Avian Influenza
Avian Influenza
Avian Influenza
AUSVETPLAN
Disease Strategy
Avian influenza
Version 3.4, 2011
AUSVETPLAN is a series of technical response plans that describe the proposed Australian
approach to an emergency animal disease incursion. The documents provide guidance based on
sound analysis, linking policy, strategies, implementation, coordination and emergency-
management plans.
AUSVETPLAN Edition 3
Preface
This disease strategy for the control and eradication of avian influenza (AI) is an integral part of
the Australian Veterinary Emergency Plan, or AUSVETPLAN (Edition 3). AUSVETPLAN
structures and functions are described in the AUSVETPLAN Summary Document.
This manual has been produced in accordance with the procedures described in the
AUSVETPLAN Summary Document and in consultation with Australian national, state
and territory governments and the poultry industry. It has been endorsed out of session by
the Animal Health Committee (AHC OOS 2007).
Avian influenza (AI) is included on the OIE (the World Organisation for Animal Health) list of
notifiable diseases. This obliges OIE member countries that had been free from the disease to
notify the OIE within 24 hours of confirming the presence of highly pathogenic avian influenza
(HPAI) in birds and low pathogenicity avian influenza (LPAI) in poultry (as defined by the OIE).
OIE-listed diseases are diseases with the potential for international spread, significant mortality
or morbidity within the susceptible species and/or potential for zoonotic spread to humans. 1
The strategies in this document for the diagnosis and management of an outbreak of AI are based
on the recommendations in the OIE Terrestrial Animal Health Code 2 and the OIE Manual of
Diagnostic Tests and Vaccines for Terrestrial Animals. 3
The detection of active or recent infection with HPAI virus in wild, cage or zoo birds and the
detection of active infection with LPAI (H5/H7) virus in cage or zoo birds are addressed, as they
would lead to the implementation of arrangements consistent with this manual. This manual also
contains a response policy for LPAI (not H5/H7) detections caused by subtypes of AI virus other
than H5 and H7 and not classified as HPAI. Responses to the detection of these subtypes are not
covered by the EAD Response Agreement.
Where in this manual text has been placed in square brackets [xxx], this indicates that that
aspect of the manual remains contentious or is under development; such text is not part of
the official manual. The issues will be worked on by experts and relevant text included at a
future date.
Detailed instructions for the field implementation of AUSVETPLAN are contained in the disease
strategies, operational procedures manuals, management manuals and wild animal manual.
Industry-specific information is given in the relevant enterprise manuals. The full list of
AUSVETPLAN manuals that may need to be accessed in an emergency are shown below.
1 These criteria are described in more detail in Chapter 2.1.1 of the OIE Terrestrial Animal Health Code
(http://www.oie.int/eng/normes/mcode/en_chapitre_2.1.1.htm).
2 2 http://www.oie.int/eng/normes/mcode/en_chapitre_4.5.6.htm
3 3 http://www.oie.int/eng/normes/mmanual/A_00035.htm
4 http://www.animalhealthaustralia.com.au/programs/eadp/eadra.cfm
In addition, Exotic Diseases of Animals: A Field Guide for Australian Veterinarians by WA Geering, AJ
Forman and MJ Nunn, Australian Government Publishing Service, Canberra, 1995 (to be
updated) is a source for some of the information about the aetiology, diagnosis and epidemiology
of the disease.
AUSVETPLAN documents 5
Disease strategies Enterprise manuals
Individual strategies for each of 35 Artificial breeding centres
diseases Dairy processing
Response policy briefs (for diseases not Feedlots
covered by individual manuals) Meat processing
Poultry industry
Operational procedures manuals Saleyards and transport
Decontamination Zoos
Destruction of animals
Disposal Management manuals
Public relations Control centres management
Valuation and compensation (Parts 1 and 2)
Livestock welfare and management Laboratory preparedness
Wild animal manual Summary document
Wild animal response strategy
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Contents
Preface ....................................................................................................................................3
2.1 Introduction......................................................................................................34
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Glossary ...............................................................................................................................85
Abbreviations .....................................................................................................................94
References ...........................................................................................................................96
Tables
Table 1.1 Diagnostic tests currently available at CSIRO-AAHL for
avian influenza ..............................................................................................18
Table 1.2 Examples of the use of vaccines in recent overseas outbreaks
of avian influenza ..........................................................................................21
Table 1.3 Cooking temperatures and times for various poultry products ............25
Table 1.4 Pasteurisation procedures for egg products .............................................26
Table 1.5 OIE Terrestrial Code recommendations for the inactivation
of AI virus in eggs and egg products .........................................................26
Table 4.1 Movement controls for declared premises ................................................65
Table 4.2 Movement controls for declared areas .......................................................68
Avian influenza (AI) is a highly contagious viral infection, primarily in avian species.
Clinical manifestations range from inapparent in waterfowl to a rapidly fatal condition
characterised by gastrointestinal, respiratory and/or nervous signs in chickens and turkeys.
Recent outbreaks of highly pathogenic avian influenza (HPAI) in eastern Asia have been
devastating for local economies (FAO 2004a). In addition, recent changes in the
epidemiology of AI virus infections, particularly in the capacity of AI virus to infect
humans, have led to a reassessment of the classification and management of such infections.
AI virus infections show a continuous spectrum of pathogenicity in gallinaceous poultry,
from no pathogenicity to high pathogenicity (see Section 1.1.2).
From 1955, the disease was known as either ‘virulent avian influenza’ or ‘fowl plague’ until
an international meeting on AI in 1984 recommended that the name ‘highly pathogenic
avian influenza’ be used to describe the most pathogenic form of infection, as assessed from
inoculation of chickens.
This manual considers the consequences that may arise from the infection of poultry with
any AI virus, and distinguishes between HPAI, low pathogenicity avian influenza (LPAI
(H5/H7)) and LPAI (not H5/H7) infections, as defined by the OIE (World Organisation for
Animal Health); see Section 1.1.3.
The OIE defines poultry as: ‘all domesticated birds, including backyard poultry, used for
the production of meat or eggs for consumption, for the production of other commercial
products, for restocking supplies of game, or for breeding these categories of birds, as well
as fighting cocks used for any purpose.'
Influenza A viruses are further divided into subtypes determined by haemagglutinin (H)
and neuraminidase (N) antigens. At present, 16 H subtypes and 9 N subtypes have been
identified. Each virus has one of each subtype in any combination.
1.1.2 Pathogenicity
The species in the orders Anseriformes (ducks, geese, swans) and Charadriiformes
(shorebirds, waders, gulls) are regarded as important reservoir hosts and disseminators of
influenza viruses, but rarely display clinical signs of infection. There is extreme variation in
virulence among subtypes of AI viruses, and a variety of subtypes is widespread
throughout wild aquatic bird populations.
In poultry, HPAI due to H5 and H7 subtypes can cause severe clinical disease, and even
subtypes of low pathogenicity, including H5 and H7, can be associated with severe clinical
disease in the presence of other infectious agents (eg infectious bronchitis, infectious
laryngotracheitis).
The pathogenicity of AI viruses depends on the genetic properties of the virus and the
species of the host. Only viruses with H5 and H7 antigens have been isolated so far from
HPAI in poultry. These two subtypes of AI virus are considered to be high-risk strains for
antigenic drift towards HPAI, even if the clinical picture seen in poultry is of lesser or no
pathogenicity. The cleavability of viral haemagglutinins by proteolytic enzymes also
correlates with the virulence of virus strains for chickens (see Section 1.4.2).
LPAI infections of chickens and turkeys with H5 and H7 subtype that have been allowed to
continue without adequate control or eradication procedures have ultimately turned into
virulent HPAI infections (Pennsylvania, United States, 1982–83; Mexico, 1994; Italy, 1999–
2000). The change in virulence of the virus is associated with the acquisition of additional
basic amino acids at the cleavage site of the haemagglutinin protein.
The tests required to meet these OIE criteria are described in Section 1.4.4. However, the
IVPI and chicken mortality tests have the disadvantage of being slow to perform.
Genotyping of the haemagglutinin cleavage site is faster and more precise and is the test of
choice in Australia.
Molecular pathotyping, as well as subtyping (see Section 1.4.4), is needed for all AI viruses
isolated, to determine the likelihood of an H5 or H7 virus mutating to a virulent form.
For the purposes of international trade, the AI chapter in the OIE Terrestrial Code deals not
only with the occurrence of clinical signs caused by notifiable AI (NAI) virus, but also with
the presence of infection with NAI virus in the absence of clinical signs. NAI virus infection
occurs when:
• HPNAI or LPNAI virus has been isolated and identified as such;
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• viral antigen or viral RNA specific to HPNAI or LPNAI has been identified; or
• antibodies to H5 or H7 subtype of NAI virus that are not a result of vaccination have
been detected in poultry.
Outbreak of HPAI
An outbreak of HPAI in poultry in Australia is defined as:
• clinical disease in poultry, with an influenza virus that meets the OIE criterion for
lethality to 4- to 8-week-old chicks (where such a virus will probably, but not
necessarily, be of H5 or H7 subtype); or
• clinical disease in poultry, with an influenza virus that meets the other OIE criteria for
HPNAI (ie H5 or H7 subtype and has basic amino acid sequences at the
haemagglutinin cleavage site that are close to those observed in HPAI isolates).
In these cases, the AI virus involved would meet the OIE definition of HPNAI (see
Section 1.1.3). An emergency disease outbreak would be declared under the terms of the
Government and Livestock Industry Cost Sharing Deed In Respect of Emergency Animal Disease
Responses (EAD Response Agreement), and control measures would be initiated to protect
animal and public health. HPAI (H5/H7) is a Category 2 emergency animal disease (EAD)
and HPAI (not H5/H7) is a Category 3 EAD (see Section 3.4).
In this case (LPAI (H5/H7)), the virus does not have an amino acid sequence that is similar
to that observed for HPAI isolates. However, action to control the spread of infection is
necessary, particularly if the virus is highly transmissible and is spreading in poultry, since
it is likely that the virus will mutate and become highly pathogenic for chickens.
LPAI (H5/H7) is a Category 3 EAD under the EAD Response Agreement (see Section 3.4).
Cage birds are defined as birds that are confined within an enclosure and maintained for
purposes other than food production. Zoo birds are cage birds that are maintained at a zoo
premises.
The detection of active or recent infection with HPAI virus in cage or zoo birds would lead
to an emergency disease outbreak being declared under the terms of the EAD Response
Agreement. However, the detection of HPAI or LPAI in cage or zoo birds has not been
categorised under the EAD Response Agreement with regard to cost sharing. The action to
be taken following the detection of active infection with LPAI (H5/H7) virus in cage or zoo
birds would be determined after an assessment of the situation.
Outbreaks of HPAI due to a highly pathogenic H5N2 subtype virus have occurred in
ostriches in South Africa in the past few years.
AI has also been associated with a syndrome characterised by respiratory signs, enteritis,
weakness and death of ostriches in South Africa (Allwright et al 1993) and in Denmark
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(Jorgensen et al 1998). An outbreak with over 20% mortality was reported to the OIE in
April 1994. In Italy in 2000, young ostriches suffered 30% mortality when infected with
H7N1 virus during an HPAI outbreak (Capua et al 2000a). An AI virus that was virulent for
chickens was isolated from an emu in Texas, United States, in 1993. This virus did not cause
clinical signs of HPAI when inoculated into ostriches, but was isolated widely from internal
organs (Clavijo et al 2001).
Field surveys have suggested that many species of waterfowl, particularly ducks, geese and
swans, are the natural hosts of AI viruses. AI viruses have also been recovered from gulls,
terns and shearwaters. Intensive surveillance of wild birds during the 1983–84 AI outbreak
in Pennsylvania, United States, confirmed that aquatic birds harbour many influenza
viruses. Subsequent reports on the prevalence of AI infection in waterfowl range from 0.6%
to 26% (Alfonso et al 1995). Crows have become infected with and died from H5N1 subtype
virus infection in Japan (ProMED 2004a).
AI viruses of many H and N subtypes have been isolated from, or demonstrated in, a wide
range of wild waterbirds, including migratory species in well-separated locations
throughout Australia. Thus, a virus that is virulent for poultry could emerge from the pool
of viruses in wild birds at any time, particularly AI viruses of subtypes H5 and H7.
Representatives of H1, H3, H4, H5, H6, H11, H12 and H15 AI viruses have been isolated
from wild aquatic birds in Australia (Arzey 2004). The source of virus in outbreaks of H7 AI
viruses in Australia is not known, as there have been no reports of the isolation of H7 AI
viruses from wild birds in Australia (Cross 1987, Peroulis and Arzey 2004, O’Riley 2004,
C Morrow, Victorian Institute of Animal Science, pers comm, 1996).
Mammals
Human volunteers inoculated with a number of H subtypes of AI viruses (not H5 or H7)
showed mild disease but did not produce an antibody response (Beare and Webster 1991).
There was no field evidence that avian-derived viruses infected humans until the Hong
Kong incident of 1997. Since then, more infections with H5N1 viruses have been recorded in
Hong Kong, and in Vietnam and Thailand in 2004 and 2005 when more than half of those
infected died. In the Netherlands in 2003, 89 people became infected with H7N7 virus, with
a veterinarian dying, and Hong Kong and China have recorded human infections with
H9N2 virus (Peiris et al 1999, Lin et al 2000). Canada recorded human infections with H7N3
subtype virus. A serological survey of poultry workers in Hong Kong found that 17% had
antibody without known clinical signs of infection with H5N1.
Human infections have usually required direct contact with infected poultry, although a
small number of relatives in contact with infected workers during the Netherlands H7N7
outbreak became infected (3 of 83 tested; Koopmans et al 2004). A retrospective study in the
Netherlands has suggested that an estimated 1000 people, possibly more, became infected
with the H7N7 virus. The serological study showed that about 50% of people who handled
infected poultry became infected, and antibody was detected in 59% of the members of
infected poultry workers’ families, indicating much more human-to-human transmission
than supposed in the initial study (ProMED 2004b). The antiviral drug oseltamivir protected
against infection, but mouth and nose masks did not provide protection. In southern China,
a small number of influenza cases have been associated with infection from H9N2. Human-
to-human spread of H5N1 AI virus was recorded in Hong Kong (Katz et al 1999, Bridges
et al 2000, Katz 2003).
Infection of pigs with H7N7 subtype was evidenced by detection of antibody in the sera of
pigs during the Netherlands outbreak in 2003 (ProMED 2003); herds with positive serology
rates above 2.6% were slaughtered. Reports of infection in pigs with H5N1 subtype in Asia
have been confirmed (ProMED 2004c).
A snow leopard and a white tiger were reported to have died with HPAI infection in a Thai
zoo, and three domestic cats were reported as having died with H5N1 infection in Thailand
in 2004. A large number of tigers became infected with H5N1 virus following the feeding of
infected carcases in Thailand (ProMED 2004a). Inoculated cats and cats fed infected chicken
meat became infected with H5N1 virus and died with severe alveolar disease; in-contact
cats also acquired infection (Kuiken et al 2004).
The last two large outbreaks of HPAI in North America (Mexico 1995 and United States
1983), the 1999 outbreak in Italy, and outbreaks in the Netherlands, Chile, Canada and
Australia all initially involved LPAI. In each case the AI infection became widespread and
HPAI virus emerged by mutation, after which decisive depopulation had to be undertaken.
In Italy, LPAI infection was detected in the summer of 1999. By late in 1999, HPAI virus had
emerged and 13 million poultry died of HPAI infection in four months; HPAI was
eradicated in April 2000. In August 2000, viruses of lesser pathogenicity reappeared in meat
turkeys and rapidly spread in an area of high poultry density (Capua et al 2000b). This
outbreak was eradicated using vaccination with the other control measures (Capua and
Marangon 2003).
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Since December 2003, there have been outbreaks of highly pathogenic H5N1 AI in poultry
and other birds in Korea, Japan, Vietnam, Thailand, Cambodia, Laos, Myanmar, Indonesia,
China and Malaysia. In 2005, H5N1 was reported in birds in Kazakhstan, Mongolia and
Russia, and the disease then spread westwards into Romania, Turkey and the Ukraine.
Since early 2006, there have been reports of H5N1 virus in wild and domestic birds in some
European Union Member States, domestic birds in India, and in domestic and wild birds in
the Middle East (Iraq, Iran and Israel). The virus has also been reported in domestic birds in
some countries in Africa (Niger, Nigeria, Egypt, the Ivory Coast and Cameroon), and in
Afghanistan.
For the latest information on the distribution of avian influenza, refer to the OIE website. 6
The five outbreaks of AI that occurred in Australia between 1976 and 1997 all involved
HPAI viruses, and this has made decisions on dealing with the infections clear cut. HPAI
viruses caused clinical disease in commercial poultry in Victoria in 1976, 1985 and 1992, in
Queensland in 1994, and in New South Wales in 1997. Each time, there was severe disease
in affected chicken flocks and all had obvious or circumstantial evidence of contact with
waterfowl. All the Australian outbreaks to date have involved H7 subtype viruses.
However, there is some evidence that, initially, LPAI may have been involved in the 1976
outbreak (Westbury 1998), the 1992 Victorian outbreak (Victorian Department of
Agriculture records) and the 1997 outbreak (Selleck et al 2003).
[In future, this Section will also address the diagnosis of AI in birds other than poultry.]
• Mortality ranges from 3% in caged layers to 15% in meat chickens; high mortalities to
90% have been recorded in young turkey poults.
• Egg production in layers can drop by up to 45%, with recovery to normal in 2–4 weeks.
6 http://www.oie.int/downld/AVIAN%20INFLUENZA/A_AI-Asia.htm
• The last eggs laid after the onset of illness frequently have no shells.
• In peracute cases involving sudden death, clinical signs may not be seen and mortalities
occur as early as 24 hours after the first signs of the disease, and frequently within 48
hours. In other cases, more diverse visible signs are seen, and mortalities can be delayed
for as long as a week. Overall mortality rates for peracute/acute cases of nearly 100%
have been reported. Chickens in cages may have a prolonged incubation period of up to
16 days, as evidenced in Italy in 1999–2000 (I Capua, OIE and National Reference
Laboratory for Avian Influenza, Italy, pers comm).
• Some severely affected hens may recover, but rarely come back into lay.
The disease in turkeys is similar to that seen in chickens, but is often complicated by
secondary infections such as fowl cholera, turkey coryza and colibacillosis.
1.4.2 Pathogenesis
Most HPAI viruses isolated from poultry have come from chickens and turkeys. Clinical
signs result from the replication of the virus in the respiratory tract and subsequent
systemic replication in the visceral organs and brain. The viruses that are nonpathogenic
replicate only on the surfaces of the respiratory and intestinal tracts.
The major determinant of virulence of AI viruses is the cleavability of the H protein. If the
H cleavage site has the right configuration of basic amino acids, the protease enzymes
found in internal organs are able to cleave the protein resulting in a higher likelihood of
systemic spread. Without this configuration, however, the protein can only be cleaved by
trypsin-like enzymes, which have a more restricted distribution on endodermal surfaces,
such as the respiratory and intestinal tracts (Swayne and Suarez 2000). Non-highly
pathogenic viruses cannot produce plaques in cell cultures unless trypsin is added to the
substrate medium.
1.4.3 Pathology
Gross lesions
In many cases, poultry dying from the peracute form of the disease lack visible gross
lesions; such chickens die on day 1 or day 2 after infection. With the acute infections seen in
chickens in Hong Kong and Italy in 1997, there was severe lung congestion, haemorrhage
and oedema in dead chickens; other organs and tissues appeared normal.
With the acute form of infection, seen 3–5 days after inoculation, more diverse visible
lesions are evident. Chickens have ruffled feathers, congestion and/or cyanosis of the comb
and wattles, and swollen heads. The changes in the comb and wattles progress to dark red,
then to blue depressed areas of ischaemic necrosis. Internally, the characteristics of acute
infections with viruses causing HPAI are haemorrhagic, necrotic, congestive and
transudative changes. The oviducts and intestines often have severe haemorrhagic changes.
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As the disease progresses, the pancreas, liver, spleen, kidney and lungs can display
yellowish necrotic foci.
Haemorrhages (petechial and ecchymotic) cover the abdominal fat, serosal surfaces and
peritoneum. The peritoneal cavity is frequently filled with yolk from ruptured ova,
associated with severe inflammation of the air sacs and peritoneum in birds that survive 7–
10 days. Haemorrhages may be present in the proventriculus, particularly at the junction
with the gizzard (Swayne and Suarez 2000).
In infections such as mildly pathogenic AI, lesions may be seen in the sinuses, characterised
by catarrhal, serofibrinous, mucopurulent or caseous inflammation. The tracheal mucosa
may be oedematous with an exudate varying from serous to caseous. The air sacs may be
thickened and have a fibrinous to caseous exudate. Catarrhal to fibrinous peritonitis and
egg yolk peritonitis may be seen. Catarrhal to fibrinous enteritis may be seen in the caeca
and/or intestine, particularly in turkeys. Exudates may be seen in the oviducts of laying
birds (Easterday et al 1997).
Specimens should initially be sent to the state or territory diagnostic laboratory, from where
they will be forwarded in packaging that complies with International Air Transport
Association requirements to the CSIRO Australian Animal Health Laboratory (CSIRO-
AAHL), Geelong for emergency disease testing, after obtaining the necessary clearance
from the chief veterinary officer (CVO) of the state or territory of the disease outbreak and
after informing the CVO of Victoria about the transport of the specimens to Geelong.
Specimens required
Samples should be taken both from live, clinically affected birds and from recently dead
birds. Cloacal and tracheal swabs and/or fresh faeces and serum should be taken from live
birds. From dead birds, alimentary tract tissues (proventriculus, pancreas, intestine, caecal
tonsil) and respiratory tract tissues (trachea, lung) should be collected. For details of sample
collection, transport, storage and processing, see Geering et al (1995) and the Laboratory
Preparedness Manual.
Transport of specimens
Fresh tissues and/or swab samples in transport medium need to be chilled and forwarded
with frozen gel packs (Geering et al 1995).
Laboratory diagnosis
Tests currently available at CSIRO-AAHL are shown in Table 1.1.
Table 1.1 Diagnostic tests currently available at CSIRO-AAHL for avian influenza
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• Molecular pathotyping. The gene encoding the haemagglutinin protein of the virus at the
cleavage site is sequenced. There are well-recognised differences between the gene
sequences of highly pathogenic and lesser pathogenic viruses.
Because time is of the essence for diagnosis, molecular pathotyping is the preferred method
of determining the pathogenicity of an AI virus in Australia. Once an outbreak virus has
been characterised, immunohistochemistry, immunofluorescence, virus detection and virus
isolation can be used to confirm virulent infections.
The Texas, United States outbreak virus was reported as having basic amino acids at the
cleavage site consistent with other HPAI viruses, but it was later reported as having no
pathogenicity by the chicken pathogenicity test (OIE 2004a). Canada similarly reported a
probable H7 infection detected by surveillance as HPAI and subsequently reported that the
virus was nonpathogenic by the chicken pathogenicity test, but the virus from a separate
site later proved to be fully HPAI (OIE 2004b).
HPAI should be suspected whenever sudden bird deaths occur with severe depression, loss
of appetite, nervous signs, watery diarrhoea, severe respiratory signs and/or a drastic drop
in egg production, with production of abnormal eggs. The likelihood of AI is increased by
the presence of facial subcutaneous oedema, swollen and cyanotic combs and wattles, and
petechial haemorrhages on the internal membrane surfaces.
Young chickens, or those dying from the peracute form of the disease, may not show any
lesions.
Other work has demonstrated that birds infected with nonpathogenic viruses were
protected against challenge with virulent strains having similar surface antigens.
1.5.3 Vaccination
Human and animal AI vaccines are under development and assessment, as overseas there
have been human infections with H5 and H7 AI virus, and human deaths associated with
H5N1 virus. While new technologies will influence poultry vaccines in the future, at
present the types of vaccine licensed by overseas authorities for use in poultry include:
Table 1.2 gives examples of the use of vaccines in recent overseas outbreaks of avian
influenza.
Many vaccines used recently around the world are inactivated whole AI virus antigen in an
oil-based emulsion adjuvant, produced according to OIE standards. Inactivated vaccines
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are made by formalin treatment of infected allantoic fluids from chicken embryos and
adjuvanted by making a water-in-oil emulsion using mineral oil. Immunity results
primarily from response to the H protein and, to a lesser degree, the N antigen. These
vaccine technologies produce safe, pure and potent vaccines, and commercial inactivated
vaccines have been shown to protect against disease and prevent mortality. However, they
require the handling and injection of individual birds. A second disadvantage is that they
are not able to prevent virus shedding in chickens challenged with antigenically different
viruses. This may aid virus persistence in the field and demonstrates the need for regular
review of vaccine viruses for their antigenic relatedness to field strains.
Table 1.2 Examples of the use of vaccines in recent overseas outbreaks of avian influenza
The inactivated vaccines use homologous H determinants (eg H5) and either a homologous
or heterologous N determinant to provide protection against known current field strains of
AI virus. The use of heterologous N subtype vaccines provides an opportunity to use
serological surveillance to detect circulating field virus by detecting antibodies to the N
subtype of the field virus, in what is known as a differentiating infected from vaccinated
animals (DIVA) strategy. Vaccine technologies are being developed which will enable
DIVA testing based on viral proteins other than the N antigen, obviating the need for using
heterologous N subtypes for DIVA purposes.
Inactivated whole virus vaccines which may be appropriate for use in Australia during an
emergency have been identified and are undergoing regulatory assessment. Following
importation, they would be held in quarantine until vaccination is authorised by the
Effective vaccination reduces susceptibility to infection and, where infection does occur,
reduces the amount of virus shed into the environment. These two factors mean that, under
some circumstances, vaccination may provide valuable assistance in eradication programs.
Vaccination may be considered to assist in managing particular compartments of birds
considered to be at risk of infection such as captive endangered species; the cost-sharing
agreement may not apply in some of these circumstances.
1.6 Epidemiology
AI viruses are not very resistant to warm temperatures, but they remain viable for longer
periods in cold and humid environments (see Section 1.6.2); as a consequence, the number
of outbreaks in Italy increased with the onset of winter (Capua and Marangon 2000). It was
noted in these outbreaks that the circulation of AI viruses of varying pathogenicity
complicated the interpretation of diagnostic results, leading to delays in initiating
eradication procedures for HPAI. Similar events were recorded in the outbreaks in
Pennsylvania, United States in 1983–84 (Webster and Kawaoka 1988).
General properties/environment
Environmental conditions have a marked effect on virus survival outside the bird. Survival
is prolonged in aerosols by high relative humidity and low temperature, and low
temperature and high moisture levels prolong survival in faeces.
AI virus can survive in faeces for at least 35 days at 4°C, and survival of virus in dust in
poultry houses has been reported for two weeks after depopulation. AI virus can survive
within the poultry house environment for up to five weeks (Webster et al 1978).
AI virus can be isolated from lake water where waterfowl are present (Hinshaw et al 1979).
Virus may remain infective in lake water for up to four days at 22°C and for over 30 days at
0°C (Webster et al 1978).
The presence of lipid in the AI virus envelope makes the virus highly susceptible to
disinfectants, including detergents (but only if items have been properly cleaned before
they are disinfected; see Section 2.2.10).
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Wild birds
As indicated in Section 1.2, AI virus is infective for almost all wild avian species, which
form an important reservoir for the virus. A virus that is highly pathogenic for poultry
could emerge from the pool of viruses in wild birds at any time.
Waterfowl
Wild aquatic birds, such as waterfowl and seabirds, are important reservoirs and can shed
AI virus for up to one month, compared with two weeks in domestic species.
AI virus from waterfowl can remain viable in faeces and water for up to 32 days.
During the 2003 Netherlands outbreak, 85 samples from waterfowl yielded seven H7N7
viruses — four were from ducks and three were from mute swans. This infection rate
would be similar to the rate of isolation recorded by random sampling when there is no
outbreak.
China has reported heavy mortalities in domestic ducks, geese and chickens from H5N1
virus infection in 2004; the acquisition of pathogenicity for waterfowl is a significant change
in the virus, indicating mutations (WHO 2004a).
Crows were reported dead in the repeated outbreaks in Japan (ProMED 2004a).
Game birds
AI virus was recovered from pheasants, partridges and guinea fowl for up to seven days
after infection during the outbreak in the United States in 1983–84.
In the Italian HPAI and LPAI outbreaks, quail showed few clinical signs and did not always
produce an antibody response to infection, and infection spread slowly — all of which
made detection of infection less straightforward (I Capua, OIE and National Reference
Laboratory for Avian Influenza, Italy, pers comm).
Live poultry
Viruses with the potential to be highly pathogenic for chickens and turkeys can be carried
by birds and shed in faeces and from the respiratory tract for at least two weeks and up to
30 days after recovery from the disease, while the virulent viruses can be carried by other
avian species without signs of clinical disease (Webster et al 1978). The importance of
spread by live poultry became apparent in the 2004 eastern Asia epidemic.
Cloacal shedding can continue for longer than 30 days after infection in the presence of
immunosuppressive diseases or other physical stresses.
Backyard poultry were extensively surveyed in the Netherlands outbreak of H7N7 subtype;
the eradication program depopulated about 150 000 pet birds on about 15 000 premises, and
infection was detected by virus isolation retrospectively on 14 sites and by serology on
eight sites.
Mammals
As indicated in Section 1.2, AI viruses can replicate in mammals and have been recovered
from experimentally infected pigs, ferrets and cats for several days after infection.
Carcases
AI virus survives for several days in carcases at ambient temperatures, compared with a
few weeks at refrigeration temperatures (Easterday et al 1997). There are insufficient data
on the spread of virus from fresh, frozen and processed meat, but this has not been
highlighted as an important method of transmission in outbreaks. Birds processed during
the viraemic stage will contaminate other carcases with blood or faecal material containing
virus. Packaging and the drips that develop during storage are also important, as both can
be contaminated with virus from infected carcases. On the basis of the Australian
experience, however, there is no evidence that carcases and animal products have
contributed to recycling virus back to poultry. All Australian outbreaks were controlled
soon after infection became established in poultry, leaving little opportunity for spread to
occur by this route.
AI viruses have been isolated from duck meat following export to other countries (Tumpey
et al 2003). The isolated viruses were pathogenic for chickens but did not produce clinical
disease in ducks, although the virus multiplied to high titres in many tissues and the
oropharynx.
Meat products
Virus can persist in poultry meat products.
In setting minimum processing conditions for cooked chicken-meat imports from New
Zealand, the Australian Quarantine and Inspection Service reviewed the published
literature on thermal inactivation of AI viruses in 1991 (AQIS 1991). Although the
inactivation times were found to vary between virus strains, the following agreed
minimum core temperatures for imports of cooked poultry meat from New Zealand are
considered sufficient to kill AI viruses:
• 70°C for a minimum of 30 minutes;
• 75°C for a minimum of 5 minutes; or
• 80°C for a minimum of 1 minute.
The actual cooking temperatures and times used for poultry products are shown in
Table 1.3.
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Table 1.3 Cooking temperatures and times for various poultry products
Nuggets
– fully cooked 210 1 minute (average) 75
– partially cookeda 196–207 27 seconds (–1)b
– further cooking at 182 10–15 minutes 85
fast-food outlets
Roast chicken
– chicken loaf 215 60 minutes 85–90
a Flash fried
b Nuggets are held at –1°C before partial cooking and then subjected to a short period at a high temperature. They are
further cooked at fast-food outlets.
Source: Arzey (1989)
Industry sources claim that precooked products for the retail market such as roasted and
smoked poultry and poultry rolls, and secondary products such as poultry stock cubes,
soup mixes, and canned and dried pet foods, all satisfy the minimum core temperature
requirements. However, for flash-fried products, such as nuggets, the cooking time is so
short that the internal temperature is unlikely to be raised sufficiently to kill the virus.
Further cooking at fast-food outlets, however, should be sufficient to kill the virus. The
virus may also survive in fully cooked nuggets, as they only reach a core temperature of
75°C for one minute. However, fully cooked nuggets are recooked by the consumer before
serving.
The OIE Terrestrial Code’s recommendation for the inactivation of AI virus in poultry meat
is that the meat reaches a core temperature of 70°C for one second.
The World Health Organization (WHO) INFOSAN website states that ‘the virus is
inactivated at temperatures reached during conventional cooking (at least 70°C at the centre
of the product … or when the meat is not pink in any part)’. 8
7 http://www.daff.gov.au/ba/ira/current-animal/chicken-meat
8 See http://www.who.int/foodsafety/micro/avian/en/index1.html#section%201
Egg pulp products could be another source of the virus. Current pasteurisation procedures
and cooking procedures for egg products are shown in Table 1.4.
However, these conditions are not sufficient to inactivate AI virus, which requires at least
4.5 minutes at 64°C, 5 minutes at 60°C or over 15 minutes a 55°C (Moses et al 1948).
The OIE Terrestrial Code recommendations for the inactivation of AI virus in eggs and egg
products are shown in Table 1.5.
Table 1.5 OIE Terrestrial Code recommendations for the inactivation of AI virus in eggs and egg
products
Fertile eggs
AI virus has been isolated from eggs laid by infected breeding hens.
Poultry byproducts
Rendered meals, produced from frames (boned-out skeletons), viscera, blood, feathers, feet,
heads, necks, offcuts, birds dead in trucks and discarded live birds, are added to poultry
feed as poultry offal meal and tallow. They may also be added to pet foods.
Poultry offal meal and pet foods are usually cooked at above 100°C for from several
minutes to more than one hour, which is sufficient to kill AI virus. However, if the
procedure is not carried out properly or cooked product is subsequently contaminated by
unprocessed product, AI virus could persist in the byproduct for several weeks.
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Waste products
Waste can be any of the unwanted byproducts of processing. All products that go into the
production of rendered meals may also be discarded as waste. In addition, there will be
wastes from hatcheries, laboratories (cultures and specimens, dead birds), farms and egg
marketing establishments (unsaleable eggs, egg shells after pulping, solid egg fillers), as
well as chicken manure and litter. AI virus has the potential to persist in these products and
could be spread by vehicles that transport them unless the products are treated before
movement. Composting infected carcases and internal organs for 10 days has been reported
to eliminate HPAI infection (Senne et al 1994).
Fomites
Persistence of the virus in faeces and respiratory secretions (see Live poultry above) is of
major importance. Their stickiness facilitates spread over a wide geographical area on
footwear, clothing, equipment and other fomites. This is the main way infection is
transmitted between premises.
Not all strains of AI viruses are highly transmissible for poultry; highly and lesser
pathogenic viruses can begin with low transmissibility but, following passage through
flocks, transmissibility as well as virulence for the host can increase in the field.
In the early part of the twentieth century, live bird movements through markets and the
shipping trade were the principal means of the epidemic spread of infection. The
significance of live poultry markets in generating and spreading HPAI has been observed in
Hong Kong in 1997, 2001 and 2002, in the northeastern United States from the 1990s to the
present, and in Southeast Asia in 2004. Live market movements have also assisted the
dissemination of LPAI viruses in the United States. Infection from contact with fresh
poultry, meat or eggs has not been recorded in either the Netherlands (2003) or eastern Asia
(1997–2004).
In recent times, dissemination of HPAI virus between flocks has been primarily attributed
to:
• the movement of infected birds (including vaccinated birds); and
• the actions of humans in moving feedstuff, personnel, equipment and vehicles into and
from premises that are contaminated with infected faeces or respiratory secretions.
Reductions in, and controls on, the movement of live commercial poultry and improved
biosecurity have meant that spread by live birds is now less important. Contamination of
personnel and fomites is now the principal way that infection spreads during outbreaks.
Epidemiological studies in the northeastern United States have shown that AI viruses
detected in the live bird trade usually remain LPAI, but they have been a source of infection
for commercial poultry in New York, Pennsylvania, Delaware and New Jersey from the
1990s to 2004 (Davison et al 2003, Henzler et al 2003, Panigrahy et al 2003, ProMED 2004d).
Outbreaks in commercial poultry were dealt with by slaughtering birds on infected
premises (IPs) and cleaning and disinfection, for fear that HPAI would develop through
passage in domestic chickens. It was noted that depopulating IPs quickly led to infection on
nearby properties; this was reduced by orderly marketing of the birds through slaughter
after infection had died down, rather than rapid slaughter (Henzler et al 2003).
Studies of the live bird markets of the northeastern United States showed that markets
operating the most intensive schedules, and selling both birds and animals, had the highest
risk of AI infection (Bulaga et al 2003).
Although aerosols may have caused some secondary spread during the New South Wales
outbreak in 1997, aerosols and windborne contamination have not been regarded as
important in the spread of infection (Swayne and Suarez 2000).
Wild birds
Direct or indirect contact with waterfowl is the most likely source of infection in poultry
(see Sections 1.2, 1.6.2 and 1.7). Studies have been undertaken in Italy, the Netherlands and
the United States on the isolation of AI viruses from wild waterfowl; over a period, nearly
every H and N subtype virus can be isolated from waterfowl throughout the year, with AI
viruses being isolated from 0.5% to 26% of samples (Alfonso et al 1995, De Marco et al 2003,
Fouchier et al 2003, Hansen et al 2003). An Australian study in 2001–02, of samples from
wild birds in Victoria, isolated H3N2 viruses from wild ducks (Peroulis and O’Reilly 2004).
During the 1985 AI outbreak in Victoria, a virus of the same serotype was isolated from a
starling trapped on the infected farm (Morgan and Kelly 1990).
Monitoring for HPAI in wild birds was undertaken in Italy in 1999–2000, when there were
outbreaks on 413 premises and 13 million poultry died. Some 103 dead wild birds were
collected in the winter, and virulent virus was isolated from only two samples: one from
sparrows that died in an infected poultry shed and one from a dove that died 1 kilometre
from an IP. Therefore, in this widespread and virulent outbreak, wild birds did not appear
to be an important means for disseminating virus (Capua et al 2000c). Monitoring wild
birds during the Netherlands outbreak in 2003 enabled virus isolation from four ducks and
three mute swans from 85 samples.
In the H5N1 epidemic in eastern Asia (1997–2004), deaths of waterbirds were reported in
Hong Kong in 2002 and a dead falcon was reported infected in 2004. There were reports of
deaths in overwintering birds in areas of Thailand near outbreaks among chickens, but no
investigation appears to have been made into the cause of death.
Live poultry
Transmissibility in poultry varies enormously between AI virus strains. Contact with faeces
or respiratory secretions is important, while airborne spread is not considered significant.
Work in the United States has detected virus in air samples only, to 45 metres downwind of
infected flocks, indicating limited spread through aerosols. However, Henzler et al (2003)
believed that depopulating IPs early in the infection cycle led to spread of infection to
nearby properties; this spread was reduced by orderly marketing of the birds in the normal
production cycle after infection had died down.
Experimental work in turkeys showed that infection readily passed to susceptible birds on
contact, but not to birds housed one metre off the floor. Westbury et al (1981) also showed
that A/duck/Victoria/76 (H7N7) was able to spread quickly to contact chickens but
A/chicken/Victoria/76 (H7N7) spread slowly. The methods of spread from bird to bird are
therefore poorly understood. Field outbreaks are further complicated by having to
distinguish between direct transmission and secondary spread by people and fomites.
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Overall, access of naive birds to fomites contaminated with infected faecal material poses
the greatest risk of spreading infection.
Eggs
Vertical transmission via infected eggs has never been proved, although AI virus has been
detected on the shell surface and in the yolk and albumen of eggs, suggesting that the
potential for spread exists. Normal incubation temperatures of 38.7°C in the early stages of
embryo development may be lethal to AI virus, or infected embryos may be killed by the
virus early during incubation. Persistence through the incubation process is most likely
through shell contamination.
Fomites
Overseas experience has shown that AI can spread very rapidly and can be carried over
long distances by transport of contaminated materials such as bird cages, pallets, egg filler
flats, manure and feed, and on contaminated clothing, equipment and vehicles.
Other vectors
There is no evidence to suggest that invertebrates are involved in the interepidemic
maintenance of transmission (Easterday and Beard 1984). However, there is a possibility of
mechanical transmission by either invertebrate or vertebrate vectors through contact with
infected faeces, although such transmission would be infrequent.
Virus spreads more efficiently in winter than in summer because lower temperatures and
higher relative humidity favour virus survival.
Improving biosecurity is the most important way that poultry producers, zoo personnel
and the owners of cage birds can prevent the spread of virus. This includes:
• biocontainment — containment of the virus on IPs; and
• bioexclusion — prevention of introduction of the virus to naive premises (Swayne and
Suarez 2000).
The reservoir for all 16 haemagglutinins (H) and 9 neuraminidases (N) of influenza viruses
is wild aquatic birds, particularly waterfowl, in which they multiply in the gastrointestinal
tract to produce large amounts of virus, usually without clinical signs. Influenza viruses
with new combinations of H and N genes are generated by genetic re-assortment (‘antigenic
shift’), which occurs when cells of the host are co-infected with two genetically different
viruses.
In wild waterbirds, the H and N subunits appear to be stable (Reid et al 2003) and the
viruses do not cause disease. However, when viruses with new H and N combinations
infect chickens and turkeys, a proportion tend to mutate and produce strains that cause
severe disease in those species. Epidemics of AI have occurred when an HPAI virus with
either an H5 or an H7 H is introduced to a naive poultry population. Similarly, influenza
epidemics occur in humans when there is antigenic drift in the H gene of human influenza
viruses; pandemics occur when there is a major antigenic shift, such as when the H is
changed.
It is not clear why AI virus H5N1, which had been present in China since at least 1997,
subsequently broke out across eastern Asia, but there were various gene assortments and
mutations (Shortridge 2003).
In influenza terminology, it is thought that the antigenic shift in a human virus that
occurred in 1918–19 was caused by the H of an avian virus entering the pig population
through co-infection with pig and avian influenza viruses in the respiratory tract cells of a
pig. The new pig virus then underwent a similar re-assortment in human respiratory tract
cells, producing a virus with the pig (formerly avian) H that was capable of spreading in
humans. However, some recent research has shown that the 1919 virus may have had an H
of direct avian origin, rather than an avian-to-pig origin (Stevens et al 2004).
In 1997, H5N1 AI virus infection of 18 humans (mostly children) occurred in Hong Kong.
All had had close contact with AI-infected chickens; six died. After the outbreak, 17% of
poultry workers showed evidence of inapparent infection (OIE 2003). Further cases were
recorded in Hong Kong in 1999 and 2003 (including one case of H9N2 strain). Also in 2003,
453 people reported health complaints associated with the management and depopulation
of chicken flocks infected with the H7N7 virus in the Netherlands; 89 became mildly
infected with the virus and one died (Koopmans et al 2004). In early 2004, human infections
occurred in Vietnam and Thailand (H5N1) and in Canada (H7N7). Further human
infections have occurred in Vietnam, Cambodia, China, Indonesia and Thailand since early
2005. Since 2006, cases have also been confirmed in Egypt, Turkey, Laos, Nigeria,
Azerbaijan, Djibouti and Iraq. 9.
Infected people have high levels of chemokines in their blood, and it is thought that
cytokine dysfunction contributes to the pathogenicity of the disease in humans, as opposed
to the generalised infection that occurs in poultry (Peiris et al 2004). Many of those who
have become ill and died with H5N1 infection have been children.
Antigenic characterisation of the viruses from people and birds in Hong Kong in 1997 and
2003, and Vietnam in 2004, indicates that the virus has mutated (WHO 2004bc); the Vietnam
strains of H5N1 are resistant to the antiviral drugs amantadine and rimantadine (WHO
2004d).
Human infection with H5 and H7 AI viruses has caused the World Health Organization to
consider whether a new pandemic human influenza virus could be derived directly from
birds, rather than through the intermediary infection of pigs (WHO 2004b). Fortunately, in
these outbreaks, there were no cases of sustained person-to-person transmission of AI
9 http://www.who.int/csr/disease/avian_influenza/en/
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viruses: all the people hospitalised were exposed to live poultry in the week before
becoming ill. There was also no association between infection and eating or preparing
poultry products (WHO 2004e).
It was claimed that chicken depopulation in Hong Kong in 1997, 2001 and 2002 averted the
re-assortment of avian and human influenza viruses and therefore prevented a pandemic of
human influenza (Mounts et al 1999, WHO 2004bc).
In an outbreak of AI involving the poultry industry, the main losses will be from
mortalities, which can be high, and reduced productivity. The stamping-out policy will
cause further loss of income for an extended period. Disruption to the flow of product and
reduced consumption and production may cause job losses on farms and in service and
associated industries, depending upon the time it takes to bring the outbreak under control.
Even a small outbreak will result in dislocation of the industry and its normal marketing
patterns. Infection in grandparent and foundation flocks would cause loss of some valuable
genetic material.
Export markets for poultry products are likely to close if the outbreak becomes established,
but the period of closure may be reduced by the adoption of a zoning strategy.
If the disease is allowed to become widespread and national production is affected, it is
possible that domestic supply will not meet demand; it is in preventing this situation that
vaccination has a role.
The eradication strategy and the movement controls that will need to be imposed and
rigorously enforced if a zoning or compartmentalisation policy is to be pursued will likely
result in severe disruption to many industry practices, including breeding programs and
sales of eggs, chicks, poults, pullets, turkeys and meat birds. Any delays beyond the
marketing age of the various commodities can cause greatly increased production costs and
losses over a short time, and affect producers not directly involved in the outbreak through
loss or disruption of supply.
Zoos and premises holding cage birds, including pet shops and aviaries may be affected
directly by the outbreak or indirectly through movement controls.
It is important that restrictions be eased as soon as the control strategy and circumstances
permit, so viable commerce can be resumed as soon as possible by as many premises as
possible.
If the CCEAD is satisfied that the actions taken are adequate to contain the disease within
the declared areas, and zoning or compartmentalisation procedures are in place, then all
birds and avian products from the free area should be allowed to move unimpeded
(overseas or interstate). Birds and avian products from the declared areas may be moved by
permit, subject to an assessment of the risks involved and to efficient implementation of an
industry national management plan and agreed standard operating procedures.
Poultry products are considered unlikely to transmit infection between countries and flocks
(Swayne and Suarez 2000).
The likelihood of the poultry epidemic in eastern Asia spreading to Australia has been
estimated to remain low because:
• migratory birds return to Australia from the northern hemisphere without incident; and
• the Australian poultry industry operates with good biosecurity compared with that in
Asian countries, where a large part of the poultry industry is free range.
If an Asian poultry epidemic were to spread to Australia, the risk of the general public
becoming infected as a result of contact with live infected poultry would be very low. Sales
of live poultry in Australian markets are very small, and such sales would be prohibited in
the event of an epidemic.
Surveillance in the areas outside the restricted area (RA) and control area (CA) needs to
include testing of flocks that show any clinical signs suggesting infection with AI viruses.
Surveillance needs to include virological and/or serological investigations.
Establishing proof of freedom from AI can best be achieved by clinical observations and
dead-bird sampling of repopulated sheds and possible disease outbreaks, rather than by
widespread biological testing. Further testing may be considered in the light of
epidemiological information; such testing will become important if an AI outbreak becomes
widespread and mild or low pathogenicity strains of the virus are detected during the
outbreak. Failure to take decisive action could lead to such modified strains again becoming
widespread, with possible later reversion to virulence and HPAI.
The OIE Terrestrial Code allows for the status of a country, zone or compartment to be
determined on the basis of a risk assessment, provided that ‘notifiable avian influenza’
(NAI, which includes HPNAI and LPNAI) is notifiable in the country and appropriate
surveillance is in place. Based on surveillance, a country, zone or compartment may be
considered to be free from NAI when HPNAI and LPNAI have not been present for at least
the previous 12 months, based on surveillance in accordance with OIE guidelines. The
surveillance may need to be adapted to parts of the country or existing zones or
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If NAI infection occurs in a previously NAI-free country, zone or compartment, free status
can be regained three months after a stamping-out policy (including disinfection of all
affected establishments) is applied, provided that surveillance in accordance with OIE
guidelines has been carried out during the three-month period.
These time periods apply irrespective of whether vaccination is carried out. If Australia
were to move into a vaccination program as part of the eradication strategy, the earliest that
freedom from disease could be declared would depend on whether or not stamping out is
carried out on all IPs, as follows:
Importing countries may be prepared to accept less than the OIE standard and allow
imports of Australian live birds, hatching eggs and avian products as part of normal
bilateral agreements if infected and free zones, or free compartments have been established.
2.1 Introduction
Infection of commercial poultry flocks with highly pathogenic avian influenza (HPAI) virus
would be recognised quickly. However, infection of poultry with avian influenza (AI)
strains that are of low pathogenicity (LPAI (H5/H7) or LPAI (not H5/H7); see Sections 1.1.3
and 1.1.4), infection of cage or zoo birds with any strain of AI virus or the presence of HPAI
virus in wild birds may not be recognised easily without ongoing surveillance. Although it
would be desirable to eradicate all HPAI and LPAI (H5/H7) viruses isolated from
commercial poultry or cage or zoo birds, the virulence of any isolate needs to be
determined so that an appropriate control strategy can be formulated. The detection in
Australian poultry or cage or zoo birds of an AI virus classified as LPAI (H5/H7) is taken
seriously because spread of the virus may lead to HPAI virus arising by mutation and
causing a much larger outbreak, with high mortalities as occurred in Pennsylvania, Mexico
and Italy.
As some strains of H5, H7, H9 and H10 subtypes of AI viruses have been shown to be
capable of infecting humans, the public health implications of any outbreak of HPAI, LPAI
(H5/H7) or LPAI (not H5/H7)) should be assessed.
AI virus is stable under a range of environmental conditions, particularly cool and humid
conditions, allowing it to be spread directly from flock to flock by live birds, fomites or
drinking water contaminated with infected faeces (see Sections 1.6.3 and 1.6.4).
The basis for eradication of HPAI in poultry flocks by stamping out is, therefore:
• the rapid imposition of effective quarantine;
• stamping out by isolation of infected and potentially infected birds, followed as rapidly
as possible by the killing of the birds and the sanitary disposal of carcases;
• decontamination;
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These principles will need to be combined with the following other strategies:
• comprehensive, integrated national surveillance and diagnostic programs;
• enhanced biosecurity practised at all levels of production and processing by all
employees of companies, diagnostic laboratories and government agencies that have
contact with poultry or equipment from poultry operations; and
• education of poultry farmers and other workers about AI control, and sharing of
information on surveillance and control strategies at all levels in the production
process.
Rapid reporting and diagnosis of suspected cases together with swift imposition of effective
eradication and movement controls will be the key to achieving these objectives. These
procedures have been recognised as effective in previous outbreaks of HPAI in Australia
and elsewhere (Swayne and Suarez 2000).
In some specific circumstances, where other control and eradication measures are not
succeeding, vaccination, with government control, may be considered as one element of a
comprehensive control program (Swayne and Suarez 2000).
Similar principles and procedures apply to the stamping out of HPAI following the
detection of virus in cage or zoo birds.
For this reason, quarantine needs to be imposed on suspect premises (SPs) and dangerous
contact premises (DCPs), at least until the extent of infection spread is determined. In the
past, it may have taken several weeks of strategic surveillance before confidence was
obtained that other properties in the area were not incubating the disease. Rapid diagnostic
technology such as real-time PCR and direct antigen tests can now assist with rapid
evaluation of the extent of infection.
Risk assessment of DCPs will identify premises that have received live birds or avian
products from an IP and therefore have a higher risk of being infected than premises with
indirect contact with an IP through personnel, equipment or vehicles. This difference in risk
needs to be reflected in the management of the DCPs. Very high-risk DCPs should be
slaughtered-out before the flocks excrete virulent virus. Lower risk poultry DCPs may be
process slaughtered.
The possible AI infection of workers who are in contact with live birds, faeces and
contaminated materials means that such workers need protection in an outbreak; worker
protection is discussed in Section 2.2.15 and Section 4.2.
The declaration of a control area (CA) around the RA will help to control the spread of the
outbreak from within the RA. The CA is a buffer zone between the RA and the rest of the
domestic bird population where normal operations can continue. If the outbreak involves
commercial poultry and if the CA contains an appropriate place for poultry slaughter,
permission should be given to remove meat birds from DCPs and SPs, following inspection,
within 24 hours for slaughter where no sign of infection has developed during the declared
incubation period and surveillance has been in place.
The RA and CA are defined in Section 4.1. Recommended movement controls are given in
Section 4.2.
If an outbreak of HPAI is spreading quickly, declaration of the RA and CA will allow the
rapid investigation of the extent of infection and scaling up of the response. It is important
that the extent of area declarations in Australia be limited to as small an area as necessary to
cover the likely extent of infection. The size of the declared areas can be reduced after initial
investigations have determined the likely extent of infection. If the outbreak involves
commercial poultry, delaying the slaughter of meat birds inevitably places pressure on the
routine of orderly processing. While restricting movement provides distinct advantages for
disease control, it may be necessary to implement a ‘welfare slaughter’ if overcrowding
becomes a problem.
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Zoning/compartmentalisation
Zoning or compartmentalisation could be used by some jurisdictions outside the CA to
establish a free area that, after the required serosurveillance to prove freedom from AI,
could be accepted by other countries as separate from the other parts of Australia for trade
purposes. Section 1.9 gives information on establishing proof of freedom.
2.2.4 Tracing
The information obtained from tracing will help to decide the extent of the RA and CA and
identify any additional DCPs and SPs. Information should be requested on Animal
Emergency Information System (ANEMIS) forms.
• The critical date is determined as the earliest time the virus could have entered the IP,
and should be consistent with the maximum incubation period of 21 days for poultry,
designated in the OIE Terrestrial Code.
• As a first priority, movements to and from IPs and, where possible, DCPs should be
traced for at least 21 days before the first observation of unusual morbidity or
mortality. High-risk movements that need to be traced are those of birds, eggs, poultry
products, manure, litter and waste. Movements of feed, equipment (including egg
fillers, cages, trolleys and pallets) and people also need to be traced and contact flocks
assessed for infection for the 3 days before unusual morbidity or mortality was
observed on the IP.
• People involved with feed delivery, vaccinating crews, bird handling crews,
tradespeople, company service people and veterinarians should be interviewed, and
lists should be compiled of all their possible contacts for the 3 days after they visited
any SP or DCP.
• The original source of likely introduction of the virus to the birds should be traced, as it
could remain a source of further virus dissemination.
2.2.5 Surveillance
Ongoing strategic surveillance will aid the early detection of AI. Active surveillance should
be initiated as soon as HPAI is suspected. Initially, the location of all commercial and
backyard poultry, zoo birds and significant holdings of cage birds in the RA should be
identified and mapped. A sample of birds of any domestic species that die in the RA should
be checked for AI lesions, and specimens submitted to approved laboratories for virus
isolation. The use of real-time PCR and tests such as the DirectigenTM test provides the
opportunity to conduct rapid diagnostic surveillance.
Field surveillance examinations should seek to detect changes in flock health. To avoid
spread of virus, visits by local disease control centre (LDCC) officers should be limited to
the investigation of reports of increased mortality and/or morbidity.
Intensive surveillance aims to identify potential new cases of AI. Because of the risk of
spread of virus by personnel, equipment and vehicles, the following procedures should be
adopted to enable continuing surveillance while minimising multiple farm visits by
inspectors and other authorised personnel to premises in the RA and CA:
• dead bird pick-up and transport to a laboratory, or sampling and sending of samples to
a laboratory;
• reporting on flocks by telephone or fax;
• telephone survey; and
• serological/virological testing.
Training needs
Surveillance officers or other authorised officers must be:
• familiar with the poultry industry, zoo operations or the cage bird world; or
• able to pass information to appropriate experts for interpretation.
If the investigation of wild birds becomes necessary, surveillance officers would need to be
aware of the natural movements and behaviour of wild birds, or be able to draw upon the
expertise of ornithologists.
Surveillance officers must have access to:
• for domestic and zoo birds, flock health records expected for the class of stock under
normal circumstances; and
• a summary of the disease — a list, pictures and video of clinical signs and an example
of how health and production records would change in flocks infected with AI virus.
Information required
Information from records and from owners/personnel will be required for high-risk flocks
in the RA and CA. These could be flocks of any of the following types:
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Decisions should be made locally on which laboratory will be responsible for laboratory
testing, managing the reporting system and evaluating the results for the situations
described below.
All reports of a decline in the health of birds (decline in feed or water consumption or egg
production, increase in mortality, depression or respiratory disease) should be investigated.
A standard reporting procedure is outlined in Section 1.9.
The most appropriate method of destruction will depend on such factors as the species of
bird, the type of premises involved, the weather, the availability of expertise and skilled
workers, and physical resources. Handling dead birds produces less airborne
contamination than catching and handling live birds, reduces the exposure of workers to
contamination, and makes working in the recommended protective equipment more
bearable.
Whether to gas birds in their cages depends on the nature of the buildings, the species and
size of the birds, the number of birds per cage and the timespan before they are removed (as
it can be extremely difficult to remove dead birds from cages once rigor mortis is
established). It may be better to remove birds from their cages alive and gas them in an
enclosed trailer or container (skip) before rendering, burial or incineration.
For OHS requirements for personnel involved in destruction of birds, see Appendix 3.
Although these preventive and monitoring measures are voluntary, personnel who do not
agree to them should not be engaged in activities in which they could come into contact
with infected birds or premises.
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be contained to IPs. In addition, attention needs to be paid to ensuring that products from
other premises in the area of infection do not transfer AI virus before infection is diagnosed
on those premises.
2.2.9 Disposal
One of the major objectives of the eradication program is prompt and effective disposal of
contaminated material that cannot be effectively treated (eg dead birds, eggs, litter, manure,
fresh or frozen carcases, plant and equipment, and building materials). Disposal requires
consideration by an expert group using a decision-making framework to define and
document the most appropriate option (see the Disposal Manual). Available methods
include burial, incineration, burning, rendering and composting.
The removal of very large numbers of birds in a short time presents environmental and
logistical problems. A poultry shed full of meat birds close to market weight contains about
75–90 tonnes of organic material, of which 75% is water. If infected material must be
transported for disposal, particular attention should be paid to preventing the spread of the
virus. For example, truck body trays must be waterproof and all loads carefully covered
with tarpaulins to ensure that material cannot be blown out.
Disposal may be either on or off the IP. Burial in a common site would be considered if a
number of IPs in a given area have to be depopulated and decontaminated.
Incineration is a good method of disposal, but incinerators are mostly too small to be useful
for poultry flocks and may not be near IPs. Burning in pits or on pyres has been used where
no burial site is available, but is expensive because of the high water content of carcases and
may also be environmentally unacceptable.
Rendering is a good method of disposal if the rendering plant has enough capacity and if it
can be effectively decontaminated afterwards. However, private rendering plants may not
be willing to handle infected birds and eggs. A disadvantage is that infectious material
would need to be transported from IPs to the plant.
Composting is an effective way to deal with dead birds, manure and litter waste. Material
can be composted inside sheds or otherwise on site, eliminating the risk of spreading the
virus during transport.
If litter is to be removed, it will be necessary to moisten the surface with a disinfectant and
possibly heap the litter in mounds under plastic before removal.
2.2.10 Decontamination
Decontamination entails cleaning and disinfection of the infected site to remove all infective
material.
Particular attention should be paid to the decontamination of litter. As the AI virus can
survive up to 35 days at 4ºC in faecal material, it is necessary to quickly disinfect the surface
of the litter and to use measures such as composting to thermally inactivate the virus
(composting inside sheds has some advantages).
Contaminated fomites, such as clothing, footwear, crates, feed sacks, egg fillers and other
equipment should be decontaminated, if possible, or destroyed.
2.2.11 Vaccination
Vaccination is an option in the control of HPAI and LPAI (H5/H7), and has been used
successfully in control of the disease in some countries (China, Canada, Vietnam and Italy).
However, vaccination alone will not ensure AI eradication but it should only be used in
addition to culling, the adoption of appropriate biosecurity procedures and monitoring.
Although inactivated vaccines may protect against clinical disease and reduce mortality
and environmental contamination, they do not prevent infection in vaccinated birds which
may shed low levels of virus without showing clinical signs.
In addition, when vaccine is used during an outbreak, the masking of infection and the risk
of vaccination crews spreading infection remain of concern. In all vaccinated flocks there is
a need to perform virological and serological tests to monitor for virus circulation and to
provide evidence of the effectiveness of the vaccination program.
In Australia, vaccination could be part of a response where the disease is likely to spread
and is unable to be rapidly controlled by stamping out and other measures. Any decision
regarding possible vaccination needs to be made as early as possible in the course of the
incident to allow for the time lag inherent in making arrangements for field use of the
vaccine. The decision whether to vaccinate and the options chosen in Australia will be
determined by factors such as the species and types of birds at risk, the density and
characteristics of the surrounding avian population (wild and domesticated), geographic
considerations, epidemiological factors, the virus subtypes involved, public health
concerns, the resources available and the availability of appropriate vaccines.
• Suppressive vaccination — to reduce the virus load through the vaccination of animals
that are at high risk of exposure to infection, for example in an infected area. Vaccination
can reduce morbidity and mortality, and while it may not prevent infection in
vaccinated birds, it can reduce the volume of virus produced by infected flocks. This
approach is more likely to be used in intensive farming situations, particularly where
resource constraints have created rate-limiting situations for destruction and disposal,
for example a delay in carcase disposal. Under this regime, vaccinated birds are likely to
be destroyed. Vaccination can involve all at-risk birds or a selected subset based on area
or production type.
• Buffer vaccination — to create a population of less susceptible birds around the infected
region to slow virus transmission and minimise spread beyond a defined area. Clearly,
movement control is essential to prevent infectious material passing beyond the buffer.
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The location and shape of the vaccinated population may be influenced by geography
and by the demographics of the animal population at risk. Buffer size is dependent on
the epidemiology of the pathogen involved, the livestock density, the resources available
and other factors.
• Targeted vaccination — to assist the management of specific compartments such as free-
range birds, breeding stock of high genetic value, and rare birds.
In conjunction with the biosecurity requirements applying generally, specific requirements
may need to be imposed on all vaccinated flocks and individual birds. These should remain
in place until destruction or process slaughter, or until freedom from infection is confirmed,
and should include:
• movement restrictions on live birds and other things from vaccinated flocks to manage
any increased risk that might be a result of vaccination concealing the presence of virus;
• evaluation of vaccine effectiveness by monitoring post-vaccination titres, where
appropriate;
• use of methods differentiating infected from vaccinated animals or other clinical and
virological monitoring, including use of sentinel birds, to look for evidence of infection
in vaccinated flocks;
• for commercial poultry, designated timeframes for process slaughter or destruction of
vaccinates;
• identification of vaccinated birds/flocks to ensure all are accounted for; and
• any other measures as required by the chief veterinary officer to manage risks in the
particular situation.
Suitable exit strategies would be required for vaccinated birds and the controls placed on
vaccinated flocks must include a clear endpoint:
To minimise the risk of infection from wild birds, it is essential to practise high-level
biosecurity on such premises. During eradication procedures, bird-proofing of quarantined
and other bird houses and protection of contaminated sites from wild birds are essential
disease control strategies and need to be rigorously enforced.
The detection of HPAI virus in a wild bird or birds would lead to epidemiologically based
investigations being commenced in the area in which the bird was found. Such
investigations may include sampling of live or dead wild birds and ensuring that
public/private enterprises in the area holding birds are aware of the need for enhanced
biosecurity. If widespread HPAI infection is found in wild birds, it may be necessary to
proclaim restricted areas, to conduct broad surveillance and to consider the use of
vaccination.
Joint FAO/OIE/WHO meetings have recommended that slaughter of wild birds, including
waterfowl, should not be part of control/eradication activities in eastern Asia (FAO
2004bc). AI virus cannot feasibly be eradicated from these populations, and it is the
responsibility of bird owners to protect their birds from infection by preventing contact
between domestic birds and wild birds or their faeces.
Flying insects can spread the disease mechanically (see Section 1.6.3). If practical, steps
should be taken to reduce flying insect numbers and minimise the chance of flies entering
bird sheds.
Experience in the United States and Australia has shown that dead-bird sampling of
repopulated sheds is more efficient for monitoring than placing sentinel birds in the
buildings from the time of depopulation to repopulation.
WHO has recommended taking steps to halt the further spread of epidemics in poultry
populations in eastern Asia and giving high priority to the rapid elimination of H5N1 virus
in bird populations as a matter of international public health importance. To limit the
possibility of starting a human influenza pandemic, it has also recommended prudent steps
to protect workers involved in controlling outbreaks (WHO 2004bfg).
The OHS measures to be taken in Australia have been agreed nationally; human aspects
will be coordinated by local public health authorities, who will be guided and coordinated
by the National Pandemic Influenza Action Committee (see Appendix 3). Treatment of
workers with antiviral drugs and/or collection of blood samples will require the consent of
each person and the knowledge and agreement of local public health workers.
Care will need to be taken to provide adequate training to personnel recruited from the
general public about the measures needed to ensure their safety in the workplace. Poultry
10 http://www.who.int/csr/disease/avian_influenza/guidelinestopics/en/index3.html
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industry workers, zoo personnel and government officers recruited to depopulate infected
premises will also need adequate training.
Details of any imposed movement controls need to be made available and clearly
explained. Poultry industry workers, zoo personnel and cage bird owners need to be made
aware that illness, such as symptoms of mild influenza or colds, may follow contact with
infected birds, and that they should seek medical assistance should any symptoms of
influenza follow such contact.
Further information must be provided to the public to address concerns about the safety of
poultry products.
Further information on how to manage a public relations and media campaign in the event
of an emergency animal disease outbreak is provided in the Public Relations Manual.
The WHO recommendation for a stamping-out policy currently applies only to HPAI
outbreaks in poultry and where there is a risk of human infections, which could arise from
HPAI (WHO 2004b). The OIE has made both HPAI and LPAI (H5/H7) notifiable diseases
(HPNAI and LPNAI) and subject to international trade rules (see Section 1.1.3). LPAI
(H5/H7) has not been recorded as producing clinical or inapparent infections in humans.
If LPAI (H5/H7) is detected in Australian poultry flocks, or in cage or zoo birds, the
following risk factors will need to be assessed in arriving at a control/eradication program
which may include vaccination:
• the species involved;
• the nature and severity of the clinical disease;
• whether the virus produces clinical illness or infection in humans;
• the rapidity with which the virus is spreading within or between flocks;
• the proximity to commercial poultry or other significant avian establishments;
• the density of bird populations especially poultry in the area of the outbreak;
• the possibility of spread to other areas;
• the possibility of a mixed population of viruses being present, with apparent LPAI
(H5/H7) viruses masking subpopulations of HPAI viruses;
• the impact that the disease will have on the marketing of poultry products;
• the possibility of creating a vaccination zone and process slaughtering infected poultry
flocks when major disease control activities can be undertaken, such as in the
favourable, low-spread, summer months; and
• the costs and impacts of alternative response options.
The methods for the control of LPAI (H5/H7) infections in poultry are essentially the same
as those for HPAI (see Section 2.2). The preferred control and eradication option will be
stamping out for IPs, if the infection is detected early and immediate surveillance in the
area using rapid diagnostic technology indicates no significant spread. Ongoing
surveillance for LPAI (H5/H7) infections in at-risk premises will give confidence that
infection has been contained and is not establishing widely. These control measures will
need to be supported by strict biosecurity by poultry farmers and industry actions to limit
the spread of virus in the industry.
However, where immediate surveillance indicates there has been some spread from the
index property, vaccination needs to be considered. The principles of vaccination for LPAI
are the same as for HPAI (see 2.2.11).
Further surveillance may be required if LPAI (H5/H7) causes few or no clinical signs and
vaccination is being used as an adjunct to eradication. For surveillance, rapid techniques
can be used for virus detection, followed by confirmatory testing to identify field viruses.
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3.1.1 Overall policy for avian influenza classified as HPAI (except in wild birds)
Highly pathogenic avian influenza (HPAI) is a OIE (World Organisation for Animal Health)
notifiable disease (HPNAI) that is highly lethal to poultry and has the potential to infect
humans. An uncontrolled outbreak of HPAI would cause severe production losses with
consequent dislocation and financial losses in the poultry and associated service and sales
industries. It may also lead to morbidity and mortality in large numbers of cage and zoo
birds.
• stamping out by destruction of all birds on infected premises (IPs) where there is clinical
disease or evidence of active infection with HPAI virus, and the sanitary disposal of
destroyed birds and contaminated avian products to remove the source of infection;
• possible pre-emptive slaughter of birds on other premises, depending on information
derived from tracing, surveillance and study of the behaviour of the disease;
• quarantine and movement controls on birds, avian products and associated items in
declared areas to prevent spread of infection (a national standstill is not necessary for
containment of AI);
• decontamination of facilities, products and associated items to eliminate the virus on IPs
and to prevent spread in declared areas;
• tracing and surveillance to determine the source and extent of infection, and to establish
proof of freedom from the disease;
• enhanced biosecurity at poultry establishments, and premises holding cage or zoo birds;
• zoning and compartmentalisation to define infected and disease-free areas;
• a public awareness campaign to communicate risk and promote cooperation from
industry, zoos, cage bird owners and the community; and
• protection of public health, by requiring that personnel engaged in eradication activities
be vaccinated (with the currently available human vaccine), be treated with antivirals
(if appropriate) and wear protective clothing.
Vaccination may be considered if an outbreak of HPAI is likely to spread or has spread out
of control.
Under the Government and Livestock Industry Cost Sharing Deed In Respect of Emergency Animal
Disease Responses (EAD Response Agreement) for cost sharing, HPAI (H5/H7) is a
Category 2 emergency animal disease (EAD) and HPAI (not H5/H7) is a Category 3 EAD.
Category 2 EADs are those for which costs will be shared 80% by government and 20% by
industry; Category 3 EADs are those for which costs will be shared 50% by government and
50% by industry.
When HPAI is confirmed on or threatens to spread to premises on which rare poultry, cage
or zoo birds are present, the prime objective is eradication of the virus. A modified
approach, including consideration of vaccination, may be appropriate, however, taking into
account factors such as biosecurity, movement controls, ongoing tracing and surveillance,
and timeliness in achieving disease eradication.
3.1.2 Overall policy for avian influenza classified as LPAI (H5/H7) in poultry
Low pathogenicity avian influenza (LPAI (H5/H7)) is an infection caused by a strain of
avian influenza virus that is of H5 or H7 subtype and produces mild or no clinical disease
in poultry. LPAI could mutate to HPAI and cause significant disease problems in the
poultry industry, and lead to morbidity and mortality in large numbers of cage and zoo
birds.
Such virus strains in poultry are classified as notifiable (LPNAI) according to OIE criteria,
and because of the potentially severe consequences of an uncontrolled outbreak of these
strains of AI mutating to HPAI, they are categorised under the EAD Response Agreement.
LPAI (H5/H7) of subtypes H5 or H7 is a Category 3 EAD under the EAD Response
Agreement for cost sharing. Category 3 diseases are those for which costs will be shared
50% by government and 50% by industry.
When CCEAD determines that an infection is caused by an AI virus that meets the
definition of LPAI (H5/H7), the policy is to control and eradicate the disease, while limiting
spread and potential for mutation to HPAI, using a combination of strategies, including:
• tracing and surveillance to determine the source and extent of infection and to
establish proof of freedom from the disease; followed by
either
• stamping out either as for HPAI, if the infection is limited in distribution in the
poultry industry and destruction of infected flocks is manageable or by modified
stamping out using process slaughter if processing capacity is available;
or
• vaccination and a modified approach to eradication, if the infection is likely to
spread or has spread out of control;
and
• quarantine and movement controls on poultry, poultry products and associated items
in known IPs to prevent spread of infection;
• decontamination of facilities, products and associated items to eliminate the virus on
IPs;
• enhanced biosecurity at poultry establishments and premises holding cage or zoo
birds in the vicinity;
• zoning and compartmentalisation to define infected and disease-free areas; and
• a public awareness campaign to communicate risk and promote cooperation from
industry and the community.
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3.1.3 Overall policy for avian influenza classified as LPAI (H5/H7) in cage or zoo birds
LPAI (H5/H7) is an infection caused by a strain of avian influenza virus that is of H5 or H7
subtype and produces mild or no clinical disease. LPAI could mutate to HPAI and lead to
morbidity and mortality in large numbers of cage and zoo birds.
Because of the potentially serious consequences of the spread of these strains of AI, LPAI
(H5/H7) in cage or zoo birds is a Category 3 EAD.
When CCEAD determines that an infection in cage or zoo birds is caused by such a virus,
an assessment of the risks to animal and public health will be carried out, taking into
account the species of bird involved, the clinical status of the birds, and their proximity to
commercial poultry and other significant bird establishments and populations, and to
public amenity areas. The policy is to limit the spread of the infection and its potential for
mutation to HPAI, and the response will depend upon the assessed risk. A combination of
strategies may be employed, including:
• tracing and surveillance to determine the source and extent of infection and to
establish proof of freedom from the disease;
• quarantine and movement controls on birds and associated items in known IPs to
prevent spread of infection;
• stamping out as for LPAI in poultry, or a modified approach to control in accordance
with the risk assessment; this may include vaccination if the infection is likely to
spread or has spread out of control;
• decontamination of facilities, products and associated items to eliminate the virus on
IPs;
• enhanced biosecurity at avian establishments in the vicinity; and
• a public awareness campaign to communicate risk information and promote
cooperation from industry, zoos, cage bird owners and the community.
3.1.4 Overall policy for avian influenza infections classified as LPAI (not H5/H7) in
poultry, or in cage or zoo birds
Avian influenza caused by a strain of virus that is neither HPAI nor LPAI subtype H5 or
H7, and which is producing no or mild clinical disease, is not considered an immediate
threat to Australia’s domestic or zoo birds or public health. Such AI virus strains are
classified as LPAI (not H5/H7), and their detection in Australia would not be treated as an
emergency disease outbreak.
When the CVO determines that an infection is caused by such a virus, an assessment of the
risks to animal and public health will be carried out, taking into account the virus subtype,
the species of bird involved, the clinical status of the birds, and their proximity to
commercial or other significant bird establishments and populations, and to public amenity
areas. No action will be required unless the risk assessment indicates an unacceptable threat
to animal or public health. When a response is necessary, it may include:
These AI subtype viruses (LPAI (not H5/H7)) are not categorised under the EAD Response
Agreement for cost-sharing arrangements.
3.1.5 Overall policy for avian influenza infections classified as HPAI or LPAI in wild birds
Avian influenza infections classified as HPAI or LPAI in wild birds are not considered to
pose an immediate threat to Australia’s domestic or zoo birds, or public health. Their
detection would therefore not be treated as an emergency disease outbreak in Australia.
However, HPAI infections in domestic or zoo birds could have serious consequences for
avian and/or public health.
Therefore, if HPAI infection is detected in wild birds, the CCEAD will be convened and an
assessment of the risks to animal and public health will be carried out, taking into account
the circumstances under which sampling occurred, the possible source of the virus, the
species of bird involved, the clinical status of the sampled birds/population, and their
proximity to commercial and other significant bird establishments and populations, and to
public amenity areas.
The response to a finding of HPAI infection in wild birds will be measured, commensurate
with the level of assessed risk posed to domestic and wild bird populations, and to public
health. No destruction of wild birds will occur, other than for reasons such as animal
welfare. For further details, see Appendix 2.
If widespread HPAI infection is found in wild birds only (ie not in poultry, cage or zoo
birds), it may be necessary to proclaim restricted areas, to conduct broader surveillance and
to consider the use of vaccination in domestic and zoo birds in the immediate vicinity.
The CVO in the state or territory in which the incident occurs is responsible for developing
an EAD Response Plan for the particular incident.
The CCEAD convened for the incident assesses the response plan drawn up by the CVO for
technical soundness and consistency with AUSVETPLAN, and endorses or seeks
modifications to it. Overall operational management of the incident rests with the CVO of
the affected jurisdiction, with oversight by the CCEAD.
The NMG, also convened for the specific incident, decides on whether cost sharing will be
invoked (following advice from the CCEAD) and manages the national policy and
resourcing needs.
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CVOs will implement disease control measures as agreed in the EAD Response Plan and in
accordance with relevant legislation. They will make ongoing decisions on follow-up
disease control measures in consultation with the CCEAD and the NMG, based on
epidemiological information about the outbreak(s).
For information on the responsibilities of the state or territory disease control headquarters
and local disease control centres, see the Control Centres Management Manual, Part 1.
While vaccination was not considered an option for control programs in the past, in some
circumstances vaccines may now have a role in an eradication strategy (see Sections 1.5.3
and 2.2.11). If HPAI is not being controlled effectively, a vaccination strategy can be
developed for Australian conditions to dampen virus spread and protect elite flocks and
other rare birds if a suitable effective vaccine has been identified and is available in the
required quantities and within the time required (see Section 3.2.5).
It will be necessary to ensure regular and ongoing liaison, through the industry liaison
officer, with industry, poultry owners and farm managers, and with zoos and cage bird
owners to seek their involvement, cooperation and support for eradication, particularly
with regard to stamping out, disposal, decontamination and improved biosecurity.
Effective involvement with the media will also be needed to ensure informed reporting,
and with the public to provide information and clear explanations.
When HPAI is confirmed on a premises on which rare poultry, cage or zoo birds are
present, the primary objective is eradication of the virus. A modified approach may be
appropriate, taking into account factors such as biosecurity, movement controls (such as
lifetime quarantine), ongoing tracing and surveillance, and timeliness in achieving disease
eradication.
The important first steps to control the spread of infection will be to define the bounds of
infection and place restrictions in that area to slow the spread of infection and prevent it
getting out of the defined infected area. Pre-emptive destruction of birds on close-contact
premises, including DCPs and suspect premises (SPs), can be undertaken to control
infection spread in the infected area if the infection is spreading rapidly, and there are
resources available to destroy and safely dispose of the birds and carry out
decontamination. Where premises design and other factors allow, birds may be destroyed
by gassing in skips, modified truck trays or sheds (see Sections 2.2.7 and 2.2.9). The
Destruction of Animals Manual and the Disposal Manual must be consulted when
deciding on the most appropriate means of destruction and disposal.
IPs, DCPs and SPs will be declared (see Section 4.1), and will be subject to quarantine and
movement controls on items as outlined in Section 4.2. Movements of manure and litter off
these premises will be prohibited unless, in exceptional circumstances, a permit is issued.
Equipment (egg fillers, trolleys, pallets, etc) and eggs (table and fertile) may need to be
destroyed on site, or they may be moved under permit after decontamination or
sanitisation (see Section 4.2). Movements of people and vehicles will be controlled, and
personal and vehicle decontamination will be required before leaving the premises. The
access of wild birds to premises and water supplies will be restricted. Bird-proofing will
begin as soon as possible. Pets will be confined. Infected poultry will not be allowed to be
moved for process slaughter, but process slaughter should be used for uninfected flocks
where feasible. Movement controls need to be applied as specified in Section 4.2.
DCPs will be subject to movement controls during investigations into the status of the
premises and during the OIE-prescribed incubation period of 21 days. These restrictions
will ease as the situation is better defined. It is important that restrictions on declared
premises be eased as soon as circumstances permit.
The initial boundary of the CA may correspond with the state/territory or other
geopolitical border, but the boundary will be amended on the basis of epidemiological
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evidence obtained over time to allow as much commercial activity as possible, in line with
accepted disease control measures.
Within the CA, movements of birds, avian products and other items will be allowed.
Processing establishments and markets may be able to continue to operate under permit
after inspection and upgrading of hygiene and management practices. Sales, zoos, shows,
pet shops, aviaries and pigeon races may be able to continue to operate under exceptional
circumstances permits.
Permits will be required for movements out of the RA and CA of birds, avian products and
other items. Permitted movements must meet the specific conditions in Section 4.2. Birds
and avian products from the free area may enter the CA under permit.
If the CA contains an appropriate place for poultry slaughter, permission should be given
to remove meat chickens from DCPs and SPs for slaughter within 24 hours following
inspection and/or testing if no sign of infection has developed during the declared
incubation period and surveillance has been in place. Risk of spread of infection is further
reduced by supervised heat processing (cooking) of meat and offal from these birds (see
Table 1.3, Section 1.6.2 and Section 4.2) and strict supervision of quarantine and the hygiene
of the vehicles and equipment used to move them.
Movement controls should not hinder the movements of the general public unless human
infection with the outbreak virus is occurring. Quarantine arrangements for humans will
need to be agreed with health authorities.
See Section 4 for further details of declared areas, quarantine and movement controls.
Industry support for the eradication program through enhanced biosecurity measures on
poultry farms and assistance with eradication procedures will be vital.
Zoning/compartmentalisation
To regain the earliest access to international markets, zoning or compartmentalisation
should be implemented as soon as possible after the epidemiological investigations have
been completed and the extent and severity of the disease have been determined. Zoning
and compartmentalisation should be implemented in accordance with OIE standards
(Chapters 2.7.12 and 1.3.5 (Zoning and compartmentalisation) of the OIE Terrestrial Code).
Zones or compartments may be established on the basis of geographical areas, management
practices in enterprises, infection status and/or vaccination policies. Potential free zones
will be those areas outside CAs while free compartments could lie within CAs. To achieve
free zone or compartment status, surveillance to prove freedom from infection within the
zone or compartment will be required (see Section 1.9).
If an outbreak of an HPAI virus is rapidly spreading, establishing RAs and CAs containing
all IPs as soon as possible will allow rapid investigation of the extent of infection and the
later application of zoning or compartmentalisation. It is important that the declared
infected areas in a country the size of Australia be limited to as small an area as necessary to
cover the likely extent of infection.
The OIE defines a compartment as: ‘One or more establishments under a common
biosecurity management system containing an animal subpopulation with a distinct health
status with respect to a specific disease or diseases for which required surveillance, control
and biosecurity measures have been applied for the purpose of international trade.’
The notifiable avian influenza (NAI) status of a country, zone or compartment can be
determined on the basis of the following criteria:
• A risk assessment has been undertaken to identify all potential factors for NAI
occurrence and their historic perspective.
• NAI is notifiable in the whole country, an ongoing NAI awareness program is in place,
and all notified suspect occurrences of NAI are subjected to field and, where
applicable, laboratory investigations.
• Appropriate surveillance is in place to demonstrate the presence of infection in the
absence of clinical signs in poultry, and the risk posed by birds other than poultry; this
may be achieved through an NAI surveillance program in accordance with
Appendix 3.8.9 of the OIE Terrestrial Code.
People engaged in product treatment should be protected from infection (see Section 3.2.8
and Appendix 3).
3.2.5 Vaccination
Stamping out is the preferred control measure for HPAI unless the spread or likely spread
of infection indicates that stamping out alone is not going to achieve eradication.
Vaccination has not been a necessary option in past Australian outbreaks, but its usefulness
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has been demonstrated in overseas outbreaks (see Sections 1.5.3 and 2.2.11). If the disease is
spreading at a significant rate (as determined by the CCEAD and agreed by the NMG),
vaccination, enhanced biosecurity and the other infection control measures will be
implemented to protect flocks from infection. Further details on how vaccination might be
used are provided in the National Operating Policy and Procedures for the Use of Avian Influenza
(AI) Vaccine in the Event of an AI Outbreak in Australia (National AI Vaccine Guidance;
NAIVE Group 2010). 11
Vaccination will be in accordance with a decision of CCEAD. Vaccination will be under the
control of the CVO of the affected jurisdiction. Depending on the circumstances, specific
requirements will be imposed on vaccinated flocks and/or birds as outlined in the National
AI Vaccine Guidance (NAIVE Group 2010). It will be essential to maintain all the other
strategies of the control/eradication program simultaneously.
The matters which will need to be considered in developing a response plan using
vaccination include:
11www.animalhealthaustralia.com.au/aahc/index.cfm?BDA6CF7D-A00F-3670-2401-
D1FA0F0C1421
from the IP will be traced from at least 21 days before the first signs of disease until the
imposition of full quarantine on the IP. The original source of the virus should be traced, as
it could remain a source for more outbreaks.
During the outbreak, surveillance will be undertaken on those premises considered at risk,
and include the following arrangements:
In the RA
Arrangements should be made for local laboratories to autopsy samples from all species of
bird that are found dead. Flock health can be monitored by:
• twice weekly (or more frequently if needed) reporting by telephone/fax by poultry
handlers, cage bird owners and zoo personnel, and dead bird pick-up, with field visit if
needed;
• twice weekly (or more frequently if needed) telephone surveillance of SPs and dead
bird pick-up, and field visit if needed;
• immediate serological/virological testing of breeding flocks (paired samples 12 two
weeks apart, then weekly);
• swabbing of dead birds weekly for virus isolation (trachea and cloaca) in at least 50%
of the commercial flocks in the RA; and
• quarantine of suspicious flocks, virus isolation and resampling of flocks after
seven days;
• investigation of unusual disease conditions in wild birds.
In the CA
Backyard poultry, and cage and zoo birds will be included in the surveys, although the
main means of controlling the disease and gaining knowledge of its spread will be by
defining the extent of infection in the commercial poultry flock (see Section 2.2.5). The
sampling of live or dead wild birds may be necessary. Proof of freedom from HPAI can best
be achieved by clinical observations and sampling of dead birds in repopulated sheds and
in possible disease outbreaks, rather than by widespread testing.
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See Section 1.9 for further information about the measures that need to be taken to support
a declaration of freedom from disease.
3.2.7 Decontamination
The Decontamination Manual must be consulted when deciding on the most appropriate
means of decontamination and disposal.
As AI virus is relatively stable in faeces and litter, buildings, equipment, vehicles, manure
and litter on IPs must all be cleaned and disinfected, or destroyed. People should undergo
personal decontamination procedures. Other premises will be decontaminated as
considered necessary. All items to be disinfected must be thoroughly cleaned before
disinfection (see Section 2.2.10).
Decontamination should include standard insect vector and rodent control measures to
minimise mechanical spread of the agent to nearby premises.
Personnel showing symptoms consistent with influenza must not come into contact with
infected birds, in order to reduce the chance of combination of AI virus with a human
strain.
Personnel may also be asked to take part in monitoring involving the collection of blood
samples by the state/territory health department to see if they have become infected.
Personnel who do not agree to preventive and monitoring measures should not be engaged
in activities in which they could come into contact with infected birds.
See Appendix 3 for national guidelines for the protection of people exposed to infected
birds.
More information about the possible infection of humans with AI viruses is given in
Section 2.2.15.
See Section 2.2.16 for further details of what to include in a public awareness campaign.
Therefore, if HPAI infection is detected in wild birds, an assessment of the risks to animal
and public health will be carried out taking into account the circumstances under which
sampling occurred, the possible source of the virus, the species of bird involved, the clinical
status of the sampled birds/population, and their proximity to commercial and other
significant bird establishments and populations, and to public amenity areas. Appropriate
testing and diagnosis are important components of the policy. Confirmation of HPAI
infection is obtained from the isolation and typing of an HPAI virus or the detection of
genetic material from an HPAI virus. Because serology is not evidence of current infection,
response action will not be taken based solely on serological results.
The response to a finding of HPAI infection in wild birds will be measured, commensurate
with the level of assessed risk posed to domestic and wild bird populations, and to public
health. If HPAI infection is detected, the CCEAD will be convened to consider the outcomes
of the risk assessment including the value in further sampling, management of domestic
birds in the vicinity, a communications strategy and any other appropriate measures. The
extent of these activities is dependent on the likely spread of the virus and the
consequences. If the initial laboratory testing is negative, or subsequent preliminary
surveillance is negative, no further action will be undertaken. For further details of the
response, see Appendix 2.
If LPAI infection only is detected in wild birds, no further action is required, however
consideration may be given to increasing surveillance in commercial poultry and zoo birds
in the immediate vicinity of the wild bird LPAI detection.
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The detection of LPAI infection in cage or zoo birds will lead to an assessment of the risks to
animal and public health, taking into account the species of bird involved, the clinical status
of the birds, and their proximity to commercial and other significant bird establishments
and populations, and to public amenity areas. The policy is to limit the spread of the
infection and its potential for mutation to HPAI and the response will be dependent upon
the assessed risk.
When LPAI (H5/H7) is confirmed on a premises on which rare poultry, cage or zoo birds
are present, enhanced biosecurity, movement controls (such as lifetime quarantine), and
ongoing tracing and surveillance will be implemented.
An application for recognition of free zones or compartments in the country will require
appropriate surveillance for the disease agent and the institution of controls on the
movement of birds and avian products between infected areas and free
zones/compartments. The surveillance carried out after zoning or compartmentalisation
has been proclaimed, including surveillance for the detection of infection in an infected
zone and for freedom from infection in a free zone or compartment, will be structured using
the known epidemiology of AI infection in domestic and zoo birds. Quail and free-range
flocks of chickens, turkeys, ostriches and ducks, especially where they are farmed near
chickens, might be used as indicators for the passage of AI virus from waterfowl to poultry.
Further information is provided in Section 3.5 about the measures that will be taken to
support a declaration of freedom from disease.
Section 4.2 lists movement controls for products and byproducts. For LPAI (H5/H7), some
of the restrictions on the movement of birds and products might be less stringent than for
HPAI.
3.3.5 Vaccination
The points to be considered in developing a vaccination strategy for LPAI (H5/H7) are as
for those discussed in Section 3.2.5.
Proof of freedom from LPAI (H5/H7) on IPs can best be achieved by clinical observations
and sampling of dead birds in repopulated sheds and in possible disease outbreaks, rather
than by widespread testing.
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3.3.7 Decontamination
The Decontamination Manual must be consulted when deciding on the most appropriate
means of decontamination and disposal.
HPAI caused by virus of subtypes not H5 and H7 is classified as a Category 3 disease. LPAI
caused by virus of subtypes H5 or H7 is also classified as a Category 3 disease, and control
and eradication arrangements are required. Category 3 diseases are EADs that have the
potential to cause significant (but generally moderate) national socioeconomic
consequences through international trade losses, market disruptions involving two or more
states and severe production losses to affected industries, but have minimal or no effect on
human health or the environment. For this category, the costs will be shared 50% by
governments and 50% by the relevant industries (refer to the EAD Response Agreement for
details).
The detection of HPAI or LPAI in cage or zoo birds has not been categorised under the EAD
Response Agreement.
AI infections classified as LPAI (not H5/H7) are not subject to the EAD Response
Agreement; nor are they designated diseases in the disease control legislation of all states
13 http://www.animalhealthaustralia.com.au/programs/eadp/eadra.cfm
and territories. This means that the costs of the control of such infections, including
compensation to owners for the destruction of birds, will not be shared by governments
and industry.
While a vaccination policy would assist the poultry industry economically, it may have
implications for Australia’s trading status, and the CCEAD would need to develop
strategies to re-establish Australia’s status of freedom from HPAI infection.
The movement of HPAI or LPAI (H5/H7) viruses into Australia’s native bird populations
may have unfortunate consequences if the viruses prove to be virulent or later acquire
virulence.
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Infected premises
Premises classified as IPs will be defined areas (which may be all or part of a property) in
which highly pathogenic avian influenza (HPAI) or low pathogenicity avian influenza
(LPAI (H5/H7)) infection exists, or is believed to exist. An IP is subject to quarantine served
by notice and to eradication and control procedures.
Suspect premises
Premises classified as suspect premises (SPs) will be those that contain birds that have
possibly been exposed to an HPAI or LPAI (H5/H7) virus, such that quarantine and
surveillance, but not pre-emptive destruction, are warranted; or birds not known to have
been exposed to an HPAI or LPAI(H5/H7) virus but showing clinical signs requiring
differential diagnosis.
Restricted area
An RA will be a relatively small declared area (compared to a CA) around IPs that are
subject to intense surveillance and movement controls. Multiple RAs may exist within one
CA.
The RA does not need to be circular but can have an irregular perimeter provided the
boundary is initially an appropriate distance from the nearest IP, DCP or SP. This distance
will vary with the size and nature of the potential source of virus, but will be between one
and five kilometres from the IP, depending on the density of bird, especially poultry,
premises. The boundary could be the perimeter fence of the IP if the IP is in an isolated
location. The boundary in a densely populated area will take into account the distribution
of susceptible birds, traffic patterns to markets, service areas and abattoirs, and natural
barriers to movement. If possible, hatcheries should be kept out of the RA.
Control area
The CA will be a larger declared area around one or more RAs and, initially, possibly as
large as a state or territory, where restrictions will reduce the risk of disease spreading from
the RA. In general, surveillance and movement controls will be less intense (see Section 4.2),
allowing reasonable commercial activities to continue.
The declaration of a CA helps control the spread of the outbreak from within the RA. The
CA is a buffer zone between the RA and the rest of the bird population. The CA boundary
does not have to be circular or parallel to that of the RA but should be 2–10 kilometres from
the boundary of the RA.
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NOTES:
(1) This type of movement is approved, under permit, provided that the chief veterinary
officer has cleared this type of movement (ie generally not each individual
movement) with the Consultative Committee on Emergency Animal Diseases. Risk
materials, vehicles and equipment would need to be disinfected.
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(2) If the CA contains an appropriate abattoir, permits can be issued to move meat
chickens from SPs and from the RA following inspection (no birds showing clinical
signs) and negative serosurveillance, for immediate slaughter (within 24 hours). The
movement of the live birds requires careful selection of transport routes and
disinfection of vehicles and equipment. The product from poultry will be permitted
to move to approved premises outside the CA where it is subject to heat treatment
sufficient to kill virus before being sold to consumers. Waste is to be subject to
approved disposal.
(5) If a processing plant has received birds from an IP or DCP since the date when they
were infected or exposed to infection, the plant must be cleaned and decontaminated,
under supervision, before operating again. Staff must undergo disinfection
procedures before leaving the premises. Advice must be given to staff about poultry,
cage and aviary birds or pigeons kept at their homes.
(6) The vehicle must be disinfected on site, at a central point or back at the mill.
(7) The refuse must be buried at an approved site and the vehicle cleaned and
disinfected. The refuse must not be fed to or brought into contact with other birds.
(8) Heat treatment must attain product core temperatures sufficient to kill virus before
the product leaves the approved premises (see Section 1.6.2).
(9) For the purposes of quarantine and movement controls, vaccinated birds will be
treated the same as unvaccinated birds.
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NOTES:
(1) This type of movement is approved, under permit, provided that the chief veterinary
officer has cleared this type of movement (ie generally not each individual
movement) with the Consultative Committee on Emergency Animal Diseases. Risk
materials, vehicles and equipment would need to be disinfected.
(2) If the CA contains an appropriate abattoir, permits can be issued to move meat
chickens from SPs and from the RA following inspection (no birds showing clinical
signs) and negative serosurveillance, for immediate slaughter (within 24 hours). The
movement of the live birds requires careful selection of transport routes and
disinfection of vehicles and equipment. The product from poultry will be permitted
to move to approved premises outside the CA where it is subject to heat treatment
sufficient to kill virus before being sold to consumers. Waste is to be subject to
approved disposal.
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(5) If a processing plant has received birds from an IP or DCP since the date when they
were infected or exposed to infection, the plant must be cleaned and decontaminated,
under supervision, before operating again. Staff must undergo disinfection
procedures before leaving the premises. Advice must be given to staff about poultry,
cage and aviary birds or pigeons kept at their homes.
(6) The vehicle must be disinfected on site, at a central point or back at the mill.
(7) The refuse must be buried at an approved site and the vehicle cleaned and
disinfected. The refuse must not be fed to or brought into contact with other birds.
(8) Heat treatment must attain product core temperatures sufficient to kill virus before
the product leaves the approved premises (see Section 1.6.2).
(9) For the purposes of quarantine and movement controls, vaccinated birds will be
treated the same as unvaccinated birds.
Ap p e n d i x 1 Disease summary
Species affected
All commercial, domestic and wild bird species are susceptible, but disease outbreaks occur
more frequently in chickens and turkeys. Infection may be brought into Australia by
migratory wild birds. Many species of waterfowl, especially geese, ducks and swans, carry
the virus but usually show no signs of disease. Historically, humans have not been affected,
but more than 150 humans have died in the current H5N1 epidemic, principally in
Southeast Asian countries.
Distribution
Avian influenza (AI) viruses are probably ubiquitous throughout the world in wild
waterbirds, with outbreaks of disease in poultry occurring as sporadic events. Since
December 2003, there have been outbreaks of highly pathogenic H5N1 AI in poultry and
other birds in Korea, Japan, Vietnam, Thailand, Cambodia, Laos, Indonesia, China and
Malaysia. In 2005, H5N1 was reported in birds in Kazakhstan, Mongolia and Russia, and
the disease then spread westwards into Romania, Turkey and the Ukraine. By early 2006,
there were reports of H5N1 virus in wild and domestic birds in some European Union
Member States, domestic birds in India, and in domestic and wild birds in the middle East
(Iraq, Iran, Israel). The virus has also been reported in domestic birds in some countries in
Africa (Niger, Nigeria, Egypt, Cameroon), and in Afghanistan and Myanmar. The virus has
been the cause of clinical disease in commercial poultry in Australia in Victoria (1976, 1985
and 1992), Queensland (1994) and New South Wales (1997).
Key signs
The clinical signs of HPAI in birds are variable and can be affected by the existence of other
diseases, the age of the birds, the environment and the virulence of the virus. In very severe
forms, the disease appears suddenly and all birds may die quickly. Some may appear
depressed, egg production falls and soft-shelled eggs are produced. There may be profuse
watery diarrhoea, combs and wattles may become blue and respiration may be laboured. In
less severe forms, the clinical signs may include decreased egg production, depression,
respiratory signs suggestive of a cold, swelling of the face, nervous signs, and diarrhoea.
The severity of signs can vary when the virus mutates during an outbreak.
Spread
Direct or indirect contact with migratory waterfowl (probably through drinking water) is
the most likely source of HPAI infection in poultry. The virus can be isolated from lake
water where waterfowl are present. Spread can also occur through contact with
contaminated equipment or humans. Although the virus has been found inside the egg,
transmission through the egg is not known to occur, but the shell can be contaminated. The
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virus is highly concentrated in the manure and in nasal and eye discharges, and spreads
more easily in winter.
Control strategy
The strategy is to eradicate HPAI in poultry, cage and zoo birds by immediate stamping out
(killing of the birds) and disposal of infected and exposed birds to remove the major source
of virus. When HPAI is confirmed on a premises on which rare poultry, cage or zoo birds
are present, the primary objective is eradication of the virus. A modified stamping-out
approach may be appropriate, taking into account requirements for biosecurity, ongoing
tracing and surveillance, and timeliness in achieving disease eradication.
The response to a finding of HPAI in wild birds will be measured, commensurate with the
level of assessed risk posed to domestic and wild bird populations, and to public health.
There will also be strict quarantine and movement controls to prevent the spread of
infection; decontamination to remove and reduce the virus; tracing and surveillance to
locate the source of infection, locate other infected premises and determine the extent of the
infection; and zoning to define infected and disease-free areas. The potential for human
infection has led to greater emphasis on eradication as a public health measure.
In Australia, vaccination could be part of a response where the disease is likely to spread
and is unable to be rapidly controlled by stamping out and other measures. The decision
whether to vaccinate and the options chosen in Australia will be determined by factors such
as the species and types of birds at risk, the density and characteristics of the surrounding
avian population (wild and domesticated), geographic considerations, epidemiological
factors, the virus subtypes involved, public health concerns, the resources available and the
availability of appropriate vaccines.
There is potential for low pathogenicity strains (LPAI) to mutate into HPAI, so control
measures will be applied if those strains are detected.
The Australian government–industry agreement for sharing the costs of emergency animal
disease control applies to HPAI and to LPAI subtypes H5 and H7.
Overall policy for avian influenza classified as HPAI (except in wild birds)
Highly pathogenic avian influenza (HPAI) is a OIE (World Organisation for Animal Health)
notifiable disease (HPNAI) that is highly lethal to poultry and has the potential to infect
humans. An uncontrolled outbreak of HPAI would cause severe production losses with
consequent dislocation and financial losses in the poultry and associated service and sales
industries. It may also lead to morbidity and mortality in large numbers of cage and zoo
birds.
• stamping out by destruction of all birds on infected premises (IPs) where there is clinical
disease or evidence of active infection with HPAI virus, and the sanitary disposal of
destroyed birds and contaminated avian products to remove the source of infection;
• possible pre-emptive slaughter of birds on other premises, depending on information
derived from tracing, surveillance and study of the behaviour of the disease;
• quarantine and movement controls on birds, avian products and associated items in
declared areas to prevent spread of infection (a national standstill is not necessary for
containment of AI);
• decontamination of facilities, products and associated items to eliminate the virus on IPs
and to prevent spread in declared areas;
• tracing and surveillance to determine the source and extent of infection, and to establish
proof of freedom from the disease;
• enhanced biosecurity at poultry establishments, and premises holding cage or zoo birds;
• zoning and compartmentalisation to define infected and disease-free areas;
• a public awareness campaign to communicate risk and promote cooperation from
industry, zoos, cage bird owners and the community; and
• protection of public health, by requiring that personnel engaged in eradication activities
be vaccinated (with the currently available human vaccine), be treated with antivirals
(if appropriate) and wear protective clothing.
Vaccination may be considered if an outbreak of HPAI is likely to spread or has spread out
of control.
Under the Government and Livestock Industry Cost Sharing Deed In Respect of Emergency Animal
Disease Responses (EAD Response Agreement) for cost sharing, HPAI (H5/H7) is a
Category 2 emergency animal disease (EAD) and HPAI (not H5/H7) is a Category 3 EAD.
Category 2 EADs are those for which costs will be shared 80% by government and 20% by
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industry; Category 3 EADs are those for which costs will be shared 50% by government and
50% by industry.
When HPAI is confirmed on or threatens to spread to premises on which rare poultry, cage
or zoo birds are present, the prime objective is eradication of the virus. A modified
approach, including consideration of vaccination, may be appropriate, however, taking into
account factors such as biosecurity, movement controls, ongoing tracing and surveillance,
and timeliness in achieving disease eradication.
3.1.2 Overall policy for avian influenza classified as LPAI (H5/H7) in poultry
Low pathogenicity avian influenza (LPAI (H5/H7)) is an infection caused by a strain of
avian influenza virus that is of H5 or H7 subtype and produces mild or no clinical disease
in poultry. LPAI could mutate to HPAI and cause significant disease problems in the
poultry industry, and lead to morbidity and mortality in large numbers of cage and zoo
birds.
Such virus strains in poultry are classified as notifiable (LPNAI) according to OIE criteria,
and because of the potentially severe consequences of an uncontrolled outbreak of these
strains of AI mutating to HPAI, they are categorised under the EAD Response Agreement.
LPAI (H5/H7) of subtypes H5 or H7 is a Category 3 EAD under the EAD Response
Agreement for cost sharing. Category 3 diseases are those for which costs will be shared
50% by government and 50% by industry.
When CCEAD determines that an infection is caused by an AI virus that meets the
definition of LPAI (H5/H7), the policy is to control and eradicate the disease, while limiting
spread and potential for mutation to HPAI, using a combination of strategies, including:
• tracing and surveillance to determine the source and extent of infection and to
establish proof of freedom from the disease; followed by
either
• stamping out either as for HPAI, if the infection is limited in distribution in the
poultry industry and destruction of infected flocks is manageable or by modified
stamping out using process slaughter if processing capacity is available;
or
• vaccination and a modified approach to eradication, if the infection is likely to
spread or has spread out of control;
and
• quarantine and movement controls on poultry, poultry products and associated items
in known IPs to prevent spread of infection;
• decontamination of facilities, products and associated items to eliminate the virus on
IPs;
• enhanced biosecurity at poultry establishments and premises holding cage or zoo
birds in the vicinity;
• zoning and compartmentalisation to define infected and disease-free areas; and
• a public awareness campaign to communicate risk and promote cooperation from
industry and the community.
3.1.3 Overall policy for avian influenza classified as LPAI (H5/H7) in cage or zoo birds
LPAI (H5/H7) is an infection caused by a strain of avian influenza virus that is of H5 or H7
subtype and produces mild or no clinical disease. LPAI could mutate to HPAI and lead to
morbidity and mortality in large numbers of cage and zoo birds.
Because of the potentially serious consequences of the spread of these strains of AI, LPAI
(H5/H7) in cage or zoo birds is a Category 3 EAD.
When CCEAD determines that an infection in cage or zoo birds is caused by such a virus,
an assessment of the risks to animal and public health will be carried out, taking into
account the species of bird involved, the clinical status of the birds, and their proximity to
commercial poultry and other significant bird establishments and populations, and to
public amenity areas. The policy is to limit the spread of the infection and its potential for
mutation to HPAI, and the response will depend upon the assessed risk. A combination of
strategies may be employed, including:
• tracing and surveillance to determine the source and extent of infection and to
establish proof of freedom from the disease;
• quarantine and movement controls on birds and associated items in known IPs to
prevent spread of infection;
• stamping out as for LPAI in poultry, or a modified approach to control in accordance
with the risk assessment; this may include vaccination if the infection is likely to
spread or has spread out of control;
• decontamination of facilities, products and associated items to eliminate the virus on
IPs;
• enhanced biosecurity at avian establishments in the vicinity; and
• a public awareness campaign to communicate risk information and promote
cooperation from industry, zoos, cage bird owners and the community.
3.1.4 Overall policy for avian influenza infections classified as LPAI (not H5/H7) in
poultry, or in cage or zoo birds
Avian influenza caused by a strain of virus that is neither HPAI nor LPAI subtype H5 or
H7, and which is producing no or mild clinical disease, is not considered an immediate
threat to Australia’s domestic or zoo birds or public health. Such AI virus strains are
classified as LPAI (not H5/H7), and their detection in Australia would not be treated as an
emergency disease outbreak.
When the CVO determines that an infection is caused by such a virus, an assessment of the
risks to animal and public health will be carried out, taking into account the virus subtype,
the species of bird involved, the clinical status of the birds, and their proximity to
commercial or other significant bird establishments and populations, and to public amenity
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areas. No action will be required unless the risk assessment indicates an unacceptable threat
to animal or public health. When a response is necessary, it may include:
These AI subtype viruses (LPAI (not H5/H7)) are not categorised under the EAD Response
Agreement for cost-sharing arrangements.
3.1.5 Overall policy for avian influenza infections classified as HPAI or LPAI in wild birds
Avian influenza infections classified as HPAI or LPAI in wild birds are not considered to
pose an immediate threat to Australia’s domestic or zoo birds, or public health. Their
detection would therefore not be treated as an emergency disease outbreak in Australia.
However, HPAI infections in domestic or zoo birds could have serious consequences for
avian and/or public health.
Therefore, if HPAI infection is detected in wild birds, the CCEAD will be convened and an
assessment of the risks to animal and public health will be carried out, taking into account
the circumstances under which sampling occurred, the possible source of the virus, the
species of bird involved, the clinical status of the sampled birds/population, and their
proximity to commercial and other significant bird establishments and populations, and to
public amenity areas.
The response to a finding of HPAI infection in wild birds will be measured, commensurate
with the level of assessed risk posed to domestic and wild bird populations, and to public
health. No destruction of wild birds will occur, other than for reasons such as animal
welfare. For further details, see Appendix 2.
If widespread HPAI infection is found in wild birds only (ie not in poultry, cage or zoo
birds), it may be necessary to proclaim restricted areas, to conduct broader surveillance and
to consider the use of vaccination in domestic and zoo birds in the immediate vicinity.
1. The response to a finding of HPAI in wild birds will be measured, commensurate with the
level of assessed risk posed to domestic and wild bird populations, and the risk posed to the
community in general.
2. Testing for AI in wild birds will be performed only in laboratories that are competent and
are using appropriate methods. Testing for HPAI will be undertaken in accordance with the
Procedures for Transmission of Diagnostic Specimens for Suspect Emergency Animal Diseases
(October 2006) agreed by the Animal Health Committee, and as set out in AHC08 OOS27
Reporting and Laboratory Testing Protocols for AI.
3. Confirmation of HPAI infection is obtained from the isolation and typing of an HPAI virus
or the detection of genetic material from an HPAI virus. Sero-evidence of H5 or H7
antibodies is not evidence of infection with HPAI and response action will not be taken
based on the results of serological testing only.
4. As the opportunity for follow-up sampling and testing of individual wild birds is rarely
available, sampling of wild birds for AI will include appropriate cloacal and/or tracheal
samples for virus detection. Collection of serum samples only should generally be avoided
given the difficulties of interpretation and the inability to collect further meaningful samples
from the sampled birds at a later time.
5. At the time of sampling, all relevant details will be recorded, including date, location,
species, circumstances and the clinical status of the bird(s) sampled.
6. If blood samples are all that is available, animal health authorities will consider all available
information, including clinical signs, and determine the value and feasibility of further
investigations, including ability to identify the target population and collect further samples.
7. Where evidence of infection with HPAI virus has been found in the situations described in
the following table, the actions identified in the table will be considered. The actions
implemented will be dependent on available information and the assessed risk, and will be
those agreed by the CCEAD.
8. Risk assessment will include considerations of the circumstances under which sampling
occurred, the possible source of the virus, the species involved, the clinical status of the
sampled birds/population, the proximity to commercial and other significant bird
establishments, and proximity to public amenity areas.
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A. If HPAI virus is detected in a wild bird, the CVO of the state/territory of origin of the
sampled bird(s) should immediately notify the Australian Chief Veterinary Officer
(ACVO), who will convene a meeting of CCEAD.
CCEAD will consider the following matters in deciding upon the further action to be
taken:
B. If HPAI virus is detected in more than one wild bird in a group or area, CCEAD may
further consider:
C. If further investigations prove widespread HPAI infection in wild birds only (ie not
domestic birds) then CCEAD should consider whether further actions may be justified:
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Note: These guidelines are being updated by the Australian Government Department of
Health and Ageing
These guidelines are based on material developed by the World Health Organization, the
United States Centers for Disease Control and Prevention, and the Australian Government
departments of Agriculture, Fisheries and Forestry, and Health and Ageing.
The guidelines are intended for use by people who are in a high-risk situation at the time of
a response to an outbreak of HPAI in birds in Australia.
The guidelines aim to minimise the risk of spread of virus via people and are for use in
addition to normal workplace occupational health and safety (OHS) operations, including
good hygiene practices. AUSVETPLAN sets out comprehensive infection control,
containment and eradication procedures, including OHS advice that should be read in
conjunction with these guidelines. 14
It is important that both the animal/agricultural and the human health sectors work
together to implement the measures below.
Before participating in the response, personnel should be trained in the use of personal
protective equipment (PPE) and procedures for dealing with sick or dead birds.
Vaccination
All workers who are or will be directly exposed to infected or potentially infected poultry
or poultry products and waste must be vaccinated with the seasonal human influenza
vaccine (that is, the human influenza vaccine that is currently available). The vaccine
usually becomes available in March. Although the human influenza vaccine will not protect
workers against AI, it may prevent simultaneous infection with human influenza and AI.
There is a small possibility that if a person is infected with both these viruses at the same
time, the viruses could share genetic material to produce a new and highly transmissible
virus that would pose a threat to the wider community.
Children should not have contact with infected or exposed poultry or any other affected
birds.
People with weakened immune systems (from such causes as some cancers, cancer
treatments or high-dose steroids), people aged over 60 years and people with known
chronic heart or lung disease should avoid contact with affected birds or their environment.
Selection of personnel to work on IPs should include procedures to identify and exclude
people at high risk.
It is important that personnel know the symptoms of AI infection in humans and seek
medical advice if they become unwell.
Any worker who does not agree to abide by these guidelines must not be exposed to
infected poultry or contaminated areas and should be excluded from handing infected
poultry or working in a contaminated environment.
Protective overalls should be worn and, where gross contamination of clothing is likely, an
impermeable apron. Disposable protective clothing is preferred, and this clothing should be
kept separate from street clothes. If nondisposable clothing is used, it should be cleaned and
disinfected according to AUSVETPLAN recommendations.
Disposable gloves or rubber work gloves that can be disinfected should be worn. Gloves
must be changed if they become torn or damaged.
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Reusable items such as rubber gloves, boots and PAPRs should be cleaned and disinfected
according to AUSVETPLAN recommendations. AI virus is susceptible to detergents and to
a range of disinfectant products.
After cleaning and disinfection, PPE should be stored in a clean place to avoid
contamination.
Antiviral drugs
Antiviral drugs are recommended for workers in direct contact with infected poultry or
contaminated materials for the duration of their exposure and for seven days after their last
exposure. 17
Public health authorities will provide the drug of choice and product use and safety
information, and arrange supervised dosing of antiviral medications daily at the workplace.
Antivirals should not be taken for more than 42 days. 18 If the exposure period (culling and
clean-up) will be prolonged, personnel should be rotated off site.
Workers who develop any of these symptoms should seek medical advice, indicating that
they may have been exposed to AI. In addition, workers should report their illness to health
and safety officials at the workplace, who in turn should notify public health authorities.
Workers who are unwell should stay at home until 24 hours after any fever resolves, or
until given a medical clearance.
If any worker becomes unwell, close contacts (eg household members) will be contacted by
public health authorities and advised according to public health management protocols. 19
Household members should also monitor their health, although transmission from person
to person is extremely rare.
index.htm
Serological testing may be arranged for people who are exposed to potentially infected
poultry. This involves testing the blood for evidence of exposure to the AI virus. The
purpose of this would be to provide public health authorities with more information about
the disease in humans.
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Glossary
Animal byproducts Products of animal origin that are not for consumption but
are destined for industrial use (eg hides and skins, fur,
wool, hair, feathers, hooves, bones, fertiliser).
Animal Health Committee A committee comprising the CVOs of Australia and New
Zealand, Australian state and territory CVOs, Animal
Health Australia, and a CSIRO representative. The
committee provides advice to PIMC on animal health
matters, focusing on technical issues and regulatory policy
(formerly called the Veterinary Committee).
See also Primary Industries Ministerial Council of Australia
and New Zealand (PIMC)
Animal products Meat, meat products and other products of animal origin
(eg eggs, milk) for human consumption or for use in
animal feedstuff.
Chief veterinary officer The senior veterinarian of the animal health authority in
(CVO) each jurisdiction (national, state or territory) who has
responsibility for animal disease control in that
jurisdiction.
See also Australian Chief Veterinary Officer
Critical date The earliest time the pathogen entered the premises. The
critical date is determined by the CVO in consultation
with laboratory staff and epidemiologists and should be
consistent with the apparent incubation period of the
current outbreak.
Cyanosis (adj: cyanotic) Blueness of the skin and/or mucous membranes due to
insufficient oxygenation of the blood.
Dangerous contact animal An animal showing no clinical signs of disease but which,
by reason of its probable exposure to disease (revealed by
tracing and epidemiological investigation), will be
subjected to disease control measures (which may require
slaughter of some or all such animals).
See also Suspect animal.
Dangerous contact premises Premises that contain dangerous contact animals or other
serious contacts.
See Section 4 for further details
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Disease Watch Hotline 24-hour freecall service for reporting suspected incidences
of exotic diseases — 1800 675 888.
Egg marketing premises Premises where table eggs are graded and packed for the
retail market. The premises may also contain a pulp plant
and facilities for manufacture of egg-based products.
Egg pulp A homogenous liquid made from either whole liquid egg,
egg albumen or egg yolk, pasteurised for marketing as a
liquid or frozen product.
Emergency animal disease A disease that is (a) exotic to Australia or (b) a variant of
an endemic disease or (c) a serious infectious disease of
unknown or uncertain cause or (d) a severe outbreak of a
known endemic disease, and that is considered to be of
national significance with serious social or trade
implications.
See also Endemic animal disease, Exotic animal disease
Endemic animal disease A disease affecting animals (which may include humans)
that is known to occur in Australia.
See also Emergency animal disease, Exotic animal disease
Further processing plant A plant that receives fresh carcases from an abattoir for
cutting up, processing into poultry nuggets, rolls, etc and
cooking or partial cooking for fast-food outlets and retail
markets.
Galliformes (adj: The order of birds that includes poultry, turkey, pheasant
gallinaceous) and peafowl.
In-contact animals Animals that have had close contact with infected animals,
such as noninfected animals in the same group as infected
animals.
Incubation period The period that elapses between the introduction of the
pathogen into the animal and the first clinical signs of the
disease.
Index property The property on which the first or original case (index
case) in a disease outbreak is found to have occurred.
Local disease control centre An emergency operations centre responsible for the
(LDCC) command and control of field operations in a defined area.
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Modified stamping out The process where stamping out is not implemented in
full (eg the animals may be sent for process slaughter over
a period of time, or some animals may be vaccinated, held
under an appropriate level of biosecurity and killed at a
later date). Details of the modifications should be
provided.
See also Process slaughter
OIE Terrestrial Code OIE Terrestrial Animal Health Code. Reviewed annually at
the OIE General Session in May and published on the
internet at:
http://www.oie.int/eng/normes/mcode/a_summry.htm
OIE Terrestrial Manual OIE Manual of Standards for Diagnostic Tests and Vaccines for
Terrestrial Animals. Describes standards for laboratory
diagnostic tests and the production and control of
biological products (principally vaccines). The current
edition is published on the internet at:
http://www.oie.int/eng/normes/mmanual/a_summry.htm
Petechial haemorrhage Tiny, flat, red or purple spots in the skin or mucous
membrane caused by bleeding from small blood vessels.
Poultry Defined by the OIE as ‘all domesticated birds used for the
production of meat or eggs for consumption, for the
production of other commercial products, for restocking
supplies of game, or for breeding these categories of
birds’.
Primary Industries The council of Australian national, state and territory and
Ministerial Council (PIMC) New Zealand ministers of agriculture that sets Australian
and New Zealand agricultural policy (formerly the
Agriculture and Resource Management Council of
Australia and New Zealand).
See also Animal Health Committee
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State or territory disease The emergency operations centre that directs the disease
control headquarters control operations to be undertaken in that state or
territory.
Susceptible animals Animals that can be infected with a particular disease; for
HPAI and LPAI (H5/H7), all avian species.
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Wild animals
Ab b r e vi a t i o n s
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References
Akey BL (2003). Low pathogenicity H7N2 avian influenza outbreak in Virginia during 2002.
Avian Diseases 47:1099–1103.
Alfonso CP, Cowen BS and Campen HV (1995). Influenza A viruses isolated from
waterfowl in two wildlife management areas of Pennsylvania. Journal of Wildlife
Diseases 31(2):179–185.
Allwright DM, Burger EP, Geyer A and Terblanche AW (1993). Isolation of influenza A
virus from ostriches (Struthio camelus). Avian Pathology 22:59–65.
FSANZ (Food Stanadards Australia New Zealand) (2011). Australia New Zealand Food
Standards Code.
http://www.foodstandards.gov.au/foodstandards/foodstandardscode/
AQIS (Australian Quarantine and Inspection Service) (1991). Discussion paper on the
importation of fresh frozen and cooked chicken meat and products from the USA,
Denmark, Thailand and New Zealand, Department of Primary Industries and Energy,
Canberra.
Arzey GC (1989). Mechanisms of Spread of Newcastle Disease. NSW Agriculture and Fisheries,
Technical Bulletin 42.
Arzey G (2004). The role of wild aquatic birds in the epidemiology of avian influenza in
Australia. Australian Veterinary Journal 82:277–388.
Beare AS and Webster RG (1991). Replication of avian influenza viruses in humans. Archives
of Virology 119:37–42.
Bridges CB, Katz JM, Seto WH, Chan PKS, Tsang D, Ho W, Mak KH, Lim W, Tam JS, Clarke
M, Williams SG, Mounts AW, Bresee JS, Conn LA, Rowe T, Hu-Primmer J, Abernathy
RA, Lu X, CoxNJ and Fukuda K (2000). Risk of influenza A (H5N1) infection among
health care workers exposed to patients with influenza A (H5N1), Hong Kong. Journal
of Infectious Diseases 181:344–348.
Bulaga LL, Garber L, Senne DA. Myers TJ, Good R, Wainwright S, Trock S and Suarez DL
(2003). Epidemiologic and surveillance studies on avian influenza in live-bird markets
in New York and New Jersey 2001. Avian Diseases 47:996–1001.
Capua I and Marangon S (2000). The avian influenza epidemic in Italy, 1999–2000. Avian
Pathology 29:289–294.
Capua I and Marangon S (2003). The use of vaccination as an option for the control of avian
influenza. Avian Pathology 32:335–343.
Capua I and Mutinelli F (2001). Mortality of Muscovy ducks (Cairina moschate) and domestic
geese (Anser anser var. domestica) following natural infection with highly pathogenic
avian influenza of the H7N1 subtype. Avian Pathology 30:179–183.
96 AUSVETPLAN (Edition 3)
AI3.4-07FINAL(16Feb11).doc
Capua I, Mutinelli F, Bozza MA, Terregino C and Cattoli G (2000a). Highly pathogenic
avian influenza (H7N1) in ostriches (Struthio camelus). Avian Pathology 29:643–646.
Capua I, Marangon S, Dalla Pozza M and Santucci U (2000b). Vaccination for avian
influenza in Italy. Veterinary Record 147:751.
Capua I, Grossele B, Bertoli E and Cordioli P (2000c). Monitoring for highly pathogenic
avian influenza in wild birds in Italy. Veterinary Record 147:640.
Clavijo A, Riva J, Copps J, Robinson Y and Zhou E-M (2001). Assessment of the
pathogenicity of an emu-origin influenza AH5 virus in ostriches (Struthio camelus).
Avian Pathology 30:83–89.
Cross GM (1987). The status of avian influenza in poultry in Australia. In: Proceedings of the
Second International Symposium on Avian Influenza, US Animal Health Association,
Richmond, Virginia, 96–103.
De Marco MA, Foni GE, Campitelli L, Raffini E, Di Trani L, Delogu M, Guberti V, Barigazzi
G and I. Donatelli I (2003). Circulation of influenza viruses in wild waterfowl wintering
in Italy during the 1993–99 period: evidence of virus shedding and seroconversion in
wild ducks. Avian Diseases 47:861–866.
Easterday BC and Beard CW (1984). Influenza. In: Diseases of Poultry, 8th edition, (Calnek
BW et al, eds), Iowa State University Press, USA, 482.
Easterday BC, Hinshaw VL and Halvorsen DA (1997). Influenza. In: Diseases of Poultry, 10th
edition, (Calnek BW et al, eds), Iowa State University Press, USA, 583–605.
FAO (Food and Agriculture Organization) (2004a). Avian influenza: a threat to rural
livelihoods, agricultural production and human health. 6 February 2004, FAO, Rome.
http://www.fao.org/newsroom/en/focus/2004/36467/index.html .
Fouchier RAM, Olsen B, Bestebroer TM, Herfst S, van der Kemp L, Rimmelzwaan GF and
Osterhaus ADME (2003). Influenza A virus surveillance in wild ducks in northern
Europe in 1999 and 2000. Avian Diseases 47:857–860.
Geering WA, Forman AJ and Nunn MJ (1995). Exotic Diseases of Animals: A Field Guide for
Australian Veterinarians. Bureau of Resource Sciences, Australian Government
Publishing Service, Canberra.
Hansen BA, Stallknecht DE, Swayne DE, Lewis LA and Senne DA (2003). Avian influenza
viruses in Minnesota ducks during 1998–2000. Avian Diseases 47:867–871.
Henzler DJ, Kradel DC, Davison S, Ziegler AF, Singletary D, DeBok P, Castro AE, Lu H,
Eckroade R, Swayne D, Lagoda W, Schmucker B and Nesselrodt A (2003).
Epidemiology, production losses and control measures associated with an outbreak of
avian influenza virus subtype H7N2 in Pennsylvania (1996–98). Avian Diseases 47:1022–
1036.
Jorgensen PH, Nielsen OL, Hansen HC, Manvell RJ, Banks J and Alexander DJ (1998).
Isolation of influenza A virus, subtype H5N2, and avian paramyxovirus type 1 from a
flock of ostriches in Europe. Avian Pathology 27:15–20.
Katz JM (2003). The impact of avian influenza viruses on public health. Avian Diseases
47:914–920.
Katz JM, Lim W, Bridges CB, Rowe T, Hu-Primmer J, Lu X, Abernathy RA, Clarke M, Conn
L, Kwong H, Lee M, Au G, Ho YY, Mak KH, Cox NJ and Fukuda K (1999). Antibody
response in individuals infected with avian influenza A (H5N1) viruses and detection
of anti-H5 antibody among households and social contacts. Journal of Infectious Diseases
180:1763–1770.
Kuiken T, Rimmelzwaan G, van Riel D et al (2004). Avian influenza in cats. Science 306:241.
Lu H, Dunn PA, Wallner-Pendleton EA, Henzler DJ, Kradel DC, Liu J, Shaw DP and Miller
P (2004). Investigation of H7N2 outbreaks in two broiler breeder flocks in
Pennsylvania, 2001–02. Avian Diseases 48:26–33.
Moses HE, Brandly CA, Jones EE and Jungherr EL (1948). The isolation and identification of
fowl plague virus. American Journal of Veterinary Research 9:314–328.
98 AUSVETPLAN (Edition 3)
AI3.4-07FINAL(16Feb11).doc
Mounts AW, Kwong H, Izurieta HS, Ho Y, Au T, Lee M, Buxton Bridges C, Williams SW,
Mak KH, Katz JM, Thompson WW, Cox NJ, and Fukuda K (1999). Case–control study
of risk factors for avian influenza A (H5N1) disease, Hong Kong, 1997. Journal of
Infectious Diseases 180(2):505–508.
NAIVE Group (National Avian Influenza Vaccine Expert Group) (2010). National Operating
Policy and Procedures for the Use of Avian Influenza (AI) Vaccine the Event of an AI Outbreak
in Australia, guidance prepared by the NAIVE Group (a working group of the Animal
Health Committee), Animal Health Australia, Canberra.
http://www.animalhealthaustralia.com.au/aahc/index.cfm?BDA6CF7D-A00F-3670-
2401-D1FA0F0C1421
Panigrahy B, Senne DA and Pearson JE (1995). Presence of avian influenza subtypes H5N2
and H7N1 in emus and rheas: virus isolation and serologic findings. Avian Diseases
39:64–67.
Panigrahy B, Senne DA and Pedersen JC (2003). Avian influenza virus subtypes inside and
outside live bird markets, 1993–2000: a spatial and temporal relationship. Avian
Diseases 47:298–307.
Peiris M, Yuen KY, Leung CW et al (1999). Human infection with influenza H9N2. The
Lancet 354:916–917.
Peroulis I and O’Reilly K (2004). Detection of avian paramyxoviruses and influenza viruses
amongst wild bird populations in Victoria. Australian Veterinary Journal 82:79–82.
ProMED (2003). Avian influenza — Netherlands (24): Pig involvement. ProMED 21 May
2003.
ProMED (2004a). Avian influenza — eastern Asia (128): Thailand, tigers. ProMED
21 October 2004.
ProMED (2004c). Avian influenza, porcine H5N1 — China (06): OIE ProMED 15 and
1 September 2004.
ProMED (2004d). Avian Influenza, H7, poultry – USA (Delaware, Maryland) 11 April 2004.
Reid AH, Fanning TG, Slemons RD, Janczewski TA, Dean J and Taubenberger JK (2003).
Relationship of pre-1918 avian influenza HA and NP sequences to subsequent avian
influenza strains. Avian Diseases 47:921–925.
Selleck PW, Arzey G, Kirkland PD, Reece RL, Gould AR, Daniels PW and Westbury HA
(2003). An outbreak of highly pathogenic avian influenza in Australia in 1997 caused
by an H7N4 virus. Avian Diseases 47:806–811.
Senne DA, Panigrahy B and Morgan RL (1994). Effect of composting poultry carcasses on
survival of exotic avian viruses: highly pathogenic avian influenza (HPAI) and
adenovirus of egg drop syndrome-76. Avian Diseases 38:733–737.
Shortridge KF (2003). The next influenza pandemic: lessons from Hong Kong. Journal of
Applied Microbiology 94:70S–79S.
Sims LD, Guan Y, Ellis TM, Liu KK, Dyrting K, Wong H, Kung NYH, Shortridge KF and
Peiris M (2003). An update on avian influenza in Hong Kong 2002. Avian Diseases
47:1083–1086.
Swayne DE and Suarez DL (2000). Highly pathogenic avian influenza. Scientific and
Technical Review, Office International des Epizooties 19:463–482.
Tumpey TM, Suarez DL, Perkins LF, Senne DA, Lee J, Lee YJ, Mo IP, Sung HW and Swayne
DE (2003). Evaluation of a high pathogenicity H5N1 avian influenza virus isolated
from duck meat. Avian Diseases 47:951–955.
Webster RG and Kawaoka Y (1988). Avian influenza. Critical Reviews in Poultry Biology
1.3:211–246.
Webster RG, Yakhno M, Hinshaw VS, Bean WJ and Murti KG (1978). Intestinal influenza:
replication and characterisation of influenza viruses in ducks. Virology 84:268–276.
Westbury HA, Turner AJ and Amon L (1981). Transmissibility of two avian influenza
viruses (H7N6) between chickens. Avian Pathology 10(4):481–487.
WHO (World Health Organization) (2004a). Avian influenza A (H5N1) — update 15, WHO
website, 2 February 2004. http://www.who.int/csr/don/2004_02_02/en/index.html
WHO (World Health Organization) (2004b). Avian influenza H5N1 infection in humans:
urgent need to eliminate the animal reservoir, WHO website, 22 January 2004.
http://www.who.int/csr/don/2004_01_22/en/index.html
WHO (World Health Organization) (2004f). WHO interim recommendations for the
protection of persons involved in the mass slaughtering of animals potentially infected
with highly pathogenic avian influenza viruses. WHO Regional Office for the Western
Pacific website, Manila, 26 January 2004
http://www.wpro.who.int/internet/resources.ashx/CSR/Publications/WHO+interi
m+recommendation+26012004.pdf
WHO (World Health Organization) (2004g). Control of avian influenza A (H5N1): public
health concerns. WHO website, 10 February 2004.
http://www.who.int/csr/disease/avian_influenza/guidelines/publichealth/en/
OIE documents
OIE (World Organisation for Animal Health) (2007). OIE Terrestrial Animal Health Code.
Updated each year . http://www.oie.int/eng/normes/en_mcode.htm?e1d10
OIE (World Organisation for Animal Health) (2004). OIE Manual of Diagnostic Tests and
Vaccines for Terrestrial Animals, 5th edition, OIE, Paris.
http://www.oie.int/eng/normes/en_mmanual.htm?e1d10
OIE (World Organisation for Animal Health) (2003). Avian influenza — brief review. Prepared
by an OIE ad hoc group.
OIE (World Organisation for Animal Health) (2004a). Highly pathogenic avian influenza in
the United States of America. Report to OIE, 23 February 2004. Follow-up report 1, 5
March 2004. Available from the OIE website (http://www.oie.int).
OIE (World Organisation for Animal Health) (2004b). Highly pathogenic avian influenza in
Canada. Report to OIE, 20 February 2004. Follow-up report 3, 12 March 2004. Available
from the OIE website (http://www.oie.int).