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Avian Influenza - Disease Card
Avian influenza (AI) has been recognised as a highly lethal
generalised viral disease of poultry since 1901. In 1955, a
specific type of influenza virus was identified as the causal
agent of what was then called fowl plague. It has since been
found that AI viruses cause a wide range of disease syndromes,
ranging from severe to mild, in domestic poultry.
Aetiology
AI viruses are members of the family Orthomyxoviridae. The
influenza viruses that constitute this family are classified
into types A, B or C based on differences between their
nucleoprotein and matrix protein antigens. AI viruses belong
to type A. Influenza viruses are further categorised into
subtypes according to the antigens of the haemagglutinin (H)
and neuraminidase (N) projections on their surfaces. There are
14 haemagglutinin subtypes and 9 neuraminidase subtypes of
influenza A viruses, and AI viruses have representatives in
all of these subtypes. However, to date all highly pathogenic
AI viruses that cause generalised rather than respiratory
disease belong to either the H5 or H7 subtypes. For example,
the classical fowl plague virus is H7N7 and the virus
responsible for the major epidemic in the eastern United
States in 1983 84 was H5N2. However, not all H5 and H7 viruses
are virulent for poultry.
The pathogenicity of AI viruses is correlated to the ability
of trypsin to cleave the haemagglutinin molecule into two
subunits. Highly pathogenic strains of H5 and H7 viruses have
several amino acid residues at the cleavage site. Trypsin
sensitivity and amino acid sequencing can be used
diagnostically to determine whether or not an isolated virus
is potentially pathogenic.
Natural hosts
Domestic fowl, ducks, geese, turkeys, guinea fowl, quail and
pheasants are susceptible. Disease outbreaks occur most
frequently in domestic fowl and turkeys. A particular isolate
may produce severe disease in turkeys but not in chickens or
any other avian species. Therefore, it would be impossible to
generalize on the host range for HPAI, for it will likely vary
with the isolate. This assumption is supported by reports of
farm outbreaks where only a single avian species of several
species present on the farm became infected. Many species of
wild birds particularly waterbirds and seabirds - are also
susceptible, but infections in these birds are generally
subclinical.
World Distribution
AI viruses are probably ubiquitous in wild waterbirds.
Pathogenic strains could emerge and cause disease in domestic
poultry in any country at any time without warning. In fact,
outbreaks have occurred at irregular intervals on all
continents. The most serious epidemic in recent times was in
Hong Kong 1997-1998 and 2003, The Netherlands 2003,
South-Korea 2003.
Epidemiology
The immediate source of infection for domestic poultry can
seldom be ascertained, but most outbreaks probably start with
direct or indirect contact of domestic poultry with waterbirds.
Many of the strains that circulate in wild birds are either
non-pathogenic or midly pathogenic for poultry. However, a
virulent strain may emerge either by genetic mutation or by
reassortment of less virulent strains. Scientific evidence
indicates that the former mechanism occurredmin 1983-87 in the
Eastern United States.
Swine appear to be important in the epidemiology of infection
of turkeys with swine influenza virus when they are in close
proximity. Other mammals do not appear to be involved in the
epidemiology of HPAI. The infection of humans with an H5 avian
influenza virus in Hong Hong in 1997 has resulted in a
reconsideration of the role of the avian species in the
epidemiology of human influenza.
Once AI is established in domestic poultry, it is a highly
contagious disease and wild birds are no longer an essential
ingredient for spread. Infected birds excrete virus in high
concentration in their faeces and also in nasal and ocular
discharges. Once introduced into a flock, the virus is spread
from flock to flock by the usual methods involving the
movement of infected birds, contaminated equipment, egg flats,
feed trucks, and service crews, to mention a few. The disease
generally spreads rapidly in a flock by direct contact, but on
occasions spread is erratic.
Airborne transmission may occur if birds are in close
proximity and with appropriate air movement. Birds are readily
infected via instillation of virus into the conjunctival sac,
nares, or the trachea. Preliminary field and laboratory
evidence indicates that virus can be recovered from the yolk
and albumen of eggs laid by hens at the height of the disease.
The possibility of vertical transmission is unresolved;
however, it is unlikely infected embryos could survive and
hatch. Attempts to hatch eggs in disease isolation cabinets
from a broiler breeder flock at the height of disease failed
to result in any AI-infected chickens. This does not mean that
broken contaminated eggs could not be the source of virus to
infect chicks after they hatch in the same incubator. The
hatching of eggs from a diseased flock would likely be
associated with considerable risk.
Incubation Period
The incubation period is usually 3 to 7 days, depending upon
the isolate, the dose of inoculum, the species, and age of the
bird.
Clinical signs
The clinical signs are very variable and are influenced by
factors such as the virulence of the infecting virus, species
affected, age, sex, concurrent diseases and environment.
In virulent (or highly pathogenic) AI of the type
traditionally associated with fowl plague, the disease appears
suddenly in a flock and many birds die either without
premonitory signs or with minimal signs of depression,
inappetence, ruffled feathers and fever. Other birds show
weakness and a staggering gait. Hens may at first lay
soft-shelled eggs, but soon stop laying. Sick birds often sit
or stand in a semi-comatose state with their heads touching
the ground. Combs and wattles are cyanotic and oedematous, and
may have petechial or ecchymotic haemorrhages at their tips.
Profuse watery diarrhoea is frequently present and birds are
excessively thirsty. Respiration may be laboured. Haemorrhages
may occur on unfeathered areas of skin. The mortality rate
varies from 50 to 100%.
In broilers, the signs of disease are frequently less obvious
with severe depression, inappetence, and a marked increase in
mortality being the first abnormalities observed. oedema of
the face and neck and neurological signs such as torticollis
and ataxia may also be seen. The disease in turkeys is similar
to that seen in layers, but it lasts 2 or 3 days longer and is
occasionally accompanied by swollen sinuses. In domestic ducks
and geese the signs of depression, inappetence, and diarrhea
are similar to those in layers, though frequently with swollen
sinuses. Younger birds may exhibit neurological signs.
Vaccination
Inactivated oil-emulsion vaccines, although fairly expensive,
have been demonstrated to be effective in reducing mortality,
preventing disease, or both, in chickens and turkeys (7).
These vaccines may not, however, prevent infection in some
individual birds, which go on to shed virulent virus. More
economical viable vaccines prepared using naturally avirulent
or attenuated strains have the disadvantage of the possible
creation of reassortant influenza viruses with unpredictable
characteristics. These reassortants could result when a single
host bird is simultaneously infected with both the vaccine and
another AI virus. Owing to the segmented nature of the
influenza virus genome, a reassortment of genetic material can
readily occur, creating new influenza viruses.
The basic drawback to any vaccine approach for the control of
HPAI is the large number of HA subtypes that can cause the
disease. Because there is no cross-protection among the 15
known HA subtypes, either a multivalent vaccine will be needed
or vaccination postponed until the prevalent disease-causing
subtype in the area is identified. A recombinant fowl pox
virus vaccine containing the gene that codes for the
production of the H5 antigen has recently been licensed. The
use of a recombinant insect virus containing the gene for
either the H5 or H7 antigen has been used to make these
vaccine proteins in insect cell cultures.
Pathology
Birds that die of peracute disease may show minimal gross
lesions, consisting of dehydration and congestion of viscera
and muscles.
In birds that die after a prolonged clinical course, petechial
and ecchymotic haemorrhages occur throughout the body,
particularly in the larynx, trachea, proventriculus and
epicardial fat, and on serosal surfaces adjacent to the
sternum. There is extensive subcutaneous oedema, particularly
around the head and hocks. The carcase may be dehydrated.
Yellow or grey necrotic foci may be present in the spleen,
liver, kidneys and lungs. The air sace may contain an exudate.
The spleen may be enlarged and haemorrhagic.
AI is characterised histologically by vascular disturbances
leading to oedema, haemorrhages and perivascular cuffing,
especially in the myocardium, spleen, lungs, brain and
wattles.Necrotic foci are present in the lungs, liver and
kidneys. Gliosis, vascular proliferaion and neuronal
degeneration may be present in the brain.
Differential diagnosis
The following diseases must be considered in the differential
diagnosis of virulent AI:
Other diseases causing sudden high mortality:
• Newcastle disease
• infectious laryngotracheitis
• duck plague
• acute poisonings
other diseases causing swelling of the combs and wattles:
• acute fowl cholera and other septicaemic diseases
• bacterial cellulitis of the comb and wattles
Less severe forms of the disease may be confused with, or
complicated by, many othe diseases with respiratory or enteric
signs. AI should be suspected in any disease outbreak in
poultry that persists despite the application of preventive
and therapeutic measures for other diseases.
Laboratory diagnostic specimens
Specimens required
Specimens should abe collected from at least six birds.
Preferably, three should be birds showing signs of the acute
disease and the other three may be recently dead.
Bacteriological swabs of tracheal and cloacal contents, brain
and heart blood should be collected aseptically. The material
collected on the swabs should be mixed into 3mL aliquots of
transport medium in sterile bottles and the swabs discarded.
The transport medium may be sterile brain-heart infusion both
containing 5000 ug of streptomycin per mL, or equal parts of
glycerol and phosphate-buffered saline with the same
antibiotics added. Tracheal and cloacal swabs should also be
collected from selected live birds in the flock.
At autopsy, unpreserved specimens of brain, trachea, spleen
and intestinal contents should be collected for isolation of
the virus. Impression smears should be made of internal
organs, including kidney and pancreas, for detection of viral
antigen.
Blood samples should be collected for serum. Samples should be
taken from several birds in the flock.
Transport of specimens
Unpreserved tissues and swab material should be chilled and
forwarded on water ice or with frozen gel packs. If delays of
greater than 48 hours are expected in transit, these specimens
should be frozen and forwarded with dry ice.
Laboratory procedures
AI virus is most commonly isolated by inoculation of swab
material or tissue homogenates into 9-11-day-old embryonated
chicken eggs by the allantoic sac route. The embryos may or
may not die, but in any case the presence of the virus can be
detected by haemagglutinin tests on harvested allantoic fluid.
Its identity is confirmed by agar gel diffusion or
haemagglutination inhibition tests using specific antiserum.
Rapid diagnosis can be made by the detection of viral antigen
in tissue impression smears using immunofluorescence, or by
antigen detection enzyme-linked immunosorbent assay (ELISA) on
tissue homogenates. Pancreas and kidney are the organs in
which antigen is most often demonstrable.
Isolates of the virus can be serotyped to determine their
haemagglutinin and neuraminidase subtypes. Pathogenicity tests
are carried out by inoculating 4-6-week-old chickens,
intravenoulsy or into the caudal thoracic air sac, with an
inoculum prepared from infectious allantoic sac fluid. A
pathogenicity index is determined from the number of healthy,
sick, paralysed and dead birds observed on each day for 10
days post inoculation. In vitro tests, based on the ability of
the virus to produce plaques in cell cultures in the absence
of trypsin, are also useful for pathotyping strains of the
virus. However, polymerase chain reaction and gene sequencing
procedures can be used for rapid determination of the
pathogenic potential of an AI virus, and this is an important
aspect in determining the role of the virus in the disease
seen in the field.
Group-specific antibody can be detected by ELISA in serum
samples from birds two weeks or more after they first show
clinical signs. Once the subtype of the virus has been
identified, haemagglutination inhibition tests can be used to
detect specific antibodies.
Source
• Exotic diseases of Animals, a field guide for Australian
veterinarians. W.A Geering, A.J. Forman and M.J. Nunn
• Foreign animal diseases, the grey book. Bayer. Committee on
Foreign Animal Diseases of the United States Animal Health
Association
FAO
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