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Datasheet

avian influenza

Summary

  • Last modified
  • 25 September 2017
  • Datasheet Type(s)
  • Animal Disease
  • Preferred Scientific Name
  • avian influenza
  • Overview
  • Influenza viruses belong to the family Orthomyxoviridae and are divided on the basis of their antigenic nature into types A, B and C. Only type A influenza viruses are of interest to veterinarians because they can inf...

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Pictures

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PictureTitleCaptionCopyright
Oedema of the wattles
TitleExternal signs
CaptionOedema of the wattles
Copyright©USDA-2002/Foreign Animal Diseases Training Set/USDA-Animal and Plant Health Inspection Service (APHIS)
Oedema of the wattles
External signsOedema of the wattles©USDA-2002/Foreign Animal Diseases Training Set/USDA-Animal and Plant Health Inspection Service (APHIS)
Cyanotic comb of an infected chicken (a) compared with a normal chicken (b).
TitleExternal signs
CaptionCyanotic comb of an infected chicken (a) compared with a normal chicken (b).
Copyright©USDA-2002/Foreign Animal Diseases Training Set/USDA-Animal and Plant Health Inspection Service (APHIS)
Cyanotic comb of an infected chicken (a) compared with a normal chicken (b).
External signsCyanotic comb of an infected chicken (a) compared with a normal chicken (b).©USDA-2002/Foreign Animal Diseases Training Set/USDA-Animal and Plant Health Inspection Service (APHIS)
Cyanosis of comb and wattles
TitleSigns
CaptionCyanosis of comb and wattles
CopyrightDirk van Aken
Cyanosis of comb and wattles
SignsCyanosis of comb and wattlesDirk van Aken
Severe (terminal) respiratory distress
TitleSigns
CaptionSevere (terminal) respiratory distress
CopyrightDirk van Aken
Severe (terminal) respiratory distress
SignsSevere (terminal) respiratory distressDirk van Aken
Diarrhoea
TitleSigns
CaptionDiarrhoea
CopyrightDirk van Aken
Diarrhoea
SignsDiarrhoeaDirk van Aken
Congestion and petechiae in the skin on the hocks and shanks.
TitleExternal signs
CaptionCongestion and petechiae in the skin on the hocks and shanks.
Copyright©USDA-2002/Foreign Animal Diseases Training Set/USDA-Animal and Plant Health Inspection Service (APHIS)
Congestion and petechiae in the skin on the hocks and shanks.
External signsCongestion and petechiae in the skin on the hocks and shanks.©USDA-2002/Foreign Animal Diseases Training Set/USDA-Animal and Plant Health Inspection Service (APHIS)
Opened oedematous wattle.
TitleInternal signs
CaptionOpened oedematous wattle.
Copyright©USDA-2002/Foreign Animal Diseases Training Set/USDA-Animal and Plant Health Inspection Service (APHIS)
Opened oedematous wattle.
Internal signsOpened oedematous wattle.©USDA-2002/Foreign Animal Diseases Training Set/USDA-Animal and Plant Health Inspection Service (APHIS)
Serofibrinous pericarditis
TitlePathology
CaptionSerofibrinous pericarditis
CopyrightDirk van Aken
Serofibrinous pericarditis
PathologySerofibrinous pericarditisDirk van Aken
Fibrinous adhesions, haemorrhages and lung congestion
TitlePathology
CaptionFibrinous adhesions, haemorrhages and lung congestion
CopyrightDirk van Aken
Fibrinous adhesions, haemorrhages and lung congestion
PathologyFibrinous adhesions, haemorrhages and lung congestionDirk van Aken
Haemorrhages in the muscle
TitlePathology
CaptionHaemorrhages in the muscle
CopyrightDirk van Aken
Haemorrhages in the muscle
PathologyHaemorrhages in the muscleDirk van Aken
Necrotic foci in the liver
TitlePathology
CaptionNecrotic foci in the liver
CopyrightDirk van Aken
Necrotic foci in the liver
PathologyNecrotic foci in the liverDirk van Aken
Necrotic foci in the spleen
TitlePathology
CaptionNecrotic foci in the spleen
CopyrightDirk van Aken
Necrotic foci in the spleen
PathologyNecrotic foci in the spleenDirk van Aken
Severe congestive and haemorrhagic lesions in the lung
TitlePathology
CaptionSevere congestive and haemorrhagic lesions in the lung
CopyrightDirk van Aken
Severe congestive and haemorrhagic lesions in the lung
PathologySevere congestive and haemorrhagic lesions in the lungDirk van Aken

Identity

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Preferred Scientific Name

  • avian influenza

International Common Names

  • English: avian influenza, AI in birds; bird flu; bird grippe; Brunswick bird plague; Brunswick disease; fowl disease; fowl grippe; fowl pest; fowl plague; high pathogenicity avian influenza; highly pathogenic avian influenza; low pathogenic avian influenza; low pathogenicity avian influenza; typhus exudatious gallinarium
  • French: grippe aviaire; peste aviaire

Local Common Names

  • Germany: Geflugelpest

English acronym

  • AI
  • HPAI
  • LPAI

Overview

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Influenza viruses belong to the family Orthomyxoviridae and are divided on the basis of their antigenic nature into types A, B and C. Only type A influenza viruses are of interest to veterinarians because they can infect birds, pigs, horses, and occasionally seals, whales and mink. Influenza viruses that infect birds are called avian influenza viruses. The first reports of the disease in chickens caused by avian influenza viruses occurred in 1878 in northern Italy. This disease was originally termed 'fowl plague' because of the devastating high mortality rate, but today, this disease is called highly pathogenic avian influenza. The pathogenicity of avian influenza viruses varies widely and clinical signs of disease range from mild respiratory signs to multi-systemic infections with near 100% mortality. Low pathogenicity avian influenza viruses cause the milder forms of avian influenza while highly pathogenic avian influenza viruses cause the more severe form. However, the presence of secondary pathogens or environmental stressors can increase the severity of disease associated with low pathogenicity avian influenza viruses.

Avian influenza viruses can infect most domestic and wild bird species. Influenza viruses have been known to be widely present in waterfowl since the 1970s and most such viruses are of low pathogenicity for poultry. An outbreak of highly pathogenic avian influenza in broilers in Pennsylvania and Virginia, USA, in 1983-1984 led to the slaughter of approximately 11 million birds at a cost of approximately US $61 million. Epidemics of highly pathogenic avian influenza (H5N2) in broilers in Mexico (1993-1995) and of both high and low pathogenic virus (H7N1 and H5N2) in various domestic poultry in Italy between 1997 and 2000 showed that the risk continues. In 1997-1998, avian influenza prompted worldwide concerns after an outbreak of the highly pathogenic H5N1 avian influenza spread from chickens in Hong Kong to humans: six people died and a further 12 were severely affected. The entire population of 1.4 million chickens in Hong Kong was slaughtered. A H5N1 highly pathogenic avian influenza virus reappeared in Hong Kong in 2001 and 2002 resulting in two additional depopulations of chickens in Hong Kong. In 2003, a highly pathogenic virus (H7N7) appeared in the Netherlands resulting in the death or slaughter of 23 million chickens.

Avian influenza viruses are further classified based on their surface proteins; i.e. haemagglutinin and neuraminidase. There are (at least) 16 different haemagglutinin and nine neuraminidase subtypes based on serological testing with the haemagglutinin-inhibition and neuraminidase inhibition tests, respectively. Low pathogenicity avian influenza viruses can be any of the 16 haemagglutinin (H1-16) and nine neuraminidase (N1-9) subtypes. However, highly pathogenic avian influenza viruses have only been of the H5 and H7 haemagglutinin subtypes. The haemagglutinin is the surface protein of greatest immunological significance and provides the basis of immunological protection. Generally, antibodies against one of the haemagglutinins offer little or no protection against a virus with a different haemagglutinin subtype. The virulence of the avian influenza viruses ranges from very low (causing low pathogenicity avian influenza, LPAI) to very high (causing highly pathogenic avian influenza, HPAI). However, some LPAI viral strains are capable of mutating under field conditions to HPAI.

Avian influenza [defined as an infection of poultry caused by any influenza A virus with high pathogenicity and by H5 and H7 subtypes with low pathogenicity] is on the list of diseases notifiable to the World Organisation for Animal Health (OIE). The distribution section contains data from OIE's WAHID database on disease occurrence. For further information on this disease from OIE, see the website: www.oie.int.

Host Animals

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Animal nameContextLife stageSystem
Anas platyrhynchosDomesticated hostPoultry: All Stages
Anser anser (geese)Domesticated hostPoultry: All Stages
Aves (birds)Wild host
Coturnix japonica (Japanese quail)Domesticated hostPoultry: All Stages
Dromaius novaehollandiaeDomesticated host, Wild hostPoultry: All Stages
Gallus gallus domesticus (chickens)Domesticated hostPoultry: All Stages
Meleagris gallopavo (turkey)Domesticated hostPoultry: All Stages
Numida meleagris (guineafowl)Domesticated hostPoultry: All Stages
Phasianus (pheasants)Domesticated host, Wild hostPoultry: All Stages
Struthio camelus (ostrich)Domesticated host, Wild hostPoultry: All Stages

Hosts/Species Affected

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Wild birds


Since the mid-1970s, avian influenza viruses have been isolated from avian species representing most of the major families of birds throughout the world. Stallknecht and Shane (1988) in their review of surveillance studies listed 88 species of birds, covering 12 orders, which have been found to excrete influenza virus. The actual number of naturally infected or susceptible species is probably much greater because these surveys have been selective with respect to the species sampled, the geographical locations examined and the time of year sampling occurred. Most avian influenza viruses have been isolated from ducks, although other wild birds may also be infected including other waterfowl, shorebirds, and gulls and other seabirds. Wild birds and their excreta are considered to be a major source of avian influenza virus. Most avian influenza virus infections of wild birds are asymptomatic.


Domestic poultry


Turkeys are more commonly infected than chickens probably because of differences in husbandry systems. Preventing direct contact with free-flying birds and protecting domestic poultry from contact with the faeces of wild birds is an important way to prevent initial introduction of avian influenza into domestic poultry. Modern commercial chicken farms are made wild bird-proof. Turkeys, however, are often raised on open ranges, and this has resulted in outbreaks of primarily low pathogenicity avian influenza. Also at risk to avian influenza are poultry raised outdoors for organic or free-range markets, domestic ducks raised on ponds frequented by wild ducks, live poultry markets with multiple bird sources and multi-directional movement of birds, and small farm enterprises that raise multiple poultry species and such birds having access to outdoor areas.

Systems Affected

Top of page digestive diseases of poultry
multisystemic diseases of poultry
nervous system diseases of poultry
reproductive diseases of poultry
respiratory diseases of poultry
urinary tract and renal diseases of poultry

Distribution

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Avian influenza viruses occur worldwide in both wild and domestic birds. Migratory birds, especially waterfowl are believed to be important reservoir hosts, and shed the virus in their respiratory and ocular secretions as well as in faeces. These birds frequently introduce avian influenza viruses into local, non-migratory, wild bird populations. Infected wild birds can transmit the virus to domestic birds such as chickens and turkeys. Asymptomatic carrier birds may also transmit the virus.

Avian influenza notifiable to OIE is defined as an infection of poultry caused by any influenza A virus with high pathogenicity (HPAI) and by H5 and H7 subtypes with low pathogenicity (H5/H7 LPAI). Influenza A viruses with high pathogenicity in birds other than poultry, including wild birds, are also notifiable.

Since 2002 a number of serious outbreaks of HPAI have occurred in different regions of the world with massive disruption to international trade, the culling of millions of birds, and transmission to humans resulting in disease and mortality.

The only country in Africa that reported cases of HPAI to the AU-IBAR in 2011 was Egypt. The country reported a total of 306 outbreaks that involved a morbidity of 218,797 and mortality of 31,851 birds. With the exception of Egypt, there has been a significant reduction in the number of HPAI outbreaks being reported on the African continent. The countries that have reported cases of HPAI in recent years include Egypt (2009, 2010, 2011), South Africa (2010) and Togo (2008).

Countries reporting avian influenza in 2011 to AU-IBAR 

Country

Outbreaks

Cases

Deaths

Slaughtered

Destroyed

Egypt

306

218,797

31,851

60,735

126,395

Total (1)

306

218,797

31,851

60,735

126,395

The distribution map associated with this datasheet illustrates occurrence of notifiable avian influenza in poultry.

Distribution Table

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The distribution in this summary table is based on all the information available. When several references are cited, they may give conflicting information on the status. Further details may be available for individual references in the Distribution Table Details section which can be selected by going to Generate Report.

Continent/Country/RegionDistributionLast ReportedOriginFirst ReportedInvasiveReferenceNotes

Asia

AfghanistanPresentOIE, 2009
ArmeniaDisease not reportedOIE, 2009
AzerbaijanDisease not reportedOIE, 2009
BahrainDisease never reportedOIE, 2009
BangladeshPresentOIE, 2009
BhutanDisease never reportedOIE, 2009
Brunei DarussalamDisease not reportedOIE Handistatus, 2005
CambodiaPresentNULLOIE, 2005d; Larkin, 2005; OIE, 2009
ChinaPresentNULLOIE, 2004b; OIE, 2009
-AnhuiLast reported2004OIE, 2004b
-GansuLast reported2004OIE, 2004b
-GuangdongLast reported2004OIE, 2004b
-GuangxiLast reported2004OIE, 2004b
-HenanLast reported2004OIE, 2004b
-Hong KongPresentNULLOIE, 2005c; Zhou et al., 1999; OIE, 2009
-HubeiLast reported2004OIE, 2004b
-HunanLast reported2004OIE, 2004b
-JiangxiLast reported2004OIE, 2004b
-JilinLast reported2004OIE, 2004b
-ShaanxiLast reported2004OIE, 2004b
-ShanghaiLast reported2004OIE, 2004b
-XinjiangLast reported2004OIE, 2004b
-YunnanLast reported2004OIE, 2004b
-ZhejiangLast reported2004OIE, 2004b
Georgia (Republic of)Disease not reportedOIE Handistatus, 2005
IndiaPresentOIE, 2009
IndonesiaPresentNULLOIE, 2004b; ProMED-mail, 2005d; Koh-Yeo et al., 1996; Larkin, 2005; OIE, 2009
IranAbsent, reported but not confirmedOIE, 2009
IraqDisease not reportedOIE, 2009
IsraelDisease not reportedOIE, 2009
JapanPresentNULLOIE, 2004a; OIE, 2009
JordanDisease not reportedOIE, 2009
KazakhstanDisease not reportedOIE, 2009
Korea, DPRDisease not reportedOIE Handistatus, 2005
Korea, Republic ofDisease not reported20080514OIE, 2004b; OIE, 2009
KuwaitDisease not reportedOIE, 2009
KyrgyzstanDisease not reportedOIE, 2009
LaosPresentNULLOIE, 2004b; OIE, 2009
LebanonDisease not reportedOIE, 2009
MalaysiaDisease not reportedOIE, 2009
-Peninsular MalaysiaReported present or known to be presentNativeLandman and Schrier, 2004; OIE Handistatus, 2005
-SabahDisease never reportedOIE Handistatus, 2005
-SarawakDisease never reportedOIE Handistatus, 2005
MongoliaDisease not reportedOIE, 2009
MyanmarDisease not reportedOIE, 2009
NepalNo information availableOIE, 2009
OmanDisease not reportedOIE, 2009
PakistanDisease not reported20080619OIE, 2004b; Perdue and Suarez, 2000; OIE, 2009
PhilippinesDisease never reportedOIE, 2009
QatarNo information availableOIE, 2009
Saudi ArabiaPresentOIE, 2009
SingaporeDisease never reportedNULLKoh-Yeo et al., 1996; OIE, 2009
Sri LankaDisease never reportedOIE, 2009
SyriaDisease not reportedOIE, 2009
TaiwanDisease never reportedOIE, 2004b; OIE Handistatus, 2005
TajikistanDisease never reportedOIE, 2009
ThailandPresentNULLOIE, 2005a; Li et al., 2004; OIE, 2009
TurkeyDisease not reportedOIE, 2009
TurkmenistanDisease never reportedOIE Handistatus, 2005
United Arab EmiratesDisease never reportedOIE, 2009
UzbekistanDisease never reportedOIE Handistatus, 2005
VietnamPresentNULLOIE, 2004b; OIE, 2005b; Koh-Yeo et al., 1996; OIE, 2009
YemenPresentOIE, 2009

Africa

AlgeriaDisease not reportedOIE, 2009
AngolaDisease never reportedOIE, 2009
BeninLast reported2008OIE, 2012
BotswanaDisease never reportedOIE, 2009
Burkina FasoLast reported2006OIE, 2012
BurundiDisease not reportedOIE, 2012
CameroonLast reported2006OIE, 2012
Cape VerdeDisease never reportedOIE, 2012
Central African RepublicDisease not reportedOIE Handistatus, 2005
ChadNo information availableOIE, 2009
CongoDisease never reportedOIE, 2009
Congo Democratic RepublicDisease not reportedOIE Handistatus, 2005
Côte d'IvoireLast reported2007OIE, 2012
DjiboutiDisease not reportedOIE, 2009
EgyptPresentOIE, 2012
EritreaNo information availableOIE, 2009
EthiopiaDisease never reportedOIE, 2009
GabonDisease never reportedOIE, 2009
GambiaNo information availableOIE, 2009
GhanaLast reported2008OIE, 2012
GuineaNo information availableOIE, 2009
Guinea-BissauDisease never reportedOIE, 2009
KenyaDisease never reportedOIE, 2009
LesothoDisease never reportedOIE, 2009
LibyaDisease never reportedOIE Handistatus, 2005
MadagascarDisease never reportedOIE, 2009
MalawiDisease never reportedOIE, 2009
MaliDisease never reportedOIE, 2012
MauritaniaDisease never reportedOIE, 2012
MauritiusDisease never reportedOIE, 2009
MoroccoDisease not reportedOIE, 2009
MozambiqueDisease never reportedOIE, 2009
NamibiaNo information availableOIE, 2009
NigerLast reported2006OIE, 2012
NigeriaLast reported2008OIE, 2012
RéunionDisease not reportedOIE Handistatus, 2005
RwandaDisease never reportedOIE, 2009
Sao Tome and PrincipeDisease not reportedOIE Handistatus, 2005
SenegalDisease never reportedOIE, 2009
SeychellesDisease not reportedOIE Handistatus, 2005
Sierra LeoneDisease not reportedOIE, 2012
SomaliaNo information availableOIE Handistatus, 2005
South AfricaPresentPfitzer et al., 2000; Swayne and Suarez, 2000; Landman and Schrier, 2004; ProMED-mail, 2004; OIE, 2012
SudanLast reported2006OIE, 2012
SwazilandDisease not reportedOIE, 2009
TanzaniaDisease never reportedOIE, 2009
TogoLast reported2009OIE, 2012
TunisiaDisease never reportedOIE, 2009
UgandaDisease never reportedOIE, 2009
ZambiaDisease not reportedOIE, 2009
ZimbabweDisease not reportedOIE, 2009

North America

BermudaDisease not reportedOIE Handistatus, 2005
CanadaDisease not reported200801OIE, 2004b; Swayne and Suarez, 2000; OIE, 2009
-British ColumbiaLast reported2004OIE, 2004b
GreenlandDisease never reportedOIE, 2009
MexicoDisease not reported199506Swayne et al., 1997; Perdue and Suarez, 2000; OIE, 2009
USADisease not reported2004OIE, 2004b; Lasley, 1987; OIE, 2009
-DelawareLast reported2004OIE, 2004b
-North CarolinaLast reported2005ProMED-mail, 2005a
-TexasLast reported2004OIE, 2004b

Central America and Caribbean

BarbadosDisease never reportedOIE Handistatus, 2005
BelizeDisease never reportedOIE, 2009
British Virgin IslandsDisease never reportedOIE Handistatus, 2005
Cayman IslandsDisease never reportedOIE Handistatus, 2005
Costa RicaDisease never reportedOIE, 2009
CubaDisease never reportedOIE, 2009
CuraçaoDisease not reportedOIE Handistatus, 2005
DominicaDisease not reportedOIE Handistatus, 2005
Dominican RepublicDisease never reportedOIE, 2009
El SalvadorDisease never reportedOIE, 2009
GuadeloupeDisease never reportedOIE, 2009
GuatemalaDisease never reportedOIE, 2009
HaitiDisease never reportedOIE, 2009
HondurasDisease never reportedOIE, 2009
JamaicaDisease never reportedOIE, 2009
MartiniqueDisease never reportedOIE, 2009
NicaraguaDisease never reportedOIE, 2009
PanamaDisease never reportedOIE, 2009
Saint Kitts and NevisDisease never reportedOIE Handistatus, 2005
Saint Vincent and the GrenadinesDisease never reportedOIE Handistatus, 2005
Trinidad and TobagoDisease never reportedOIE Handistatus, 2005

South America

ArgentinaDisease never reportedOIE, 2009
BoliviaNo information availableOIE, 2009
BrazilDisease never reportedNULLResende et al., 1990; OIE, 2009
ChileDisease not reportedOIE, 2009
ColombiaDisease never reportedOIE, 2009
EcuadorDisease never reportedOIE, 2009
Falkland IslandsDisease never reportedOIE Handistatus, 2005
French GuianaDisease never reportedOIE, 2009
GuyanaDisease never reportedOIE Handistatus, 2005
ParaguayDisease never reportedOIE Handistatus, 2005
PeruDisease never reportedOIE, 2009
UruguayDisease never reportedOIE, 2009
VenezuelaDisease never reportedOIE, 2009

Europe

AlbaniaDisease not reportedOIE, 2009
AndorraDisease not reportedOIE Handistatus, 2005
AustriaDisease not reportedOIE, 2009
BelarusDisease never reportedOIE, 2009
BelgiumDisease not reported200304Office International des Epizooties, 2003a; OIE, 2004b; OIE, 2009
Bosnia-HercegovinaDisease never reportedOIE Handistatus, 2005
BulgariaDisease not reportedOIE, 2009
CroatiaDisease not reportedOIE, 2009
CyprusDisease never reportedOIE, 2009
Czech RepublicDisease not reportedOIE, 2009
DenmarkDisease not reportedOIE, 2009
EstoniaDisease never reportedOIE, 2009
FinlandDisease never reportedOIE, 2009
FranceDisease not reported200708Luini et al., 1988; OIE, 2009
GermanyPresentNULLOIE, 2004b; Hoffrogge et al., 2003; OIE, 2009
GreeceDisease not reportedOIE, 2009
HungaryDisease not reportedOIE, 2009
IcelandDisease never reportedOIE, 2009
IrelandDisease not reported1983Banks et al., 1998; OIE, 2009
Isle of Man (UK)Disease never reportedOIE Handistatus, 2005
ItalyDisease not reported200602Zanella, 2000; Capua and Mutinelli, 2001; OIE, 2009
JerseyDisease never reportedOIE Handistatus, 2005
LatviaDisease never reportedOIE, 2009
LiechtensteinDisease not reportedOIE, 2009
LithuaniaDisease never reportedOIE, 2009
LuxembourgDisease not reportedOIE, 2009
MacedoniaDisease never reportedOIE, 2009
MaltaDisease never reportedOIE, 2009
MoldovaDisease never reportedOIE Handistatus, 2005
MontenegroDisease never reportedOIE, 2009
NetherlandsDisease not reported2003OIE, 2004b; Hoffrogge et al., 2003; OIE, 2009
NorwayDisease never reportedOIE, 2009
PolandPresentOIE, 2009
PortugalDisease not reportedOIE, 2009
RomaniaDisease not reportedOIE, 2009
Russian FederationDisease not reportedOIE, 2009
-Eastern SiberiaPresentOkazaki et al., 2000
SerbiaDisease not reportedOIE, 2009
SlovakiaDisease not reportedOIE, 2009
SloveniaDisease not reportedOIE, 2009
SpainDisease not reportedOIE, 2009
SwedenDisease not reportedOIE, 2009
SwitzerlandDisease not reportedOIE, 2009
UKPresentNULLWood et al., 1994; Perdue and Suarez, 2000; OIE, 2009
-Northern IrelandDisease never reportedOIE Handistatus, 2005
UkraineDisease not reported20080227Elkin et al., 1988; OIE, 2009
Yugoslavia (former)Disease never reportedOIE Handistatus, 2005
Yugoslavia (Serbia and Montenegro)Disease never reportedOIE Handistatus, 2005

Oceania

AustraliaDisease not reported199711Cross, 1987; Röhm, 1996; Perdue and Suarez, 2000; OIE, 2009
French PolynesiaDisease never reportedOIE, 2009
New CaledoniaDisease never reportedOIE, 2009
New ZealandDisease never reportedOIE, 2009
SamoaDisease never reportedOIE Handistatus, 2005
VanuatuDisease never reportedOIE Handistatus, 2005
Wallis and Futuna IslandsNo information availableOIE Handistatus, 2005

Pathology

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Highly pathogenic avian influenza in poultry is characterized by subcutaneous haemorrhages and oedema of the head. Vesicles to necrotic foci may be present on the comb and wattles. Haemorrhages can be seen in the serosa of all visceral organs and in the mucosa and lymphoid tissue of the intestinal and respiratory tracts. Low pathogenicity influenza results in tracheitis, pulmonary oedema and air sacculitis. Occassionally, low pathogenicity avian influenza viruses may cause sowllen kidneys (nephrosis), visceral urate deposition ('visceral gout') and exudative inflammation in the lumen of the oviduct.

Diagnosis

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Editor's note: the clinical signs table in this datasheet refers to highly pathogenic avian influenza (HPAI).

Avian influenza (AI) is difficult to diagnose and false positives are not uncommon in preliminary tests. Virus isolation in specific-pathogen-free embryonated eggs or cell cultures is conventionally considered the method of choice for the detection and identification of avian influenza viruses. This is a reliable and specific technique although it is time-consuming and expensive. However, the time between clinical suspicion and laboratory confirmation of AI can be long because of the logistics of sending samples to laboratories and their capacity for providing high throughput of sensitive and specific assays is often limited. Although very accurate, virus isolation is of limited value for control and eradication purposes, because avian influenza is a highly contagious disease and the prompt identification of infection is crucial. In order to shorten the time between receipt of samples in a laboratory and diagnosis there has been widespread application of molecular techniques based on the amplification of specific nucleic acid sequences by polymerase chain reaction (PCR), ligase chain reaction and nucleic acid sequence-based amplification (NASBA). Real-time PCR (Brown, 2006) is increasingly being used, as it enables rapid diagnosis in part due to automation, and also because the PCR products are detected, and quantified, during the DNA amplification process, without requiring a subsequent separate detection process. The development of portable instruments for application of molecular technologies in field offers prospects for radically changing diagnostic approaches for AI in the future (Cattoli and Capua, 2006).

Clinical Diagnosis


Clinical signs of avian influenza vary according to the host, strain of virus, vaccinal immunity, secondary infections and environmental conditions. In some flocks the only evidence of the infection is seroconversion, i.e. the birds infected with a LPAI virus may only develop a detectable antibody titre to avian influenza virus. Birds infected with LPAI virus often develop respiratory, enteric, or reproductive disease. Decreased feed intake and a drop in egg production are some of the earliest and most predictable signs of disease. Birds infected with LPAI may show mild depression with a significant decrease in egg production. Other clinical signs for LPAI include excessive lacrimation, sinusitis, diarrhoea, coughing and sneezing.

Birds with HPAI may show some of the clinical signs of LPAI, but infected poultry usually have swollen heads, facial oedema with swollen and cyanotic unfeathered skin (comb, wattles, snood, feet and legs) and nervous signs such as paresis, paralysis, torticollis, and opisthotonus. Other clinical signs include severe depression and inappetence as well as a significant decline in egg production. Infection with the HPAI virus may cause sudden death with little or no overt signs (mortality can reach 100%). However, none of these signs can be considered pathognomonic. Differential diagnosis should consider acute fowl cholera, velogenic Newcastle disease, and respiratory diseases such as infectious laryngotracheitis.

Laboratory Diagnosis


Diagnosis of avian influenza is made by the isolation of the virus, molecular detection of specific nucleic acids or identification of specific proteins. Serological methods may be used as additional diagnostic tools, but, used alone, are unsuitable for a detailed identification.

The virus can be isolated from variety of sources including faeces, tracheal swabs and cloacal swabs. Inoculation of embryonated SPF chicken eggs is the preferred method of growing avian influenza A viruses but avian cell tissue culture can be used. The presence of haemagglutination activity in allantoic fluids of inoculated 9- to 11-day-old embryonating chicken eggs after incubation for 4-7 days at 35-37°C indicates a high probability of either influenza A virus or Newcastle disease virus infection.

The presence of influenza A virus can be confirmed in the allantoic fluid using agar gel immunodiffusion tests by demonstrating the presence of the nucleocapsid or matrix antigens, which are common to all influenza A viruses. The method for definitive antigenic sub-typing of influenza A viruses recommended by the WHO Expert Committee (1980) involves the use of highly specific antisera against haemagglutinin and neuraminidase subtypes, generally in a reference laboratory. Alternatively, the allantoic fluid can be tested for avian influenza virus type A nucleoprotein or matrix protein by solid phase ELISA test such as Directigen or by detection of avian influenza viral nucleic acids in a reverse transcriptase polymerase chain reaction assay. The antigen or nucleic acid detection tests can also be used to identify avian influenza virus directly in respiratory or cloacal swabs, or tissue homogenates from affected birds.

Further information concerning the pathogenicity of avian influenza subtypes may be obtained by sequencing part of the genome of the virus, where the amino acid make-up of the cleavage site of the haemagglutinin has great significance as an indicator of pathogenicity. Essentially, high pathogenicity H5 and H7 subtype strains have one or more pairs of basic amino acids (arginine, lysine) at the HA1-HA2 cleavage site, rendering the haemagglutinin cleavable by ubiquitous furin proteases present in many cells of organs throughout the body of poultry species. Consequently AIVs with such cleavage sites can replicate in many visceral and other organs and are consequently highly pathogenic. In contrast, low pathogenicity strains generally have only individual basic amino acids, not pairs, in the cleavage site. Proteases able to cleave such cleavage sites are not present in organs throughout the body, thereby restricting replication largely to respiratory and enteric organs where these proteases are present.

List of Symptoms/Signs

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Digestive Signs

  • Anorexia, loss or decreased appetite, not nursing, off feed
  • Dark colour stools, faeces
  • Diarrhoea
  • Vomiting or regurgitation, emesis

General Signs

  • Cyanosis, blue skin or membranes
  • Decreased, absent thirst, hypodipsia, adipsia
  • Dehydration
  • Discomfort, restlessness in birds
  • Generalized weakness, paresis, paralysis
  • Head, face, ears, jaw, nose, nasal, swelling, mass
  • Inability to stand, downer, prostration
  • Increased mortality in flocks of birds
  • Pale comb and or wattles in birds
  • Petechiae or ecchymoses, bruises, ecchymosis
  • Sudden death, found dead
  • Swelling of the limbs, legs, foot, feet, in birds
  • Torticollis, twisted neck
  • Underweight, poor condition, thin, emaciated, unthriftiness, ill thrift
  • Weakness, paresis, paralysis of the legs, limbs in birds
  • Weight loss

Nervous Signs

  • Coma, stupor
  • Dullness, depression, lethargy, depressed, lethargic, listless
  • Head tilt

Ophthalmology Signs

  • Conjunctival, scleral, redness
  • Lacrimation, tearing, serous ocular discharge, watery eyes

Reproductive Signs

  • Decreased, dropping, egg production

Respiratory Signs

  • Abnormal breathing sounds of the upper airway, airflow obstruction, stertor, snoring
  • Abnormal lung or pleural sounds, rales, crackles, wheezes, friction rubs
  • Change in voice, vocal strength
  • Coughing, coughs
  • Dyspnea, difficult, open mouth breathing, grunt, gasping
  • Increased respiratory rate, polypnea, tachypnea, hyperpnea
  • Mucoid nasal discharge, serous, watery
  • Purulent nasal discharge
  • Sneezing, sneeze

Skin

  • Integumentary Signs/Ruffled, ruffling of the feathers
  • Integumentary Signs/Skin edema
  • Integumentary Signs/Skin necrosis, sloughing, gangrene
  • Integumentary Signs/Skin vesicles, bullae, blisters

Disease Course

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The virus is transmitted rapidly to susceptible birds through inhalation or ingestion of influenza particles in nasal and respiratory secretions and by direct contact with faeces of infected birds. Viral replication occurs in the intestinal and respiratory tracts for both low and high pathogenicity avian influenza viruses. The highly pathogenic strains spread to vascular endothelium with replication, causing viraemia and multi-focal necrosis in many visceral organs, skin and brain. These necrobiotic lesions may be accompanied by inflammatory lesions in many organs including heart, skeletal muscle, brain and pancreas. In addition, chicken and turkey succumb after several days of clinical signs, exhibiting petechial haemorrhages and serous exudates in respiratory, digestive and cardiac tissues. Neutralizing antibodies are detectable within 3-7 days after the onset of both high and low pathogenicity avian influenza viruses, reaching a peak during the second week and persisting for up to 18 months in all avian species. Most poultry infected with high pathogenicity avian influenza viruses do not survive but many infected with low pathogenicity viruses recover.

Morbidity is apparent following exposure to either low or high pathogenicity avian influenza viruses. Mortality is consistently high with high pathogenicity avian influenza viruses, but mortality is variable for low pathogenicity avian influenza viruses depending on climatic factors, the presence of secondary pathogens, and environmental conditions.


The avian influenza virus does not persist in individual birds, but within a large population of birds, the virus may spread slowly throughout a production facility; depending on level of immunity, transmissibility of the virus, infectivity of the virus, housing type and host species. A farm cannot be assumed avian influenza virus-free until the infected flock has been removed by depopulation or controlled marketing, and the facility has been thoroughly cleaned and disinfected.

Epidemiology

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Avian influenza viruses are highly infectious. Most poultry flocks affected with avian influenza are infected directly or indirectly from other infected poultry flocks. Wild waterfowl, seabirds and shorebirds serve as a reservoir of avian influenza virus, but once it enters the poultry population, these birds no longer have a role in its spread.

Avian influenza viruses show host adaptation with greatest amount of virus replication and easiest transmission occurring between birds in the same or closely related species. However, with repeated infection cycles in a new host species, the avian influenza virus adapts to a new host making transmission easier and faster. Avian influenza virus is periodically introduced into susceptible poultry flocks from wild birds, especially wild ducks. Avian influenza viruses have also been isolated in many countries from imported cage birds. The epidemiological importance of live poultry markets should not be underestimated. They serve as a reservoir and source of introduction to other commercial poultry. Influenza virus is transmitted by direct contact with respiratory secretions and faeces where the virus can survive for long periods, especially in water at low temperatures. Influenza in turkeys is principally seen in countries where they are raised in facilities where wild birds can have access or use drinking water obtained from ponds frequented by wild birds. An important way of preventing exposure to the virus is preventing contact of domestic birds with wild and migratory birds that may carry the virus. For commercial farming operations, preventing exposure to wild birds is also important, but preventing exposure to other domestic poultry that may have had direct or indirect contact with wild birds is more important. Such exposure could be through using dirty chicken crates from live poultry markets, partial load-out of poultry, employees owning backyard poultry or fighting chickens, sharing equipment between farms, lack of visitor restrictions, and failure to disinfect boots and equipment and launder dedicated work clothing on the farm.

Avian influenza is most often transmitted from infected to susceptible flocks by personnel and their equipment. Once introduced into the poultry of an area it can spread rapidly and be extremely difficult to control and/or eradicate.

Impact: Economic

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Outbreaks of high pathogenicity avian influenza result in severe losses in production, and high costs associated with disease control and prevention. The cost of the 1983-1984 eradication programme in Pennsylvania and surrounding states far exceeded any other losses attributable to avian influenza. Lasley (1987) estimated that this outbreak cost the government and farmers US $75 million. Subsequent rises in food prices may have cost the consumers an additional US $349 million. An outbreak of HPAI in Australia in 1985 was estimated to have cost more than AUS $2 million (Cross, 1987). The 1997 outbreak of H5N1 highly pathogenic avian influenza in Hong Kong cost US $13 million. The 2000 outbreak of H7N1 high pathogenicity avian influenz cost the Italian government US $100 million in conpensation to farmers (Swayne and Halvorson, 2003).

Low pathogenicity avian influenza leads to a reduction in egg production and exacerbates secondary bacterial infections. Carcass and egg quality declines following infection. Losses in trade due to embargoes and restrictions imposed by importing countries are more devastating economically for some countries than the direct losses caused by an epizootic of avian influenza. In Minnesota alone, a 1978 outbreak cost US $5 million in losses to producers. From 1978 to 1996, losses to producers in Minnesota exceeded US $22 million (Swayne and Halvorson, 2003).

Zoonoses and Food Safety

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Most avian influenza virus strains do not infect humans, even when high-risk exposures occur (Swayne and King, 2003). However, avian influenza virus can occasionally infect mammals. Seroepidemiological and virological studies since 1889 have indicated that human influenza infections were caused by H1, H2 and H3 subtypes of influenza A viruses. However, unlike previous outbreaks, an outbreak of H5 subtype of avian influenza virus in Hong Kong in 1997-1998 affected both chickens and humans. Six people died and a further 12 were severely affected in this outbreak, and the entire chicken population of Hong Kong (1.4-1.5 million birds) was slaughtered. The cause of this outbreak was avian influenza A virus, strain H5N1, which was previously thought only to infect birds. These cases represent the first documented human infections with avian influenza A (H5N1) virus. The virus appeared to have been transmitted directly from chickens to humans from contact with live birds and not from consumption of or handling poultry meat. Since then, more than 500 human cases of avian influenza virus infection due to H5, H7 and H9 subtypes have been reported, mainly as a result of poultry-to-human transmission with a fatality rate of over 50% for H5N1 infections. In 1998, seven people were infected with low pathogenicity H9N2 avian influenza virus in China and Hong Kong, but all had uneventful recoveries

The H5N1 virus re-emerged in South Korea in 2003. In that year four cases were reported in China and Viet Nam, a number that increased 10-fold in the following year, with cases in Thailand and Viet Nam. During the next year (2005) the number of reported cases doubled again, Thailand and Viet Nam being joined by Indonesia. The peak number of reports was in 2006 (115 cases, 79 deaths), with Cambodia, Djibouti, Egypt, Iraq and Turkey joining the list of affected countries. Since then the number of cases reported annually has declined, there being 48 and 53 in 2010 and 2011, respectively (as of 2ndNovember 2011), Egypt reporting more cases than any other country in each year from 2007 to 2011, inclusive. In total 569 cases had been reported from all countries since 2003, 334 of them fatal (59%). The H5N1 virus arrived in Europe in October 2005, but no human cases have been reported. Over 100 people were infected with H7N7 highly pathogenic avian influenza in the Netherlands, with one death. These outbreaks have prompted the governments of many countries to start developing contingency plans for the emergence of an influenza virus that can readily transmit between humans.


Cumulative number of confirmed human cases of avian influenza A/(H5N1) from January 2003 to 2 November 2011 (only laboratory-confirmed cases are included). Taken from the website of the World Health Organization (WHO, http://www.who.int).
 


Country/ Territory


Total cases


Deaths

Azerbaijan 8 5
Bangaldesh 3 0

Cambodia


18


16


China


40


26

Djibouti 1 0
Egypt 152 52

Indonesia


181


149


Iraq


3


2

Lao People's Democratic Republic 2 2
Myanmar 1 0
Nigeria 1 1
Pakistan 3 1

Thailand


25


17


Turkey


12


4


Viet Nam


119


59


Total


569


334

 

Disease Treatment

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There is no approved effective treatment for infected birds. Drugs for treatment of influenza in humans are expensive and not approved for use in birds. Treatments for secondary pathogens, such as antibiotics for bacteria, and improving environmental conditions can hasten natural recovery of birds from low pathogenicity avian influenza viruses.

In human medicine, the influenza virus-specific antiviral drugs oseltamivir (brand name Tamiflu®) and zanamivir (brand name Relenza®) may reduce clinical signs and accelerate recovery. Both drugs inhibit the neuraminidase (NA) and are active against various subtypes of influenza virus. They are about 70% to 90% effective. Previously several adamantane drugs were used to fight influenza A infections in humans, but these are no longer recommended, due to high levels of resistance among circulating influenza A viruses. (Source, Centres for Disease Control, USA). Jefferson et al. (2006) reviewed the efficacy and safety of registered antiviral drugs against naturally occurring influenza in healthy adults.

Scientists also believe that immunoglobulins obtained from recovered flu patients could be used as an alternative treatment if an avian influenza virus strain develops resistance to antiviral drugs.

Prevention and Control

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Prevention is based on biosecurity measures that include avoiding contact between poultry and wild birds, in particular waterfowl, avoiding introduction of birds of unknown disease status into flocks, control of human traffic, proper cleaning and disinfection procedures, and one age group per farm ('all in-all out') breeding systems.

When outbreaks have occurred, all birds in the flock must be slaughtered and the carcasses disposed. Restocking should not occur for at least 21 days.


Immunization and vaccines


Antibodies against the haemagglutinin play the major role in protection following immunization or exposure. These antibodies are protective against the homologous haemagglutinin subtype but not against heterologous subtypes; i.e. H5 vaccine protects against an H5 but not an H7 avian influenza virus.

Several types of commercial vaccines are available, listed though not necessarily endorsed by the Food and Agriculture Organisation (see: Avian Influenza Vaccine Producers and Suppliers for Poultry, June 2009). The largest type is inactivated whole AIV oil emulsion vaccines of H5 or H7 subtypes. These consist of various AIV isolates i.e. all eight genes from the respective AIV isolate, or comprise the H5 and N1 or N3 genes from AIVs plus the six internal protein genes from human A/Puerto Rico/8/34 virus, known as PR8. The PR8 virus has been used for many decades as the basis for human inactivated influenza vaccines, containing the HA and NA genes of a prevailing human influenza virus. PR8 genes confer high productivity in embryonated chicken eggs. There are also some live recombinant virus vectored vaccines against AIV. Two such vaccines comprise an avian poxvirus as the vector, producing H5 or both an H5 and N1 proteins. Another vectored vaccine comprises live Newcastle disease virus (LaSota) producing H5 haemagglutinin.

The use of AI vaccines around the world in poultry is not well documented. It is believed that the largest single use of inactivated avian influenza vaccine (H5N2 strain) has occurred in China (since December 2003 to present). Indonesia has also used H5 inactivated AI vaccine. In Mexico, both inactivated and recombinant fowlpox vaccines have been used since January 1995. Pakistan began using H7 inactivated AI vaccine following epizootics (in 1995, 1998, 2000 and 2003) of H7N3 HPAI and H9N2 LPAI (Naeem and Siddique, 2006). H9N2 inactivated vaccines are used in many countries in Asia, the Middle East and Eastern Europe. The USA also has considerable experience with the use of killed vaccines, primarily in turkeys. In the state of Minnesota in the 1980s and early 1990s vaccines were used successfully to control outbreaks of AI in turkeys. More recently, several large layer flocks have been vaccinated in Connecticut after an H7N2 LPAI outbreak (Suarez et al., 2006). H7 inactivated vaccine has been used in a high-risk area of northern Italy.

In areas where inadequate resources preclude eradication, flocks may be immunized using autogenous inactivated vaccines or recombinant vectored products. These vaccines are effective in preventing disease and reducing the amount of virus shed into the environment, but have the disadvantage of making it difficult to distinguish between infected and vaccinated birds. Vaccination suppresses clinical occurrence of disease but the virus may persist in the poultry population of the affected region unless adequate biosecurity and surveillance measures are undertaken. In most developed countries, vaccines are banned or discouraged because they may interfere with control policies and may also result in export bans on poultry products. However, during the devastating epidemics of HPAI in the 1990s and early 2000s, the mass slaughter of animals raised serious ethical questions. These epidemics showed that the use of emergency vaccination is an essential element in disease control (Clercq and Goris, 2004). With the development of tests or vaccines that will allow differentiation of vaccinated birds from those infected with the field virus, vaccines may come into greater use (Capua et al., 2003; Ellis et al., 2004; Swayne et al., 2006; Zhao et al., 2006).

Table: Types of vaccines available

 

Vaccine

Notes

inactivated avian influenza oil-emulsion vaccines made directly from AIV  isolates. Monovalent (H5 or H7) and bivalent (H5 plus H7)

 

inactivated avian influenza oil-emulsion vaccines made by reverse genetics. Monovalent (H5).

These have H5 and N1 or N3 genes from various AIVs with the other six genes from A/Puerto Rico/8/34, known as PR8.

Live recombinant fowlpox virus vectored vaccine

This vaccine has an H5 AI gene insert from AI virus A/turkey/Ireland/83 (H5N8).

Live recombinant avian pox virus vectored vaccine

NB. This vaccine has the H5 and N1 genes from A/Goose/Guangdong/1996.

Live recombinant Newcastle disease virus vectored vaccine

NB. This vaccine is Newcastle disease virus vaccine (LaSota) with the H5 gene from A/Barheaded goose/Qinghai/3/2005.

Information from the Food and Agriculture Organisation (FAO), June 2009.


Vaccines and vaccination to control avian influenza - update 2005


By kind permission of the author, Dr David Swayne, Laboratory Director, Southeast Poultry Research Laboratory, USDA/ARS, and ProMED-mail (http://www.promedmail.org), the following is provided as background information on the use of vaccines for control of avian influenza (AI) in poultry (first published as: ProMED-mail. Avian influenza, poultry vaccines: a review. ProMED-mail 2005; 7 March: 2005 16:32:05 -0500 (EST). <http://www.promedmail.org>. Accessed 7 March 2005).

"1. Vaccination should be viewed and used only as a single tool in a comprehensive control strategy that includes: 1) biosecurity, 2) education, 3) diagnostics and surveillance, and 4) elimination of AI virus infected poultry. One or more of these components are used to develop AI control strategies to achieve one of 3 goals or outcomes (Swayne, 2004): 1) Prevention - preventing introduction of AI; 2) Management - reducing losses by minimizing negative economic impact through management practices; or 3) Eradication - total elimination of AI.

2. Protection against avian influenza is the result of immune response against the hemagglutinin protein (HA), of which there are 15 different HA subtypes, and to a lesser extent against the neuraminidase protein (NA), of which there are 9 different NA subtypes (Suarez & Schultz, 2000; Swayne & Halvorson, 2003). Immune responses to the internal proteins, such as nucleoprotein or matrix protein, are insufficient to provide field protection. Therefore, there is no one universal AI vaccine. Practically, protection is provided against the individual hemagglutinin subtype(s) included in the vaccine.

3. Experimental and field studies have shown that properly used vaccines will accomplish several goals: 1) protect against clinical signs and death, 2) reduced shedding of field virus if vaccinated poultry become infected, 3) prevent contact transmission of the field virus, 4) provide at least 20 weeks protection following a single vaccination for chickens (this may require 2 or more injections in turkeys or longer-lived chickens), 5) protect against challenges by low to high doses of field virus, 6) protect against a changing virus and 7) increase a birds resistance to avian influenza virus infection (Swayne, 2003; Capua et al., 2004). These positive qualities are essential in contributing to AI control strategies. Most AI vaccine studies and field use have focused on chickens and turkeys because of their high death rates and the high concentrations of Highly Pathogenic Avian Influenza (HPAI) virus excreted into the environment by these species. However, with the changing epidemiology of the H5N1 HPAI virus in Asia, the infection of domestic ducks and geese has become a very important contributor to the maintenance and spread of the H5N1 HPAI virus. Experimentally, vaccines have been shown to significantly reduce AI virus replication and shedding in domestic ducks and geese and thus decrease environmental contamination (especially in ponds, lakes and rivers) and prevent contact transmission. Proper vaccination of domestic ducks and geese will have a positive impact on control of H5N1 HPAI in Asia.

4. A wide variety of vaccines have been developed and examined in the laboratory for potential use in the field. However, only vaccines from 2 technologies are licensed and used in poultry: inactivated whole avian influenza virus vaccines and a recombinant fowlpox virus vectored vaccine with an H5 AI gene insert (from AI virus A/turkey/Ireland/83 (H5N8)). These 2 vaccine technologies have been shown to produce safe, pure and potent vaccines. Both vaccine technologies require handling and injection of individual birds.

5. The quantity of AI vaccine used around the world in poultry is not well documented, but reliable information suggests the largest single use has been 2 billion doses of inactivated H5N2 avian influenza vaccine in China (December 2003 - present). Indonesia also uses H5 inactivated AI vaccine. In Mexico, an AI vaccination program has been used since January 1995, with over 1.3 billion doses of inactivated vaccine and 850 million doses of recombinant fowlpox have been used. H5N2 HPAI has been eradicated (last isolate was in June 1995), but H5N2 LPAI (low pathogenic avian influenza) still circulates in central Mexico. Pakistan began using H7 inactivated AI vaccine in 1995, with use in 3 regions following epizootics of H7N3 HPAI (1995, 2001 and 2004). By contrast, with low pathogenicity (LP) AI, H9N2 inactivated vaccines have been and are used in many countries within Asia, the Middle East and Eastern Europe, but the number of doses is unknown. Vaccines for control of LPAI have been used sporadically. Recently, H7 inactivated vaccine is being used in a high risk area of Northern Italy and in one chicken layer company in the USA to control LPAI.

6. Historically, AI virus strains selected for manufacturing of inactivated vaccines have been based on LPAI viruses obtained from field outbreaks that have homologous hemagglutinin protein; i.e. H5 vaccine virus obtained from an H5 LPAI outbreak. Rarely, HPAI strains have been used to manufacture inactivated vaccines, because, to be done properly, such production requires specialized high biocontainment manufacturing facilities which are uncommon in the world. Contrary to rumor, HPAI strains do replicate to sufficient titer in embryonating eggs to be used in inactivated AI vaccines, but their use is discouraged because of biosecurity and biosafety manufacturing concerns. Furthermore, LPAI strains, with fewer biosecurity and biosafety concerns for manufacturing, protect against HPAI viruses of the same hemagglutinin subtype.

7. Vaccine strains have been shown to provide protection against diverse field viruses (88-100 percent similarity to the challenge virus hemagglutinin) isolated over a 38 year period (Swayne et al., 2000b). Recently, both North American and Eurasian lineages of AI vaccine viruses from 1968-1986 have been shown to be protective against the most recent 2003-2004 Asian H5N1 HPAI viruses (Swayne, 2004). This broad and longer-term protection efficacy of poultry AI vaccines, as compared to the need for frequent change of human influenza vaccine strains, is potentially the result of the following: 1) poultry vaccines use proprietary oil-emulsion-adjuvant technology which elicits more intense and longer-lived immune response in poultry than alum-adjuvant influenza vaccines, 2) the AI virus immune response in poultry appears to be broader than in humans, 3) the immunity in the domestic poultry population is more consistent because of greater host genetic homogeneity than is present in the human population, and 4) vaccine use in poultry is targeted to a relatively young, healthy population as compared to humans, in whom the vaccine is optimized for groups with the highest risk of severe illness and death.

8. The protection efficacy of individual poultry AI vaccines should be evaluated every 2-3 years to assure they are still protective against circulating virus strains. For example, a recent study demonstrated the 1994 Mexican H5N2 vaccine strain is no longer protective against circulating H5N2 LPAI viruses in Central America, and a change in vaccine strains is needed (Lee et al., 2004a). With the H5N1 AI virus in Asia circulating as only an HP strain, future vaccines may require the use of reverse genetics (Liu et al., 2003; Lee et al., 2004b) to generate new LPAI vaccine strains, or, other molecular techniques to produce vectored vaccine products, such as new recombinant fowlpox virus vaccines. Some of these products use patented technologies and will require legal clarification before use in the field.

9. "Sterilizing immunity" is not feasible in the field. Some experiments have reported "sterilizing immunity," but closer examination indicated such studies used very few experimental birds without statistical evaluation, used a very low virus challenge, or used low sensitive virus isolation/detection methods. In the field, vaccines will reduce replication of challenge virus in respiratory and GI tracts and thus reduce the environmental load of virus and virus transmission. However, the protection in conventional poultry in the field will always be less than that seen in specific-pathogen-free poultry under laboratory conditions because of other factors, such as improper vaccination technique, reduced vaccine dose, immunosuppressive viruses and improper storage & handling of vaccines. The other 4 components of a control strategy, as presented in item 1, are essential, because vaccines and their use are not perfect.

10. Economics and animal health control drive the use of vaccines in poultry. Vaccines are used in geographic areas of highest risk and in the agricultural sector affected, or at greatest risk to be affected. In the USA, inactivated AI vaccines cost on average USD 0.05/dose and another USD 0.05-0.07 for labor and equipment to administer. In examining new vaccine technologies, such adoption will only occur when protection is as good as or better than existing technologies, and the product is cost effective (Swayne, 2004). If the cost is prohibitively high, the farmer or company will not be able to use the vaccine.

11. When deciding to use AI vaccine in poultry, a simple animal health algorithm, in decreasing order of application, should be used: 1) high risk situations - e.g. as suppressor vaccine in the outbreak zone or as ring vaccination outside the outbreak zone; 2) rare captive birds, such as those in zoological collections; 3) valuable genetic poultry stock, such as pure lines or grandparent stocks whose individual value is high; 4) long-lived poultry, such as egg layers or parent breeders; and, lastly, 5) meat production poultry.

12. Several issues which must be resolved before deciding to use AI vaccines: 1) the vaccine strain must be of the same hemagglutinin subtype and be shown in animal studies to be protective against the circulating field virus, 2) standardized manufacturing of vaccines must be followed to produce consistent and efficacious vaccines, 3) policies must be established for proper storage, distribution and administration of the vaccine; 4) adequate serological or virological surveillance must be done to determine whether the field virus is circulating in vaccinated flocks; and 5) an exit strategy must be developed to prevent permanent use of vaccine. In addition, for inactivated whole AI vaccines, the following should be addressed: 1) the need for adequate AI viral antigen content to elicit a protective immune response, either by establishing a minimum hemagglutinin protein content in the vaccine (e.g. minimum of 1-5 micrograms/dose if using generic adjuvant system, less antigen is needed if a proprietary systems gives higher titers) or by demonstration of a high level of protection as measured by _in vivo_ challenge studies or the presence of a minimal hemagglutination inhibition (HI) antibody titer in vaccinated birds (e.g. minimum of 1:32-1:40 HI test); 2) the need for a good oil emulsion adjuvant system; and 3) the establishment of a high level of biosecurity practice for vaccination crews that enter farms to prevent accidental spreading of field virus. If using recombinant fowlpox vaccine, the vaccine should only be administered to one day-old chickens in hatchery, which will give good protection, improved biosecurity and a high degree of quality control. Before new vaccine technologies should be used in the field, assessment of safety in target species, environmental impact to non-target species, purity and efficacy must be demonstrated.

13. Surveillance must be conducted on vaccinated flocks to determine whether the field virus is circulating and the control strategy is working. This should be done by both serological and virological surveillance of vaccinated and non-vaccinated flocks. For serological surveillance, several methods can be used to identify infections by field virus in vaccinated populations: 1) placement of unvaccinated sentinel birds and looking for antibodies against AI viruses, such as in ducks, 2) if using inactivated vaccine, looking for specific antibodies against the neuraminidase of the circulating field virus in vaccinated birds (if using an inactivated vaccine strain with a different neuraminidase subtype than the circulating field virus (Capua et al., 2003)) or looking for antibodies against the non-structural protein (Tumpey et al., 2005), or 3) if using recombinant fowlpox vaccine, looking for antibodies to nucleoprotein/matrix protein. For virological surveillance, examination for specific AI viral nucleic acids or proteins, or isolation of the virus, could be used to determine whether the field virus is circulating. This is best done on sentinel birds that are showing clinical signs or who die. Alternatively, examination of dead poultry from vaccinated populations will give an indication of whether the field virus is circulating.

14. Recently, 2 new vaccines for use in China have been reported (ProMED 20050207.0415 and 20050210.0456): 1) recombinant fowlpox-H5N1 AI vaccine, and 2) a reverse genetic produced influenza A inactivated vaccine. The new recombinant fowlpox vaccine is a live, injectable vaccine for chickens and uses the same technology as the previously licensed recombinant-fowlpox-virus-AI-H5 vaccine (cDNA copy of the AI hemagglutinin gene from A/turkey/Ireland/83 (H5N8)), but includes inserted cDNA copies of AI hemagglutinin (H5) and neuraminidase (N1) genes (both from A/goose/Guangdong/3/96 (H5N1)) (Qiao et al., 2003). This type of vaccine can only be used in one-day-old chickens and not in older birds in which immunity to fowlpox virus will inhibit replication of the vaccine virus and prevent development of effective immunity (Swayne et al., 2000a). The other new vaccine is a traditional inactivated oil emulsion AI vaccine, but unlike current inactivated AI vaccines, the new vaccine virus is not an H5 LP or HPAI field virus. The vaccine virus was produced by reverse genetics using the 6 internal genes from a human influenza vaccine strain (PR8) and the hemagglutinin and neuraminidase genes from A/goose/Guangdong/3/96 (H5N1) AI virus. The use of PR8 internal genes imparts the characteristic of growth to high virus content in embryonating chicken eggs used in the manufacturing process and thus produces a high concentration of the protective hemagglutinin protein in the vaccine. Another change in the vaccine virus: the portion of the gene that codes the hemagglutinin proteolytic cleavage site has been changed from a sequence of an HP to an LPAI virus, thus, the vaccine virus is a LPAI virus and can be manufactured at a lower level of biosafety. Both vaccines require handling and injection of individual birds. Data published or presented at scientific meetings indicate that these new vaccines are as efficacious as the existing licensed vaccines, but no data have been presented to demonstrate they provide superior protection."


National and international control policy



The virulent form of avian influenza (fowl plague) is included in the OIE (World Organisation for Animal Health) list of notifiable diseases, which means that outbreaks are notifiable to the OIE and restrictions to movement of birds and poultry products are enforced.

Many countries have regulations aimed at preventing avian influenza, which involve trade embargoes on importation of birds and avian products from countries not declared highly pathogenic avian influenza (HPAI) -free. HPAI virus is considered an exotic pathogen in most European countries, the USA and Australia. Exotic outbreaks of HPAI are eradicated by implementing an intensive programme comprising rapid diagnosis, slaughter and disposal of affected flocks, quarantine of the affected area and concurrent surveillance with disposal of flocks with positive antibody titres to avian influenza. Restrictions on movement of flocks and poultry products from infected areas are imposed.


Farm-level control



It is important to have adequate biosecurity to prevent AI introduction from other poultry flocks. Preventing direct contact with wild and migratory birds that may carry the virus, and protecting domestic poultry from contact with the faeces of wild birds are also ways of preventing avian influenza. Implementation of strict biosecurity measures at the local farm level can limit dissemination of avian influenza virus. However, the prevention of avian influenza in developing countries is extremely difficult because feed is delivered in bags, and because small-scale producers distribute eggs and live broilers through dealers to regional markets.


Cleaning and disinfection


The virus remains viable for a long time in tissues and faeces. Effective disinfection procedures involve complete removal of all organic material because influenza viruses are well protected from inactivation in such material. Disinfectants of many types (glutaraldehyde plus formaldehyde; glutaraldehyde and quaternary ammonium salts; chlorocresols; oxidising disinfectants; iodophores; quaternary ammonium salts) are effective against influenza virus. However, professional advice should be sought as these differ with respect to efficacy in the presence of organic matter and in relation to low temperatures.

References

Top of page

African Union-Interafrican Bureau for Animal Resources, 2011. Panafrican Animal Health Yearbook 2011. Pan African Animal Health Yearbook, 2011:xiii + 90 pp. http://www.au-ibar.org/index.php?option=com_flexicontent&view=items&cid=71&id=109&Itemid=56&lang=en

Alexander DJ, 1987. Avian influenza - historical aspects. In: Proceedings of Second International Symposium on Avian Influenza, 1986. University of Wisconsin, Madison, USA, 4-13.

Alexander DJ, 1993. Orthomyxovirus infection. Virus infections of birds., 287-316; 122 ref.

Banks J; Speidel E; Alexander DJ, 1998. Characterisation of an avian influenza A virus isolated from a human - is an intermediate host necessary for the emergence of pandemic influenza viruses?. Archives of Virology, 143(4):781-787; 23 ref.

Brown IH, 2006. Advances in molecular diagnostics for avian influenza. Developmental Biology (Basel), 124:93-97.

Capua I; Mutinelli F, 2001. Mortality in Muscovy ducks (Cairina moschata) and domestic geese (Anser anser var. domestica) associated with natural infection with a highly pathogenic avian influenza virus of H7N1 subtype. Avian Pathology, 30(2):179-183; 13 ref.

Capua I; Terregino C; Cattoli G; Mutinelli F; Rodriguez JF, 2003. Development of a DIVA (Differentiating Infected from Vaccinated Animals) strategy using a vaccine containing a heterologous neuraminidase for the control of avian influenza. Avian Pathology, 32(1):47-55.

Capua I; Terregino C; Cattoli G; Toffan A, 2004. Increased resistance of vaccinated turkeys to experimental infection with an H7N3 low-pathogenicity avian influenza virus. Avian Pathology, 33(2):158-163.

Cattoli G; Capua I, 2006. Molecular diagnosis of avian influenza during an outbreak. Developmental Biology (Basel), 124:99-105.

Cattoli G; Monne I; Fusaro A; Joannis TM; Lombin LH; Aly MM; Arafa AS; Sturm-Ramirez KM; Couacy-Hymann E; Awuni JA; Batawui KB; Awoume KA; Aplogan GL; Sow A; Ngangnou AC; Hamza IMEN; Gamatié D; Dauphin G; Domenech JM; Capua I, 2009. Highly pathogenic avian influenza virus subtype H5N1 in Africa: a comprehensive phylogenetic analysis and molecular characterization of isolates. PLos One, No.March:e4842. http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0004842

Clercq K de; Goris N, 2004. Extending the foot-and-mouth disease module to the control of other diseases. In: Control of infectious animal diseases by vaccination, Basel, Switzerland: S Karger AG, 333-340.

Cross GM, 1987. Status of avian influenza in poultry in Australia. In: Proceedings of Second International Symposium Avian Influenza, 1986. University of Wisconsin, Madison, USA, 96-103.

Daulbaeva KD; Shaikhinova TB; Yamnikova SS; Sayatov MKh; Abisheva FZh; Laptev SV; Grebenkin VA; Ter-Pogosyan VE, 1990. Characteristics of type A influenza viruses isolated from domestic ducks in Kazakhstan. Izvestiya Akademii Nauk Kazakhskoi SSR. Seriya Biologicheskaya, No.1:60-63; 3 ref.

Ducatez MF; Olinger CM; Owoade AA; Landtsheer Sde; Ammerlaan W; Niesters HG; Osterhaus AD; Fouchier RA; Muller CP, 2006. Avian flu: multiple introductions of H5N1 in Nigeria. Nature, 442:37.

Elkin VS; Podchernyaeva RYa; Sidorenko EV; Sadykhova FE; Ignatenko TA; Smogorzhevskii LA; Novruzov RM; L'vov DK, 1988. Detecting antibodies, by using recombinant strains of influenzavirus, in serum from various species of birds captured in the Ukrainian and Azerbaidzhan Republics of the USSR. Voprosy Virusologii, 33(6):674-676; 8 ref.

Ellis TM; Leung CYHC; Chow MKW; Bissett LA; Wong W; Guan Yi; Peiris JSM, 2004. Vaccination of chickens against H5N1 avian influenza in the face of an outbreak interrupts virus transmission. Avian Pathology, 33(4):405-412.

Hoffrogge W; Linn KP; Arnold JJ; Bachmeier J; Behr KP; Löhren U; Pöppel M; Reetz G; Voss M, 2003. Lessons and consequences of the Highly Pathogenic Avian Influenza outbreak in the Netherlands, Belgium and Germany for the German poultry association. (Erfahrungen und Konsequenzen aus dem HPAI-influenza-Geschehen in den Niederlanden, Belgien und Deutschland.) Archiv für Geflügelkunde, 67(6):264-283.

Jefferson T; Demicheli V; Rivetti D; Jones M; Di Petrantonj C; Rivetti A, 2006. Antivirals for influenza in healthy adults: systematic review. Lancet, 367(9507):303-313.

Koh-Yeo SC; Ng FK; Ng SK; Soh ML, 1996. Viruses isolated from captive birds imported in 1992-1995. Singapore Journal of Primary Industries, 24:91-93; 2 ref.

Landman WJ; Schrier CC, 2004. Avian influenza: eradication from commercial poultry is still not in sight. Tijdschr Diergeneeskd, 129(23):782-96.

Larkin M, 2005. Avian:flu: sites seek to respond and reassure. Lancet Infectious Diseases, 2005 March 5(3): 129-131.

Lasley FA, 1987. Economics of avianinfluenza: Control vs noncontrol. In: Proceedings of Second International Symposium Avian Influenza, 1986. University of Wisconsin, Madison, USA, 390-399.

Lee ChangWon; Song ChangSeon; Lee YounJeong; Mo InPil; Garcia M; Suarez DL; Kim SunJoong, 2000. Sequence analysis of the hemagglutinin gene of H9N2 Korean avian influenza viruses and assessment of the pathogenic potential of isolate MS96. Avian Diseases, 44(3):527-535; 27 ref.

Lee CW; Senne DA; Suarez DL, 2004. Effect of vaccine use in the evolution of Mexican lineage H5N2 avian influenza virus. J. Virol., 78(15):8372-8381.

Lee CW; Senne DA; Suarez DL, 2004. Generation of reassortant influenza vaccines by reverse genetics that allows utilization of a DIVA (Differentiating Infected from. Vaccine, 22(23-24):3175-3181.

Ley EC; Morishita TY; Harr BS; Mohan R; Brisker T, 2000. Serologic survey of slaughter-age ostriches (Struthio camelus) for antibodies to selected avian pathogens. Avian Diseases, 44(4):989-992; 16 ref.

Li KS; Guan Y; Wang J; Smith GJ; Xu KM; Duan L; Rahardjo AP; Puthavathana P; Buranathai C; Nguyen TD; Estoepangestie AT; Chaisingh A; Auewarakul P; Long HT; Hanh NT; Webby RJ; Poon LL; Chen H; Shortridge KF; Yuen KY; Webster RG; Peiris JS, 2004. Genesis of a highly pathogenic and potentially pandemic H5N1 influenza virus in eastern Asia. Nature, 430(6996):209-13.

Liu M; Wood JM; Ellis T; Krauss S; Seiler P; Johnson C; Hoffmann E; Humberd J; Hulse D; Zhang Y; Webster RG; Perez DR, 2003. Preparation of a standardized, efficacious agricultural H5N3 vaccine by reverse genetics. Virology, 314(2):580-590.

Luini M; Mortarino P; Cervio G, 1988. Isolation of influenza viruses from ducks imported [from France] for slaughter. Clinica Veterinaria, 111(1-2):83-87; 12 ref.

Murphy FA; Gibbs EPJ; Horzinek MC and Studdert MJ, 1999. Orthomyxoviridae. In: Veterinary Virology. San Diego, USA: Academic Press, 459-468.

Naem K; Siddique N, 2006. Use of strategic vaccination for the control of avian influenza in Pakistan. Developmental Biology, 124:145-150.

Office International des Epizooties, 2003. Avian influenza in Belgium additional information. Disease information, 16(31).

OIE Handistatus, 2002. World Animal Health Publication and Handistatus II (dataset for 2001). Paris, France: Office International des Epizooties.

OIE Handistatus, 2003. World Animal Health Publication and Handistatus II (dataset for 2002). Paris, France: Office International des Epizooties.

OIE Handistatus, 2004. World Animal Health Publication and Handistatus II (data set for 2003). Paris, France: Office International des Epizooties.

OIE Handistatus, 2005. World Animal Health Publication and Handistatus II (data set for 2004). Paris, France: Office International des Epizooties.

OIE, 2004. Highly pathogenic avian influenza in Japan. Disease Information, 17(8): 4.

OIE, 2004. World animal health situation. Paris, France: Office International des Epizooties. Online. www.oie.int. Accessed on 24 February 2004.

OIE, 2005. Highly pathogenic avian influenza in Cambodia. Follow-up report No. 4. Disease Information, 18(13).

OIE, 2005. Highly pathogenic avian influenza in Hong Kong, special administrative region of the People’s Republic of China in a wild bird (additional information). Disease Information, 18(8).

OIE, 2005. Highly pathogenic avian influenza in Thailand. Follow-up report No. 49. Disease Information, 18(11).

OIE, 2005. Highly pathogenic avian influenza in Vietnam. Follow-up report No. 13. Disease Information, 18(9).

OIE, 2009. World Animal Health Information Database - Version: 1.4. World Animal Health Information Database. Paris, France: World Organisation for Animal Health. http://www.oie.int

OIE, 2012. World Animal Health Information Database. Version 2. World Animal Health Information Database. Paris, France: World Organisation for Animal Health. http://www.oie.int/wahis_2/public/wahid.php/Wahidhome/Home

Okazaki K; Takada A; Ito T; Imai M; Takakuwa H; Hatta M; Ozaki H; Tanizaki T; Nagano T; Ninomiya A; Demenev VA; Tyaptirganov MM; Karatayeva TD; Yamnikova SS; Lvov DK; Kida H, 2000. Precursor genes of future pandemic influenza viruses are perpetuated in ducks nesting in Siberia. Archives of Virology, 145(5):885-893; 23 ref.

Perdue ML; Suarez DL; Swayne DE, 2000. Avian influenza in the 1990s. Poultry and Avian Biology Reviews, 11(1):1-20; 4 pp. of ref.

Pfitzer S; Verwoerd DJ; Gerdes GH; Labuschagne AE; Erasmus A; Manvell RJ; Grund C, 2000. Newcastle disease and avian influenza A virus in wild waterfowl in South Africa. Avian Diseases, 44(3):655-660; 40 ref.

ProMED-mail, 2004. South Africa: new avian flu scare. ProMED-mail 2004; 22 September 2004. 20040922.2617. <. Accessed 4 April 2005. target="_blank">http://www.promedmail.org>. Accessed 4 April 2005.

ProMED-mail, 2005. Bird flu kills quail in Indonesia’s Central Java . ProMED-mail 2005; 28 March: 20050328.0901 <. Accessed 4 April 2005. target="_blank">http://www.promedmail.org>. Accessed 4 April 2005.

ProMED-mail, 2005. Influenza found in turkey flock in Sampson County, North Carolina. ProMED-mail 2005; 8 Feb: 20050208.0432. <. Accessed 4 April 2005. target="_blank">http://www.promedmail.org>. Accessed 4 April 2005.

Qiao CL; Yu KZ; Jiang YP; Jia YQ; Tian GB; Liu M; Deng GH; Wang XR; Meng QW; Tang XY, 2003. Protection of chickens against highly lethal H5N1 and H7N1 avian influenza viruses with a recombinant fowlpox virus co-expressing H5 haemagglutinin and N1 neuraminidase genes. Avian Pathol., 32(1):25-32.

Resende JSde; Jorge MA; Oliveira RLde; Resende M, 1990. Influenza A antibodies in broilers in Brazil after American outbreak of 1983-1984. Arquivo Brasileiro de Medicina Veterinária e Zootecnia, 42(5):453-454; 6 ref.

Robles CG, 1995. Influenza as zoonosis: an overview. Philippine Journal of Science, 124(3):233-243; 52 ref.

Röhm C, 1996. The haemagglutinin genes of virulent avian influenzaviruses and demonstration of a new subtype of influenzavirus type A in birds. Charakterisierung der Hämagglutinin-Gene virulenter aviärer H7-Influenzaviren und Nachweis eines neuen Influenza-A-Subtyps in Vögeln., 161 pp.; 20 pp. of ref.

Sharp GB; Kawaoka Y; Jones DJ; Bean WJ; Pryor SP; Hinshaw V; Webster RG, 1997. Coinfection of wild ducks by influenza A viruses: distribution patterns and biological significance. Journal of Virology, 71(8):6128-6135; 43 ref.

Stallknecht DE, 1986. Ecology and epidemiology of avian influenza viruses in wild bird populations: waterfowl, shorebirds, pelicans, cormorants, etc. In: Swayne DE, Slemons RL eds. Proceedings of the Fifth International Symposium on Avian Influenza, 1986. Richmond, USA: US Animal Health Association, 61-69.

Stallknecht DE; Shane SM, 1998. Host range of avian influenza virus in free-living birds. Veterinary Research Communications, 12:125-141.

Suarez DL; Garcia M; Latimer J; Senne D; Perdue M, 1999. Phylogenetic analysis of H7 avian influenza viruses isolated from the live bird markets of the Northeast United States. Journal of Virology, 73(5):3567-3573; 31 ref.

Suarez DL; Lee CW; Swayne DE, 2006. Avian influenza vaccination in North America: strategies and difficulties. Developmental Biology (Basel), 124:117-124.

Suarez DL; Schultz CS, 2000. Immunology of avian influenza virus: a review. Dev. Comp. Immunol., 24(2-3):269-283.

Swayne DE, 2000. Understanding the ecology and epidemiology of avian influenza viruses: implications for zoonotic potential. In: Brown C, Bolin C, eds. Emerging Infectious Diseases of Animals, 2000. Washington DC, USA: ASM Press, 101-130.

Swayne DE, 2003. Vaccines for list A poultry diseases: emphasis on avian influenza. Developments in Biologics (Basel), 114:201-212.

Swayne DE, 2004. Application of new vaccine technologies for the control of transboundary diseases. Developments in Biologics (Basel), 119:219-228.

Swayne DE; Beck JR; Kinney N, 2000. Failure of a recombinant fowl poxvirus vaccine containing an avian influenza hemagglutinin gene to provide consistent protection against influenza in chickens preimmunized with a fowl pox vaccine. Avian Diseases, 44(1):132-137; 18 ref.

Swayne DE; Beck JR; Mickle TR, 1997. Efficacy of recombinant fowl poxvirus vaccine in protecting chickens against a highly pathogenic Mexican-origin H5N2 avian influenza virus. Avian Diseases, 41(4):910-922; 37 ref.

Swayne DE; Halvorson DA, 2003. Influenza. In Disease of Poultry, Saif YM, Barnes HJ, Glisson JR, Fadly AM, McDougald LR, Swayne DE (Eds). Iowa State Press, Ames, Iowa, 135-160.

Swayne DE; King DJ, 2003. Zoonosis update: avian influenza and Newcastle disease. Journal of the American Veterinary Medical Association, 222(11):1534-1540.

Swayne DE; Lee CW; Spackman E, 2006. Inactivated North American and European H5N2 avian influenza virus vaccines protect chickens from Asian H5N1 high pathogenicity avian influenza virus. Avian Pathology, 35(2):141-146.

Swayne DE; Perdue ML; Beck JR; Garcia M; Suarez DL, 2000. Vaccines protect chickens against H5 highly pathogenic avian influenza in the face of genetic changes in field viruses over multiple years. Veterinary Microbiology, 74(1/2):165-172; 15 ref.

Swayne DE; Senne DA; Beard CW, 1998. Avian influenza. In: Swane DE, Glisson JR, Jackwood MW, Pearson JE, Reed WM, eds. A Laboratory Manual for the Isolation and Identification of Avian Pathogens. American Association of Avian Pathologists, Kennett Square, Pennsylvania, 150-155.

Swayne DE; Suarez DL, 2000. Highly pathogenic avian influenza. Revue Scientifique et Technique - Office International des Épizooties, 19(2):463-482; 131 ref.

Tanyi J; Fenyvesi A; Földi J, 1988. Turkey influenza in Hungary. Tagung der Fachgruppe "Geflugelkrankheiten" in Verbindung mit der WVPA und der Abt. Geflugelkrankheiten der I. Medizinischen Klinik, Veterinarmedizinischen Universitat Wien, 18.-20. Juli 1988., 111-114.

Tumpey TM; Alvarez R; Swayne DE; Suarez DL, 2005. A diagnostic aid for differentiating infected from vaccinated poultry based on antibodies to the nonstructural (NS1) protein of influenza A virus. J. Clin. Microbiol., 43(2): 676-683.

Tumpey TM; Suarez DL; Perkins LEL et al., 2002. Characterization of a highly pathogenic H5N1 avian influenza A virus isolated from duck meat. Journal of Virology, 76: 6344-6355.

Vasfi Marandi M; Bozorgmehri Fard MH; Hassani Tabatabai SAM; Kerdabadi M; Charkhkar S; Farahmandi M, 2000. Serological monitoring of haemagglutination inhibition antibodies in a multi aged layer farm following avian influenza outbreak due to H9N2 sub-serotype in 1998 in Iran. Journal of the Faculty of Veterinary Medicine, University of Tehran, 55(3):73-81; 30 ref.

Wang HengAn; Wang ShiQiang; Yan YaXian; Wu ZuLi; Hua XiuGuo, 1999. Isolation and characterization of duck derived type A influenza virus. Jiangsu Agricultural Research, 20(4):57-60; 14 ref.

WHO, 1980. Memorandum: A revision of the system of nomenclature for influenza virus. Bull. WHO, 58:585-591.

Wood GW; Banks J; Brown IH; Strong I; Alexander DJ, 1997. The nucleotide sequence of the HA1 of the haemagglutinin of an H1 avian influenza virus isolate from turkeys in Germany provides additional evidence suggesting recent transmission from pigs. Avian Pathology, 26(2):347-355; 22 ref.

Wood GW; Banks J; McCauley JW; Alexander DJ, 1994. Deduced amino acid sequences of the haemagglutinin of H5N1 avian influenza virus isolates from an outbreak in turkeys in Norfolk, England. Archives of Virology, 134(1/2):185-194; 20 ref.

Woolcock PR; Shivaprasad HL; Rosa Mde, 2000. Isolation of avian influenza virus (H10N7) from an emu (Dromaius novaehollandiae) with conjunctivitis and respiratory disease. Avian Diseases, 44(3):737-744; 25 ref.

Yamntskova SS; Kovtun TO; Dmitriev GA; Shemyakin IG; Semenova NP; L'vov DK; Chambers T; Webster R, 1989. Antigenic variability of avian influenzavirus A/H13, isolated in the USSR. Voprosy Virusologii, 34(5):568-572; 13 ref.

Zanella A, 2000. Avian influenza: about some outbreaks of disease in light layers. Selezione Veterinaria, No. 8/9:639-644; [de=conferences]; 21 ref.

Zhao S; Jin M; Li H; Tan Y; Wang; G; Zhang R; Chen H, 2006. Detection of antibodies to the nonstructural protein (NS1) of avian influenza viruses allows distinction between vaccinated and infected chickens. Avian Diseases, 49(4):488-493.

Zhou NanNan; Shortridge KF; Claas ECJ; Krauss SL; Webster RG, 1999. Rapid evolution of H5N1 influenza viruses in chickens in Hong Kong. Journal of Virology, 73(4):3366-3374; 42 ref.

Links to Websites

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WebsiteURLComment
Avian influenza - Center for Infectious Disease Research and Policy of the University of Minnesotahttp://www.cidrap.umn.edu/cidrap/content/influenza/avianflu/index.htmlWebsite with good overview information on avian influenza, and the latest news on the disease, including advice for travellers to infected regions).
Avian influenza - Centers for Disease Control (USA)http://www.cdc.gov/flu/avian/Fact sheets containing basic information on avain influenza.
Avian influenza - European Unionhttp://ec.europa.eu/dgs/health_consumer/dyna/influenza/index.cfmWeb site with general information and links to European legislation and regulation regarding avian influenza.
Avian influenza - Health Protection Agency, UKhttp://www.hpa.org.uk/infections/topics_az/influenza/avian/default.htmInformation on the threat of avian influenza to human health and the UK Government contingency plans in the event of a human influenza epidemic.
Avian influenza - National Agricultural Library (USA)http://www.nal.usda.gov/awic/aflu/Avian%20Influenza.htmInformation recource on avian influenza created by the National Agricultural Library (USA).
Avian influenza - Naturehttp://www.nature.com/nature/focus/avianflu/index.htmlCollection of information from Nature (the international weekly science journal) on avian influenza including articles on the 1918 pandemic and the causative strain of the virus.
Avian influenza - OIE portalhttp://www.oie.int/en/animal-health-in-the-world/web-portal-on-avian-influenza/
Avian influenza - World Health Organizationhttp://www.who.int/csr/disease/avian_influenza/en/Web page providing information on avian influenza transmitted to humans.
Canadian Food Inspection Agency - Avian Influenzahttp://www.inspection.gc.ca/animals/terrestrial-animals/diseases/reportable/ai/eng/1323990856863/1323991018946General information, including fact sheets, prevention and control measures, information on disease incidents in Canada.
CFSPH: Animal Disease Informationhttp://www.cfsph.iastate.edu/DiseaseInfo/index.php"Animal Disease Information" provides links to various information sources, including fact sheets and images, on over 150 animal diseases of international significance.
FAO: Understanding avian influenzahttp://www.fao.org/avianflu/documents/key_ai/key_book_preface.htmbook by Les Sims and Clare Narrod
OIE Manual of Diagnostic Tests and Vaccines for Terrestrial Animalshttp://www.oie.int/en/international-standard-setting/terrestrial-manual/access-online/The Manual of Diagnostic Tests and Vaccines for Terrestrial Animals (Terrestrial Manual) aims to facilitate international trade in animals and animal products and to contribute to the improvement of animal health services world-wide. The principal target readership is laboratories carrying out veterinary diagnostic tests and surveillance, plus vaccine manufacturers and regulatory authorities in Member Countries. The objective is to provide internationally agreed diagnostic laboratory methods and requirements for the production and control of vaccines and other biological products.
OIE Technical Disease Cardshttp://www.oie.int/animal-health-in-the-world/technical-disease-cards/An updated compilation of 33 technical disease cards, containing summary information, mainly directed to a specialised scientific audience, including 32 OIE-listed priority diseases. USDA-APHIS (USA) are also credited with contributing to the maintenance of the cards.
Promed Listservehttp://www.promedmail.orgProvides a rapid, moderated bulletin board for new outbreaks of disease. New outbreaks of avian influenza are listed here.
USAHA: Foreign Animal Diseases. Seventh Editionhttp://www.aphis.usda.gov/emergency_response/downloads/nahems/fad.pdfCopyright © 2008 by United States Animal Health Association ALL RIGHTS RESERVED. Library of Congress Catalogue Number 2008900990 ISBN 978-0-9659583-4-9. Publication with 472pp. aimed at providing information for practitioners within the USA to prevent and or mitigate the incursion of foreign animal diseases into that country. Contains general chapters on surveillance, diagnosis, etc. as well as 48 chapters covering individual diseases, mostly those notifiable to the OIE.

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