2. Newcastle Disease Overview
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This section provides an overview of ND, focusing on these main areas:
- Susceptible species
- Global distribution
- Public health
ND is a viral disease of chickens, turkeys, and wild and pet birds. Clinically, ND varies widely, depending on the virus strain and host species. Generally, chickens are highly susceptible, whereas turkeys and pigeons are less so. Ducks and geese are refractory, with peafowl, guineafowl, pheasant, and quail exhibiting mild disease. Typically, there is no persistent infection in domestic poultry. In psittacine birds, a chronic infection may develop in the kidney with potential for long-time shedding.
ND is caused by an avian paramyxovirus Type 1 (APVM-1) virus. There are nine types of avian paramyxoviruses that are antigenically similar but can be differentiated in routine serology (HI; VN). The virus is relatively stable in nature, remaining infective for weeks at low temperatures, and surviving for several hours over a wide range of pH (3−10). Protected by associated organic matter, it can survive for days in litter (20 days), water, soil, carcasses, eggs and feathers (255 days).
APMV-1 strains are classified into three pathotypes, based on their virulence in chickens:
- Lentogenic strains are the least virulent.
- Mesogenic strains are moderately virulent.
- Velogenic strains are the most virulent.
Most strains cluster toward the two extremes of virulence, and are either lentogenic or velogenic. Velogenic viruses can be subdivided into a neurotropic form, which is typically associated with respiratory and neurologic signs, and a viscerotropic form with hemorrhagic intestinal lesions. These clinical forms overlap.
ND's first outbreak occurred in 1926 in Java, Indonesia, and in Newcastle upon Tyne, England, but also at this time slightly different strains were found in other parts of the world.
Though named "Newcastle Disease" by Doyle, the following names are also used: pseudo-fowl pest, pseudo-poultry plague, avian pest, avian distemper, and avian pneumoencephalitis.
ND is present in most countries, but velogenic strains are exotic to poultry in Canada. ND has been reported in 1995 in wild birds in Canada, and in 2002–2003, an epidemic outbreak in California (mainly) resulted in losses that were estimated at $5 billion and the death of more than 3 million birds.
Canada and the United States have seen high mortality in wild cormorants caused by ND.
2.2 Susceptible Species
ND affects primarily avian species (domestic and wild), although it may affect other species (human, rodent) either naturally or experimentally. Infections in non-avian species could spread the disease, but the significance of this is unknown. However, these animals pose a significant risk because they can act as mechanical vectors of ND.
Chickens are the most susceptible of domestic poultry species to APMV-1 and the pigeon variant.
Turkeys are as susceptible as chickens to APMV-1; however, the infection is usually less severe than that in chickens.
Pigeons are susceptible to APMV-1. The pigeon variant of APMV-1 can produce up to 80% morbidity, with nervous signs and diarrhea the most notable clinical features.
Ducks and possibly geese are readily infected with APMV-1 and are capable of spreading the virus. Ducks seem clinically resistant.
Game birds are susceptible to natural APMV-1 infection, and though mortalities have been recorded, infection usually produces only mild disease unless it occurs in quail, which are very susceptible.
Canaries are susceptible to infection, typically producing mild or inapparent disease. However, 20%–30% of mortalities have been recorded in experimental infections in which neurologic signs predominated.
Ratites are susceptible to infection; however, resistance to developing clinical signs increases with age.
Psittacines are very susceptible to ND, with budgerigars more susceptible than canaries. The disease is mainly neurological.
Tropical parrots form a reservoir of virulent ND virus and have been responsible for a number of introductions to the United States. Infected psittacines can excrete virus for at least one year.
Cormorants act as a reservoir of ND viruses. They can excrete virulent ND virus for up to 6 weeks. Several die-offs were reported in Canada, generally in remote lakes. Migratory wild birds have been strongly implicated in the spread of outbreaks across Europe.
Professionals who handle poultry may become exposed. Infection has occurred among laboratory workers and individuals who eviscerate and prepare poultry for market. Person-to-person transmission of ND virus has not been reported.
Rodents harboured ND virus in the 1974 outbreak in California.
2.3 Global Distribution
APMV-1 is endemic in Asia, the Middle East, Africa, Central and South America, and parts of Mexico. Virulent strains are endemic in wild cormorants in the United States and Canada, but commercial poultry are free of velogenic isolates. Lentogenic isolates are found in poultry throughout the world, including the Canada; mesogenic strains may also be found, but are less common.
The CFIA website lists the countries that are recognized by the CFIA as ND-free.
The World Organisation for Animal Health (OIE) website World Animal Health Information Database (WAHID) provides information on global distribution.
2.4.1 Incubation Period – Critical Period
The incubation period for the various diseases and syndromes caused by ND viruses is highly variable, ranging from 2 to 15 days. The incubation period can be 2 to 6 days in chickens infected with velogenic strains. The appearance of the initial clinical signs and the length of the incubation period are dependent on the dose and virulence of the virus strain, route of exposure, species affected, how the flock is raised (e.g. on litter or in cages), and ability to detect clinical signs. However, the OIE regulatory code uses 4 to 6 days.
An outbreak in chickens may be so severe that almost all of an affected flock may die within 72 hours without prior noticeable signs, often causing a suspicion of poisoning. The pigeon variant of paramyxovirus (PMV1) can produce morbidity up to 80%. In ducks and geese, typically refractory to ND, morbidity is usually less than 10%, but large die-offs have been reported. Canaries are susceptible, showing a mild disease, although mortalities of 20%–30% have been recorded in experimental cases.
2.4.2 Persistence in the Environment
Temperature: Inactivated by 56°C/3 hours, 60°C/30 min
pH: Inactivated by acid pH
Chemicals/Disinfectants: Ether sensitive; inactivated by formalin, phenolics, and oxidising agents (e.g. Virkon®); chlorhexidine, sodium hypochlorite (6%)
Survival: Survives for long periods at ambient temperature, especially in faeces
OIE Newcastle Disease brochure - PDF (84 kb)
APMV-1 is readily transmitted on fomites. Survival is prolonged on eggshells and especially in feces, compared with an inorganic surface (filter paper). Published information on virus survival is highly variable, likely due to its being affected by humidity, temperature, suspending agent, and exposure to light.
Based on different studies, APMV-1 may survive in contaminated, uncleaned poultry houses for:
- up to 7 days in summer, as long as 14 days in the spring, and 30 days during the winter.
- up to 16 days after depopulation of an unvaccinated flock.
- up to 255 days in a henhouse, at ambient temperatures of –11°C to 36°C.
- up to 10 to 14 days at 23–29°C in contaminated litter, and at 20°C (68°F) in soil for 22 days.
The virus has also been recovered from earthworms for 4 to 18 days and from experimentally contaminated lake water for 11 to 19 days.
ND virus is relatively heat stable – a feature of great importance in relation to its epidemiology and control. It remains infectious in bone marrow and muscles of slaughtered chickens for at least 6 months at –20°C and up to 4 months at refrigerator temperatures, and has been isolated from bone marrow held for several days at 30°C.
The virus is more susceptible to the action of alkali than to acid, and highly susceptible to detergent and disinfectants, including chlorhexidine, sodium hypochlorite (6%), phenolic disinfectants, and oxidizing agents (e.g. Virkon).
The virus may remain viable in the carcasses of wild birds until decomposition is well advanced.
2.4.3 Modes of Introduction and Transmission
Modes of Introduction
The introduction of ND virus between flocks has been attributed to the following in order of importance:
- moving live infected birds (including vaccinated birds), and infected poultry products and by-products;
- contact with other animals;
- moving people and equipment;
- moving poultry products;
- airborne spread;
- contaminated poultry feed;
- contaminated water; and
Horizontal transmission of the disease can occur by inhalation or ingestion (fecal/oral route). Birds shed virus in both feces and respiratory secretions. Predatory birds and untreated swill containing poultry meat may contribute to direct horizontal spread.
Gallinaceous birds excrete APMV-1 for only 1 to 2 weeks, but psittacine birds often shed these viruses for several months. Some species of psittacine birds can excrete virus for over 1 year. Prolonged shedding has also been reported in some members of other orders, including owls (more than 4 months) and cormorants (1 month). Shedding can be sporadic.
The survival of aerosolized virus is likely dependent on humidity and other environmental factors, as well as the concentration of infected poultry. APMV-1 was found 64 meters but not 165 meters downwind of an infected farm.
Some isolates can be transmitted vertically through the egg to hatching chicks. Egg-associated transmission of highly virulent isolates is possible but uncommon, as the embryo usually dies unless the viral titre in the egg is low.
The newly hatched chicks may become infected from direct contact with contaminated eggshells and cracked or broken eggs.
Flies may transmit APMV-1 mechanically; however, it is still uncertain whether insects can carry enough virus to infect poultry. The importance of arthropod-borne transmission may vary with the type of housing and flock management.
During replication of ND virus a precursor fusion glycoprotein F0 is produced, which must be cleaved to F1 and F2 proteins for the virus to become infectious. The prime determinant of pathogenicity in ND virus strains is possessing basic amino acids at least at positions 113, 115, and 116, and phenylalanine at position 117 of the F0 protein. All but one virulent ND virus (pigeon paramyxovirus APMV-1) also had a basic amino acid at position 112. These positions form the cleavage site of the F0 protein and correspond to the C-terminus (116) and N-terminus (117) of the F2 and F1 proteins, respectively. If the F0 protein can be cleaved by proteases, which are found in a wide variety of internal organs, including liver, spleen, brain, heart, and lymphoid tissues, the virus can replicate in a wide variety of organs. The result is systemic infection and the appearance of clinical signs, followed by death in most cases.
For viruses of lower virulence, the F0 protein can only be cleaved by trypsin-like enzymes, which are found only on endodermal surfaces, such as in the intestinal and respiratory tracts. This limits replication to these surfaces in the animal. As a distinguishing feature, these viruses also cannot produce plaques in tissue culture without trypsin being added to the overlay medium.
2.6.1 Clinical Signs
Strains of ND virus cause sudden onset of depression, rapid breathing, and anorexia in all age groups of birds, and a precipitous drop in egg production in laying hens.
Viscerotropic pathogenic strains may cause:
- edema of the head; and
- bright green or bloody diarrhea as prominent clinical features.
Neurotropic pathogenic strains are characterized by marked neurologic signs, such as torticollis, tremors, or paralysis.
Morbidity and mortality with all pathogenic strains may rapidly exceed 90% in chickens and turkeys. Infected pet birds may show mild to severe respiratory, enteric and/or neurologic signs, and virus shedding for several months.
2.6.2 Gross Pathologic Lesions
Peracute form results in a very rapid death: no gross lesions.
Viscerotropic form can result in:
- edema of the interstitial tissues of the neck;
- hemorrhages that occur in the trachea and in the proventriculus, gizzard, and Peyer's patches, cecal tonsils, and other aggregations of lymphoid tissue in the intestinal wall;
- lesions in the gastrointestinal tract that progressively become edematous, hemorrhagic, necrotic, and finally ulcerative; and
- petechial hemorrhages that may be seen on the breast muscle, heart muscle, and peritoneal adipose tissue and on serosal surfaces.
- severe hemorrhagic tracheitis; and
- hemorrhagic lesions (proventriculus).
With less virulent strains, the lesion may be limited to congestion and mucoid exudates in the respiratory tract with aerosaculitis, depending on the secondary bacterial infection.
2.6.3 Morbidity and Mortality
Similar to the clinical signs of the disease, morbidity and mortality are variable because they are dependent on many factors, such as the following:
- host susceptibility;
- virulence of the virus;
- presence of concurrent disease; and
- farm management.
Mesogenic viruses can result in mortality up to 10% and lentogenic strains cause negligible mortality, whereas velogenic strains may cause up to 100% morbidity and mortality.
2.6.4 Laboratory Diagnosis
A tentative ND diagnosis may be possible based on thorough medical history from the owner, the clinical signs, the necropsy lesions, and a high morbidity and mortality. In an ND initial investigation, obtaining a virus isolate that can be fully characterized would be ideal, though this may not always be possible. In these situations, a combination of other tests, such as real-time reverse transcription polymerase chain reaction (RRT-PCR) and sequencing would be used to characterize the virus as much as possible.
Serology, using the hemagglutination inhibition (HI) test, demonstrates infection or vaccination. Virus isolation is conducted in embryonated chicken eggs. Hemagglutination activity is assessed on bacteria-free fluids; then, the HI assay identifies the viral agent.
Pathogenicity tests: ND virus isolates are assessed for virulence by an intracerebral pathogenicity index (ICPI) and intravenous pathogenicity index (IVPI). The OIE recommends one of these four tests:
- mean death time (MDT) in eggs
- ICPI in day-old chicks
- polymerase chain reaction pathogenicity (PCRP) test
APMV-1 isolates can also be separated into two clades: class I and class II, which are based on the genetic relation between viruses. The vast majority of APMV-1 strains belong to class II, which is divided into at least nine genotypes (I to IX). Class I isolates have been found mainly in wild waterfowl, and are usually of low pathogenicity.
Laboratory tests for the diagnosis of ND that are available in Canada include the following:
Virus Isolation: to indicate an active infection.
Isolation and identification of the ND virus from tracheal or cloacal swabs, feces, or internal organs is the gold standard method of diagnosis. To attempt virus isolation, specimen samples for laboratory submission should be collected from several birds, as it is not unusual for many specimens to fail to yield virus.
Suspensions in an antibiotic solution prepared from tracheal and cloacal swabs (or feces) obtained from live birds or feces, and pooled organ samples taken from dead birds are inoculated into the allantoic cavity of 9- to 11-day-old embryonating fowl eggs. The eggs are incubated at 37°C for 4 to 7 days. The allantoic fluid of any egg containing dead or dying embryos, as they arise, and all eggs at the end of the incubation period are tested for hemagglutinating activity. Any hemagglutinating agents should be tested for specific inhibition with a monospecific antiserum to ND virus (NDV). NDV (APMV-1) may show some antigenic cross-relation with some of the other avian paramyxovirus serotypes, particularly APMV-3 and APMV-7.
Rapid Molecular Diagnostic tests: RRT-PCR to indicate an active infection.
Serological tests: to indicate a past infection or a vaccine-induced immunity.
Serological tests are used to demonstrate the presence of antibodies that may be detected 5 to 7 days post-infection. The most commonly used techniques are the HI. This type of testing is of limited value for ND, as vaccination is widely used.
2.6.5 Differential Diagnoses
For central nervous system (CNS) signs, differentials include avian encephalomyelitis (AE), Marek's disease; fowl cholera, poisonings (heavy metals), intoxications; botulism and vitamin E/Se deficiency. Respiratory differentials are infectious bronchitis (IB); infectious laryngotracheitis (ILT); avian influenza (AI); coryza; mycoplasmosis; aspergillosis; turkey rhinotracheitis; psittacosis; and a diphtheritic form of fowl pox.
Cell-mediated immunity is:
- the initial response; and
- detectable 2 to 3 days after infection.
Humoral immunity: Protective antibodies measured by virus neutralization or by HI seen after ND infection:
- antibodies are detected in the serum at 6 to 10 days;
- peak response is 3 to 4 weeks; and
- antibodies may remain detectable for up to 1 year (mesogenic strain infection).
Local immunity: Antibodies in the secretion may appear at the same time as humoral immunity. Local protection is unproven and, in fact, may interfere with early eye-drop vaccination.
Chicks from immune hens may be protected by antibody derived from the yolk, and maternal immunity is protective and may interfere with the primary vaccination timing.
Vaccination against ND induces immunity against the infection and replication of the virus; however, vaccination doesn't completely prevent virus replication and shedding.
|Mesogenic||Strain H||1.4 fall within the OIE definition of viruses causing ND|
|Mukteswar||1.4 fall within the OIE definition of viruses causing ND|
|Roakin||1.45 fall within the OIE definition of viruses causing ND|
ICPI = Intracerebral Pathogenicity Index; ND = Newcastle disease; OIE = World Organisation for Animal Health
Lentogenic virus vaccines are generally administered by eye drop, in drinking water, by aerosol, or intranasally.
Live vaccines are relatively less expensive, stimulate local immunity, and are easy to use as a mass vaccination. In addition, they protect soon after vaccination, but require multiple vaccination. Lentogenic virus vaccines may cause the disease, and concurrent infections may make it worse.
Killed inactivated vaccines are widely used and are usually injected intramuscularly. These vaccines have been used where ND is endemic to revaccinate laying and breeding birds that were previously vaccinated with a live vaccine. The double vaccination is claimed to produce a stronger and more durable immune response. Revaccination close to the point of lay, using an oil-based inactivated vaccine, is believed to provide protection for the bird during the whole of the laying period.
Simultaneous use of a live vaccine (oral spray) and subcutaneous oil-based inactivated vaccine has protected chickens that were vaccinated as day-old chicks for 12 weeks.
2.8 Public Health
ND is a zoonotic disease with symptoms of headache, flu, and mild conjunctivitis (4 to 7 days), rarely becoming severe or leading to lasting visual impairment.
Laboratory workers and vaccination crews are affected most often. Poultry workers are rarely infected, and handling or consuming poultry products does not appear a risk.
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