Diseases: Avian Infuenza Characteristics
1. Causative agent
Genus: Influenzavirus A
Family: Orthomyxoviridae
Several subtypes of the virus exist, which are divided on the basis of the glycoproteins haem o agglutinin (H) and neuraminidase (N). At present 15 H subtypes have been recognized (H1 – H15) and 9 N subtypes (N1 – N9).
Influenza A viruses infecting poultry can also be divided on the basis of their pathogenicity:
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OIE criteria for classifying an avian influenza virus as highly pathogenic:
a) Any influenza virus that is lethal for six, seven or eight of eight 4-8-week-old susceptible chickens within 10 days following intravenous inoculation with 0.2 m l L of a 1/10 dilution of a bacteria-free, infective allantoic fluid.
b) The following additional test is required of if the isolate kills from one to five chickens but is not of the H5 and H7 subtype: growth of the virus in cell culture (for example primary cells such as chick embryo cells or cell lines such as MDCK cells, although most cell cultures support the growths of HPAI influenza viruses or those of low pathogenicity in the presence of trypsin) with cytopathic effect or plaque formation in the absence of trypsin. If no growth is observed, the isolate is not considered to be a HPAI isolate.
c) For all H5 and H7 isolates of low pathogenicity and for other influenza viruses, if growth is observed in cell culture without trypsin, the amino acid sequence of the connecting peptide of the haemagglutinin must be determined. If the sequence is similar to that observed for other HPAI isolates, the isolate being tested will be considered to be highly pathogenic.
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The very virulent viruses cause highly pathogenic avian influenza (HPAI), also known as Fowl Plague. Less virulent virus strains cause a much milder disease (low pathogenic avian influenza, LPAI)
To date only viruses of H5 and H7 subtype have been shown to cause HPAI in susceptible species, but not all H5 and H7 influenza A viruses are highly pathogenic.
Influenza A viruses have a broad spectrum of antigenic diversity and virulence as well as a high capability for mutation. They are known to increase in pathogenicity after mutation1 (antigentic shift / reassortment, antigenic drift).
2. Characteristics of Avian influenza virus
Resistance to physical and chemical action
Temperature: |
Inactivation by 56 º C/3 hours; 60 º /30 min |
PH: |
Inactivated by < pH 5 or > pH 8 |
Chemicals: |
Inactivated by oxidising agents, sodium dodecyl sulphate, lipid solvents, ß -propiolactone |
Tenacity
Influenza A viruses may remain viable for long periods of time in infected faeces (up to 3 days at 20 ° C – depending on the amount of virus), but also in tissues (in carcasses a few days at ambient temperature, but up to 23 days when stored cool) and water (duck influenza virus is proofed proven to be infectious for 4 days at 22 ° C in water). Direct sunlight will also inactivate the virus.
Disinfection
Formalin, peracetic acid or any other registered disinfectant with antiviral effect can be used.
3. Transmission:
Avian influenza is highly contagious.
Influenza virus is shed mainly with the droppings but as well with any secretions from infected birds (discharge from eyes, nose or beak, eggs, semen). Virus shedding starts 24 hours before clinical symptoms can be seen. The virus might be shed for up to 30 days.
Transmission might occur through
• direct contact with secretions from infected birds, especially faeces
• contaminated feed, water, equipment and clothing
• insects, rodents and parasites as well as humans can be mechanical carriers
• clinically normal waterfowl and sea birds may introduce the virus into flocks
• broken contaminated eggs may infect chicks in the incubator
There is no proof of horizontal transmission of HPAI, but the virus might be transmitted via the egg shell.
4. Species affected
In addition to birds, several mammalian species are susceptible for to various Influenzavirus A, e.g. pigs (H1N1, H1N2, H3N2), horses (H7N7, H3N8), minks, seals, whales and humans.
Birds
All species of birds can be affected by influenza viruses. In intensive poultry rearing systems, young fattening turkeys and laying hens are usually the most affected species.
Free-living birds may carry influenza viruses without becoming ill due to a natural resistance. It is known that wild waterfowl present a natural reservoir for these viruses and can be responsible for the primary introduction of infection into domestic poultry.
Pigs
Pigs are susceptible for to avian and human Influenza viruses. They are known to act as “mixing vessels” (reassortment of avian and human virus strains) and therefore play an important role in interspecies transmission of Avian Influenza.
Humans
HPAI strains have sometimes been shown to infect man, but it must not be confused with human influenza, a common human disease. However, Avian Inlfuenza Influenza under certain circumstances could pose a serious threat to humans.
Symptoms: |
Conjunctivitis
respiratory symptoms |
Transmission: |
direct contact with a sick bird or its excretions
contact with infected persons (rarely) |
Risk: |
recombination of avian and human virus strains in humans, resulting in a new virus strain with high susceptibility in humans |
5. Clinical signs and differential diagnosis with special regard to Newcastle disease
All diseases affecting the respiratory tract and / or the central nervous system might be caused by Influenza A viruses.
Clinical signs caused by LPAI are much less evident or even absent and mortality is much lower compared to HPAI.
Newcastle disease (ND) is of major importance for differential diagnosis of HPAI.
Table 1: Comparison of HPAI and ND
|
HPAI |
ND |
Incubation period |
Several hours up to 2-3 days |
4-5 days (range 2-15 days) |
Duration of clinical disease |
About 1 week |
Maybe several weeks |
Clinical signs |
- facial oedema
- nasal, oral discharge
- distressed and noisy breathing
- greenish diarrhoea
- marked decrease in egg production a
- often nervous signs (ophistotonus, torticollis)
- high mortality (up to 100%) |
- facial oedema
- nasal, oral discharge
- distressed and noisy breathing
- greenish diarrhoea
- marked decrease in egg production a
- often nervous signs (ophistotonus, torticollis)
- high mortality (up to 100%) |
a ) can mainly be observed in commercial flocks
To be considered for differential diagnosis of HPAI besides ND:
• Infectious Bronchitis (IB)
• Infectious Laryngotracheitis (ILT)
• Mareks Disease (MD)
• Avian Encephalomyelitis (AE)
• Infections with Avian Pneumovirus 1 : Turkey Rhinotracheitis (TRT), - swollen head syndrome (SHS)
(normally diarrhoea is not present with any of these diseases)
6. Post mortem findings
Lesions might be absent in cases of sudden death.
• Subcutaneous oedema of the head and neck area
• Severe congestion of the musculature and kidneys
• Petechiae on the inside if of the sternum, on the serosa and abdominal fat, serosal surfaces and in the body cavity
• Mucous or even bloody content in trachea, sinuses and maybe in the nose
• Haemorrhages on the mucosal surface of the proventriculus, particularly at the juncture with the gizzard
• Haemorrhages and erosions of the gizzard lining
• Haemorrhagic foci on the lymphoid tissues in the intestinal mucosa
• Haemorrhages and degeneration of the ovaries
There are no pathognomonic post-mortem lesions for Avian Influenza
7. Control
Avian Influenza cannot be cured.
• slaughtering of all birds
• disposal of carcasses and all animal products
• cleaning and disinfection
• allow at least 21 days before restocking
Vaccination
In the past, it has been considered counterproductive to vaccinate against HPAI as some vaccinated individuals may, nonetheless, become infected and shed virulent virus. However, in the recent outbreaks in Pakistan, Mexico, Italy and Asia, inactivated subtype-specific vaccines have been employed to combat rapidly spreading disease.
Compiled by Dr Christine Ahlers
Veterinary Advisor
AusAID Southern Africa Newcastle Disease Project
Maputo, Mozambique
E-mail: sandcp@tropical.co.mz
September, 2004.
