Highly Pathogenic Avian Influenza (Fowl Plague)

January 23, 2004


Agent

Avian influenza can occur in two forms: highly pathogenic avian influenza (HPAI), also known as fowl plague, and low-pathogenic avian influenza (LPAI). Both forms are caused by influenza type A virus. HPAI spreads rapidly among flocks and often is highly fatal. Conversely, LPAI generally does not cause severe disease and is more commonly seen in US poultry flocks.

Viral classification and genetic composition

Family: Orthomyxoviridae
Genus: Influenza
Virions 80 to 120 nm in diameter
May be filamentous
Eight different segments of negative-stranded RNA; allows for genetic reassortments in single cells infected with more than one virus and may result in multiple strains that are different from the initial ones (see References: PHS, Voyles 2002)
Types: A, B, and C
Type designation is based on the antigenic character of the M protein located in the virus envelope and the nucleoprotein within the virus particle.
Influenza A virus causes human, swine, equine, avian, and marine mammal influenza and is the type associated with pandemic disease in humans.
Influenza B virus causes disease in humans only.
Influenza C virus causes a relatively mild illness in both humans and swine and occurs uncommonly.
HPAI and LPAI are caused by influenza A viruses.
The virus envelope glycoproteins have hemagglutinin (HA) and neuraminidase (NA) activity; these characteristics are used to subtype the A, B, and C viruses.
For influenza A viruses, there are 15 different HA antigens (H1 to H15) and nine different NA antigens (N1 to N9).
Only subtypes H5 and H7 of influenza A virus have caused HPAI.
The H5 and H7 strains also are identifiable according to a nucleic acid sequence at the hemagglutinin cleavage site (see References: PHS).
Environmental Survival of HPAI Virus

Influenza A virus remains viable at moderate temperatures for long periods in the environment and can survive indefinitely in frozen material. It can survive for 4 days in water at 22°C and for over 30 days at 0°C (see References: PHS).
Inactivation of the virus occurs under the following conditions (seeReferences: OIE 2002, PHS):
Temperatures of 56°C for 3 hours or 60°C or more for 30 minutes
Acidic pH conditions
Presence of oxidizing agents such as sodium dodecyl sulfate, lipid solvents, and B-propiolactone
Exposure to disinfectants: formalin, iodine compounds
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Hosts

It is likely that all birds are susceptible to HPAI. Species that have been shown to be susceptible either experimentally or naturally include:

Chickens
Turkeys
Ducks
Partridges
Pheasants
Quail
Pigeons
Ostriches and other ratites
Geese
Guinea fowl
Migratory waterfowl, sea birds, shore birds, and imported pet birds have been found to be carriers of highly-pathogenic influenza A viruses without clinical signs.

As noted above, influenza A viruses also cause illness in humans and other animal hosts (pigs, horses, sea mammals, and mustelids).



Epidemiology

Transmission

Routes of infection include:
Oral
Conjunctival
Respiratory
Vertical transmission is not known to occur
Common modes of infection include:
Direct transmission through secretions (feces, respiratory secretions) of infected birds
Broken contaminated eggs in incubators infecting healthy chicks (see References: OIE 2002)
Movement of infected birds between flocks
Fomites such as contaminated equipment, egg flats, feed trucks, and clothing and shoes of employees and service crews (see References: APHIS, Beard 1998)
Contact with wild birds and waterfowl, which appear to be natural reservoirs for the virus
Fecal contamination of drinking water
Garbage flies (suspected of transmitting the virus during the 1983-1984 epidemic in Pennsylvania) (see References: Beard 1998)
Airborne transmission if birds are in close proximity
The disease is highly contagious. One gram of contaminated manure can contain enough HPAI virus to infect 1 million birds (seeReferences: APHIS).

As stated above, waterfowl, ostriches and other ratites, shore birds, sea birds, and other wild birds can act as carriers of the virus. These birds may not show clinical signs but shed the virus.

Occurrence

Because HPAI usually arises from an LPAI virus that has mutated at its hemagglutinin surface proteins, it is difficult to define specific areas where the disease is endemic. HPAI types of virus have been isolated from free-living birds in Europe and other regions; however, there is no recognized wild bird reservoir for the HPAI subtypes of the virus.

Apathogenic and mildly pathogenic influenza A viruses occur worldwide.
Some H5 and H7 viruses are of low pathogenicity.
Because of a lack of appropriate laboratory facilities in many parts of the world, it is difficult to accurately determine the actual incidence of HPAI in the world's poultry flocks (see References: Beard 1998).
Outbreaks of HPAI have occurred throughout the world:

An H5 strain affected Pennsylvania in 1983 and caused severe clinical disease and high mortality rates in chickens, turkeys, and guinea fowl (see References: Beard 1998).
A serologically identical but apparently mild virus had been circulating in poultry in the area for 6 months (see References: Beard 1998).
A total of 17 million birds were culled.
Retail egg prices increased by 30 cents (see References: APHIS).
An H5N1 strain of AI was responsible for a significant outbreak of influenza in humans and domestic poultry in 1997 in Hong Kong.
Prior to this outbreak, H5N1 was not known to infect humans.
Six human deaths were attributed to this strain.
The virus was isolated from chickens, and mortality rates were high.
A total of 1.5 million birds were culled in 3 days.
A monitoring system was instituted for birds in live markets.
An H7N1 strain occurred in the Veneto region of Italy in December 1999.
A total of 30,000 turkeys died or were destroyed to contain the outbreak.
In 1998, H5N2 strains of the virus were responsible for at least eight outbreaks on Italian farms (see References: APHIS).
Other countries that have had outbreaks include Australia (H7), England (H7), South Africa (H5), Scotland (H5), Ireland (H5), Mexico (H5), and Pakistan (H7).
A Hong Kong man died in February 2003 from bird flu (H5N1), the first human case reported since 1997 (see below), and his son contracted the disease as well. Health officials are working to develop a vaccine to H5N1 in humans (see References: Cyranoski 2003).
An outbreak of HPAI occurred in the Netherlands in 2003. Over 28 million birds out of a total 100 million birds in the country were killed. There were reports of over 80 human cases, and one veterinarian died. The disease spread to Belgium but was quite rapidly contained.
An outbreak in Asia started in January 2004 and continues to spread. So far, it involves South Korea, Vietnam, Japan, Thailand, and Cambodia. Of special concern is that fact that in Vietnam and Thailand, the avian strain (H5N1) has now been confirmed in several cases of fatal human respiratory disease. Low-pathogenic avian influenza (H5N2) has been identified in Taiwan.
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HPAI As a Biological Weapon

HPAI is considered a potential biological weapon because of the following factors:

Extremely contagious
High mortality rate
Severe economic consequences of an outbreak:
Large numbers of birds are destroyed or die.
Control measures disrupt trade of poultry products from affected areas.
Prices of retail poultry products may increase significantly.
Virus has a high potential for genetic mutations and for new strains to arise and affect new species
The Hong Kong epidemic of 1997 and the associated human cases demonstrate the ability of the virus to affect humans and birds.
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Clinical Features

The clinical signs of HPAI are severe and result in high mortality rates in many species of birds, especially domestic fowl. As mentioned above, waterfowl, ratites, and other birds may not be as susceptible to clinical signs, but can act as carriers for the virus.

Clinical Features of Highly Pathogenic Avian Influenza in Animals

Feature Characteristics

CHICKENS

Incubation Period

3-7 days

Clinical signs

˜Sudden death
˜Severe depression with ruffled feathers
˜Inappetence
˜Drastic decline in egg production
˜Edema of head and neck
˜Swollen and cyanotic combs and wattles (see Gray Book figure 25 and figure 26 [References: Beard 1998])
˜Petechial hemorrhages on internal membrane surfaces
˜Excessive thirst
˜Watery diarrhea that begins as bright green and progresses to white
˜Swollen and congested conjunctiva with occasional hemorrhage
˜Diffuse hemorrhage between hocks and feet (see Gray Book figure 27 [References: Beard 1998])
˜Respiratory signs are dependent on tracheal involvement
˜Nasal and ocular discharge
˜Mucus accumulation (varies)
˜Lack of energy
˜Coughing/sneezing
˜Incoordination
˜Nervous system signs such as paralysis

Complications

˜Cessation of egg production, and eggs laid immediately prior to infection often soft-shelled and misshapen
˜Surviving birds are in poor condition and resume laying only after a period of several weeks

Case-fatality rate

˜Can be as high as 100%
˜Death may occur prior to any symptoms or as late as a week after symptoms, though it is frequently within 48 hr

TURKEYS

Incubation period

3-7 days

Clinical signs

˜Sudden death
˜Severe depression with ruffled feathers
˜Inappetence
˜Drastic decline in egg production
˜Edema of the head and neck
˜Swollen and cyanotic combs and wattles
˜Petechial hemorrhages on internal membrane surfaces
˜Excessive thirst and evidence of dehydration
˜Watery diarrhea that begins as bright green and progresses to white
˜Swollen and congested conjunctivae with occasional hemorrhage
˜Diffuse hemorrhage between hocks and feet
˜Respiratory signs are dependent on tracheal involvement
˜Nasal and ocular discharge
˜Mucus accumulation (varies)
˜Lack of energy
˜Coughing/sneezing
˜Incoordination
˜Nervous system signs such as paralysis
˜Sinusitis
˜Dehydration

Complications

˜Decrease in egg production
˜Sudden death
˜Surviving birds are in poor condition and resume laying only after a period of several weeks

Case-fatality rate

˜Can be as high as 100%
˜Most turkeys die within 3 to 10 days

DOMESTIC DUCKS AND GEESE

Incubation period

3-7 days

Clinical signs

˜Signs of depression, inappetence, and diarrhea similar to those seen in layers
˜Swollen sinuses
˜Neurologic signs in younger birds
˜Sinusitis

Complications

˜Decrease in egg production
˜Sudden death
˜Surviving birds are in poor condition and resume laying only after a period of several weeks

Case-fatality rate

As high as 100%

Adapted from Aeillo 1998, APHIS, Beard 1998, Capua 2001, OIE 2002, PHS) (see References).

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