Definition
Velogenic Newcastle disease (VND) is the most severe form of
Newcastle disease and is likely the most serious disease of poultry throughout the world
(2,4,13). In chickens it is characterized by lesions in the brain or gastrointestinal
tract, morbidity rates near 100 percent, and mortality rates as high as 90 percent in
susceptible chickens. Neurologic signs or severe depression are the most obvious clinical
sign, and some nonvaccinated birds may be found dead with no detected sign of prior
illness.
Etiology
Newcastle disease viruses (NDV's) occur as three pathotypes:
lentogenic, mesogenic, and velogenic, reflecting increasing levels of virulence. The most
virulent (velogenic) isolates are further subdivided into neurotropic and viscerotropic
types. The velogenic isolates are considered exotic to the United States, and the disease
caused by these VND isolates is the subject of this chapter.
The Newcastle disease viruses belong to the Paramyxoviridae virus family and, like other members of this group, possess two surface proteins that are
important to the identification and behavior of the virus. The first,
hemagglutinin/neuraminidase (HN) is important in the attachment and release of the virus
from the host cells in addition to its serologic identification. The other very important
surface protein is the fusion (F) protein, which has a critical role in the pathogenesis
of the disease. There are at least nine known types of avian paramyxoviruses based on the
antigenic makeup of the hemagglutinin. NDV is the prototype virus for Type 1 avian
paramyxoviruses.
Host Range
Inapparently infected carriers that are the most likely source for
introduction of VND include numerous species of exotic pet and exposition birds,
waterfowl, and domestic poultry (18). A persistent carrier state has been demonstrated in
psittacine (8) and in certain other wild birds (19) whereas virus can be recovered from
chickens for shorter periods of time, usually 14 days or less.
Geographic Distribution
Velogenic Newcastle disease is endemic in many countries of Asia,
the Middle East, Africa, and Central and South America. Some European countries are
considered free of VND. VND has caused high mortality in wild cormorants in Canada and the
United States.
Transmission
In many parts of the tropics VND is recurrent in the poultry
populations. One possibility is that they are infected from a wild bird reservoir.
Additional studies will be required before it can be established which species, if any,
are true carriers and which are only transiently infected. It is not known whether the
occurrence of VND in wild birds moving in international trade can be reduced by avoiding
the capture of certain species or their collection at certain time periods or places. Once
introduced into poultry, the virus spreads farm-to-farm by the movement of inapparently
infected poultry species; on contaminated objects such as boots, sacks, egg trays, and
crates; or by flies (5) or mice. Reports from England (11) that the virus can be
wind-borne under certain conditions should be considered even though there was no evidence
of airborne transmission between premises with the virus that caused the 1971 outbreak in
California. Free-flying wild birds apparently had no role in the spread of VND during that
outbreak (16).
Incubation Period
The incubation period for Newcastle disease after natural exposure
varies from 2 to 15 days. For VND in chickens, an incubation period of 2 to 6 days is
common. The incubation period in other species of birds may be longer.
Clinical Signs
Velogenic Newcastle disease is a devastating malady in
unvaccinated chickens of any age. The first sign in laying chickens is usually a marked
drop in egg production followed within 24 to 43 hours by high death losses. At the onset,
10-15 percent of a flock may be lost in 24 hours. After 7 to 10 days, deaths usually
subside, and birds surviving 12 to 14 days generally do not die but may display permanent
paralysis and other neurologic signs. The reproductive system may be permanently impaired,
and thus egg production does not return to previous levels. In vaccinated chickens, or
chicks protected by parental antibodies, the clinical signs are less severe and are
proportional to the level of protective antibodies.
With viscerotropic strains (VVND), edema of the head, especially
around the eyes (Fig. 107) may become
apparent after birds have been sick for 2 or 3 days (9). This edema usually does not
involve the comb and wattle to the extent of highly pathogenic avian influenza (HPAI). A
dark ring sometimes forms around the eye, probably due to cyanosis and poor blood
circulation in the edematous tissue. This "black eye" appearance is especially
visible in white chickens.
Bile-stained, greenish-dark diarrhea may be noted 2 to 3 days
after onset of illness. Some birds in an affected flock usually have diarrhea throughout
the course of the disease.
The most noteworthy clinical sign in unvaccinated flocks is sudden
death without prior indications of illness. The peracute onset often causes the owner to
suspect poisoning.
Respiratory distress and signs of neurological disturbances, such
as drooping wings, torticollis, and ataxia. may not be as marked as they are with the
neurotropic forms of the disease. However, these neurologic signs are frequently observed
in chickens that survive infection with the viscerotopic strains for 2 or 3 weeks. Because
of lack of experience with viscerotropic strains, poultry owners throughout the United
States and Canada may not consider Newcastle disease as a possible diagnosis unless they
see the neurologic signs they have seen with the domestic neurotropic viruses.
Neurotropic strains cause respiratory signs soon followed by
neurologic signs, including muscular tremors, paralysis of legs or wings, torticollis, and
opisthotonos. There is a marked decline in egg production but ususally no diarrhea.
Disease signs may differ markedly, depending on the host species. Psittacines or pigeons
infected with the viscerotropic strains of virus may display neurologic signs typical of
the disease caused by the strains of neurotropic ND in chickens (7). These same
viscerotropic viruses may cause typical signs and lesions of VVND when inoculated into
chickens (6). In some species, such as finches and canaries, clinical disease may not be
observed.
Gross Lesions
No gross lesion may be observed in many of the first birds dying
in a commercial poultry operation. Peracute deaths are generally due to collapse or
dysfunction of the reticuloendothelial system before discernible gross lesions have
developed. There is no pathognomonic gross lesion for VVND, but, generally, sufficient
lesions can be found to make a tentative diagnosis if enough birds are examined (14).
Because of the marked similarities between the gross lesions of VVND and higly pathogenic
avian influenza, a final diagnosis in the first flocks must await virus isolation and
identification. In a continuing outbreak where numerous flocks are involved, gross
observations may eventually be all that is necessary when typical lesions are present.
Edema of the interstitial tissue of the neck, especially near the
thoracic inlet, may be marked. After the trachea and esophagus are exposed during necropsy
examination, straw colored fluid may drip from these tissues. Congestion and occasionally
hemorrhage may be seen in the trachea generally corresponding to the rings of cartilage.
Proventriculus
Petechial and small ecchymotic hemorrhages may be present on the
mucosa of the proventriculus (Fig. 108).
These small hemorrhagic foci tend to be found near the base of the papillae and
concentrated around the posterior and anterior orifices.
Intestine
Peyer's patches (Fig. 109), cecal tonsils (Fig.110), and other focal aggregations of lymphoid tissue in the
gut wall usually are markedly involved and are responsible for the term viscerotropic
applied to this form of Newcastle disease. These areas progressively become edematous,
hemorrhagic, necrotic, and ulcerative. In chickens that have died from VVND, these
involved lymphoid areas can often be observed without opening the gut.
Reproductive System
Ovaries may be edematous, hemorrhagic, or degenerated. Yolk
peritonitis can frequently be observed in layers as a result of VVND, and rough, misshapen
eggs are frequently laid by recovering hens.
Neurotropic strains of VND may cause few gross lesions other than
in the trachea and lungs. There will be no gross lesion in the brain of diseased birds.
Gross lesion patterns usually differ markedly between the disease caused by the
viscerotropic and neurotropic velogenic viruses.
Morbidity and Mortality
Clinical VND is most severe in chickens, peafowl, guineas,
pheasant, quail and pigeons. Turkeys may develop a milder form of the disease. Severity of
disease in psittacine and passerine birds is variable. In susceptible chickens, the
morbidity and mortality rates can be as high as 100 percent and 90 percent, respectively.
In some species such as finches and canaries, clinical disease may not be observed.
Diagnosis
Field Diagnosis
A tentative diagnosis of VND may be made on the basis of history,
clinical signs, and gross lesions, but because of similarities to other diseases such as
fowl cholera and highly pathogenic avian influenza, confirmation requires virus isolation
and identification.
Specimens for Laboratory
Virus can readily be recovered from sick or recently dead birds.
Swabs are the most convenient way to transfer VND virus from tissues or secretions of the
suspect bird to brain and heart infusion broth or other cell culture maintenance medium
containing high levels of antibiotics (1). Trachea, lung, spleen, cloaca, and brain should
be sampled. Swabs should be inserted deeply to ensure obtaining ample epithelial tissue.
If large numbers of dead or live birds are to be sampled, cloacal swabs from up to five
birds can be pooled in the same tube of broth. An alternate technique is to place 0.5 cm3 of each tissue into the broth. If the specimens can be delivered to a laboratory within 24
hours, they should be placed on ice. If delivery will take longer, quick-freeze the
specimens and do not allow them to thaw during transit.
Laboratory Diagnosis
In the laboratory, virus isolation is attempted by inoculating 9-
to 11-day-old embryonating chicken eggs. Chorioallantoic fluid (CAF) is collected from all
embryos dying after 24 hours postinoculation and tested for hemagglutination (HA)
activity. If positive, the hemagglutination-inhibition (Hl) test is used with known
NDV-positive serum to confirm the presence of NDV in the CAF (3). If NDV is found, it is
characterized by inoculating 4- to 6-week-old chickens free of ND antibodies with the
suspect CAF by swabbing the cloaca, instilling into the nares or conjuctival sac, or
injecting into the thoracic air sac. If VVND virus is present, the inoculated chicks
usually die in 3 to 7 days, revealing typical visceral lesions on postmortem examination.
Neurotroph ic VVD viruses will cause severe neurologic and respiratory signs in inoculated
chickens but no visceral lesions. If no bird dies in 10 days, the NDV is not considered to
be the velogenic, viscerotropic type but is either a lentogen or mesogen.
Differential Diagnosis
The viscerotropic, velogenic Newcastle disease in poultry can be
confused with highly pathogenic avian influenza, infectious laryngotracheitis, fowl
cholera, and coryza.
Vaccination
Vaccination with viable or inactivated oil emulsion vaccines, or
both, can markedly reduce the losses from VND in poultry flocks. If eradication of the
virus is not the goal of the control program, vaccines can be used to lessen the impact of
the disease. Their use, however, can make the complete eradication of the virus much more
problematic by increasing the difficulty of identifying infected flocks. There is little
doubt, however, that vaccination makes the flock more refractive to infection when exposed
and reduces the quantity of virus shed by infected flocks.
Control and Eradication
Before 1972, VND was introduced into the United States on several
occasions by unrestricted introduction of exotic pet birds, especially psittacine birds.
Because pet birds are not usually associated with domestic poultry, VND outbreaks were
rare (20). Since 1973, restrictions on the importation of exotic birds requiring the
quarantining and testing of imported birds in approved quarantine facilities have reduced
but not eliminated the threat of VND in the United States. Illegally imported exotic bird
species remain the source of frequent outbreaks of VND in private or commercial aviaries.
The establishment of a strict quarantine and destruction of all
infected and exposed birds with financial indemnification for losses followed by thorough
cleaning and disinfection of premises were the main features necessary for eradication of
VND virus from the poultry producing area of southern California. Flocks may be safely and
humanely destroyed using carbon dioxide in air-tight chambers and the carcasses disposed
of by burying, composting, or rendering, depending upon the geographic area and the
numbers involved. The VND virus has been recovered from effluent water for as long as 21
days and from carcasses for 7 days when the daytime temperatures were over 90o F. It is
recommended that premises be kept free of domestic poultry for an additional 30 days after
cleaning and disinfection are completed.
Insects and mice associated with the poultry should be destroyed
before depopulation of a flock begins (5,12). Usually 48 hours is sufficient to control
these vectors. As soon as all birds are killed and the manure and feed removed, all
equipment and structural surfaces should be thoroughly cleaned using high-pressure spray
equipment. The entire premises should then be sprayed with an approved residual
disinfectant such as the cresylics or phenolics. Preliminary disinfection will probably
inactivate most of the viruses on the surface of floors, equipment, cages, etc., but no
disinfectant is effective unless it is applied to scrupulously cleaned surfaces free of
all organic material.
Cleaning and disinfecting commercial poultry premises are
time-consuming and expensive operations. All manure must be removed down to a bare
concrete floor. If the floor is earthen, at least the top inch of soil should be removed
with the manure. Manure can be safely disposed of by burying it at least 5 feet deep or by
composting. If composting is used, the manure piles should be tightly covered with black
polyethylene sheets in a manner to prevent access by birds, insects, and rodents during
composting. These piles of manure should remain tightly covered and undisturbed at least
90 days during warm weather and for longer periods during cold weather. Recent studies
indicate that proper composting can decompose carcasses and manure, and thus inactivate
viruses in only a few weeks.
Feathers, usually numerous around commercial poultry premises, can
be burned outside the buildings, and in some cases inside, with the careful use of a flame
thrower, or they can be removed and the area wet down with disinfectant. The hot sun and
high daytime temperatures will assist in destroying the virus in the area of the houses.
Extremely cold temperatures will make the cleaning and decontamination process much more
difficult, and the results more uncertain.
In 1997, because neither the neurotropic or viscertropic strain of
velogenic Newcastle disease was known to exist in the United States, USDA-APHIS declared
both types to be exotic and therefore indistinguishable as to the response of disease
control officials should they occur in the United States.
Surveillance
The most difficult part of the VND eradication program is locating
inapparently infected and exposed birds.
Repeated vaccination at 30 to 50 day intervals protects most
chickens against clinical manifestation of VND. However, vaccine does not prevent all
chickens in a flock from becoming infected, showing no disease sign, or shedding virulent
virus. As individual chickens become susceptible and get exposed to the virus, they become
infected and also shed the virus for a time. Thus, the virulent virus continues to be
present in apparently healthy, vaccinated flocks. The advantages of using vaccines as part
of a VND eradication program must be weighed against the difficulty created in finding
asymptomatic but infected and virus-shedding flocks. In such instances owners should be
encouraged to observe strict biosecurity measures to reduce the chances of their flocks
being exposed to VND virus.
Infected carriers in vaccinated flocks can be detected using one
of two systems. In the first, all birds dying during a 24-hour period are collected twice
a week, and cloacal swabs and brains are collected and cultured for the presence of VND
virus using the diagnostic sampling procedures described earlier. Birds in VND-infected
flocks that die from Marek's disease, leukosis, gout, and numerous other disease
conditions may yield VND virus—especially if their immune system was impaired by
those diseases before death. In the second virus detection system, susceptible sentinel
birds are placed in vaccinated flocks (18). The sentinel birds must be unvaccinated and
obtained from a specific pathogen-free source to be certain that they do not inadvertently
serve as a source of diseases for the suspect flock. In most instances the sentinel birds
die from VND within a week or so after placement if there is VND virus present in the
flock; however, in some cases it is sometimes difficult to place sentinel birds so they
are adequately exposed to any VND virus that may be in the flock — especially in
caged-layer flocks.
Public Health
Although people may become infected with VND virus, the resulting
disease is typically limited to a conjunctivitis. Recovery is usually rapid, and the virus
is no longer present in eye fluids after 4 to 7 days. Infections have occurred mostly in
laboratory workers and vaccinating crews with rare cases in poultry handlers. No instance
of transmission to humans through handling or consuming of poultry products is known.
Individuals with conjunctivitis from VND virus should not enter poultry premises or come
in contact with live avian species.
GUIDE TO THE LITERATURE
1. ALEXANDER, D. J. 1989. Newcastle Disease. In A Laboratory
Manual for the Isolation and Identification of Avian Pathogens. 3rd. H. G. Purchase, L
H. Arp, C. H. Domermuth, and J. E. Pearson (eds.), Kennett Square, PA: Amer. Assoc. Avian
Pathologist,.pp 114-120.
2. ALEXANDER, D. J. 1997. Newcastle Disease and Other
Paramyxovirus Infections. In Diseases of Poultry, 10th ed., B. W. Calnek, H. J.
Barnes, C. W. Beard, L.R. McDougal, and Y.M. Saif, eds., Ames, IA:Iowa State University
Press, pp 541-569.
3. BEARD, C. W. 1989. Serologic Procedures. In A Laboratory
Manual for the Isolation and Identification of Avian Pathogens. 3rd. H. G. Purchase, L
H. Arp, C. H. Domermuth, and J. E. Pearson (eds.), Kennett Square, PA: Amer. Assoc. Avian
Pathologist,.pp 192-200.
4. BEARD, C. W. and HANSON, H. P. 1984. Newcastle Disease. In Diseases
of Poultry, 8th ed. M. S. Hofstad, H. J. Bames, B. W. Calnek, W. M. Reid, andH. W.
Yoder, eds., ., Ames, IA:Iowa State Univ. Press, pp. 452-470.
5. BRAM, R. A., WILSON, S. W., and SARDESAI, J. B. 1974. Fly
control in support of the exotic Newcastle disease eradication program in southern
California. Bull Entomol. Soc. Amer., 20:(3)228280.
6. BRUGH, M., and BEARD, C. W. 1984. Atypical disease produced in
chickens by Newcastle disease virus isolated from exotic birds. Avian Dis., 28(2):482-488.
7. ERICKSON, G. A., BRUGH, M., and BEARD, C.W. 1980. Viscerotropic
velogenic Newcastle disease in pigeons: Clinical disease and immunization. Avian Dis.,
24(1):256-267.
8. ERICKSON, G. A., MARE, C. J., GUSTAFSON, G. A., MILLER, L. D.,
PROCTOR. S.J. and CARBREY, E. A, 1977. Interactions between viscerotropic velogenic
Newcastle disease and pet birds of six species. 1. Clinical and serologic responses and
viral excretions. Avian Dis., 21:264-272.
9. HANSON, R. P., SPALATIN, J., and JACOBSON, G. S. 1973. The
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10. HAYES, F. A. 1976. Role of Wildlife in Exotic Diseases. In Proc.
FAD Sem. January 15-16, 1976, Athens, GA, pp. 99-105.
11. HUGH-JONES, M. E., ALLAN, W. H., DARK, F. A., and HARPER, G.
J. 1973. The evidence for airborne spread of Newcastle disease. J. Hygiene, Cambridge,
71:325-339.
12. JOHNSON, D. C., COOPER. R. S., and ORSBORN, J. S. 1974.
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633-636.
13. LANCASTER, J. E., and ALEXANDER, D. J. 1975. Newcastle Disease
Virus and Spread. Canada, Dept. Agric., Monograph No. 11, 79 pp.
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velogenic viscerotropic Newcastle disease. J.A.V.M.A., 163(9):1075-1079.
15. OMOHUNDRO, R. E. 1972. Exotic Newcastle Disease Eradication.
In Proc. 76th Ann. Meet. U. S. Anim. Health Assoc., pp. 264-268.
16. SHARMAN, E. C., and LAMONT, J. D. 1974. The Velogenic
Viscerotropic Newcastle Disease Eradication Program in Southern California. (Presented at
the XV World Poultry, Congress, Aug. 11-16, 1974, New Orleans, LA.)
17. SHARMAN, E. C., and Walker, J. W. 1973. Regulatory aspects of
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18. UTTERBACK, W. W., and SCHARTZ, J. H. 1973. Epizootiology of
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163(9): 1080-1088.
19. VICKERS, M. L, and HANSON, R. P. 1979. Experimental Newcastle
disease virus infections in three species of wild birds. Avian Cis., 23:70-79.
20. WALKER, J. W., HERON, B. R., and MIXSON, M. A. 1973. Exotic
newcastle disease eradication programs in the United States. Avian Dis., 17: (3) 486-503.
Charles W. Beard, D.V.M., M.S., Ph.D., USDA, ARS, Southeast
Poultry Research Laboratory, Athens, GA
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