Avian Notifiable Disease- Newcastle Disease & Avian Influenza

Notifiable disease in birds:

• Newcastle Disease (paramyxovirus).
• Avian Influenza (orthomyxovirus)
• Pigeon paramyxovirus. 

Both ND and AI are enveloped RNA viruses with surface glycoproteins. 

Morphology

Avian Influenza:

• H & N glycoprotein spikes.
• Helical nucleocapsid.
• ssRNA genome. 
• Segmented genome.
• Antigenic shift.
• Antigenic drift.

Newcastle Disease 

• H, N & F glycoprotein spikes.
• Helical nucleocapsid.
• ssRNA genome.
• No segmented genome, and only undergoes antigenic drift. 

The diseases caused by both appear very similar:

• Highly infectious and affect a wide range of avian species.
• Range from apathogenic to highly virulent.
• Can cause respiratory, enteric and sometimes nervous signs. 
• Can cause high mortality without specific signs. 

Avian Influenza

Type A is of veterinary importance. 

Disease-> man, horse, pig and poultry.

Only virulent strains of avian influenza are notifiable. 

Huge reservoirs in wild birds. 

8 gene segments which code for 10 proteins. 

H= haemaglutinin. NA= Neuraminidase. 

The subtype is defined by the 'spike' glycoproteins. H (1-16) and N(1-9). Any combination is H & N is possible in birds e.g. H5N1. They are not stable properties and antigenic shift (reassortment, I think of this as the BIG change) and antigenic drift (SMALL point mutations) can occur at any time. 

The subtype controls the pathogenesis, diagnosis, immunity and control for that strain. 

Like FMD, there is no cross-immunity between strains which makes vaccination control almost impossible. 

Genetic reassortment (shift)-> separate molecules of NA in segmented genomes are exchanged and the progeny contain NA molecules from each parent. New virus may even have different properties. Pigs are considered to be the main 'mixing vessel' for new viruses, but cats could be important as were tested seropositive where humans were infected with H5N1. 

It is made notifiable by any infection of poultry caused by type A influenza virus of H5 or H7 subtypes or by any virus categorised as HPAI (highly pathogenic). This is where they have an IVPI (intravenous pathogenicity index) of above 1.2 in 6 week old chickens or 75% or above mortality in 4-8 week old chickens. 

H5 and H7 are associated with high pathogenicity but low pathogenicity types can mutate to become high pathogenicity due to alterations in the H gene. 

Clinical Signs 

• Necrosis, congestion and haemorrhage after replication in a wide range of tissues.
• Death without obvious signs- great variation in clinical picture and severity.
• Respiratory distress, lack of appetite, diarrhoea and egg production drop. 
• Cyanosis of comb, wattle and shanks (blue colouration).
• Tracheal haemorrhages alongside intestinal and mesenteric haemorrhages.

Ducks, geese and swans act as reservoirs, especially the mallard.

Diagnosis

• Clinical signs/increased mortality (notify DEFRA).
• Samples to VLA.
• RT-PCR and then H5 and H7 specific primers.
• Virus isolation in eggs, HA activity indicates AI or ND.
• Subtyping.
• Pathogenicity testing via IVPI and HA cleavage site sequence. 

Control

• Not very stable outside the host- killed by formalin, phenol etc.
• Survives 2 weeks in dust, but longer in cold, moist conditions.
• Difficult to control via vaccines.
• Control aimed at HPAI viruses.
• 'Stamping out.' 

Transmission

• Aerosol/respiratory secretions. Faecal excretion with high titres.
• Waterfowl carry virus.
• Migratory waterfowl-> poultry.
• No egg transmission but surface contamination.
• Easily spread by fomites (people etc).
• Feathers.
• Contamination of water.

Human concern= reassortment between human influenza and HPAI H5N1 with no human to human spread into a pig/human host as coinfection. This could result in reassortment which could spread from human to human. This could also be generated by mutation of the AI virus. 

Should we vaccinate?

• Killed vaccines offer protection against disease but not infection.
• Vaccination can mask infection.
• Adverse effect on exports.
• Killed vaccines need individual vaccination and are too labour intensive. 

Free range layers= high risk. 

Outbreaks

• 1991. Norfolk. Turkeys H5N1 birds destroyed.
• 2006 H5N1 in whooper swan in Scotland. 
• 2007 Norfolk H7N3 LPAI in three premises. Restrictions and culling. Two free range places and Norfolk= near migratory route.
• 2007 Suffolk Turkeys (east anglia connection). H5N1. 5 days to confirm virus identity. At outbreak all poultry culled, restricted access and visitors disinfected. In the 3km protection zone poultry were kept indoors and tested. In the 10km surveillance zone no poultry movements apart from slaughter, bird fairs and markets banned, domestic birds not to use same water as wild birds, people in towns not affected unless they kept poultry. Restriction zone had isolation of poultry from wild birds, and licensed poultry movements. 
• 2008- H7N7 Banbury laying hens. January, Dorst wild birds and canada goose. 

Newcastle Disease

HN spikes and F protein. Single serotype and no antigenic shift. Codes for 7 proteins.

• Severe form= viscerotropic-velogenic which causes acute lethal infection and gut haemorrhagic lesions.
• Second most severe form= respiratory and neurologic disease, gut lesions absent but high mortality. 
• Asymptomatic= least severe. Primary replication in the gut. 

Clinical Signs 

• Loss of appetite.
• Thirst.
• Dehydration.
• Emaciation.
• Ruffled feathers.
• Huddling.
• Listlessness.
• Depressed.

Neurotropic

• Tremors.
• Star Gazing.
• Twisted neck.
• Convulsions.
• Inco-ordination.
• Wing and leg paralysis.

Pneumotropic

• Mild rales and snick.
• Sneezing and coughing.
• Nasal Discharge.
• Laboured breathing.
• Open mouth breathing.
• Head shaking.
• Green-yellow diarrhoea.

Viscerotropic

• Green yellow diarrhoea.
• Haemorrhage of intestine.
• PM lesions in proventricularis and lymph nodules.

Diagnosis

• Clinical signs- long differential diagnosis.
• Serology- HI preferred but ELISA common.
• Live birds- OP swabs, VI but mostly RT-PCR.
• Lesions not characteristic but suggestive.
• Samples- trachea, lungs, brain, proventricularis and caecal tonsil. 

Lab Diagnosis

• Egg inoculation.
• Pathogenicity index (ICPI & IVPI)
• Monoclonal antibodies.
• RT-PCR if positive do virulence determination. Sequence fusion protein.

Control & Prevention

• Endemic countries= continuous threat
• High standard of biosecurity and management. 
• Increase flock resistance by case exposure. Good flock management, nutrition, and avoid or minimise immunosuppression from Infectious Bronchitis and mycotoxins. Use a vaccination. Nutrition and good vaccine administration etc are very important. 
• Type of vaccine depends on severity of NDV challenge (the virulence). The type of chicken for withdrawal periods e.g. broiler vs layer. Management, multi ages, technical knowledge for storage, handling etc. A big factor is cost.
• 'STAMP OUT' if affected.