Avian influenza viruses and avian paramyxoviruses in wintering and breeding waterfowl populations in North Carolina, USA.

Although wild ducks are recognized reservoirs for avian influenza viruses (AIVs) and avian paramyxoviruses (APMVs), information related to the prevalence of these viruses in breeding and migratory duck populations on North American wintering grounds is limited. Wintering (n=2,889) and resident breeding (n=524) ducks were sampled in North Carolina during winter 2004-2006 and summer 2005-2006, respectively. Overall prevalence of AIV was 0.

Evidence for a new avian paramyxovirus serotype 10 detected in rockhopper penguins from the Falkland Islands.

The biological, serological, and genomic characterization of a paramyxovirus recently isolated from rockhopper penguins (Eudyptes chrysocome) suggested that this virus represented a new avian paramyxovirus (APMV) group, APMV10. This penguin virus resembled other APMVs by electron microscopy; however, its viral hemagglutination (HA) activity was not inhibited by antisera against any of the nine defined APMV serotypes. In addition, antiserum generated against this penguin virus did not inhibit the HA of representative viruses of the other APMV serotypes.

Avian paramyxoviruses in shorebirds and gulls.

There are nine serotypes of avian paramyxovirus (APMV), including APMV-1, or Newcastle disease virus. Although free-flying ducks and geese have been extensively monitored for APMV, limited information is available for species in the order Charadriiformes. From 2000 to 2005 we tested cloacal swabs from 9,128 shorebirds and gulls (33 species, five families) captured in 10 states within the USA and in three countries in the Caribbean and South America.

Antiviral susceptibility of avian and swine influenza virus of the N1 neuraminidase subtype.

Influenza viruses of the N1 neuraminidase (NA) subtype affecting both animals and humans caused the 2009 pandemic. Anti-influenza virus NA inhibitors are crucial early in a pandemic, when specific influenza vaccines are unavailable. Thus, it is urgent to confirm the antiviral susceptibility of the avian viruses, a potential source of a pandemic virus.

Validation of a real-time reverse transcriptase-PCR assay for the detection of H7 avian influenza virus.

This report describes the validation of an avian influenza virus (AIV) H7 subtype-specific real-time reverse transcriptase-PCR (rRT-PCR) assay developed at the Southeast Poultry Research Laboratory (SEPRL) for the detection of H7 AI in North and South American wild aquatic birds and poultry. The validation was a collaborative effort by the SEPRL and the National Veterinary Services Laboratories. The 2008 H7 rRT-PCR assay detects 10(1) 50% embryo infectious doses per reaction, or 10(3)-10(4) copies of transcribed H7 RNA.

Avian influenza in North and South America, the Caribbean, and Australia, 2006-2008.

Between 2006 and 2008, only one outbreak of highly pathogenic notifiable avian influenza (AI) was reported from the Americas, the Caribbean, and Australia. The outbreak, caused by H7N3, occurred in September 2007 in a multiage broiler breeder facility (approximately 49,000 birds) near Regina Beach in southern Saskatchewan, Canada. The disease was confined to a single farm; the farm was depopulated.

Viral and bacterial serology of six free-ranging bearded seals Erignathus barbatus.

Serum or heparinized plasma samples were obtained from 3 male (2 adult and 1 weaned calf) and 3 adult female free-ranging bearded seals Erignathus barbatus in May of 1994, 1995, or 1996. Blood samples were obtained from animals taken in subsistence hunts near St. Lawrence Island, Alaska and screened for antibodies to a suite of bacteria and viruses potentially pathogenic for pinnipeds and/or humans.

The evolutionary genetics and emergence of avian influenza viruses in wild birds.

We surveyed the genetic diversity among avian influenza virus (AIV) in wild birds, comprising 167 complete viral genomes from 14 bird species sampled in four locations across the United States. These isolates represented 29 type A influenza virus hemagglutinin (HA) and neuraminidase (NA) subtype combinations, with up to 26% of isolates showing evidence of mixed subtype infection. Through a phylogenetic analysis of the largest data set of AIV genomes compiled to date, we were able to document a remarkably high rate of genome reassortment, with no clear pattern of gene segment association and occasional inter-hemisphere gene segment migration and reassortment.

Evaluation of routine depopulation, cleaning, and disinfection procedures in the live bird markets, New York.

During the past years surveillance for avian influenza has been conducted in the live bird markets (LBMs) in New York as well as other states along the east coast. Repeated attempts to eradicate H5 and H7 influenza from the New York markets have focused efforts on the LBMs themselves. Despite repeated mandatory market closures accompanied by cleaning and disinfecting (C/D) procedures, avian influenza virus continued to be isolated.

Phylogenetic diversity among low-virulence newcastle disease viruses from waterfowl and shorebirds and comparison of genotype distributions to those of poultry-origin isolates.

Low-virulence Newcastle disease viruses (loNDV) are frequently recovered from wild bird species, but little is known about their distribution, genetic diversity, or potential to cause disease in poultry. NDV isolates recovered from cloacal samples of apparently healthy waterfowl and shorebirds (WS) in the United States during 1986 to 2005 were examined for genomic diversity and their potential for virulence (n = 249). In addition 19 loNDV isolates from U.

Characterization of low-pathogenicity H5N1 avian influenza viruses from North America.

Wild-bird surveillance in North America for avian influenza (AI) viruses with a goal of early identification of the Asian H5N1 highly pathogenic AI virus has identified at least six low-pathogenicity H5N1 AI viruses between 2004 and 2006. The hemagglutinin (HA) and neuraminidase (NA) genes from all 6 H5N1 viruses and an additional 38 North American wild-bird-origin H5 subtype and 28 N1 subtype viruses were sequenced and compared with sequences available in GenBank by phylogenetic analysis. Both HA and NA were phylogenetically distinct from those for viruses from outside of North America and from those for viruses recovered from mammals.

Avian influenza in North and South America, 2002-2005.

Between 2002 and 2005, three outbreaks of highly pathogenic avian influenza (HPAI) occurred in the Americas: one outbreak in Chile (H7N3) in 2002, one outbreak in the United States (H5N2) in 2004, and one outbreak in Canada (H7N3) in 2004. The outbreak in Chile was limited to a large broiler breeder operation and a nearby turkey flock and represented the first outbreak of HPAI in that country. The outbreak of HPAI in the United States occurred in Texas and was limited to one premise where chickens were raised for sale in nearby live-bird markets.

Development of an internal positive control for rapid diagnosis of avian influenza virus infections by real-time reverse transcription-PCR with lyophilized reagents.

We developed an internal positive control (IPC) RNA to help ensure the accuracy of the detection of avian influenza virus (AIV) RNA by reverse transcription (RT)-PCR and real-time RT-PCR (RRT-PCR). The IPC was designed to have the same binding sites for the forward and reverse primers of the AIV matrix gene as the target amplicon, but it had a unique internal sequence used for the probe site. The amplification of the viral RNA and the IPC by RRT-PCR were monitored with two different fluorescent probes in a multiplex format, one specific for the AIV matrix gene and the other for the IPC.

Pathogenic potential of North American H7N2 avian influenza virus: a mutagenesis study using reverse genetics.

An H7N2 subtype avian influenza virus (AIV) first appeared in the live bird marketing system (LBMS) in the Northeastern United States in 1994. Since then this lineage of virus has become the predominant subtype of AIV isolated from the LBMS and has been linked to several costly commercial poultry outbreaks. Concern for this low pathogenicity isolate mutating to the highly pathogenic form has remained high because of the increasing number of basic amino acids at the hemagglutinin (HA) cleavage site, which is known to be associated with increased pathogenicity of AIV.

Development and application of reference antisera against 15 hemagglutinin subtypes of influenza virus by DNA vaccination of chickens.

Reference antisera were produced against 15 influenza hemagglutinin (HA) subtypes using DNA vaccination to produce a high-quality polyclonal serum to the HA protein without antibodies to other influenza viral proteins. The HA gene from each of 15 different HA subtypes of influenza virus was cloned into a eukaryotic expression vector and injected intramuscularly, together with a cationic lipid, into 3- to 4-week-old specific-pathogen-free chickens. Birds were boostered twice at 4-week intervals after the initial injection, and in general, antibody titers increased after each boost.

Avian influenza viruses and paramyxoviruses in wintering and resident ducks in Texas.

Cloacal swabs were collected from teal (Anas crecca, Anas cyanoptera, Anas discors), mottled duck (Anas fulvigula) and northern pintail (Anas acuta) in Brazoria County, Texas, USA, during February 2001, mottled ducks during August 2001, and blue-winged teal (A. discors) during February 2002. Prevalence of avian influenza virus (AIV) infections during each sampling period were 11, 0, and 15%, respectively.

H5N2 avian influenza outbreak in Texas in 2004: the first highly pathogenic strain in the United States in 20 years?

In early 2004, an H5N2 avian influenza virus (AIV) that met the molecular criteria for classification as a highly pathogenic AIV was isolated from chickens in the state of Texas in the United States. However, clinical manifestations in the affected flock were consistent with avian influenza caused by a low-pathogenicity AIV and the representative virus (A/chicken/Texas/298313/04 [TX/04]) was not virulent for experimentally inoculated chickens. The hemagglutinin (HA) gene of the TX/04 isolate was similar in sequence to A/chicken/Texas/167280-4/02 (TX/02), a low-pathogenicity AIV isolate recovered from chickens in Texas in 2002.

Evaluation of risk factors for the spread of low pathogenicity H7N2 avian influenza virus among commercial poultry farms.

Objective: To identify risk factors associated with the spread of low pathogenicity H7N2 avian influenza (AI) virus among commercial poultry farms in western Virginia during an outbreak in 2002.

Design: Case-control study.

Procedure: Questionnaires were used to collect information about farm characteristics, biosecurity measures, and husbandry practices on 151 infected premises (128 turkey and 23 chicken farms) and 199 noninfected premises (167 turkey and 32 chicken farms).

Genomic sequences of low-virulence avian paramyxovirus-1 (Newcastle disease virus) isolates obtained from live-bird markets in North America not related to commonly utilized commercial vaccine strains.

Avian paramyxovirus 1 (APMV-1), also referred to as Newcastle disease virus (NDV), variants of low virulence were isolated from chickens, ducks and other unidentified species found in live-bird markets of the northeastern United States. These isolates were characterized as APMV-1 by the hemagglutination-inhibition (HI) assay utilizing NDV-specific polyclonal antisera. However, the isolates failed to react with a monoclonal antibody that has specificity for a wide variety of APMV-1 isolates.

Generation of reassortant influenza vaccines by reverse genetics that allows utilization of a DIVA (Differentiating Infected from Vaccinated Animals) strategy for the control of avian influenza.

Vaccination of poultry with inactivated influenza vaccine can be an effective tool in the control of avian influenza (AI). One major concern of using inactivated vaccine is vaccine-induced antibody interference with serologic surveillance and epidemiology. In the United States, low pathogenicity H5 and H7 subtype AI viruses have caused serious economic losses in the poultry industry.

Effect of vaccine use in the evolution of Mexican lineage H5N2 avian influenza virus.

An outbreak of avian influenza (AI) caused by a low-pathogenic H5N2 type A influenza virus began in Mexico in 1993 and several highly pathogenic strains of the virus emerged in 1994-1995. The highly pathogenic virus has not been reported since 1996, but the low-pathogenic virus remains endemic in Mexico and has spread to two adjacent countries, Guatemala and El Salvador. Measures implemented to control the outbreak and eradicate the virus in Mexico have included a widespread vaccination program in effect since 1995.

Characterization of recent H5 subtype avian influenza viruses from US poultry.

In the US, the isolation of H5 subtype avian influenza (AI) viruses has been uncommon in commercial chickens and turkeys, although sporadic isolations have been made from the live bird markets or its supply chain since 1986. In 2002, two different outbreaks of H5 AI occurred in commercial chicken or turkey operations. The first occurred in Texas and was identified as a H5N3 subtype AI virus.

Recombination resulting in virulence shift in avian influenza outbreak, Chile.

Influenza A viruses occur worldwide in wild birds and are occasionally associated with outbreaks in commercial chickens and turkeys. However, avian influenza viruses have not been isolated from wild birds or poultry in South America. A recent outbreak in chickens of H7N3 low pathogenic avian influenza (LPAI) occurred in Chile.