Animal Influenza E-Book
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- Herausgeber: John Wiley & Sons
- Kategorie: Fachliteratur
- Sprache: Englisch
Animal Influenza, Second Edition is a comprehensive text on animal influenza. Organized by species, coverage includes avian, swine, equine and mammals, with each section including data on influenza viruses, the infection and disease they cause, and strategies used in control.
- Covers the full range of topics within avian, swine, equine and mammalian influenzas in one comprehensive and authoritative text
- Provides a summarization of peer-reviewed and empirical data on influenza viruses, the infection, and diseases they cause
- Discusses strategies used in control of the disease
- Leading experts are drawn together to provide an international and multi-disciplinary perspective
- Fuses latest developments in basic scientific research with practical guidance on management of the disease
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Veröffentlichungsjahr: 2016
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Table of Contents
Title Page
Copyright
Dedication
List of contributors
Foreword
Preface
Section I: Common aspects of animal influenza
Chapter 1: Influenza A virus
Introduction
Etiology
Virus life cycle
Virus genetics
Clinical disease in poultry
Antigenic drift and shift
Conclusions
References
Chapter 2: Diagnostics and surveillance methods
Introduction
Sample types
Sample collection, transport, and storage
Virus detection
Serological methods
Characterization of influenza isolates
Education and training
Conclusion
References
Chapter 3: The economics of animal influenza
Introduction
Benefits and costs of controlling animal influenza
The potential impact of human influenza
The globalized livestock sector
Market shocks
Food and livelihoods insecurity
Impacts of outbreak stamping-out measures
Post-outbreak rehabilitation
Longer-term measures for prevention and control of animal influenza
Conclusions
References
Chapter 4: Trade and food safety aspects for animal influenza viruses
Global production and trade of horses, pigs, poultry, and their products
Risk of the spread of animal influenza A virus through trade
Mitigation of trade risks
Food safety risks?
Conclusions
Acknowledgments
References
Chapter 5: Public health implications of animal influenza viruses
Introduction
Diagnosis of animal-origin influenza A virus infections
Human infections with LPAIVS
Human infections with HPAIVs
Recommended measures for responders to LPAI and HPAI outbreaks
Human infections by influenza A variant viruses
Conclusions
References
Section II: Influenza in animals of the class aves
Chapter 6: The innate and adaptive immune response to avian influenza virus
Overview of immunity
Innate immune responses to avian influenza virus
Immunological basis for vaccination of poultry
Immunology of antigen recognition and processing
References
Chapter 7: Wild bird infections and the ecology of avian influenza viruses
Introduction
Host range
Species susceptibility
Wild bird reservoirs
Spatial and temporal variation in AIV infection
Susceptibility to subsequent infections
Subtype diversity
Genetic diversity
Mechanisms for AIV maintenance and transmission
Viruses shared between poultry and wild birds: an H5N1 HPAI case study
Future directions
References
Chapter 8: The global nature of avian influenza
Introduction
General history
Regulatory aspects
Low-pathogenicity avian influenza in poultry and captive birds
High-pathogenicity avian influenza (1959–2015)
Conclusions
References
Chapter 9: Multi-continental panzootic of H5 highly pathogenic avian influenza (1996–2015)
Introduction
Genetic studies and nomenclature of GS/GD-lineage H5 HPAIVs
The history of the GS/GD-lineage H5 panzootic
Sources of infection and reasons for spread
Pathology of H5 HPAI
Diagnostic aspects
Disease control
Conclusions and the future
Acknowledgments
References
Chapter 10: High-pathogenicity avian influenza outbreaks since 2008, excluding multi-continental panzootic of H5 Goose/Guangdong-lineage viruses
Introduction
Ostrich HPAIV infections in South Africa during 2004–2011
H7N7 high-pathogenicity avian influenza in the UK in 2008
H7N7 high-pathogenicity avian influenza in Spain in 2009
Highly pathogenic avian influenza H7N3 outbreak in Mexico
Highly pathogenic avian influenza H7 in Australia during 2012–2013
H5N2 high-pathogenicity avian influenza in Chinese Taipei in 2012
H7N7 High-pathogenicity avian influenza in Italy in 2013
H7N7 high-pathogenicity avian influenza in the UK in 2015
H7N7 high-pathogenicity avian influenza in Germany in 2015
Addendum
References
Chapter 11: Low-pathogenicity avian influenza
Introduction
Low-pathogenicity avian influenza virus (LPAIV) in natural and agricultural host systems
H9N2 influenza A viruses: the paradigm of live poultry market-adapted LPAIVs
The contribution of H9N2 influenza A viruses to the diversity of avian influenza viruses that pose a public health risk
Molecular markers of the host range of H9N2 and H7N9 LPAIVs
The other side of the coin: perpetuation of LPAIV H5N2 in commercial poultry production systems: the experience in Mexico
Summary
References
Chapter 12: Epidemiology of avian influenza in agricultural and other man-made systems
History of humans and birds
General ecology and epidemiology of influenza A viruses
Concepts for understanding pathobiology
Infections within agricultural and other man-made systems
Conclusions
References
Chapter 13: Pathobiology of avian influenza in domestic ducks
Introduction
General concepts in avian influenza pathobiology
Influenza A in domestic ducks
Conclusions
References
Chapter 14: Avian influenza control strategies
Introduction
Goals of avian influenza control, and components of a control strategy
Economic costs
The role of international animal health organizations
Conclusions
References
Chapter 15: Vaccines and vaccination for avian influenza in poultry
Introduction
History of avian influenza vaccines
Features of the ideal avian influenza vaccine for birds
Immunological basis for protection
Laboratory criteria for assessing vaccine protection
Types of avian influenza vaccines
Field use of vaccine and special issues
Surveillance
Conclusions
References
Section III: Influenza in animals of the class mammalia
Section IIIA: Swine influenza
Chapter 16: The clinical features, pathobiology, and epidemiology of influenza infections in pigs
Introduction
History
Virology
Clinical disease
Pathology of IAV in pigs
Transmission and epidemiology of influenza A virus in pigs
References
Chapter 17: Immunity, diagnosis, and intervention strategies for influenza infections in pigs
Immunity
Diagnosis
Intervention strategies
References
Chapter 18: Global evolution of influenza A viruses in swine
Introduction
Geographic distribution of swine IAV genotypes
Antigenic evolution of IAV in swine
Swine in the ecology of IAV and interaction with other host species
Determinants of virulence and host range
Conclusions
References
Chapter 19: Vaccines and vaccination for swine influenza: differing situations in Europe and the USA
Introduction
A primer on SIV evolution and vaccine immunology
Commercial inactivated SIV vaccines
Novel SIV vaccines
Conclusions and perspectives
Acknowledgments
References
Section IIIB: Equine influenza
Chapter 20: The clinical features, pathobiology, and epidemiology of influenza infections in horses
History
Economic implications
Transmission to other mammalian hosts
Clinical features of infection and disease
Epidemiology
Diagnosis, treatment, and control
References
Chapter 21: Vaccines and vaccination to control equine influenza
Goals of vaccination
Criteria and models for measuring efficacy and protection
Tests and strategies for detecting EIV-specific immune responses to vaccines and infections
Correlates of protection and evaluation of vaccination success
Types of vaccines and methods of administration
Improving EIV vaccines and vaccine coverage
References
Section IIIC: Sporadic and miscellaneous mammalian influenza
Chapter 22: Canine influenza
H3N8 canine influenza virus
H3N2 canine influenza
Other influenza infections of dogs (and cats)
Summary
References
Chapter 23: Sporadic influenza A virus infections of miscellaneous mammal species
Introduction
H5N1 HPAIV infections in miscellaneous mammal species
Other influenza A virus infections in miscellaneous mammal species
References
Chapter 24: Mammalian experimental models and implications for understanding zoonotic potential
Introduction
Factors relating to choice of an appropriate model
Mammalian models of traditional intranasal and intratracheal inoculation
Variation of inoculation route and dose
The importance of established models for public health
Conclusion
References
Index
End User License Agreement
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Guide
Table of Contents
Preface
Begin Reading
List of Illustrations
Chapter 1: Influenza A virus
Figure 1.1 Diagrammatic representation of the source and movement of influenza A viruses or their genes within avian and mammalian ecological and epidemiological situations (updated from [160]). H = hemagglutinin subtype, ( ) = subtype previously common but no longer circulating.
Figure 1.2 Phylogenetic tree of 17 hemagglutinin subtypes. The complete amino acid sequence of representative isolates for all 16 avian HA subtypes and the H17 bat subtype are included, with a representative North American and Eurasian isolate where available. The tree was midpoint rooted using the Influenza Research Database PhyML program, version 3.0 [144].
Figure 1.3 Phylogenetic tree of the matrix gene. The tree is based on the complete nucleotide sequence of representative isolates for major groups of type A influenza viruses. The tree is rooted to equine/Prague/1/56, which is the most divergent type A influenza virus. CK = chickens, DK = ducks, TK = turkeys. Standard two-letter abbreviations are used for states from isolates from the USA.
Chapter 2: Diagnostics and surveillance methods
Figure 2.1 Swab pooling for specimens from avian species. Up to 11 oropharyngeal/tracheal swabs or cloacal swabs may be pooled per vial if they are collected from the same species and the birds are housed together as part of the same flock or at the same location or market.
Figure 2.2 Outline of common approaches to influenza A virus (IAV) diagnostic testing. Active virus infection may be detected from swab material, oral fluids, or tissue by antigen capture immunoassay (ACIA), which needs to be confirmed by reverse transcriptase polymerase chain reaction (RT-PCR) or virus isolation (VI), or may be directly tested by RT-PCR or VI. Positive samples and isolates are further characterized by subtype-specific RT-PCR and/or genome sequencing and, in some cases,
in-vivo
pathogenesis studies. Exposure to IAV may be evaluated by antibody detection by agar gel immunodiffusion (AGID) or enzyme-linked immunosorbent assay (ELISA). The subtype specificity of positive samples may then be determined by hemagglutination inhibition (HI) assay or neuraminidase inhibition (NI) assay.
Chapter 3: The economics of animal influenza
Figure 3.1 Poultry system continuum in 2006 with country examples. Modified from World Bank, FAO, IFPRI, and OIE. 2006.
Enhancing Control of Highly Pathogenic Avian Influenza in Developing Countries through Compensation: Issues and Good Practice
. World Bank: Washington, DC, USA. Available at www.fao.org/docs/eims/upload//217132/gui_hpai_compensation.pdf
Figure 3.2 Poultry meat market chains in Thailand, 2003, and layer market chains in Egypt, 2006. Boxes in gray show integrated systems. Modified from Rushton, J. 2006.
Compensation for HPAI in Egypt
. Report produced for the FAO ECTAD Socio-Economics Working Group, November 2006. FAO: Rome, Italy.
Figure 3.3 World poultry market prices and simulated impacts from 50% demand decline and export ban in Asia. Source: OECD-FAO. 2013.
OECD-FAO Agricultural Outlook 2013
. OECD Publishing. Available at 101718/agr_outlook-2013-en. Holger Matthey, Market and Trade Division. Used with permission from the FAO.
Figure 3.4 National pork and poultry prices in 2013 in China [12].
Chapter 5: Public health implications of animal influenza viruses
Figure 5.1 Geographic distribution of human H5N1 HPAI cases reported to the World Health Organization between November 2003 and December 2014. Source: World Health Organization (WHO) and Centers for Disease Control and Prevention (CDC).
Figure 5.2 Epidemic curve of human H5N1 HPAI cases, by onset date and country, from November 2003 to December 2014. Source: Centers for Disease Control and Prevention (CDC).
Figure 5.3 Chest radiographic findings in a fatal case of clade 2.1 H5N1 HPAI virus infection in a 37-year-old woman. Bilateral lower lobe consolidation with patchy infiltrates in the upper lung fields were evident at admission on day 7 of the illness. Despite mechanical ventilation, the patient progressed to acute respiratory distress syndrome (ARDS) on day 10, and died on day 11. Source: T. Uyeki, Centers for Disease Control and Prevention (CDC).
Figure 5.4 Chest radiographic findings in the case of a clade 2.1 H5N1 HPAI virus infection of a 21-year-old man who survived. Infiltrates are present in the left mid-lung field at admission on day 5 of the illness. One week later, consolidation and diffuse infiltrates are present throughout all of the lung fields. The patient made a full recovery without mechanical ventilation. Source: T. Uyeki, Centers for Disease Control and Prevention (CDC).
Chapter 7: Wild bird infections and the ecology of avian influenza viruses
Figure 7.1 Variables that affect the host, agent, and environmental components of the AIV maintenance cycle in wild bird populations.
Chapter 8: The global nature of avian influenza
Figure 8.1 Numbers of avian influenza surveillance tests conducted under the National Poultry Improvement Plan in the USA for the years 2005 and 2007–2014.
Chapter 9: Multi-continental panzootic of H5 highly pathogenic avian influenza (1996–2015)
Figure 9.1 Phylogenetic relationships of the HA gene of Gs/GD-lineage H5N1 HPAIVs over time. The WHO/OFFLU H5 Evolution Working Group has kept under continuous review the nomenclature for Gs/GD-lineage H5 HPAIVs as they have evolved since their first emergence and detection in 1996. Discrete monophyletic groups appear within a specific clade, and when those groups meet the nucleotide divergence criteria (as well as having bootstrap values greater than 60, and within-clade average pairwise distances of less than 1.5%) they are split into second-order clades (but still considered part of the first-order clade). As a second-order clade continues to evolve it may reach a similar level of genetic diversity, at which point it may be split into third-order clades, and so on. The same clade designation criteria apply to first-, second-, and any higher-order clade designations. Extinct clades that are believed to be no longer circulating are shown without color, clades that have only been reported in avian species are shown in blue, and clades that include viruses which have been detected both in humans and in avian species are shown in green. Courtesy of Todd Davis, CDC Atlanta.
Figure 9.2 Distribution of Gs/GD-lineage H5 HPAIV HA clades during the period 1996–2002. Source: Adapted from World Map centered at the Pacific Ocean, $200inaire, 4 July 2012. https://commons.wikimedia.org/wiki/Category:Blank_maps_of_the_world_without_Antarctica#/media/File:White_World_Map(Pacfic-centered)_Blank.png Used under CC BY-SA 3.0. http://creativecommons.org/licenses/by-sa/3.0/.
Figure 9.3 Distribution of Gs/GD-lineage H5 HPAIV HA clades during the period 2003–2004. Source: Adapted from World Map centered at the Pacific Ocean, $200inaire, 4 July 2012. https://commons.wikimedia.org/wiki/Category:Blank_maps_of_the_world_without_Antarctica#/media/File:White_World_Map(Pacfic-centered)_Blank.png Used under CC BY-SA 3.0. http://creativecommons.org/licenses/by-sa/3.0/.
Figure 9.4 Distribution of Gs/GD-lineage H5 HPAIV HA clades during the period 2005–2008. Source: Adapted from World Map centered at the Pacific Ocean, $200inaire, 4 July 2012. https://commons.wikimedia.org/wiki/Category: Blank_maps_of_the_world_without_Antarctica#/media/File:White_World_Map(Pacfic-centered)_Blank.png Used under CC BY-SA 3.0. http://creativecommons.org/licenses/by-sa/3.0/.
Figure 9.5 Distribution of Gs/GD-lineage H5 HPAIV HA clades during the period 2009–2012. Source: Adapted from World Map centered at the Pacific Ocean, $200inaire, 4 July 2012. https://commons.wikimedia.org/wiki/Category:Blank_maps_of_the_world_without_Antarctica#/media/File:White_World_Map(Pacfic-centered)_Blank.png Used under CC BY-SA 3.0. http://creativecommons.org/licenses/by-sa/3.0/.
Figure 9.6 Distribution of Gs/GD-lineage H5 HPAIV clades during the period 2013–September 2014. Source: Adapted from World Map centered at the Pacific Ocean, $200inaire, 4 July 2012. https://commons.wikimedia.org/wiki/Category:Blank_maps_of_the_world_without_Antarctica#/media/File:White_World_Map(Pacfic-centered)_Blank.png Used under CC BY-SA 3.0. http://creativecommons.org/licenses/by-sa/3.0/.
Figure 9.7 Distribution of Gs/GD-lineage H5 HPAIV clades during the period October 2014–April 2015. Source: Adapted from World Map centered at the Pacific Ocean, $200inaire, 4 July 2012. https://commons.wikimedia.org/wiki/Category:Blank_maps_of_the_world_without_Antarctica#/media/File:White_World_Map(Pacfic-centered)_Blank.png Used under CC BY-SA 3.0. http://creativecommons.org/licenses/by-sa/3.0/.
Chapter 10: High-pathogenicity avian influenza outbreaks since 2008, excluding multi-continental panzootic of H5 Goose/Guangdong-lineage viruses
Figure 10.1 Maximum likelihood trees of full gene sequences derived from South African HPAI H5N2 isolates (shown in red), other southern African wild duck and ostrich isolates (shown in orange), and Eurasian strains (shown in black).
See Plate section for color representation of this figure
.
Figure 10.2 Distribution of H5N2 LPAI-affected premises in Chinese Taipei during 2012. Courtesy of the World Organisation for Animal Health.
See Plate section for color representation of this figure
.
Chapter 11: Low-pathogenicity avian influenza
Figure 11.1 H9 HA phylogenetic tree showing major phylogenetic groups. Phylogenetic analyses were performed using online tools available at the Influenza Research Database (www.fludb.org). The unrooted tree was generated using the Archaeopteryx software tool as described elsewhere [337]. Labeling and colors were added using PowerPoint software (Microsoft, Inc.).
Figure 11.2 H9 HA phylogenetic tree showing major phylogenetic relationships of H9N2 viruses isolated from various animal species. Phylogenetic analyses and editing were performed as described for Figure 11.1. H9 HA position 226 in the receptor-binding site (site) with leucine is shown in red, with glutamine is shown in black, and with mixed virus populations carrying leucine and/or glutamine is shown in green. Note that a single virus isolate from a human case with methionine 226 is shown in blue. Light red box corresponds to G1-lineage viruses, and light brown box corresponds to Y280-lineage viruses.
Figure 11.3 H5 HA phylogenetic tree showing major phylogenetic relationships of H5N2 viruses of North American (light orange) and Eurasian (light blue) lineages. Phylogenetic analyses and editing were performed as described for Figure 11.1. The Mexican viruses (shown in light green) form an independent evolutionary path stemming from an ancestor in the North American lineage. Mexican H5N2-vaccine-derived viruses were isolated from independent outbreaks of LPAI in Japan and Taiwan. In Taiwan, Mexican-derived H5N2 surface gene segments have reassorted with Taiwanese LPAIVs, and their endemic nature remains uncertain.
Chapter 12: Epidemiology of avian influenza in agricultural and other man-made systems
Figure 12.1 Pathobiology concepts for understanding AI in poultry. Source: D. Swayne, U.S. Department of Agriculture/Agricultural Research Service.
Figure 12.2 Six means or modes by which AIVs are introduced into poultry. Source: K. Carter, University of Georgia, and D. Swayne, U.S. Department of Agriculture/Agricultural Research Service.
Figure 12.3 Four proven sources responsible for introduction of LPAIV into commercial turkeys within the USA from the 1960s to 2000. Source: K. Carter, University of Georgia, and D. Swayne, U.S. Department of Agriculture/Agricultural Research Service.
Figure 12.4 Epidemiology of LPAIVs and HPAIVs between free-living aquatic birds and poultry. Source: D. Swayne, U.S. Department of Agriculture/Agricultural Research Service.
Figure 12.5 Relative importance of different means of initial introduction of AIVs from free-living aquatic birds to poultry. Source: K. Carter, University of Georgia, and D. Swayne, U.S. Department of Agriculture/Agricultural Research Service.
Chapter 13: Pathobiology of avian influenza in domestic ducks
Figure 13.1 Two-week-old Pekin ducks showing severe neurological signs at 3 days after IN inoculation with A/egret/HK/757.2/02 H5N1 HPAIV. Reprinted with permission from
Avian Diseases
. Copyright held by the American Association of Avian Pathologists, Athens, Georgia, USA. Source: USDA – M. Pantin-Jackwood [103].
Figure 13.3 Bile-stained loose droppings from a 2-week-old Pekin ducks at 3 days after IN inoculation with A/egret/HK/757.2/02. Reprinted with permission from
Avian Diseases
. Copyright held by the American Association of Avian Pathologists, Athens, Georgia, USA. Source: USDA – M. Pantin-Jackwood [103].
Figure 13.4 Moderate necrotizing rhinitis, with submucosal congestion and edema, and glandular hyperplasia of the nasal epithelium of a 2-week-old duck that died 3 days after IN inoculation with A/crow/Thailand/04 H5N1 HPAIV. HE. Inset. Demonstration of viral antigen in the epithelial cells (shown in red). Reprinted with permission from
Avian Diseases
. Copyright held by the American Association of Avian Pathologists, Athens, Georgia, USA. Source: USDA – M. Pantin-Jackwood [103].
Figure 13.15 Severe multifocal cellular swelling and necrosis of the pancreatic acinar epithelium with viral staining (shown in red) of a 2-week-old duck IN infected with A/chicken/Egypt/08124S-NLQP/2008.
Figure 13.5 AI viral antigen (shown in red) in the epithelium and pulp of feathers of a 2-week-old duck IN infected with A/duck/Vietnam/218/2005.
Figure 13.10 Extensive intranuclear and intracytoplasmic AI viral antigen (shown in red) in degenerated and necrotic myocytes of the heart of a 2-week-old duck IN inoculated with A/Thailand PB/6231/04 H5N1 HPAIV and found dead at 5 days after inoculation. Reprinted with permission from
Avian Diseases
. Copyright held by the American Association of Avian Pathologists, Athens, Georgia, USA. Source: USDA – M. Pantin-Jackwood [103].
Figure 13.13 Vacuolar degeneration and AI viral staining (shown in red) of the Harderian gland epithelia of a 2-week-old duck IN infected with A/chicken/Egypt/08124S-NLQP/2008.
Figure 13.7 AI viral staining (shown in red) of phagocytic cells and air capillary epithelium of the lung of a 2-week-old duck IN inoculated with A/chicken/Egypt/08124S-NLQP/2008.
Figure 13.6 Degeneration and necrosis of the tracheal epithelium with mucocellular exudate containing sloughed epithelial cells of the trachea of a 2-week-old duck IN inoculated with A/crow/Thailand/04 and found dead at 4 days after inoculation. HE. Inset. AI viral antigen staining (shown in red) present in the epithelial cells. Reprinted with permission from
Avian Diseases
. Copyright held by the American Association of Avian Pathologists, Athens, Georgia, USA. Source: USDA – M. Pantin-Jackwood [103].
Figure 13.9 Strongly positive AI viral staining (shown in red) present in neurons of the cerebrum of a 2-week-old duck IN inoculated with A/Vietnam/1203/04 H5N1 HPAIV and found dead at 4 days after inoculation. Reprinted with permission from
Avian Diseases
. Copyright held by the American Association of Avian Pathologists, Athens, Georgia, USA. Source: USDA – M. Pantin-Jackwood [103].
Figure 13.8 Viral staining (shown in red) in hepatocytes and Kupffer cells in the liver of a 2-week-old duck IN infected with A/chicken/Egypt/08124S-NLQP/2008.
Figure 13.11 AI viral staining (shown in red) of the myocytes of skeletal muscle of a 2-week-old duck IN inoculated with A/crow/Thailand/04 and euthanized at 4 days after inoculation. Reprinted with permission from
Avian Diseases
. Copyright held by the American Association of Avian Pathologists, Athens, Georgia, USA. Source: USDA – M. Pantin-Jackwood [103].
Figure 13.14 AI viral antigen (shown in red) in resident and infiltrating phagocytes in a bursa follicle of a 2-week-old duck IN infected with A/chicken/Egypt/08124S-NLQP/2008.
Figure 13.12 AI viral staining (shown in red) of the corticotrophic cells of the adrenal gland of a 2-week-old duck IN inoculated with A/Vietnam/218/05, 2 days after inoculation. Reprinted with permission from
Avian Diseases
. Copyright held by the American Association of Avian Pathologists, Athens, Georgia, USA. Source: USDA – M. Pantin-Jackwood [103].
Chapter 15: Vaccines and vaccination for avian influenza in poultry
Figure 15.1 Example of protection metrics related to egg-laying poultry using egg production (3-day average of percentage of eggs/hen/day), hen mortality (percentage); and virus-positive eggshell surface, yolk, and albumin samples (percentage positive for virus) for sham-vaccinated and once or twice H5-vaccinated chickens challenged with A/chicken/Pennsylvania/1370/83 (H5N2) HPAIV. Swayne
et al
.,
Vaccine
30(33):4964–4970, 2012 [11]. Used with permission of Elsevier.
Figure 15.2 Reduction in titer of HPAIV shed from the oropharynx and cloaca of vaccinated chickens 2 days post challenge. See Table 15.3 for details. Minimum limit of detection 10
1
ELD
50
/ml. Source: David E. Swayne.
Figure 15.3 Summary of H5 vaccine doses used in poultry by the 15 countries that vaccinated poultry against HPAI from 2002 to 2010.
Avian Diseases
56(4):818–828, 2012; [341]. Used with permission of the American Association of Avian Pathologists.
Figure 15.4 Concepts for application of AI vaccine in the field during an emergency vaccination program. Source: David E. Swayne.
Figure 15.5 Flow diagram for virological and serological surveillance of vaccinated flocks for detection of AIV infection (i.e. DIVA strategies). Source: David E. Swayne.
Chapter 16: The clinical features, pathobiology, and epidemiology of influenza infections in pigs
Figure 16.1 Pulmonary bronchioles during different stages of swine AIV infection. Courtesy of Juliane Deubner and University of Saskatchewan.
Figure 16.1a.
Normal bronchiole (A) that has a thin layer of epithelial cells (B) with apical cilia (C) and peribronchiolar lymphoid tissue (D).
Figure 16.1b.
Early influenza lesions of vacuolar degeneration (E) and necrosis (F) of the epithelial cells with loss of the apical cilia are seen as early as 24 hours post infection (PI).
Figure 16.1c.
Influenza lesions at 72 hours PI with necrotic epithelial cells sloughing, a small influx of inflammatory cells (G), attenuation of the remaining epithelial cells (H), and mild lymphoid hyperplasia (I).
Figure 16.1d.
Influenza lesions 5–7 days PI, showing varying degrees of epithelial hyperplasia (J), and mitotic Figure in some of the epithelial cells.
Figure 16.2 Experimental inoculation of a 4-week-old pig with A/swine/Texas/4199-2/1998 H3N2 virus 48 hours PI. Courtesy of Susan Detmer.
Figure 16.2a.
Severe, necropurulent bronchiolitis with mild interstitial pneumonia; hematoxylin and eosin (H&E), 200×.
Figure 16.2b.
Moderate bronchiolar epithelial cell and intraluminal immunoreactivity to anti-Influenza A nucleoprotein; immunohistochemistry (IHC) with diaminobenzidine (DAB), 200×.
Figure 16.2c.
Necropurulent bronchiolitis with severe alveolar pneumonia (lobular consolidation); H&E, 200×.
Figure 16.2d.
Strong bronchiolar and alveolar immunoreactivity to anti-Influenza A nucleoprotein; IHC with DAB, 200×.
Figure 16.3 Macroscopic lesions in the lung of a 4-week-old pig experimentally inoculated with A/swine/Illinois/02450/2008 H1N1 virus 5 days PI. The depressed, dark red, multifocal to coalescing lobular lesions are in the cranioventral portions of the lungs, and reflect the microscopic lesions (shown in inset) of atelectasis. Courtesy of Susan Detmer.
Chapter 18: Global evolution of influenza A viruses in swine
Figure 18.1 The number of hemagglutinin (HA) gene sequences available in the public database GenBank is not consistent with the geographic distribution of live pig populations. Although Asia currently has around 60% of the world's live pig population, only 10% of the HA gene sequences available from IAVs isolated from swine during 2012–2013 were from this region. In contrast, North America has approximately 10% of the world's pig population, but reported around 90% of the global IAV HA sequences from swine. Relatively few sequences were available from pigs in Central and South America, Europe, and Africa. The Oceania region has few pigs and very few sequences from IAVs from pigs.
Figure 18.2 The major H1 and H3 genetic lineages and their geographic distribution in swine. (a) The phylogenetic relationships of H1 sequences. (b) H3 sequences are depicted in respective trees and color coded by lineage. In Europe, the HA genes are derived from Eurasian avian-like H1N1 (shown in blue), a human-like H3N2 (shown in green), or a human-like H1N2 (shown in yellow). Classical H1 (shown in brown), human-like H1 (shown in yellow), and human-like H3-TRIG (shown in purple) co-circulate. In Asia, the predominant HA lineages reflect the dynamics observed in North America and Europe, with co-circulating viruses classified as a classical swine lineage, human-like H3, or Eurasian avian-like H1. The H1N1pdm09 arose from the classical swine-lineage H1 (shown in red), and underwent global dissemination through human-to-swine transmission. Used with permission from Vincent, A. L., K. M. Lager, and T. K. Anderson. 2014. A brief introduction to influenza A virus in swine.
Methods in Molecular Biology
1161:243–258.
Figure 18.3 Putative generation of H3N2 variant in pigs. Pigs infected with two strains of IAV—H3N2-TRIG (shown in blue) and H1N1pdm09 (shown in pink)—allowed for reassortment of each parent virus's specific whole-genome constellation to generate novel progeny virions. One virus resulting from the potential reassortment patterns contained seven gene segments derived from the H3N2-TRIG and a single gene segment derived from H1N1pdm09 (the M gene shown in light green). An H3N2 with the genome constellation depicted here has been found in almost 350 human cases in the USA since 2010, termed H3N2 variant (H3N2v). Reassortants between endemic swine viruses and the H1N1pdm09 have been detected frequently in pig populations around the world since 2009.
Chapter 20: The clinical features, pathobiology, and epidemiology of influenza infections in horses
Figure 20.1 Phylogenetic tree of EIV H3N8 HA1 nucleotide sequences. This maximum-likelihood tree was generated using PhyML version 3. Bootstrap values obtained after 100 replicates are shown at major nodes. Amino acid substitutions are shown in parentheses or indicated at branch points. Phylogenetic groups (Pre-divergence, American lineage, Eurasian lineage, and Florida sub-lineage clades 1 and 2) are shown on the right. Sequences are color coded by date of isolation for the years 2010 (green), 2011 (red), and 2012 (blue), with the older isolates shown in black. The present OIE-recommended representative vaccine strains A/eq/Richmond/1/07 and A/eq/South Africa/4/03 are shown in bold. Reassortant strains that were identified containing HA from one Florida clade and NA from the other are highlighted in yellow. Reprinted from Woodward A. L.
et al
., Development of a surveillance scheme for equine influenza in the United Kingdom and characterisation of viruses isolated in Europe, Dubai and the USA from 2010–2012.
Veterinary Microbiology
169:113–127, 2014, with permission from Elsevier. We thank Dr. Adam Rash for providing the figure.
Figure 20.2 Equine influenza virus-infected horse exhibiting typical mucopurulent nasal discharge. Experimental infection with A/equine/Ohio/2003 (H3N8) virus, 5 days post infection. The horse was not febrile at this point, but had a cough and was still shedding detectable virus. Some horses in this study developed secondary spikes of pyrexia, and mucopurulent nasal discharge persisted as late as 9 days post infection. Photo courtesy of Thomas Chambers.
Figure 20.3 Acute severe bronchointerstitial pneumonia with edema and hemorrhage in a horse with equine influenza A virus infection and secondary bacterial infection. Photo from Noah's Arkive, University of Georgia.
Chapter 22: Canine influenza
Figure 22.1 Phylogenies showing the origins of the widely circulating CIVs, namely the H3N8 virus that emerged in North America around 2000 as a variant of EIV, and the H3N2 virus that emerged in China and Korea around 2005 as a variant of an avian virus. (A) The H3N8 CIV HA and (C) the MP sequences, compared with the H3N8 EIV sequences from viruses collected from horses at various times after that virus emerged around 1963. Equine viruses are shown in black, and canine isolates in blue. (B) The H3N2 HA and (D) the MP sequences, compared with the sequences of different avian influenza viruses that are in the databases. The CIV sequences are shown in red, the Eurasian avian viruses are shown in green, and the American viruses are shown in blue. Modified from Figure 1 of Hayward, J. J., E. J. Dubovi, J. M. Scarlett, S. Janeczko, E. C. Holmes, and C. R. Parrish. 2010. Microevolution of canine influenza virus in shelters and its molecular epidemiology in the United States.
Journal of Virology
84:12636–12645, and Figure 1 of Zhu, H., J. Hughes, and P. R. Murcia. 2015. Origins and evolutionary dynamics of H3N2 canine influenza virus.
Journal of Virology
89:5406–5418.
Figure 22.2 The time course of H3N2 canine virus replication in dogs. Virus shedding and the serological response of beagles after experimental contact transmission of H3N2 CIV in dogs. EID, egg infectious dose; PI, percentage inhibition. Source: Figure 1 from Song, D., C. Lee, B. Kang, K. Jung, T. Oh, H. Kim, B. Park, and J. Oh. 2009. Experimental infection of dogs with avian-origin canine influenza A virus (H3N2).
Emerging Infectious Diseases
15:56–58, with permission.
Figure 22.3 Infection and replication of the H3N8 CIV in dogs after natural or experimental infection. (A) Bronchus from greyhound spontaneously infected with canine influenza virus. There is focal epithelial erosion of the surface epithelium. The epithelial cell cytoplasm and luminal macrophage cytoplasm are positive for hemagglutin antigen (arrows). Immunohistochemistry staining is for H3 viral antigen. (B) Trachea from a dog 5 days after inoculation with canine influenza virus. Viral hemagglutinin antigen is present in the cytoplasm of ciliated and non-ciliated cells as well as basal cells. Immunohistochemistry for H3 viral antigen. Derived from Figure 3 and 7 of Castleman, W. L., J. R. Powe, P. C. Crawford, E. P. Gibbs, E. J. Dubovi, R. O. Donis, and D. Hanshaw. 2010. Canine H3N8 influenza virus infection in dogs and mice.
Veterinary Pathology
47:507–517, with permission of Sage.
Chapter 23: Sporadic influenza A virus infections of miscellaneous mammal species
Figure 23.1 Natural infection of tigers with H5N1 highly pathogenic avian influenza virus in Sri Racha, Thailand, in 2004. Affected animals had high fever, respiratory distress, and (in some cases) nervous signs, and died with serosanguinous nasal discharge. Photograph courtesy of Dr. Roongroje Thanawongnuwech, Chulalongkorn University, Thailand.
Figure 23.2 Systemic histological lesions in domestic cats after experimental HPAIV H5N1 infection. The left-hand column shows necrotizing inflammatory foci present in multiple tissues stained with hematoxylin and eosin. The right-hand column shows influenza virus antigen (red-brown staining) present in serial sections of the same tissues, stained for nucleoprotein by immunohistochemistry. Reprinted from
The American Journal of Pathology
, January 2006, Vol. 168, No. 1, pp. 176–183, Rimmelzwaan G. F., van Riel D., Baars M., Bestebroer T. M., van Amerongen G., Fouchier R.A., Osterhaus, A. D., Kuiken, T. Influenza A virus (H5N1) infection in cats causes systemic disease with potential novel routes of virus spread within and between hosts, with permission from Elsevier.
Figure 23.3 Low pathogenic avian influenza A virus (H7N7), human seasonal influenza A virus (H3N2), and human influenza B virus show different degrees of attachment to the trachea and bronchiole of a harbor seal (
Phoca vitulina
). Red staining indicates virus attachment to the epithelial cell surface. Reprinted from Ramis A. J., van Riel D., van de Bildt M. W. G., Osterhaus A., Kuiken T. Influenza A and B virus attachment to respiratory tract in marine mammals.
Emerging Infectious Diseases
[serial on the Internet]. 2012 May [date cited]. Available from 10.3201/eid1805.111828. With permission of EID.
Figure 23.4 Phylogenetic trees displaying the hemagglutinin (HA) and neuraminidase (NA) genes of bat-derived H17N10 and H18N11 influenza viruses (denoted by asterisks) compared with the relative distance of HAs and NAs of all previously known influenza A virus subtypes. Reprinted from
Trends in Microbiology
, April 2014, Vol. 22, No. 4, pp. 183–191, Wu Y., Wu Y., Tefsen B., Shi Y., Gao G. F. Bat-derived influenza-like viruses H17N10 and H18N11, with permission from Elsevier.
Chapter 24: Mammalian experimental models and implications for understanding zoonotic potential
Figure 24.1 Laboratory modeling of influenza virus infection in mammals. Examples of different research platforms that can contribute towards a greater understanding of influenza virus pathogenicity, transmissibility, and tropism.
In spiritus
= in breath.
Figure 24.2 Advantages and disadvantages of mouse, ferret, and guinea pig models for use in influenza virus research.
Figure 24.3 Binding of influenza virus to host epithelial cell. The influenza hemagglutinin (HA) binds to sialic acids present on the epithelia of host cells in the respiratory tract. Source: Dan Higgins/PHIL CDC.
Figure 24.4 Use of the ferret model to study H5N1 virus pathogenesis. Numerous virus and host features studied in the laboratory in ferrets following infection with avian influenza viruses such as H5N1 are shown. Many LPAI viruses exhibit similar features to the low virulent H5N1 viruses depicted in the top panel. Illustration by Alissa Eckert. From Belser, J. A. and T. M. Tumpey. 2013. H5N1 pathogenesis studies in mammalian models.
Virus Research
178:168–185, with permission of Elsevier.
List of Tables
Chapter 1: Influenza A virus
Table 1.1 Hemagglutinin subtype distribution
a
of influenza A viruses between different birds (class: Aves) and mammals (class: Mammalia)
Table 1.2 Examples of genetic mechanisms for LP to HP change based on deduced amino acid sequence of HA proteolytic cleavage sites in H5 and H7 AIV
Chapter 2: Diagnostics and surveillance methods
Table 2.1 Characteristics of selected IAV diagnostic assays
Chapter 3: The economics of animal influenza
Table 3.1 Influenza A virus subtypes that circulated in birds and were found sporadically in people [26, 54, 82]
Table 3.2 Phases of disease and socio-economic issues for notifiable animal influenza outbreaks
Table 3.3 Production and international trade of pig and poultry meat during the period 2002–2011
Table 3.4 Yellow broiler wholesale market prices (in yuan/kg) in different provinces in China
Table 3.5 Timeline for an H5N1 HPAI outbreak in Turkey
Chapter 4: Trade and food safety aspects for animal influenza viruses
Table 4.1 Global production and export of agricultural animals and their derived products for species that have endemic or high susceptibility to influenza A viruses (FAO statistics)
Table 4.2 Data for specific-pathogen-free chickens vaccinated subcutaneously at 1 day of age with either a recombinant fowl poxvirus containing an H5 AI gene insert (rFP-AI-H5) or inactivated H5N9 AI oil-emulsified vaccine (A/turkey/Wisconsin/68), and challenged intranasally 3 weeks later with H5N1 HPAIV (A/chicken/South Korea/ES/03). Meat samples were taken on day 2 after inoculation from euthanatized (vaccine) or dead (sham) chickens
Table 4.3 Time predicted for an 8.7-log
10
reduction of Korea/03 HPAIV titer in chicken meat at a given internal temperature, and number of log
10
reductions of Korea/03 HPAIV titer achieved in chicken meat cooked according to minimum current USDA FSIS time–temperature guidelines for a 7-log
10
reduction in
Salmonella
[91]
Table 4.4 Estimated pasteurization times for eggs contaminated with HPAIV, and estimated number of log
10
reductions in HPAI achieved by industry pasteurization standards
Table 4.5 Estimated pasteurization times for eggs artificially contaminated with H5/H7 LPAIV
a
and estimated number of log
10
reductions in H5/H7 LPAIV achieved by industry pasteurization standards
Chapter 5: Public health implications of animal influenza viruses
Table 5.1 Subtypes of animal influenza A viruses causing zoonotic infections and subtypes causing influenza pandemics since 1900
Table 5.2 Infections with LPAIVs reported to cause human illness (from data up to December 2014
a
)
Table 5.3 Infections with HPAIV subtypes reported to cause human illness (from data up to December 2014)
Table 5.4 Gene composition of influenza A H3N2v viruses, 2011–2014
Chapter 7: Wild bird infections and the ecology of avian influenza viruses
Table 7.1 Free-living species from which low-pathogenic avian influenza viruses have been isolated
Table 7.2 Predominant HAs and HA/NA combinations reported from ducks, gulls, and shorebirds. The three predominant HA subtypes detected in each study are highlighted
Chapter 8: The global nature of avian influenza
Table 8.1 Details of the 37
a
documented pandemics, epidemics, or limited outbreaks of HPAI since the discovery of AIVs as the cause of fowl plague in 1955
Chapter 9: Multi-continental panzootic of H5 highly pathogenic avian influenza (1996–2015)
Table 9.1 Variability in HA0 cleavage site motifs of selected H5 HPAIVs
Chapter 10: High-pathogenicity avian influenza outbreaks since 2008, excluding multi-continental panzootic of H5 Goose/Guangdong-lineage viruses
Table 10.1 Summary of ostrich HPAI infections in South Africa during the period 2004–2011
Table 10.2 Summary of H7N7 HPAI infections in the UK in 2008
Table 10.3 Summary of laboratory results of serological, PCR, and sequencing analyses on samples from the infected premises
Table 10.4 Summary of H7N7 HPAI infections in Spain in 2009
Table 10.5 Summary of high-pathogenicity avian influenza H7N3 outbreak in Mexico
Table 10.6 Summary of H7 HPAI infections in Australia during the period 2012–2013
Table 10.7 Summary of H5N2 HPAI infections in Chinese Taipei in 2012
Table 10.8 Summary of H7N7 HPAI infections in Italy in 2013
Chapter 12: Epidemiology of avian influenza in agricultural and other man-made systems
Table 12.1 Pathobiological terms
Chapter 13: Pathobiology of avian influenza in domestic ducks
Table 13.1 Variability in intranasal infectivity of several LPAIVs and HPAIVs for domestic ducks as mean bird infectious dose (BID
50
) and lethal infectious dose (LID
50
)
Table 13.2 Mortality, mean death time (MDT), and viral replication titers from oropharyngeal and cloacal swabs of 2-week-old ducks inoculated intranasally with 10
6
EID
50
of Gs/GD-lineage H5N1 HPAIVs. Data from previously published and unpublished experiments [78, 94, 103, 106, 107, 147, 153]
Table 13.3 Morbidity, mortality, mean death time (MDT), and viral shedding in ducks inoculated with Gs/GD-lineage H5N1 HPAIVs
Chapter 15: Vaccines and vaccination for avian influenza in poultry
Table 15.1 Properties of ideal avian influenza vaccines and vaccination methods for poultry (modified from Swayne and Spackman [339])
Table 15.2 AI vaccine protection as measured by prevention of clinical signs (morbidity) and death (mortality) of vaccinated chickens following challenge with different doses of HPAIV (mean embryo infectious [EID
50
] and mean chicken lethal [CLD
50
] doses)
Table 15.3 AI vaccine protection as measured by reduction in the number of vaccinated chickens shedding HPAIV from the oropharynx and cloaca
Table 15.4 AI vaccine protection as measured by interruption of contact transmission
Table 15.5 Compiled information on AI experimental and field vaccine studies in poultry and other birds
Table 15.6 Current vaccines technologies licensed and used in the field for H5 and H7 avian influenza vaccines (compiled from available information [81, 82, 118–120, 133, 157, 158, 179, 180, 186, 285, 296, 311, 346] (www.nibsc.org/documents/ifu/07-252.pdf, http://onehealth.org.vn/influenza-vaccine-manufacturing-in-viet-namreport-on-the-apaci-satellite-session.new, www.fao.org/3/a-ai326e.pdf, www.navetco.com.vn/vi/sanpham/navet-vifluvac)). Information on seed strains for other subtypes was unavailable
Table 15.7 Positive serological results against specific AI viral proteins following AIV infection or vaccination with different types of AI vaccines
Chapter 19: Vaccines and vaccination for swine influenza: differing situations in Europe and the USA
Table 19.1 Major SIV lineages in Europe and North America
Table 19.2 Major commercially available SIV vaccines in Europe in 2015
Table 19.3 Major commercially available SIV vaccines in North America in 2011
Chapter 21: Vaccines and vaccination to control equine influenza
Table 21.1 Licensed commercial EIV vaccines available throughout the world
Chapter 23: Sporadic influenza A virus infections of miscellaneous mammal species
Table 23.1 Virological evidence of natural influenza A virus infection in mammals of the suborder Caniformia (dog-like carnivores). Only reports where the virus was detected by virus isolation or RT-PCR are listed
Table 23.2 Virological evidence of natural influenza A virus infection in mammals of the suborder Feliformia (cat-like carnivores). Only reports where the virus was detected by virus isolation or RT-PCR are listed
Table 23.3 Virological evidence of natural influenza A virus infection in mammals of the orders Perissodactyla (Equidae), Artiodactyla (Bovidae, Camelidae, and Cervidae), and Cetacea (Balaenopteridae and Delphinidae). Only reports where the virus was detected by virus isolation or RT-PCR are listed
Table 23.4 Serological evidence of natural influenza A virus infection in marine mammals of the order Carnivora, clade Pinnipedia (Phocidae, Otariidae, and Odobenidae), and of the order Cetacea (Balaenopteridae and Delphinidae). Only reports where antibody to influenza A virus in serum was detected are listed
Table 23.5 Virological evidence of natural influenza A virus infection in mammals of the order Primates (Cercopithecidae and Hylobatidae) and Chiroptera (Vespertilionidae and Phyllostomidae). Only reports where the virus was detected by virus isolation or RT-PCR are listed
Table 23.6 Serological evidence of natural influenza A virus infection in mammals of the order Primates (Homidae, Hylobatidae, and Cercopithecidae). Only reports where antibody to influenza A virus in serum was detected are listed
Chapter 24: Mammalian experimental models and implications for understanding zoonotic potential
Table 24.1 Differential virulence of closely related influenza viruses in different species
Animal Influenza
Second Edition
Edited by
David E. Swayne DVM, MSc, PhD, Dipl ACVP, Dipl ACPV
Exotic and Emerging Avian Viral Diseases Research Unit
Southeast Poultry Research Laboratory
US National Poultry Research Center
Agricultural Research Service
United States Department of Agriculture
Athens, Georgia, USA
This edition first published 2017 © 2017 by John Wiley & Sons, Inc
The following chapters remain with the US Government: 1, 2, 4, 5, 6, 8, 10, 12, 13, 14, 15, 18, 19, 24
First edition © 2008 Blackwell Publishing, Inc.
Editorial offices: 1606 Golden Aspen Drive, Suites 103 and 104, Ames, Iowa 50010, USA The Atrium, Southern Gate, Chichester, West Sussex, PO19 8SQ, UK 9600 Garsington Road, Oxford, OX4 2DQ, UK
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Library of Congress Cataloging-in-Publication Data
Names: Swayne, David E., editor.
Title: Animal influenza / [edited by] David E. Swayne.
Other titles: Avian influenza (Swayne)
Description: 2nd edition. | Ames, Iowa : John Wiley and Sons, Inc., 2016. |
Preceded by Avian influenza / edited by David E. Swayne. 2008. | Includes
bibliographical references and index.
Identifiers: LCCN 2016015390 (print) | LCCN 2016034176 (ebook) | ISBN
9781118907467 (cloth) | ISBN 9781118924327 (pdf) | ISBN 9781118924334
(epub)
Subjects: LCSH: Avian influenza. | Influenza. | Mammals–Virus diseases. |
Influenza A virus. | MESH: Influenza in Birds–prevention & control |
Influenza, Human–prevention & control | Influenza A virus–pathogenicity
| Disease Outbreaks–prevention & control
Classification: LCC SF995.6.I6 A92 2016 (print) | LCC SF995.6.I6 (ebook) |
NLM SF 995.6.I6 | DDC 636.5/0896203–dc23 LC record available at https://lccn.loc.gov/2016015390
This book is dedicated to the veterinarians and veterinary scientists whose long and distinguished careers focused on studying influenza for the benefit of animal health, and whose discoveries have laid the scientific foundation for all who have followed in the concept of “One World, One Health” for influenza. This book is dedicated to Dennis J. Alexander, Charles W. Beard, Bernard (Barney) C. Easterday, David A. Halvorson, Yoshihiro (Yoshi) Kawaoka, Hans D. Klenk, Rudolph Rott, Werner Schäfer, Richard Slemons, David Stallknecht, and Robert G. Webster.
List of contributors
Celia Abolnik MSc, PhD
Department of Production Animal Studies,
Faculty of Veterinary Science,
University of Pretoria,
Onderstepoort, South Africa
Jessica A. Belser PhD
Influenza Division,
National Center for Immunization and Respiratory Diseases,
Centers for Disease Control and Prevention,
Atlanta, Georgia, USA
Ian H. Brown PhD
Virology Department,
Animal and Plant Health Agency,
Addlestone, UK
Justin D. Brown DVM, PhD
Pennsylvania Game Commission,
Animal Diagnostic Laboratory,
Department of Veterinary and Biomedical Science,
College of Agricultural Sciences,
Pennsylvania State University,
Pennsylvania, USA
Giovanni Cattoli DVM, PhD
Istituto Zooprofilattico Sperimentale delle Venezie,
Research and Innovation Department,
OIE and National Reference Laboratory for Avian Influenza and Newcastle Disease,
FAO Reference Centre for Animal Influenza and Newcastle Disease,
Padova, Italy
Thomas M. Chambers PhD
OIE Reference Laboratory for Equine Influenza,
Maxwell H. Gluck Equine Research Center,
Department of Veterinary Science,
College of Agriculture, Food and Environment,
University of Kentucky,
Lexington, Kentucky, USA
Nancy J. Cox PhD
Influenza Division,
Centers for Disease Control and Prevention,
Atlanta, Georgia, USA
Susan E. Detmer DVM, PhD
Department of Veterinary Pathology,
Western College of Veterinary Medicine,
University of Saskatchewan,
Saskatoon, Saskatchewan, Canada
J. J. (Sjaak) de Wit DVM, PhD, dipl. ECPVS
Department of Research and Development,
GD Animal Health,
Deventer, The Netherlands
Edward J. Dubovi MA, PhD
Department of Population Medicine and Diagnostic Sciences,
College of Veterinary Medicine,
Cornell University,
Ithaca, New York, USA
Juan Garcia-Garcia DVM, PhD
Independent Consultant,
Chalco, Estado de México, Mexico
Jan Hinrichs PhD
Food and Agriculture Organization of the United Nations (FAO),
Regional Office for Asia and the Pacific,
Bangkok, Thailand
Darrell R. Kapczynski MSc, PhD
Exotic and Emerging Avian Viral Diseases Research Unit,
Southeast Poultry Research Laboratory,
US National Poultry Research Center,
Agricultural Research Service,
US Department of Agriculture,
Athens, Georgia, USA
Thijs Kuiken DVM, PhD, DACVP
Department of Viroscience,
Erasmus Medical Center,
Rotterdam, The Netherlands
Kelly M. Lager DVM, PhD
Virus and Prion Research Unit,
National Animal Disease Center,
Agricultural Research Service,
US Department of Agriculture,
Ames, Iowa, USA
Gabriele A. Landolt DVM, MS, PhD, DACVIM
Department of Clinical Sciences,
Colorado State University,
Fort Collins, Colorado, USA
Nicola Lewis BSc, BVetMed, PhD, MRCVS
Centre for Pathogen Evolution,
Department of Zoology,
University of Cambridge,
Cambridge, UK
Sam McCullough BVSc, PhD, MRCVS
Deputy Director,
CSIRO Australian Animal Health Laboratory,
Geelong, Victoria, Australia
Anni McLeod MBA, PhD
Private Consultant,
Edinburgh, UK
Mary J. Pantin-Jackwood DVM, PhD, DACPV
Exotic and Emerging Avian Viral Diseases Research Unit,
Southeast Poultry Research Laboratory,
US National Poultry Research Center,
Agricultural Research Service,
US Department of Agriculture,
Athens, Georgia, USA
Colin R. Parrish PhD
Baker Institute for Animal Health, and Department of Microbiology and Immunology,
College of Veterinary Medicine,
Cornell University,
Ithaca, New York, USA
Daniel R. Perez PhD
Georgia Research Alliance Distinguished Investigator and Caswell Eidson Chair in Poultry Medicine,
Department of Population Health,
Poultry Diagnostic and Research Center,
College of Veterinary Medicine,
University of Georgia,
Athens, Georgia, USA
Leslie D. Sims BVSc (Hons), MANZCVS
Asia Pacific Veterinary Information Services,
Montmorency, Victoria, Australia
Erica Spackman PhD
Exotic and Emerging Avian Viral Diseases Research Unit,
Southeast Poultry Research Laboratory,
US National Poultry Research Center,
Agricultural Research Service,
US Department of Agriculture,
Athens, Georgia, USA
David E. Stallknecht MSc, PhD
Southeast Cooperative Wildlife Disease Study,
Department of Population Health,
College of Veterinary Medicine,
University of Georgia,
Athens, Georgia, USA
David L. Suarez DVM, PhD, Dipl. ACVM
Exotic and Emerging Avian Viral Diseases Research Unit,
Southeast Poultry Research Laboratory,
US National Poultry Research Center,
Agricultural Research Service,
US Department of Agriculture,
Athens, Georgia, USA
David E. Swayne DVM, MSc, PhD, Dipl. ACVP, Diplo. ACPV
Exotic and Emerging Avian Viral Diseases Research Unit,
Southeast Poultry Research Laboratory,
US National Poultry Research Center,
Agricultural Research Service,
US Department of Agriculture,
Athens, Georgia, USA
Montserrat Torremorell DVM, PhD
Department of Veterinary Population Medicine,
College of Veterinary Medicine,
University of Minnesota,
Saint Paul, Minnesota, USA
Susan C. Trock DVM
Influenza Division,
Centers for Disease Control and Prevention,
Atlanta, Georgia, USA
Terrence M. Tumpey PhD
Influenza Division,
National Center for Immunization and Respiratory Diseases,
Centers for Disease Control and Prevention,
Atlanta, Georgia, USA
Timothy M. Uyeki MD, MPH, MPP
Influenza Division,
National Center for Immunization and Respiratory Diseases,
Centers for Disease Control and Prevention,
Atlanta, Georgia, USA
Kristien van Reeth DVM, PhD
Laboratory of Virology,
Faculty of Veterinary Medicine,
Ghent University,
Merelbeke, Belgium
Edwin J. B. Veldhuis Kroeze DVM, DECVP
Department of Viroscience,
Erasmus Medical Center and Viroclinics Biosciences B.V.,
Rotterdam, The Netherlands
Lonneke Vervelde PhD
The Roslin Institute and the Royal (Dick) School of Veterinary Studies,
Easter Bush Campus,
University of Edinburgh,
Midlothian, UK
Amy L. Vincent DVM, PhD
Virus and Prion Research Unit,
National Animal Disease Center,
Agricultural Research Service,
US Department of Agriculture,
Ames, Iowa, USA
John Weaver MA, Vet MB, MSc
Senior Veterinary Advisor,
Australia Indonesia Partnership for Emerging Infectious Diseases (AIP-EID),
Jakarta, Indonesia
Richard Webby PhD
Department of Infectious Diseases,
Saint Jude Research Children's Hospital,
Memphis, Tennessee, USA
Foreword
Over the last two decades, influenza has arguably become the most important
