Highly Pathogenic Avian Influenza Standard Operating Procedures: 1. Overview of Etiology and Ecology
Highly Pathogenic Avian Influenza Standard Operating Procedures: 1. Overview of Etiology and Ecology
Highly Pathogenic Avian Influenza Standard Operating Procedures: 1. Overview of Etiology and Ecology
The Foreign Animal Disease Preparedness and Response Plan (FAD PReP) Standard Operating
Procedures (SOPs) provide operational guidance for responding to an animal health emergency
in the United States.
These draft SOPs are under ongoing review. This document was last updated in September
2015. Please send questions or comments to:
National Preparedness and Incident Coordination Center
Veterinary Services
Animal and Plant Health Inspection Service
U.S. Department of Agriculture
4700 River Road, Unit 41
Riverdale, Maryland 20737
Fax: (301) 734-7817
E-mail: FAD.PReP.Comments@aphis.usda.gov
While best efforts have been used in developing and preparing the FAD PReP SOPs, the U.S.
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Inspection Service and other parties, such as employees and contractors contributing to this
document, neither warrant nor assume any legal liability or responsibility for the accuracy,
completeness, or usefulness of any information or procedure disclosed. The primary purpose of
these FAD PReP SOPs is to provide operational guidance to those government officials
responding to a foreign animal disease outbreak. It is only posted for public access as a reference.
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Disease
Highly pathogenic avian influenza (there is also low-pathogenic avian influenza
[LPAI]), also known as fowl plague.
Susceptible Species
Many susceptible species: chickens, turkeys, ducks, geese, pheasants, dogs, swine,
other mammals, and some non-mammalian species.
Reservoir
Migratory waterfowl are a key natural reservoir of LPAI, but there is no evidence of
HPAI generation in reservoir hosts to-date.
Transmission
Direct exposure to infected birds, excrement, or other secretions. Poultry generally
become infected thru direct or indirect contact with waterfowl. HPAI occurs following
transmission of LPAI strains from reservoirs into poultry followed by virus mutation to
high pathogenicity.
In the 2014–2015 HPAI outbreak in the United States, H5N2 was the most common subtype of
HPAI followed by H5N8; the outbreak resulted in the loss of nearly 50 million birds. Initially
introduced through wild waterfowl, H5N2 adapted and ultimately spread rapidly through
domestic poultry flocks in the Midwest.
However, HPAI can affect other mammal species and is zoonotic: HPAI H5N1 has infected
humans and caused fatalities. As of July 17, 2015, there have been 449 human deaths, and over
844 human cases, reported as a result of laboratory confirmed HPAI H5N1.1 While HPAI has a
relatively high species-specific transmission barrier, other strains have also infected humans. No
HPAI infections in humans (including responders to the incident) were reported during the
2014–2015 HPAI outbreak in the United States.
As a response goal, the Unified Command and stakeholders will have a common set of etiology
and ecology definitions and descriptions, to ensure proper understanding of HPAI when
establishing or revising goals, objectives, strategies, and procedures.
1.2 Purpose
The purpose of this document is to provide responders and stakeholders with a common
understanding of the disease agent.
1
World Health Organization (WHO). “Cumulative Number of Confirmed Cases of Avian Influenza A/(H5N1)
Reported to the WHO.” 2015. http://www.who.int/influenza/human_animal_interface/EN_GIP_20150717
cumulativeNumberH5N1cases.pdf.
Influenza A virus is further classified on the basis of the surface glycoproteins, hemagglutinin
(HA or H) and neuraminidase (NA or N). Sixteen H subtypes and nine N subtypes of influenza A
virus have been identified.
1.3.3 Morphology
The influenza A virus particle or virion is 80–120 nanometers in diameter and usually spherical,
although filamentous forms may occur. The influenza A genome is unusual as it contains eight
pieces of segmented, single stranded negative-sense ribonucleic acid (RNA).
2
Center for Food Security and Public Health (CFSPH), Iowa State University & Institute for International
Cooperation in Animal Biologics. “High Pathogenicity Avian Influenza.” 2014.
http://www.cfsph.iastate.edu/Factsheets/pdfs/highly_pathogenic_avian_influenza.pdf.
3
World Organization for Animal Health (OIE). Highly Pathogenic Avian Influenza, Technical Disease Card. 2014.
www.oie.int.
4
CFSPH, Iowa State University & Institute for International Cooperation in Animal Biologics. “High Pathogenicity
Avian Influenza.” 2014. http://www.cfsph.iastate.edu/Factsheets/pdfs/highly_pathogenic_avian_influenza.pdf.
1.4 Ecology
1.4.1 Susceptible Species
Many avian species are susceptible to infection with HPAI viruses, including:
chickens,
turkeys,
ducks,
geese,
guinea fowl, and
a wide variety of other birds, including migratory waterfowl and shorebirds.
HPAI has primarily been isolated from chickens and turkeys.6 Psittacine birds (such as parrots
and cockatiels) are more rarely affected. Mammalian hosts, including humans, may be
vulnerable to infection by some AI strains, including HPAI H5 and HPAI H7 subtypes.
Infection in birds can give rise to a wide variety of clinical signs that may vary according to the
host, strain of virus, host’s immune status, presence of any secondary exacerbating organisms,
and environmental conditions. Preliminary diagnosis is made through serology or molecular
probe (for example, a real-time reverse transcriptase polymerase chain reaction [rRT-PCR]).
Diagnostic confirmation is done by isolation and characterization of the virus through
sequencing.
1.4.2 Reservoirs
AI viruses usually infect migratory waterfowl, particularly Anseriformes (ducks and geese) and
Charadriiformes (shorebirds) that can carry LPAI viruses without showing illness. Infection rates
in these populations peak at autumn migratory staging locations, where large numbers of
immunologically naive juvenile birds congregate.7 LPAI virus strains occur worldwide, and have
been isolated from more than 100 different species of birds.8,9 The wild bird reservoir of LPAI
viruses is considered a major potential source of infection for domestic birds, particularly
5
OIE. “Update on Highly Pathogenic Avian Influenza in Animals (Type H5 and H7).” 2014–2015.
http://www.oie.int/animal-health-in-the-world/update-on-avian-influenza/.
6
OIE. Highly Pathogenic Avian Influenza, Technical Disease Card. 2014. www.oie.int.
7
Hall, Jeffrey S., Robert J. Dusek, and Erica Spackman. “Rapidly Expanding Range of Highly Pathogenic Avian
Influenza Viruses.” Emerging Infectious Diseases 21, no. 7 (2015): 1251-252.
8
Swayne, David E. “Epidemiology of Avian Influenza in Agricultural and Other Man-Made Systems.” Avian
Influenza, (2015): 59-85. doi:10.1002/9780813818634.ch4.
9
Olsen, B. “Global Patterns of Influenza A Virus in Wild Birds.” Science 312, no. 5772 (2006): 384-88.
There is not currently evidence of HPAI generation in a reservoir. However, HPAI viruses,
particularly HPAI H5N, have occasionally been isolated from free living wild birds, suggesting
that dissemination of HPAI by wild waterfowl may be possible. 11 It remains unclear how long
and to what extent wild birds can maintain HPAI viruses, but there is evidence that certain
species of Anseriformes can carry and shed certain HPAI viruses without clinical signs. 12 This
poses a serious transmission risk to commercial poultry.
HPAI virus is usually transmitted via direct exposure to HPAI infected birds, feces, or secretions
from infected birds. Transmission of the virus can also result from movement of contaminated
fomites, including by people, on contaminated clothing, equipment, and vehicles. Airborne
transmission is not likely a primary mode of transmission, although it may occur over short
distances as an aerosol.13,14 When a hen is infected, the HPAI virus is also likely to be present on
the eggshell and internal egg contents, though to date, there is no evidence demonstrating vertical
transmission of the virus.15 Transmissibility can also vary by HPAI strain. 16
HPAI can be transmitted mechanically by invertebrate and vertebrate vectors. However, there is
no evidence to suggest that invertebrates are involved in biological transmission.
It is possible for a bird to shed the virus before and after the appearance of clinical signs. The
infectious period is particularly important in outbreak response measures because some species,
such as domestic ducks, may not show clinical signs so the incubation period may not be
known. 20
18
OIE. Article 10.4.1: General Provisions, Terrestrial Animal Health Code. 2015. www.oie.int.
19
Swayne, David E. “Epidemiology of Avian Influenza in Agricultural and Other Man-Made Systems.” Avian
Influenza, (2015): 59-85. doi:10.1002/9780813818634.ch4.
20
Swayne, David E. “Epidemiology of Avian Influenza in Agricultural and Other Man-Made Systems.” Avian
Influenza, (2015): 59-85. doi:10.1002/9780813818634.ch4.
21
CFSPH, Iowa State University & Institute for International Cooperation in Animal Biologics. “High Pathogenicity
Avian Influenza.” 2014. http://www.cfsph.iastate.edu/Factsheets/pdfs/highly_pathogenic_avian_influenza.pdf.
22
Swayne, David E., and Colleen Thomas. “Trade and Food Safety Aspects for Avian Influenza Viruses.” Avian
Influenza, (2008): 499-512.
23
FAO. “Avian influenza A (H5N6): the latest addition to emerging zoonotic avian influenza threats in East and
Southeast Asia.” http://www.fao.org/3/a-i4199e.pdf.
24
WHO. “Antigenic and genetic characteristics of zoonotic influenza viruses and development of candidate vaccine
viruses for pandemic preparedness.” 2013. http://www.who.int/influenza/vaccines/virus/201309_h5h7h9_
vaccinevirusupdate.pdf.
25
Doyle, M.P., and M.C. Erickson. “Emerging Microbiological Food Safety Issues Related to Meat.” Meat Science,
74, no. 1 (2006): 98-112.
26
Perdue, Michael L. “Molecular Determinants of Pathogenicity for Avian Influenza Viruses.” Avian Influenza,
(2008): 23-41. doi:10.1002/9780813818634.ch2.
27
Reid, A. H., et al. “Relationship of Pre-1918 Avian Influenza HA and NP Sequences to Subsequent Avian
Influenza Strains.” Avian Diseases 47, (2003): 921-25.
Subtypes of influenza A have adapted to both humans and swine, and currently circulate. 30
Human infections with AI viruses have led the World Health Organization (WHO) to consider
the possibility that a new human pandemic may be derived directly from birds. However, the
evidence and triggers which cause an influenza A virus to adapt to a mammalian host remain less
clear than the transition of an influenza A virus from a low pathogenicity to a highly pathogenic
form in poultry. 31
Temperature: Pasteurization and cooking inactivate the AI virus. Cooking whole eggs at
60 ºC for 188 seconds and 507 seconds for poultry meat will inactivate the virus.
Cooking meat to a core temperature of 70 ºC for 3.5 seconds will also inactivate AI. AI
virus can survive indefinitely if frozen.
pH: Inactivated by acidic pH of ≤ 2.
Chemicals: Inactivated by organic solvents and detergents, such as sodium desoxycholate
and sodium dodecylsulphate. If organic matter is present, aldehydes, β-propiolactone and
binary ethyleneimine should be used for inactivation. After organic matter has been
removed, phenolics, quaternary ammonium compounds, oxidizing agents (such as
sodium hypochlorite), dilute acids (if pH≤ 2), hydroxylamine, and lipid solvents should
be used.
Disinfectants: For clean surfaces with no organic matter, use sodium hypochlorite
(5.25 percent), sodium hydroxide (2 percent), phenols, acidified ionophors, chlorine
dioside, or strong oxidizing agents to inactivate.
28
Suarez, David L. “Influenza A Virus.” Avian Influenza, (2008): 1-22.
29
CFSPH, Iowa State University & Institute for International Cooperation in Animal Biologics. “High Pathogenicity
Avian Influenza.” 2014. http://www.cfsph.iastate.edu/Factsheets/pdfs/highly_pathogenic_avian_influenza.pdf.
30
Perdue, Michael L. “Molecular Determinants of Pathogenicity for Avian Influenza Viruses.” Avian Influenza,
(2008): 23-41. doi:10.1002/9780813818634.ch2.
31
Perdue, Michael L. “Molecular Determinants of Pathogenicity for Avian Influenza Viruses.” Avian Influenza,
(2008): 23-41. doi:10.1002/9780813818634.ch2.
32
Swayne, David E. “Epidemiology of Avian Influenza in Agricultural and Other Man-Made Systems.” Avian
Influenza, (2015): 59-85. doi:10.1002/9780813818634.ch4.
33
OIE. Highly Pathogenic Avian Influenza, Technical Disease Card. 2014. www.oie.int.
The OIE Terrestrial Animal Health Code (2015) states that the listed temperature achieves a
7-log kill.
Because AI virus can persist on the surface of eggs and fillers, these items also need to be
sanitized.36,37
34
OIE. Terrestrial Animal Health Code. 2015. www.oie.int.
35
Swayne, David E., and Joan R. Beck. “Heat Inactivation of Avian Influenza and Newcastle Disease Viruses in
Egg Products.” Avian Pathology 33, no. 5 (2004): 512-18.
36
OIE. Highly Pathogenic Avian Influenza, Technical Disease Card. 2014. www.oie.int.
37
Swayne, David E. “Epidemiology of Avian Influenza in Agricultural and Other Man-Made Systems.” Avian
Influenza, (2015): 59-85. doi:10.1002/9780813818634.ch4.
38
OIE. Terrestrial Animal Health Code. 2015. www.oie.int.
39
Swayne, David E., and Joan R. Beck. “Heat Inactivation of Avian Influenza and Newcastle Disease Viruses in
Egg Products.” Avian Pathology 33, no. 5 (2004): 512-18.
40
OIE. Terrestrial Animal Health Code. 2015. www.oie.int.
1.5.4 In Carcasses
AI viruses can survive in bird carcasses for several days at ambient temperatures, and a few
weeks at refrigeration temperatures. Titers in carcasses will vary depending on the strain of the
virus, species of bird, and time of death in relation to clinical stage of infection. Burying,
incineration, or composting (virus inactivated in less than 10 days) is recommended for
carcasses.41,42
The current H5 HPAI viruses, defined as novel Eurasian lineage clade 2.3.4.4, began rapidly
spreading in January 2014 from South Korea to China and Japan. By November 2014, clade
2.3.4.4 H5N1 was present in Germany, the Netherlands, and the United Kingdom. Also in
November 2014, a novel HPAI H5N2 virus consisting of a reassortment of Eurasian 2.3.4.4, four
other Eurasian genes, and three North American wild bird lineage genes was reported in British
Columbia, Canada. With the detection of very similar H5N8 Eurasian viruses in three continents
(Asia, Europe, and North America), there is evidence that this particular reassortant is not only
well adapted to specific species of waterfowl, it is able to survive extended migration periods.46
The HPAI H5N8 virus has adapted to wild waterfowl hosts as few or no clinical signs have been
reported in these hosts when infected with the virus. Thus, it seems probable that the virus was
disseminated out of Russia into Europe, East Asia, and North America by migrating waterfowl
during autumn 2014.47
41
Swayne, David E. “Epidemiology of Avian Influenza in Agricultural and Other Man-Made Systems.” Avian
Influenza, (2015): 59-85. doi:10.1002/9780813818634.ch4.
42
OIE. Highly Pathogenic Avian Influenza, Technical Disease Card. 2014. www.oie.int.
43
Miller, Mark P., et al. “Intercontinental Genetic Structure and Gene Flow in Dunlin (Calidris Alpina), a Potential
Vector of Avian Influenza.” Evolutionary Applications 8, no. 2 (2015): 149-71.
44
Nallar, et al. “Demographic and Spatiotemporal Patterns of Avian Influenza Infection at the Continental Scale,
and in Relation to Annual Life Cycle of a Migratory Host.” PLoS ONE, (2015). doi:10.1371/journal.pone.0130662.
45
Scotch, M., et al. “Diffusion of Influenza Viruses among Migratory Birds with a Focus on the Southwest United
States.” Infection, Genetics and Evolution, (2014): 185–193.
46
Ip, Hon S., et al. “Novel Eurasian Highly Pathogenic Avian Influenza A H5 Viruses in Wild Birds, Washington,
USA, 2014.” Emerging Infectious Diseases 10, no. 5 (2015): 886–90.
47
Hall, Jeffrey S., Robert J. Dusek, and Erica Spackman. “Rapidly Expanding Range of Highly Pathogenic Avian
Influenza Viruses.” Emerging Infectious Diseases 21, no. 7 (2015): 1251-252.
HPAI continues to be a threat in the United States after the latest 2014–2015 outbreak as the
virus could still be present in asymptomatic wild waterfowl. With the 2015 fall migration of
waterfowl approaching, chances of potential carriers of HPAI coming in contact with poultry
increases. The real problem arises when HPAI is introduced into vulnerable poultry populations
where the virus amplifies and spreads, resulting in extremely high morbidity and mortality, and
associated significant, detrimental economic consequences.
Ip, Hon S., et al. “Novel Eurasian Highly Pathogenic Avian Influenza A H5 Viruses in Wild Birds, Washington,
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