid patches
ND (VVND) pathotype viruses affect the viscera or internal in the intestines. Other lesions include enlarged and mottled
organs. Although the most noticeable signs are in the digestive spleen, haemorrhages in the caudal part of the pharynx and
tract; the heart, liver, and kidneys are also affected. VVND virus proximal trachea, and pulmonary oedema. In case of velogenic
usually produces marked congestion in the trachea, ulcer and ero- neurotropic strains, even though neurological signs are present,
sions on the soft palate and upper oesophagus, and inflammation all tissues including the brain, may be grossly normal. With
and haemorrhages in the proventriculus (Alexander, 1998). Mor- neurotropic strains, microscopic lesions are present most regu-
tality can reach up to 100% in susceptible chickens. In velogenic larly in the brain stem and cerebellum (Alexander, 1988). The
neurotropic ND (VNND) pathotype viruses, the neurological predominant microscopic lesions in the brain consist mostly of
signs are more prominent. Usually, other signs of VVND are multifocal neuronal necrosis, non-suppurative encephalitis char-
absent. The morbidity may be 100%, but the mortality is gener- acterized by lymphocytic perivascular cuffing, plump vascular
ally lower, up to 50% in adult birds and 90% in young chickens endothelium, and multifocal astrogliosis (Brown et al., 1999;
(Alexander, 1988). Ecco et al., 2011).
Mesogenic strains of NDV usually cause respiratory disease
in adult chickens. Neurological signs are rarely seen in adult
chickens. These strains sometimes kill young chickens, but rarely Diagnosis
kill older birds. Lentogenic viruses usually do not cause disease A definitive diagnosis of ND requires isolation and characteriza-
in young and adult chickens. But in rare cases some lentogenic tion of the virus. However, in an enzootic area, clinical signs and
strains, such as LaSota, can cause serious respiratory disease in gross lesions may be highly suggestive of the disease. For virus iso-
young birds (Alexander, 2003). lation, tracheal and cloacal swabs are good sources of virus from
The susceptibility of different breeds of chickens to NDV is living birds. Spleen, lung, trachea, brain and intestines (especially
unclear. Some studies found no difference in ND susceptibil- caecal tonsils) are usually collected for virus isolation from dead
ity between local breeds and imported breeds (Higgins and or moribund birds. Although NDV grows well in primary chicken
Shortridge, 1988), whereas, other studies found native chicken cells and many established cell lines, ECE are universally used for
breeds more resistant to ND compared with imported chicken virus isolation. ECE is an extremely sensitive and convenient
breeds (Lee, 1989; Ratanasethakul, 1989). system for propagation of all NDV isolates. Although all NDV
The clinical signs of ND vary widely in other avian species. isolates replicate well in chicken embryo kidney cells, lentogenic
Turkeys are highly susceptible to NDV, but the generalized signs isolates require supplementation of exogenous protease in the
are less severe with predominating respiratory and nervous signs medium for replication in avian fibroblast and established cell
(Box et al., 1970; Alexander et al., 1999). Ducks and geese show lines. In most instances, acetylated trypsin (1 µg/ml) or 5–10%
subclinical signs when infected with mesogenic or velogenic fresh allantoic fluid is used as the source of exogenous protease.
strains of NDV (Higgins, 1971). Psittacine species are highly sus- Nine-day-old ECE are injected with 0.1 ml of the sample into the
ceptible to ND, but the signs are always confined to the nervous allantoic cavity. The eggs are incubated at 37ºC and examined
system. Pigeons and cormorants commonly show central nervous twice daily. Dead eggs as well as eggs after 5–7 days of incubation
system signs, which include paralysis of legs and wings (Barton et are chilled at 4ºC and the allantoic fluid is harvested. The pres-
al., 1992; Kuiken et al., 1998). Pheasants of all ages are suscepti- ence of virus in the allantoic fluid is determined by the HA assay
ble to ND. The clinical disease in pheasants include nervous and (Alexander, 2009). It is important to note, however, that some
respiratory signs (Aldous and Alexander, 2008). PPMV-1 strains can only be isolated by cell culture, not by ECE.