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This article was published in 1966
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INSTITUTE OF INSPECTORS OF STOCK OF N.S.W. YEAR BOOK.
Clinical and Post-Mortem Findings in the Diagnosis of Newcastle Disease
C. A. W. JACKSON, B.V.Sc., Veterinary Research Officer, Glenfield
Recent confirmation of the existence of Newcastle Disease virus (NDV) in Australia requires appreciation by all veterinarians of the need to identify outbreaks as early as possible.
General opinion is that clinical and autopsy findings are a very unreliable basis for diagnosis. This is emphasised by the disease showing a wide variation in symptomatology and all degrees of severity from 100 per cent mortality to asymptomatic cases.
In order to overcome these difficulties in diagnosis it is necessary to have in mind all forms the disease may take together with knowledge of disease conditions already existent in this country and the value of laboratory confirmation.
Symptomatology in Chickens
A number of strains of NDV have been isolated overseas and have been grouped on the basis of pathogenicity. For convenience, symptoms are described on a similar basis as follows:
1. Velogenic (Virulent) Form. Strains responsible have been isolated from the original outbreak in Great Britain in 1926, from Asian countries and in Victoria in 1931. The first symptom is dullness followed by depression. The disease spreads rapidly and birds show diarrhoea, gasping, cyanosis of the comb, progressive weakness and prostration, may die without premonitory symptoms. Most birds die within a week but those surviving may show involvement of the central nervous system indicated by leg weakness, paralysis, chronic spasms, circling, torticollis, opisthotonos or emprosthotonos, A sharp fall in egg production occurs and soft and imperfectly shelled eggs may be laid.
Birds of all ages are affected and mortality is usually greater than 90 per cent. The surviving paralytic birds seldom recover.
2. Mesogenic (less virulent) Form. Strains responsible have been isolated from outbreaks in U.S.A. and Europe and are used for vaccine production in U.S.A. Birds initially show depression followed by diarrhoea, coughing and gasping. Appetite is reduced and egg production falls rapidly. Respiratory symptoms subside in two to three weeks and are followed by nervous symptoms especially in chickens. Some chickens may show haemorrhages on the legs ("red-legs"). A feature of this form is the effect on egg quality; the shell may be imperfect, discoloured or absent and many eggs may be abnormally shaped. Later there may be a reduction in egg weight.
Chickens are more susceptible and the mortality rate may exceed 50 per cent. In adults, mortality rate usually varies from 5 to 50 per cent.
3. Lentogenic (mild) form. Strains responsible have been isolated from outbreaks in Canada, South Africa, Europe and other countries and are used for vaccine production. Affected chickens show mild respiratory symptoms with nasal discharge and rales. There is usually a drop in egg production for a few weeks.
Young chickens can show up to 50 per cent mortality, but losses in adults are negligible.
4. Asymptomatic Form. Serological diagnosis in the absence of clinical signs has been made in U.S.A. and Great Britain. Spread of this form has been shown to occur. Titres of birds were found to be very variable and a large number of sera were needed to confirm the presence of NDV.
Autopsy Findings
1. Velogenic Form
The lesions are mainly haemorrhagic and inflammatory. Petechial haemorrhages are usually seen in the proventricular and gizzard mucosa and less frequently in the trachea, intestine, mesentery and in the muscles. Commonly the lymphoid follicles are haemorrhagic and necrotic. (Some birds may die with no gross pathological changes.) Embryos may show stunting with congestion of the legs ("red-legs").
2. Mesogenic Form
There is marked variation in pathology and in some outbreaks a large percentage of the birds show no gross pathology. Typically, haemorrhages are seen in the proventriculus. Birds with respiratory involvement commonly show a cloudiness of the air sacs and this is often followed by secondary infection with E. coli. Vesicles on the skin and nephritis are sometimes seen.
Embryos may show the "red-leg" syndrome.
3. Lentogenic Form
Usually no macroscopic changes are seen although early cases in chickens may show a mild tracheitis.
Other Poultry
Other species of poultry are relatively more resistant.
1. Turkeys
Poults show initial depression, inappetence and respiratory symptoms. Nervous symptoms are uncommon. Adults may show respiratory symptoms, egg production is commonly reduced and deformed and soft shelled eggs produced. Mortality up to 60 per cent has been seen in the poults.
Autopsy findings are few and only a cloudiness of the air sacs may be seen.
2. Ducks and Geese
These species are usually unaffected but locomotory disturbances were reported in the outbreaks in Victoria in 1931.
Differential Diagnosis
The following diseases recognised in Australia could resemble an outbreak of Newcastle Disease at one time or another during its course.
1. Diseases causing a high mortality rate over a short period such as Fowl Cholera and poisoning.
2. Respiratory diseases such as IB, ILT, CRD, vitamin A deficiency, Coryza, Pullorum, Infectious Sinusitis (in turkeys), Leucosis, Mycosis and Fowl Cholera, can cause gasping and other respiratory symptoms as seen in ND.
3. Nervous diseases such as Mareks Disease (Fowl Paralysis), Avian Encephalomyelitis, riboflavin deficiency, Encephalomalacia, Pullorum, "X" Disease, Botulism, insecticidal and heavy metal poisons.
4. Diseases causing a fall in egg production such as IB, CRD, Avian Monocytosis and stress. The fall in production due to ND to almost zero in ten days is more dramatic than occurs in other diseases.
5. Diseases causing similar autopsy findings such as proventriculitis due to non-specific causes and phosphorus poisoning, tracheitis due to CRD, IB and ILT, haemorrhages as in Fowl Cholera, Haemorrhagic Disease and septicaemias, or sacculitis and pericarditis as in CRD, Colibacillosis and IB. Non-specific proventriculitis found in N.S.W. could not be attributed to any infectious cause. Initially depression and inappetence are seen. The bird usually starves to death and mortalities may reach 30 per cent. The proventriculus shows thickened walls and haemorrhages around numerous small ulcers in the mucosa.
1966 Outbreak
The relationship of the N.S.W. and Queensland isolates to overseas strains is difficult to evaluate until further tests are done to determine the pathogenicity. There is little evidence at present that it is causing any trouble in the field. Recent examination of the virus in U.S.A. indicates a very mild strain to be present. With this in mind we should consider the possible effect of the strain in our flocks. The virus could easily be clouded by respiratory diseases already present in Australia and could be a complicating factor with CRD and IB in other diseases as is the case in U.S.A. In this case the disease would be extremely difficult to recognise in the field. The virus is certainly widespread in N.S.W. as indicated by serological tests.
Diagnosis
1. Field Examination
The following features could be regarded together or individually as suggestive of ND.
(a) Respiratory symptoms in chickens followed by the development of nervous symptoms.
(b) "Red-legs" syndrome.
(c) A sharp fall in egg production in adults.
(d) Haemorrhages in the proventriculus.
2. Laboratory Examination
Isolation of the virus is necessary for a positive diagnosis although confirmation by serology and histopathology is made in enzootic areas in U.S.A.
(a) Isolation of Virus. The forwarding of live birds should be avoided. Specimens of tissue should be collected from at least six birds preferably from three showing signs of the acute disease and three recently dead. Tissue should be spleen, lung and trachea, brain and proventriculus collected as free from contamination as possible. Tissue should be sealed in a jar and forwarded in ice in a thermos flask.
(b) Serology. The haemagglutination-inhibition (H.I.) test will detect birds that have experienced ND infection. At least 20 birds should be bled from each pen or group. Birds should be aged 10-20 weeks old. The H.I. antibody appears about four to eight days after infection and usually lasts about one year.
(c) Histopathology. Changes are seen in most tissues with more pathogenic strains. Changes in the brain are considered to be a valuable diagnostic aid.
(d) Differential Diagnosis. Pipettes of heart blood and liver should be forwarded to eliminate bacterial infections.
Conclusion
The variability of symptomatology and autopsy findings in ND requires exacting examination of all suspect outbreaks. Although it is thought that there is little chance of a change in virulence of the virus, the possibility still exists and all forms of ND should be kept in mind.