1. Newcastle disease (NDV) is avian paramyxovirus type 1.
2. Virulent or velogenic NDV (vNDV) occurred in Victoria in the 1930s as part of a world wide panzootic. It was eradicated by slaughter.
3. Lentogenic NDVs (lNDV) were isolated from Australian poultry in the 1960s and found to be widespread, but not ubiquitous. These belong to an Australian sub-group within phylogenetic group I of NDV. The poultry isolates are distinct from wild bird isolates thus far studied.
4. V4 is a specific strain of lNDV, but derivatives in different laboratories vary in biological characteristics. lNDV isolates from poultry are frequently referred to as 'V4-like' but not characterised further, and may be quite distinct.
5. Haemagglutination inhibition (HI) titres of 1/8 induced by V4 are protective against vNDV.
6. 'Late broiler respiratory disease' has been well recognised in Australian poultry since the late 1980s and involves a lNDV with some respiratory trophism along with reduced immunocompetence, stress, and other respiratory pathogens such as infectious bronchitis virus and coliforrns. Deaths are due to bacterial septicaemia.
7. Since the mid 1990s the Australian poultry industry has experienced a serious problem with virulent Marek's disease (MD) in susceptible genotypes manifest as reduced immunocompetence and secondary problems in broilers, and as mortality in point of lay pullets and breeders due to tumours manifested as weakness, weight loss and occasional nervous signs with losses exceeding 25% from 18-30 weeks and thereafter >1% per week. Only in the last year has this come under control with different vaccines and vaccination procedures.
In late August 1998 a broiler farm of 6 sheds @ 24,000 chickens each suffered a rapid rise in mortality to 2-3% per day in two sheds at 33-37 days. Birds examined had respiratory distress, tracheal congestion and lung consolidation. Histologically there was severe lymphocytic tracheitis and NDV was isolated from a pool of lungs and spleens submitted for avian influenza exclusion. This virus had an intracerebral pathogenicity index (ICPI) of 0.4-0.5 and was thus lNDV. The affected birds had low or negative HI titres to NDV, whereas sera collected at slaughter a week later had titres of 1/16-1/32. This virus is the only recent isolate of lNDV from late broiler respiratory disease which AAHL have studied and probably is a single representative of a more widespread virus. It was distinct from previous isolates of lNDV.
98/1IP (Dean Park) A mortality problem commenced in early August in one group of a split delivery of 5,000 started pullets onto a mixed enterprise poultry farm. Initially this was manifest as weight loss, weakness, shell-less and soft-shelled eggs, and poor feed consumption. Necropsy revealed mild peritonitis which was diagnosed as fowl cholera although Pasteurella multocida was not isolated, and there was some amelioration with antibiotic treatment. Histological examination revealed widespread focal lymphoid accumulations tentatively diagnosed as MD although affected birds with gross lesions of MD were rare. The syndrome spread to the remainder of this particular delivery of birds, but not to the other 80,000 caged layers or 1,400 free range layers. By mid September, 6 weeks after first investigation 30% of the flock had died or been culled, and several hundred birds were noted to have torticollis. A tentative diagnosis of neurotrophic ND was made and vNDV was isolated. This virus was closely related to but distinct at crucial sites from the so-called 'progenitor virus'. Histologically there was non-suppurative encephalitis with perivascular lymphoid cuffs in the brain stem and cerebellum, a few small foci of gliosis, and Wallerian degeneration of peripheral (sciatic) nerves. Retrospectively there were some negative titres amongst these birds early in the outbreak, and a few high titres (>1/1024), but only moderate titres at the final investigation (1/64-1/128). At this investigation the birds remaining in this infected flock appeared healthy, were coming into lay, and only 2 birds were found with vague nervous signs.
The farm had received 76,000 broilers in mid August, and these were collected for abattoir slaughter the week before vNDV was diagnosed. In retrospect some of these flocks had been experiencing a high mortality with poor growth and 'leg weakness' with daily mortality in some sheds of >5%, and grow out mortalities of >50%. vNDV was isolated from carcasses. In the final week, the disease gained access to 10,500 6-week-old layer pullets in another shed: 20% showed weakness and paralysis, and <5% with torticollis. There were no gross lesions but brain histopathology was as for the older birds. 65% of the affected pullets were seronegative and the others had low titres. vNDV was isolated from tracheal swabs. NDV was not isolated from ostriches, geese or feral racing pigeons on the farm.
98/2IP (Glenorie) A serviceman who had examined affected birds at 98/1IP in mid September during the week before imposing quarantine noted a few similar birds on another farm where a point outbreak of disease was occurring in recently caged pullets. Some 60 birds out of a group of 200 died from a flock of 4,000. Most showed weakness and flaccid paralysis, only a few had torticollis. On necropsy there was empty gastrointestinal tracts, mild peritonitis and congestion of the caecal tonsils. Histologically there was non-suppurative encephalitis in the brain stem and cerebellum. The affected birds had low to moderate titres to NDV (up to 1/256) but outside the area of affected birds the pullets were seronegative. vNDV was isolated from these birds and shown to be similar to the virus form 98/1IP. 15,000 other caged layers and 1,000 free-range birds had low titres to NDV and were clinically normal. The probable source of infection was eggs purchased from 98/1LP to make up orders. These eggs were delivered to the farm on cardboard egg fillers which were then recycled without disinfection into the sheds to collect eggs.
98/81IP (Rylestone) This farm had about 2,500 free range broilers. 700 4-week-old birds had been purchased from 98/1IP in late August. A week after arrival mortality commenced and by late September 90% of this group had died. A few paralysed birds were necropsied, besides one bird with gross lesions typical of MD, the others had mild pericarditis and focal non-suppurative nephritis. The surviving birds had titres of 1/32-1/512. vNDV was not isolated, but PCR demonstrated virulence sequence in the parenchyma and pericardial surface of one heart. The birds in the adjacent pens were clinically normal and seronegative.
99/1IP (Mangrove Mountain) This was a rearing farm for a large independent layer farm and housed 27,000 pullets in cages. A disease syndrome characterised by respiratory noise commenced at the doorway of one shed and spread over 4-5 days in early April to involve about 1,000 10-week-old birds distributed in a fan shaped pattern within the shed. Mortality was rising to 25-35 birds per day, most were depressed and weak, about a dozen showed nervous signs such as tremors and torticollis. On necropsy there was mucoid tracheitis and congestion of the caecal tonsils. Histologically there was non-suppurative lesions of meningoencephalitis mainly involving the brain stem and cerebellum, cervical myelitis, pericarditis and some myocarditis and nephritis; along with severe tracheitis, splenic lymphoid necrosis and equivocal caecal tonsil microhaemorrhage. A notable feature compared to the 1998 outbreak was the very severe tracheitis in these birds, and the severe encephalitis which besides lymphoid perivascular cuffs also involved multiple foci of gliosis and neuronal necrosis. Birds from the affected area had low moderate titres to NDV (1/8-1/512) whereas birds elsewhere in the shed, and in the other sheds were seronegative. vNDV was isolated but this virus was more closely related to the so- called 'progenitor virus' than the isolates from the 1998 outbreak. In the subsequent weeks vNDV was diagnosed in several adjacent farms, of particular interest was 99/8IP.
99/8IP (Mangrove Mountain) This was a broiler farm with 4 sheds recently thinned out and approximately 50,000 chickens at 42 days of age remained. In a 36 hour period in mid April, 45,000 (90%) of these birds died; the remaining 10% showed vague nervous signs such as tremors, star gazing and pecking at the air. No gross lesions were reported. Histologically there was severe non-suppurative encephalomeningitis with multifocal gliosis and neuronal necrosis, mainly in the brain stem and cerebellum. Other tissues were not examined.
The 1998 outbreak was controlled by slaughter of infected and in-contact birds, and disinfection: no further extension of the outbreak occurred. The 1999 outbreak is being controlled in the same manner, but as at time of writing has not been eradicated.
NDV on release from the cell has a fusion protein (Fo) which requires separation by action of tissue enzymes before it can attach to host cells and become infectious. The more virulent viruses have basic amino acids at the cleavage site thus allowing them to be cleaved by a wider range of tissue enzymes in the host. The vNDV isolates from 1998 have an identical pattern to exotic vNDV. In addition, they are more closely related to the so-called 'progenitor virus' than to V4.
The amino acid sequences at the cleavage site of the fusion protein of NDV are:
1. vNDV occurred on 98/1IP, 98/2IP & 99/1IP as point outbreaks in antibody free caged birds. Disease initially spread slowly within sheds.
2. Spread amongst susceptible birds on litter or free range was far more rapid, and on some farms devastating.
3. The initial 1998 outbreak was against a background of high mortalities from MD, and the 1999 outbreak occurred in an area with severe respiratory disease.
4. The vNDV isolates were derived from Australian lNDV strains: the 1998 and 1999 isolates were not identical.
5. The clinical signs were death, weakness and flaccid paralysis: torticollis was spectacular but occurred in a minority of affected birds.
6. There were no characteristic gross lesions, except mild peritonitis in adult layers.
7. Histological lesions in the 1999 outbreak were more florid and more widespread than in 1998 with main concentration being brain stem and cerebellum. Severe tracheitis, conjunctivitis, nephritis, pericarditis, myocarditis and serositis were noted.
(this being a slightly modified version of Proceedings of the Australian Society for Veterinary Pathology, Annual Scientific Meeting, May 1999. Pp44-46.)