Avian Influenza

Also know as: Fowl Plague

Introduction

Avian influenza (AI) is a notifiable disease. It is part of the Orthomyxoviridae family, possessing a single negative sense RNA strand. Within the influenza virus family there are 3 subtypes; A, B and C, with only A causing disease in birds. Type A can then be further subdivided based on the haemagglutinin (HA) and neuraminidase (N) envelope glycoproteins present, with subtype antigens H1-17 and N1-9. Each virus possesses one HA and one N antigen. Each isolate can then be further subdivided into viral lineages called clades.

Influenza A viruses affecting birds are divided into two groups based of the severity of clinical disease; highly pathogenic avian influenza (HPAI) and low pathogenic avian influenza (LPAI). HPAI viruses are found within (though not all of) H5 and H7 subtypes. HPAI viruses are thought to be a result of mutations within an LPAI strain. HPAI is defined by the ability to infect and kill chickens using a standardized dose given intravenously (World Organization for Animal Health, 2006). The mutation occurs after the virus has moved from the wild bird host into the poultry population and may take days to months to occur. The longer the virus persists the more likely it is to adapt and mutate into a highly pathogenic strain, and once in poultry in can then spread to other species.

Initially AI cases were found to decrease as the ambient temperature increased but in 2009 cases were documented all year round with increased cases during the warmer months of the year. AI viruses can persist for long periods of time at low temperatures in water, and therefore can reinfect migratory water fowl in the spring and lead to further spread. Geographical separation of the virus can also increase independent evolution of the virus and potentially increase virulence.

AI Spread

Wild birds (in particular aquatic birds) are the main reservoir for the virus, and hence are responsible for its continuous spread and maintenance, which is easy and quick. The migration of many wild birds across distances has led to long distance spread and the introduction of AI into other countries. Different species of wild birds have different genetic pools of virus and different susceptibilities. Most infection within Europe has been detected in dead wild birds. A majority of cases, especially in developing countries, have been the result of secondary spread within poultry, most of which is human mediated. Most AI viruses are well adapted to their host species, so when they infect a new species they replicate and transmit poorly. Domestic poultry (especially ducks) are reservoirs for HPAI, and, in some cases, birds can produce the virus for weeks with no clinical signs.

AI is spread by movement of birds, direct contact with respiratory secretions or faeces as well as via fomites (inanimate objects). AI can also be transmitted by eating uncooked infected bird products, including uncooked eggs. AI virus has been found on the surface of eggs but so far there has been no evidence of transmission to people by the consumption of egg products. The practice of manure spreading also increases the possibility of disease transmission.

Recent Outbreaks

H5N1 is an HPAI strain that can persist in wild bird populations. In April 05 this strain caused high mortality in ducks and gulls in Qinghai Lake in China. Wild bird migration led to the virus being carried to Europe and Africa and over winter 2006 a large number of wild birds were found to be infected. Migratory birds in Egypt tested positive for H5N1 three months before the outbreak in poultry. The virus is thought to still be present in wild bird populations but at a lower level. This subtype proved harder to control due to the maintenance of infection within wild birds and the increased susceptibility of poultry to the strain (as shown by a low MID50, meaning that only a small amount of virus is needed to produce infection). H5N1 has spread to over 60 countries and is currently endemic in China, Egypt, Vietnam, India, Bangladesh and Indonesia.

The most recent cases reported in China on the 29th March 2013 involve the H7N9 subtype, which has been shown to be more virulent in people than poultry. Currently no animal outbreaks have been identified in the area surrounding the confirmed cases and only a small proportion of birds have tested positive for the virus; however 77% of those people infected have been exposed to poultry/swine (including live bird markets). Three family clusters of 2-3 cases each have been identified where limited human to human transmission may have occurred.

At the moment it is thought that H7N9 was transmitted from healthy poultry or swine to people either directly or through contaminated environments. As few H7N9 positive birds have been detected, this may indicate that the virus is widespread in poultry and is asymptomatic which could lead to silent spread of the virus.

The complete virus is a recombination of three viruses found in Asia, H7 of the virus has been found to be closest to that found in domestic ducks in Zhejiang and the N9 closest to the wild bird strain in South Korea. Genetic changes have also been found that lead to increased virus binding and replication in mammalian respiratory cells and thus increased severity of infection. The virus has been shown to be weakly pathogenic in poultry and testing of different populations for H7N9 specific antibodies may be helpful in finding the source, though viruses with H7 HA may not trigger a strong antibody response. No cases have been reported outside of China.

Signalment

There is a higher risk of LPAI on farms housing ducks, geese and game birds as compared to chickens, turkeys and indoor layer farms. This may be due to the rearing methods, as birds reared outside have a higher risk of coming into contact with wildfowl and thus becoming infected with LPAI. Contaminated drinking water, including water that wild birds have access to, increases the risk of infection, as does feeding uncooked meat and offal. Turkeys and ducks appear more susceptible to AI, as are many gallinaceous species. LPAI has been shown to be present in low levels in turkeys but HPAI rarely found, only five cases of HPAI since 1959 have been found to result primarily from turkeys. HPAI viruses are well adapted to poultry. Wild pigeons may not be as susceptible to AI as other wild birds. Psittacine birds are rarely affected and viruses found in ratites show a low level of virulence to chickens. The density of lamellae and feeding style within ducks has been shown to be associated with AI infection, suggesting feeding methods may have an effect on exposure to AI virus. AI has also been detected in asymptomatic swine and donkeys.

Clinical Signs

LPAI viruses cause milder disease, most commonly respiratory symptoms (e.g. rales, coughing) combined with reduced egg production and depression, though clinical signs can range from none to death. Other signs can include swelling of the infraorbital sinuses, pyrexia and loss of appetite. If other bacteria or viruses (e.g. Pasteurella spp, Newcastle disease, Mycoplasma spp, Escherichia coli) are present along with LPAI the consequences of infection can be more serious, often causing high mortality. The age, immune status and species of the infected bird can also have an impact on the severity of disease, as can the environment the bird is housed in. Many flocks are infected with LPAI every year and are only recognised due to seroconversion as the disease is asymptomatic. Most infections are transient due to lack of host adaptation, though some establish due to virus variation.

By contrast, HPAI infection may only be recognised by sudden onset mortality within the flock, which can reach 100% within a couple of days. If the birds are still alive symptoms can include those of LPAI (though egg laying has often stopped) and excessive lacrimation, sinusitis, oedema of the head, subcutaneous haemorrhage, cyanosis of the skin (including comb and wattles), diarrhoea and occasional neurological signs. Severity of signs depends on the species and strain of the virus, for example some ducks infected with HPAI rarely showed clinical signs.

Diagnosis

Laboratory diagnosis is essential when dealing with suspected cases of AI due to the lack of classical clinical signs, zoonotic potential, and need to differentiate between HPAI and LPAI as well as the virus subtype. The diagnosis is based on isolation and characterisation of the virus. Tracheal/ cloacal swabs or faeces are taken from live birds and suspended in antibiotic solution before being inoculated into the allantoic cavity of 9-11 day old embroyanted chicks. Taking lower respiratory tract samples is important, as the virus may not be found in the upper respiratory tract. Faecal or organ samples from dead birds can also be used. Following incubation the allantoic fluid is tested for haemagglutination, a positive result (i.e. haemagglutination is present) indicating viral infection. An immunodiffusion test can be used to confirm the presence of influenza A virus, using antiserum to the nucleocapsid or matrix antigens. Polyclonal chicken antisera can be used to further identify the virus subtype by observing which specific antiserum inhibits the haemagglutinating activity of the virus (haemagglutination inhibition).

Virulence assessment can be performed by injecting chickens with infective allantoic fluid and observing the presence/absence and severity of disease for 10 days.

Paired serum samples can be taken in order to identify seroconversion. One sample is taken in the acute phase of infection before antibodies are produced and another 2-3 weeks later. A fourfold increase in antibody levels (usually identified by haemagglutination inhibition) will show that infection with the virus has occurred. This can only provide a retrospective diagnosis but can be useful in identifying which flocks have been exposed to AI, especially in cases where it is an asymptomatic infection.

Due to continual antigenic drift and shift specificity and sensitivity of diagnostics is a big problem.

Control

All birds must be slaughtered immediately and all birds on the premises must also be destroyed. The premises must be isolated and mass disinfection before new stock are brought in should occur. There must be a firebreak cull in local poultry farms or poultry keepers in a certain radius from the infected farm to control the spread.

Prevention is by proper hygiene and preventing contact with the wild bird population, such as ensuring housing is of excellent quality so as no wild birds can land in or on it and defaecate into it etc.

Vaccination is not currently practiced for the following reasons:

• Eradication policy prevents it from being allowed.
• Vaccination favors the evolution of the virus, which might increase its virulence and drift.

References

Blood, D.C. and Studdert, V. P. (1999) Saunders Comprehensive Veterinary Dictionary (2nd Edition) Elsevier Science

Bridger, J and Russell, P (2007) Virology Study Guide, Royal Veterinary College

Cowart, R.P. and Casteel, S.W. (2001) An Outline of Swine diseases: a handbook Wiley-Blackwell

Jordan, F, Pattison, M, Alexander, D, Faragher, T (1999) Poultry Diseases (Fifth edition) W.B. Saunders

Saif, Y.M, (2008) Diseases of Poultry (Twelfth edition) Blackwell Publishing

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