Highly Pathogenic Avian Influenza Virus (H5N1) Outbreak in Captive Wild Birds and Cats, Cambodia

Desvaux, Stéphanie; Marx, Nick; Ong, Sivuth; Gaidet, Nicolas; Hunt, Matt; Manuguerra, Jean Claude; Sorn, San; Peiris, Malik; Werf, Sylvie van der; Reynes, J.

doi:10.3201/eid1503.071410

Cited by 37 publications

(25 citation statements)

References 11 publications

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“…Infection with the virus has been recorded in a growing number of bird species in open zoos (Ellis et al, 2004), sanctuaries (Desvaux et al, 2009) and other captive populations (Khan et al, 2009). Captive conditions may provide opportunities for HPAI H5N1 to expand its host range due to the artificially high concentration and assemblage of species.…”

Section: Wild Birds As Victimsmentioning

confidence: 99%

Victims and Vectors: Highly Pathogenic Avian Influenza H5N1 and the Ecology of Wild Birds

Takekawa

Prosser

Newman

et al. 2010

Avian Biology Research

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The emergence of highly pathogenic avian influenza (HPAI) viruses has raised concerns about the role of wild birds in the spread and persistence of the disease. In 2005, an outbreak of the highly pathogenic subtype H5N1 killed more than 6,000 wild waterbirds at Qinghai Lake, China. Outbreaks have continued to periodically occur in wild birds at Qinghai Lake and elsewhere in Central China and Mongolia. This region has few poultry but is a major migration and breeding area for waterbirds in the Central Asian Flyway, although relatively little is known about migratory movements of different species and connectivity of their wetland habitats. The scientific debate has focused on the role of waterbirds in the epidemiology, maintenance and spread of HPAI H5N1: to what extent are they victims affected by the disease, or vectors that have a role in disease transmission? In this review, we summarise the current knowledge of wild bird involvement in the ecology of HPAI H5N1. Specifically, we present details on: (1) origin of HPAI H5N1; (2) waterbirds as LPAI reservoirs and evolution into HPAI; (3) the role of waterbirds in virus spread and persistence; (4) key biogeographic regions of outbreak; and (5) applying an ecological research perspective to studying AIVs in wild waterbirds and their ecosystems.

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Section: Wild Birds As Victimsmentioning

confidence: 99%

Victims and Vectors: Highly Pathogenic Avian Influenza H5N1 and the Ecology of Wild Birds

Takekawa

Prosser

Newman

et al. 2010

Avian Biology Research

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“…It was also evident in the isolation of HPAI (H5N1) viruses from apparently healthy Tree Sparrows (Passer montanus) in China in 2003and 2004(Kelly et al, 2008. In addition, large-scale outbreak of HPAI (H5N1) was reported in a zoological institution in Cambodia that affected a variety of species of captive wild birds including eagles and owls (Desvaux et al, 2009). The maiden outbreak of HPAI H5N1 in 2006 in Nigeria was blamed on trade in poultry and migratory wild birds as likely sources of introduction (Brown, 2006;Ducatez et al, 2006).…”

Section: Introductionmentioning

confidence: 98%

Detection of avian influenza antibodies and antigens in poultry and some wild birds in Kogi state, Nigeria

Ameji¹,

Lawal²,

Abdu³

2017

Sokoto J. Vet. Sc.

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The global spread of HPAI (H5N1) between 2005 and 2006 was blamed on movement of migratory wild birds and trade in live poultry across continents from infected regions. A survey was carried out to detect the presence of avian influenza (AI) antibodies in wild birds and AI viruses in poultry and wild birds from Kogi state, Nigeria. Haemagglutination inhibition (HI) test and enzyme link immunosorbent assay (ELISA) were used to detect AI antibodies in some species of apparently healthy wild birds during the survey. Using HI test, the wild birds were negative for AI (H5) antibodies but ELISA detected AI (NP) antibodies in Black Stork (Ciconia nigra) with an overall seroprevalence of 4.5% and mean titre of 24.50±2.400 EU. Cloacal swabs from the same species of wild birds that were tested for antibodies and 710 oropharyngeal swabs from poultry were tested for AI viruses using RT-PCR with primers targeting the AI matrix proteins but were negative for AI viruses. The detection of AI (NP) antibodies in wild birds but failure to detect the viruses showed that the exposure might not be recent. We recommend that poultry should be prevented from contact with wild water birds and a broad based surveillance for AI viruses in poultry and wild birds should be carried out in Kogi state, Nigeria.

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“…Clade 2.2 H5N1 viruses had first been identified in May 2005 in dead bar-headed geese (Anser indicus) at the Qinghai Lake in China (6,31,67) followed by inter-and transcontinental transmission to Mongolia, the Middle East, Africa, and Europe (5,10,44,48,60). These strains induced lethal disease in several mammalian species, including tigers (Pantherus tigris) and leopards (Pantherus pardus) at zoos in Thailand (25,58), domestic cats (Felis catus) in Cambodia, Iraq, Indonesia, and Germany (9,26,61), masked palm civets (Paguma larvata) in Vietnam (42), a dog (Canis familiaris) in Thailand (3,49), and a stone marten (Martes foina) in Germany (26,61).…”

mentioning

confidence: 99%

Reversion of PB2-627E to -627K during Replication of an H5N1 Clade 2.2 Virus in Mammalian Hosts Depends on the Origin of the Nucleoprotein

Bogs

Kalthoff

Veits

et al. 2011

J Virol

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H5N1 highly pathogenic avian influenza viruses (HPAIV) of clade 2.2 spread from Southeast Asia to Europe. Intriguingly, in contrast to all common avian strains specifying glutamic acid at position 627 of the PB2 protein (PB2-627E), they carry a lysine at this position (PB2-627K), which is normally found only in human strains. To analyze the impact of this mutation on the host range of HPAIV H5N1, we altered PB2-627K to PB2-627E in the European isolate A/Swan/Germany/R65/2006 (R65). In contrast to the parental R65, multicycle growth and polymerase activity of the resulting mutant R65-PB2 K627E were considerably impaired in mammalian but not in avian cells. Correspondingly, the 50% lethal dose (LD 50 ) in mice was increased by three orders of magnitude, whereas virulence in chicken remained unchanged, resulting in 100% lethality, as was found for the parental R65. Strikingly, R65-PB2 K627E reverted to PB2-627K after only one passage in mice but did not revert in chickens. To investigate whether additional R65 genes influence reversion, we passaged R65-PB2 K627E reassortants containing genes from A/Hong Kong/156/97 (H5N1) (carrying PB2-627E), in avian and mammalian cells. Reversion to PB2-627K in mammalian cells required the presence of the R65 nucleoprotein (NP). This finding corresponds to results of others that during replication of avian strains in mammalian cells, PB2-627K restores an impaired PB2-NP association. Since this mutation is apparently not detrimental for virus prevalence in birds, it has not been eliminated. However, the prompt reversion to PB2-627K in MDCK cells and mice suggests that the clade 2.2 H5N1 HPAIV may have had a history of intermediate mammalian hosts.

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Highly Pathogenic Avian Influenza Virus (H5N1) Outbreak in Captive Wild Birds and Cats, Cambodia

Cited by 37 publications

References 11 publications

Victims and Vectors: Highly Pathogenic Avian Influenza H5N1 and the Ecology of Wild Birds

Victims and Vectors: Highly Pathogenic Avian Influenza H5N1 and the Ecology of Wild Birds

Detection of avian influenza antibodies and antigens in poultry and some wild birds in Kogi state, Nigeria

Reversion of PB2-627E to -627K during Replication of an H5N1 Clade 2.2 Virus in Mammalian Hosts Depends on the Origin of the Nucleoprotein

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