See discussions, stats, and author profiles for this publication at: https://www.researchgate.

net/publication/368858178

Epidemiology and Pathogenesis of Avian Influenza Type a Virus Infection in

Poultry, A Review

Article · January 2023

DOI: 10.23880/oajvsr-16000233

CITATIONS READS
0 86

1 author:

Moges Eriso Blate

19 PUBLICATIONS 7 CITATIONS

SEE PROFILE

All content following this page was uploaded by Moges Eriso Blate on 20 May 2023.

The user has requested enhancement of the downloaded file.

 Open Access Journal of Veterinary Science & Research
ISSN: 2474-9222
MEDWIN PUBLISHERS
Committed to Create Value for Researchers

Epidemiology and Pathogenesis of Avian Influenza Type a Virus

Infection in Poultry, A Review

Blate ME*
Research Article
College of Veterinary Medicine, Haramaya University, Ethiopia
Volume 8 Issue 1
Received Date: January 05, 2023
*Corresponding author: Moges Eriso Blate, College of Veterinary Medicine, Haramaya
Published Date: February 08, 2023
University, P.O. Box: 138, Dire Dawa, Ethiopia, Tel: +251910214953; Email: mogosereso99@
DOI: 10.23880/oajvsr-16000233
gmail.com

Abstract

Avian influenza (Bird flu) is a highly infectious disease caused by an Orthomyxovirus of the family Orthomyxoviridae. Avian
influenza viruses are classified in the genus influenza virus A that infects wide variety of domestic and wild animal species.
Aquatic birds are the natural hosts of avian influenza viruses as asymptomatic carriers. Mode of transmission of this virus in
poultry flock is through ingestion, inhalation and mechanical transmissions and its clinical signs are variable. Avian influenza
is distributed worldwide. According to disease severity avian influenza is classified into two forms: highly pathogenic avian
influenza (HPAI) also known as fowl plague, and low pathogenic avian influenza (LPAI). HPAI viruses are highly virulent
representing the greatest concern for public health and economic importance and categorized as List a disease by OIE.
Diagnosis mainly depends on isolation and identification of viruses. Serological tests and RT-PCR are also used. The disease
is not treatable except trials for secondary microbial complications. Biosecurity is the most useful method for prevention and
control.

Keywords: Avian; Influenza; Pathogen; Virus

Abbreviations: HPAI: Highly Pathogenic Avian Influenza; influenza viruses emerge. Avian influenza has therefore a
LPAI: Low Pathogenic Avian Influenza; HPAIV: Highly high impact on both animal and human health.
Pathogenic Avian Influenza Virus; HP: High Pathogenicity; LP:
Low Pathogenicity; HA: Hemagglutinin; NP: Nucleoprotein; The best known disease caused by an avian influenza
M: Matrix; HA: Hemagglutinin; NA: Neuraminidase; CNS: virus is fowl plague. Fowl plague was first reported in 1978
Central Nervous System; AI: Avian Influenza. and in 1901, causing severe loses in poultry, and in 1955
it was identified as avian influenza virus. From the 1970s
Introduction onward surveillance indicates the ubiquitous presence of
avian influenza virus in water fowl and the risk these birds
Avian influenza, which is caused by influenza a viruses, posed to commercial chicken industries. In 1997 a highly
can affect variety of domestic and wild bird species. Avian pathogenic avian influenza virus (HPAIV) emerged in Hong
influenza viruses are the causative agents of periodically Kong that had killed close to 150 million birds in Asia up
occurring disease outbreaks in birds with high damage to the beginning of 2005 [1]. Type an influenza viruses are
to the poultry industry. In addition, these viruses provide notorious for their ability to undergo antigenic change with
the genetic pool from which human and other mammalian time and to give rise to new viral subtypes. When different

Epidemiology and Pathogenesis of Avian Influenza Type a Virus Infection in Poultry, A Review J Vet Sci Res
2
Open Access Journal of Veterinary Science & Research

subtypes infect the same animal host genetic recombinants antigenically distinct types of influenza viruses. These
may occur: Some of the genes from one virus strain may are Type A, Type B and Type C influenza viruses. The type
replace those within another strain, giving rise to a new viral specificity is determined by antigenic nature of nucleoprotein
subtype. (NP) and matrix (M) antigens which are closely related
among all influenza [6].
Many combinations of hemagglutinin and neuraminidase
antigens in influenza A viruses are represented in isolates Type an influenza viruses are further divided into
from avian species, particularly from water fowl. Influenza subtypes based on the antigenic relationships of the surface
sub types are distributed worldwide and are frequently glyco proteins, hemagglutinin (HA) and neuraminidase (NA).
recovered from clinically normal birds. Outbreaks of severe To date, 16HA subtypes (H1-H16) and 9NA subtypes (N1-
clinical disease, usually caused by subtypes expressing H5 N9) have been recognized. Each virus has one HA and one
and H7 determinants, occur periodically in chicken and NA antigen apparently in any combination. All influenza
turkeys. In these species acute infection is often referred subtypes in the majority of possible combinations have been
to as fowl plague or highly pathogenic avian influenza and isolated from avian species. Thus far, only virus of H7, H5 and
categorized as List a disease by OIE [2]. H10 subtypes have been shown to cause highly pathogenic
avian influenza (HPAI) in susceptible species [7]. Based on
Avian influenza is classified by the World Organization pathotype (pathogenicity), avian influenza viruses from
for Animal Health (OIE) in to two forms, High pathogenicity poultry are classified into two pathotypes, highly pathogenic
(HP) and low pathogenicity (LP), based on virulence in and low pathogenic avian influenza. These terminologies are
chicken. H7 is one of the two economically important avian originally based on lethality in experimentally inoculated
influenza virus subtypes because historically all highly chicken [8].
pathogenic avian influenza viruses have been either H7 or
H5 subtype and it is among the most common subtype in To date, apart from the H10 isolates, only viruses of H5
commercial poultry in the world. In numerous cases the high and H7 subtypes have been shown to cause HPAI. It appears
pathogenic form mutated from a low pathogenic H7 or H5 that most of these viruses arose by mutation after wild bird
virus that was circulating in chickens or turkeys. However, reservoir. Highly Pathogenic avian influenza viruses arose by
not all H7 LPAI viruses become high pathogenic [3]. Influenza mutation after wild bird reservoir. Most HPAI viruses appear
A viruses are highly contagious pathogens that have been to have arisen as a result of spontaneous duplication of purine
isolated from a wide variety of animals including man, birds, triplets, which is the insertion of basic amino acids at the
swine, horses, minks, seals and most recently from cats and cleavage site. This most likely occurred due to transcription
dogs. Influenza A viruses are rarely known to cross species error by the polymerase complex [9]. The factors that bring
barriers, however their interspecies transmission has always about mutation from low pathogenic to high pathogenic
been a major concern. Although determinants of inter species avian influenza are not known. However, it can be reasonably
transmission are still not fully identified, many studies assumed that the wider the circulation of LPAI in poultry, the
showed that the compatibility between the hemagglutinin higher the chance that there will be a mutation to HPAI. In
(HA) protein of the virus and its corresponding receptor on some cases, low pathogenic avian influenza (LPAI) viruses
the host cell is essential for establishment of an infection in of the H5 or H7 subtypes circulated for very long periods of
a specific host [4]. time without mutating to highly pathogenic form Sfakianos
et al., [10].
The objective of this paper is:
 To review the epidemiology and pathogenesis of avian Morphology and Chemical Composition of Avian Influenza
influenza type A virus infection in poultry. Viruses:Virions are typically spherical to pleomorphic but
can be filamentous. Individual virions range in diameter
A General Overview of Avian Influenza Type from 80-120 nm, but the filamentous forms can have lengths
a Virus Infection In Poultry up to several hundreds of nm [6]. A helical nucleocapsid is
enclosed within the viral envelope. The surface is covered by
Etiology two types of glycoprotein projections, rod shaped trimer of
HA and mushroom shaped trimers of NA. The virions may
Avian influenza is caused by an orthomythovirus of the be disintegrated with detergents, resulting in the release
family orthomythoviridae. An orthomythoviridae contains 5 of spikes, which retain their respective activities. The HA is
genera, 3 of which contain influenza viruses. Influenza virus responsible for the attachment of the virion to cell surface
A is the main cause of avian influenza in poultry [5]. receptors (Sialyl oligosaccharides) and is responsible for
the hem agglutinating activity of the virus. Neuraminidase
Classification: Based on antigenicity, there are three enzyme activity is responsible for the release of new virus

Blate ME. Epidemiology and Pathogenesis of Avian Influenza Type a Virus Infection Copyright© Blate ME.
in Poultry, A Review. J Vet Sci Res 2023, 8(1): 000233.
3
Open Access Journal of Veterinary Science & Research

from the cell by its action on the neuromeric acid in the geographic region, country, species and age of birds, time of
receptors [7]. year and the environment or agricultural system occupied
[7].
All influenza viruses have eight different gene segments
that encode at least 10 different viral proteins. The structural The primary introduction of low pathogenic avian
proteins in the mature virion can be divided into the surface influenza viruses into a poultry population is a result of
proteins that include hemagglutinin (HA), neuraminidase wild bird activity, usually water fowl, but gull and sore birds
(NA), membrane ion channel proteins and the internal have also been implicated. Similarly backyards reared in the
proteins including nucleoprotein (NP), matrix protein and Italy have been shown to harbor the same viruses isolated
polymerase complex composed of the polymerase basic from water fowl during the same period. In considering
protein 1, polymerase basic protein 2 and polymerase acidic prevalence and distribution of influenza viruses in avian
protein. Two additional proteins produced by influenza species, it becomes clear that many viruses circulate in birds
viruses are nonstructural protein 1 and nonstructural throughout the world [7].
protein 2, which is also known as the nuclear export protein.
The nonstructural protein 2 is primarily found in host cells, Most often the wild birds that are host to the virus do
but some protein can be found in the virion [11]. not get sick, but they can spread influenza to other birds.
Infection with certain avian influenza A viruses (for example,
Influenza virions are composed of 0.8-1.1% RNA, 70-75% some H5 and H7 strains) can cause wide spread disease and
protein, 5-8% carbohydrates and 20-24% lipids. The lipids disease among some species of domestic birds (Center for
are located in the viral membrane; most are phospholipids Disease Control and Prevention; http://www.cdc.gov). Over
with smaller amount of cholesterol and glycolipids. Several the past two decades, the incidence of avian subtypes of
carbohydrates including ribose, galactose, mannose and influenza a virus directly infecting humans has dramatically
glucosamine are present in the virion mainly as glycoprotein increased. Land use changes, cultural practices and
or glycolipids. The composition of the lipid and carbohydrate worldwide outbreaks have contributed this increase [14].
chains linked to glycoproteins or glycolipids of the viral
membrane are determined by the host cell [7]. Host Range and Reservoir Host: The natural reservoir
of influenza a viruses is aquatic birds, in which the viruses
Antigenic Variation: Influenza A viruses can undergo appear to have achieved an optimal level of host adaptation
antigenic variation in two ways, antigenic drift and antigenic and do not cause disease. The exception is the H5N1 strain
shift. Antigenic drift involve minor point mutations resulting which had already crossed to humans in 1997 (in Hongkong)
in RNA replication errors. The mutations will be expressed in and those crossing have gradually increased in frequency
the new virions produced. Although such mutations may be and distribution in recent years. Avian influenza viruses have
detrimental, on occasion one might have a subtype change in been shown to infect birds and mammals. Generally speaking
shape (that is the structural shape has “drifted”) so they are the former are infected more readily and efficiently than the
not recognized by the host’s immune system [12]. later and the interspecies and interspecies transmission with
in the class Mammalia. One of the main factors that influence
Antigenic shift occurs only among influenza A viruses susceptibility to infection is the receptor conformation on
in two ways. In the first, influenza A viruses of two different the host cells [15].
subtypes simultaneously infect the same host allowing
reassortment, of exchange of viral RNA segments in the host’s Influenza viruses have been shown to infect great
cells. The second possible mechanism involves the direct variety of birds and highly pathogenic avian influenza was
transmission of influenza virus from avian or other animal a disease of domesticated birds and those wild birds usually
species to humans with subsequent adaptation by mutation only harbored the low pathogenic avian influenza. It seems
to the new human host. Genetic reassortment between likely that part of influenza gene pool is maintained in shore
human and avian viruses is suggested as the mechanism by birds and from which the predominant number of isolated
which new human pandemic strains arise [13]. influenza viruses are of subtype different from those isolated
from ducks. Pigs have an important role in the ecology
Epidemiology of the Disease and epidemiology of influenza viruses and are regarded as
“mixing vessel” for the introduction of reassorted viruses
Incidence and Distribution: Influenza viruses are into the human population, primarily because of their
distributed throughout the world in many domestic birds, susceptibility to human and avian viruses [16].
including turkeys, chicken, guinea fowl, quail, pheasants,
geese and ducks and in wild bird species. However, incidence Risk Factors: There are several recognized risk factors
and distribution of avian influenza varies greatly with for the introduction of influenza A viruses into a domestic

Blate ME. Epidemiology and Pathogenesis of Avian Influenza Type a Virus Infection Copyright© Blate ME.
in Poultry, A Review. J Vet Sci Res 2023, 8(1): 000233.
4
Open Access Journal of Veterinary Science & Research

poultry. These include 1) direct access of poultry to wild birds is through active or passive immunity. Principally against
infected with avian influenza viruses, especially wild ducks. avian influenza virus HA, and to a lesser extent, the NA, but
Outbreaks of multiple subtypes of avian influenza occurred such protection for the first one to three weeks post hatching,
routinely in the fall when infected ducks had the opportunity while active immunity was effective for longer periods of
to contact with turkeys. Once the virus was introduced to a time [11].
turkey farm, the virus could become adapted to turkeys and
spread to other turkey farms by the movement of infected Active immunity develops via infection with avian
birds and contaminated materials. 2) Infection through avian influenza virus as well as immunization with vaccines that
influenza virus contaminated drinking water. 3) Exposure elicits a humeral antibody response at both systemic and
of turkeys to pigs infected with the swine influenza virus. mucosal level. This includes a systemic IgM response by
Turkeys are susceptible to swine influenza viruses and 5 days post infection, followed shortly by an IgG response.
having turkey farm and swine farm in a close proximity The intensity of antibody response against surface proteins
is a risk factor for the introduction of swine influenza to varies with bird species. While passive immunity studies on
turkeys. 4) Live bird marketing system is a risk factor for the protection by maternal antibody to homologous HA or
the introduction of avian influenza virus into commercial NA have not been reported. Based on evidence available for
poultry. Domestic water fowl, primarily ducks are often other avian pathogens, protection against clinical signs and
raised on ponds where exposure to wild birds, including death from homologous avian influenza viral challenge is
ducks is common. This provides high risk for domestic ducks probable for the first two weeks after hatching [20].
to be infected with avian influenza [17].
Pathogenesis
Modes of Transmission: Influenza Type a viruses normally
seen in one species across over and cause illness in another The pathogenesis of avian influenza virus varies widely
species. It is transmitted by direct contact between infected depending on strain of virus, age and species infected
and susceptible birds or indirect contact through aerosol concurrent infections and husbandry. Avian influenza
droplets or exposure to virus contaminated fomites. Thus viruses can infect wide range of domestic and wild birds
avian influenza viruses are readily transported to other including chicken, ducks, turkeys, geese, quail, pheasants
premises by people (contaminated shoes and clothing) and and migratory birds. In these natural hosts, influenza viruses
equipments shared in production, live haul and live bird replicate in the gastro intestinal tract and are secreted in
marketing [18]. large amounts in to the feces [21].

Source of infection for the initial introduction of influenza Avian influenza virus hemagglutinin (HA) adsorbs
viruses in to commercial poultry flocks include other species to host cell receptors containing sialic acid bound to
of domestic poultry, exotic captive birds, wild birds and other glycoproteins, thus initiating receptor mediated endocytosis.
animals. Brocken contaminated eggs may infect chicks in the In these endosomes, low pH dependent fusion occurs via
incubator. HPAI viruses have been recovered from the egg HA mediated fusion of viral envelope with the endosome
shell and internal egg contents. Some avian influenza virus membrane. Proteolytic cleavage of HA into HA1 and HA2 is
strains can be transmitted to mammals by direct or indirect an essential pre-requisite for fusion and infectivity. The viral
contact; close contact with dead or sick birds seems to be the nucleocapsid is transported to the nucleus where the viral
principal means of transmission to humans [19]. transcriptase complex synthesizes mRNA [22].

Immunity: Immunity to influenza occurs through a Determinants of Pathogenicity of Avian Influenza

number of steps; initially, a large cytokine response Viruses:
occurs and characterized predominantly by IL-2, IL-6 and • Viral Factors: Abroad tissue tropism and the ability to
interferon gamma production. This leads to extensive local replicate systemically are hall marks of these viruses. The
inflammation with neutrophils and macrophages infiltrating most important and well-studied molecular correlate
the sub epithelium of the respiratory tract. Within the alveolar of these properties reside in the cleavability of the HA
macrophages and pneumocytes, MHC-I up regulation leads precursors of glycoprotein [23]. The viral factors that
to antigen presentation of the hemagglutinin and other sub determine the pathogenesis and virulence of influenza
capsular proteins. This eventually leads to natural killer viruses include ability to bind to host cells, ability of virus
cell destruction of infected cells and the development of shedding, escape from immunosurveilance by evolution
neutralizing antibodies largely against HA by day 14 of of antigenic variation or recombination with different
infection [14]. virus strains from zoonotic disease and modulation
of the immune response to attenuate effective host
Method to produce resistance to avian influenza viruses defense mechanism (Influenza report; http://www.

Blate ME. Epidemiology and Pathogenesis of Avian Influenza Type a Virus Infection Copyright© Blate ME.
in Poultry, A Review. J Vet Sci Res 2023, 8(1): 000233.
5
Open Access Journal of Veterinary Science & Research

influenzareport.com). tubules, pancreatic acinar epithelium and other organs with

• Host Factors: The virulence of highly pathogenic avian epithelial cells having trypsin-like enzyme [11].
influenza viruses are clearly influenced by the specific
host. Two variants of H5N1/97 virus one of which was Clinical Findings and Lesions
isolated from a human patient with mild respiratory
illness and the other form a fatal human case, displayed Clinical signs, severity of disease and mortality rates vary
similar differential pathogenicity in mice [20]. depending on avian influenza virus strain and host species.
Low pathogenic avian influenza (LPAI) viruses typically
Virions with uncleaved hemagglutinin are noninfectious. produce respiratory signs such as ocular and nasal discharge
Hemagglutinin cleavability is dependent on its primary & swollen infra orbital sinuses. Lesions in the respiratory tract
structure that the site where cleavage occurs and the presence include congestion and inflammation of trachea and lungs. In
of the right proteases in the target tissues that can carry out layers and breeders there may be decreased egg production
that cleavage. In epithelial cells lining the respiratory and or fertility, ova rupture and mucosal edema. High pathogenic
intestinal tracts, the hemagglutinin of all incoming avian avian influenza (HPAI) viruses cause severe systemic disease
influenza viruses are cleaved by host proteases, there by with high mortality in chicken, turkey and other gallinaceous
activating its fusion activity and allowing its entry. However, birds. In per-acute cases, clinical signs or gross lesions may
in other tissues, only hemagglutinins of virulent viruses are be lacking before death. However, in acute cases, lesions may
cleaved, leading to systemic disease and death [24]. include cyanosis and edema of head, comb, wattle; edema
and discoloration of shanks and feet due to subcutaneous
The pathogenesis of avian influenza is quite different echymotic hemorrhages; petechial hemorrhages on visceral
from that in mammals. Infection with the most virulent organs and in muscles; and blood tinged oral and nasal
strains is characterized by viremia and multifocal lymphoid discharges. In severely affected birds, greenish diarrhea is
and visceral necrosis, leading to pancreatitis [24]. The host common. The location and severity of microscopic lesions
factors that determine the pathogenesis and virulence of are highly variable and may consist of edema, hemorrhage,
influenza viruses include presence of target receptors on host necrosis in parenchyma cells of multiple visceral organs, skin
cells, availability of enzymes in host cells which are essential and central nervous system (CNS) [25].
for viral entry and replication, state of immunocompetence
of the individual host and ability of the immune system to Diagnosis
control the viral replication effectively without causing
serious collateral damage for the host by its inflammatory Clinical diagnosis is usually not possible except in an
response (Influenza report; http://www.influenzareport. epidemic. Virus isolation is essential not only to establish
com). the cause of an outbreak but also to assess objectively
the virulence of the causative virus [24]. A definitive
Persistence Infection: In poultry, first, the process begins diagnosis requires viral isolation and identification or the
by inhalation or ingestion of infective mild pathogenic or demonstration rising antibody titer by viral neutralization
highly pathogenic avian influenza (HPAI) virions. Multiple tests, soluble antigen fluorescent antibody test, agar gel
replication cycle occur in respiratory and/or intestinal tract precipitation or ELISA technique [18].
with release of infectious virions. In poultry the nasal cavity
is the major site of initial replication. Second, the virions Methods for virus isolation include 1) Candle 9- to 11-day-
invade sub mucosa entering capillaries. The virus replicates old embryonated fowl’s eggs to check embryo viability. Mark
with in endothelial cells and spread via the vascular/ the shell of the egg with a pen to delimit the air sac. With a
lymphatic systems to infect and replicate in variety of cell manual or electric device, drill a small hole just above the air
types in visceral organs, brain and skin. Clinical signs and sac. 2) Record the identification number of the sample, the
death are due to multiple organ failure. Damage caused by passage number (1° or 2°), the kind of sample (lung, cloacal
avian influenza virus is the result of one of the following three swabs, etc.) and the date of inoculation on five eggs. 3)
processes such as direct virus replication in cells, tissue and Inoculate 0.1–0.2 ml of clarified supernatant obtained from
organs, indirect effects from production of cellular mediators the tracheal and cloacal swabs or from the organ homogenate
(cytokines) and ischemia from vascular thrombosis. Third, into the allantoic cavity of each of the five 9- to 11-day-old
for the mild pathogenic avian influenza viruses, replication embryonated fowl’s eggs. 4) Seal the eggs with glue or wax.
usually limited to the respiratory or intestinal tracts. Illness 5) Incubate the inoculated eggs at 37°C for 7 days. Candle
or death is most often from respiratory damage, especially if the inoculated eggs daily to check embryo viability. 6) Test
accompanied by secondary bacterial infections. Occasionally, the allantoic fluid of eggs containing dead embryos for
the mild pathogenic avian influenza viruses spread haemagglutinating (HA) activity. 7) If HA activity is detected,
systemically, replicating and causing damage in kidney identify the HA agents by means of the haemagglutinating

Blate ME. Epidemiology and Pathogenesis of Avian Influenza Type a Virus Infection Copyright© Blate ME.
in Poultry, A Review. J Vet Sci Res 2023, 8(1): 000233.
6
Open Access Journal of Veterinary Science & Research

inhibition (HI) test. 8) After 7 days, chill the remaining eggs level, countries must be willing to report disease out
in a refrigerator (4°C) to end the first passage. The following breaks. The fowl plague form of avian influenza appears
day, open the eggs using sterile techniques under a laminar in list A of the International Animal Health Code of the
flow cabinet. Collect approximately 10 ml of the allantoic Office International des Epizootics; the disease is there by
fluid. 9) Test the allantoic fluid for the presence of HA activity notifiable and restrictions apply to the movement of birds
by the “rapid HA test”. 10) If bacteria are present, the fluids or avian products. At the national level, many countries have
must be passed through a 450-nm membrane filter. 11) A regulations aimed at preventing the introduction and spread
sample giving a positive result in the rapid HA test must be of virus; these are often primarily concerned with new castle
tested further [5]. disease. Policies usually involve trade embargoes to guard
against importation of infected birds or avian products from
The use of diagnostic methods based on molecular countries not declared “virus free”. At the local farm based
technology has improved substantially over the last decade; level, efforts are aimed at preventing virus introduction into
consequently, laboratory tests for the identification and chicken and turkey flocks from wild birds. Today, commercial
characterization of avian influenza (AI) viruses have become chicken facilities are always made wild bird proof [24].
available. Such tests may be used to detect the AI viral genome
directly from clinical specimens as well as to generate data There are six basic tools used to control and prevent
on the molecular characteristics of an isolate or of viral RNA avian influenza. These include farm biosecurity, stamping
present in a sample collected from an infected animal. In out, cleaning and disinfection, movement management and
addition, the current definitions of highly pathogenic AI are vaccination. None of these measures used alone is likely
based on the results of conventional and molecular techniques, to lead to elimination of infection. Control and eradication
thus, the latter are among the official methods used to identify of AI also depend on a fully functional surveillance system
virulence factors and to confirm the presence of HPAI viruses that allows early detection of infection and disease. This
in laboratory specimens. Such as RT-PCR, polymerase chain requires a well-resourced and trained veterinary service.
reaction and real-time PCR techniques [5]. Control programs should be backed by public education and
behavioral change campaigns to provide accurate and timely
As differential diagnosis, Low pathogenic avian influenza information on the nature of the disease to groups at risk. It
must be differentiated from other respiratory diseases or is important that programs fully engage all stakeholders to
causes of decreased egg production including acute to sub- ensure success [12].
acute viral diseases such as infectious bronchitis, infectious
laryngotracheits, lentogenic New castle disease, and Public Health and Economic Importance
infections with other paramyxoviruses; bacterial diseases
such as mycoplasmosis, infectious coryza and respiratory Avian influenza (Bird flu) mainly infects birds, but is
form of fowl cholera and fungal diseases such as aspergilosis. concern to humans, who have no immunity against it. The
Highly pathogenic avian influenza must be differentiated virus that causes this infection in birds can mutate and easily
from other causes of high mortality such as velogenic new infect humans and potentially start a deadly worldwide
castle disease, and sever water depression [25]. epidemic. Pandemic influenza virus has its origin in avian
influenza viruses. The highly pathogenic avian influenza
Treatment virus subtype H5N1 is already panzootic in poultry, with
attendant economic consequences. It continues to cross
Avian influenza (Bird flu) control activities there is species barriers to infect humans and other mammals,
no specific treatment. Broad spectrum antibiotics used often with fatal outcomes. Therefore, H5N1 virus has rightly
to control secondary bacterial invaders and increasing received attention as a potential pandemic threat [28].
house temperature may help to reduce mortality in poultry.
Vaccination with autogenous virus or a virus of the same Avian influenza virus which was responsible for fatal
hemagglutin in type used as prophylaxis [26]. As with human disease has the genetic formula H5N1. Meanwhile, a
any viral infections, no chemotherapeutic agent can cure second avian influenza virus (H9N2) has been isolated from
influenza in human beings. Amantadine hydrochloride is humans. Both viruses are genetically linked to influenza
used as prophylactic treatment for some high risk individuals viruses found in quail. A third avian virus, H7N7, can also
such as elderly or persons with little natural defenses [27]. infect humans [29].

Control and Prevention The biggest threat resulting from demonstrations of

direct natural infections of humans with avian influenza
Avian influenza (Bird flu) control activities operate at viruses is that pandemic viruses could emerge as a result
international, national and local levels. At the international without an intermediate host. There are two mechanisms

Blate ME. Epidemiology and Pathogenesis of Avian Influenza Type a Virus Infection Copyright© Blate ME.
in Poultry, A Review. J Vet Sci Res 2023, 8(1): 000233.
7
Open Access Journal of Veterinary Science & Research

by which this could occur: by genetic reassortment or by pathogenesis, transmission and clinical features and
progressive adaptation the first cause could occur if a person preparing for the prevention and management of its outbreak
was simultaneously infected with avian influenza virus and will help to avoid its potential devastating consequences [34-
human influenza virus. The second mechanism by which 37].
the generation of a pandemic virus may occur is through
progressive adaptation of virus entirely of avian origin. Based on the above conclusion, the following
Recent studies on the genome of H1N1”Spanish flu” influenza recommendations are forwarded:
virus, which affected a human beings at the beginning of 20th • Authorities should be notified immediately of any
century, have resulted in the speculation that this virus was suspicious cases of Highly Pathogenic avian influenza
entirely of avian origin and not generated by re-assortment (HPAI).
[30]. • While waiting for the authority or a confirmed diagnosis,
all suspect animals should be quarantined.
Variations in cell receptor specificity on respiratory • Should highly pathogenic avian influenza (HPAI) be
tract epithelium may account for some of the differences in confirmed by diagnosis?
influenza virus transmission and efficient replication. Avian • Individual and organizational awareness creation
respiratory epithelium has predominantly α- 2, 3 linkage about economically devastating nature of the disease is
while human respiratory epithelium has predominately α-2, required.
6 linkage. Two cases are exceptions with presumed exposure • To control outbreak of HPAI the premises must be
through consumption of raw duck blood and organs, and thoroughly cleaned and disinfected and there should be
defeathering H5N1 infected dead swans [9]. proper destruction of all exposed cadavers, litter and
animal products.
The highly pathogenic strain of the H5N1 avian influenza
virus was first isolated and characterized in a domestic goose References
in the southern Guangdong of china in 1996. The following
year, the first H5N1 HPAI outbreak occurred in domestic 1. Wernery U (2008) Influenza. In: Samour J (Ed.), Avian
poultry in Hongkong, resulting in the culling of 1.5 million Medicine. 2nd (Edn.), Elsevier, China, pp: 358-360.
chickens in an effort to control and eliminate the disease [31].
2. Quinn PJ, Markey BK, Leonard FC, Hartigan P, Fanning
It is likely that H5N1 virus infection among domestic poultry
S, et al. (2002) Veterinary Microbiology and Microbial
has become endemic in certain areas and that sporadic
Diseases. 2nd (Edn.), Blackwell Science, Iowa State
human infections resulting from direct contact with infected
University, USA, pp: 375-380.
poultry and/or wild birds will continue to occur (Center for
Disease Control and prevention; http://www.cdc.gov) [32]. 3. Spackman E, Gelb J, Preskenis LA, Ladman BS, Pope CR,
et al. (2010) The pathogenesis of low pathogenicity H7
The full name of H5N1 avian influenza virus is more Avian influenza viruses in chicken, ducks and turkeys.
revealing of the virus that was initially isolated by scientists. Virol J 7: 331.
The circulating H5N1 virus that is the current source of
fear throughout the world is officially named A/Goose/ 4. Yassine HM, Al-natour MQ, Lee CW, Saif YM (2007)
Guangdong/1/96(H5N1). The deadly characteristics of this Interspecies and intraspecies transmission of triple
virus in humans lead to the categorization of the virus into reassortant H3N2 Influenzaviruses. J Virol 4: 129-135.
the highly pathogenic category of influenza virus [10]. 5. Capua I, Alexander, DJ (2009) Avian influenza and New
Castle Diseases: Afield and Laboratory Manual. Springer-
In addition to the human deaths that have occurred Verlag, Italia, pp: 2-19.
due to H5N1 virus and largely as a result of that, the highly
pathogenic avian influenza panzootic caused three notable 6. Cox NJ, Fuller N, Kaverin N (2000) Orthomyxoviridae. In:
economic and social impacts. These are market shocks, Regenmortel VMH, et al. Virus Taxonomy 7th report of
negative consequences for lively hood as a result of the the International Committee on Taxonomy of Viruses.
disease and the control process applied to control it and Academic Press, Sandiego, pp: 585-597.
changes to the structure of the poultry market chains [33].
7. Easterday BC, Hinshaw VS, Halvorson DA (1997)
Influenza. In: Calnek W, et al. (Eds.), Diseases of Poultry.
Conclusion and Recommendations 10th (Edn.), Iowa State University Press, pp: 583-605.
Avian influenza (Bird flu) is a public health threat that 8. Zuckerman AJ, Banatvala JE, Griffiths P, Schoub B,
has the potential to cause serious illness and death in poultry Mortimer P (2009) Principles and Practices of clinical
as well as in humans. Understanding its epidemiology, Virology. 6th(Edn.), Black-well, Willey, USA, pp: 1042.

Blate ME. Epidemiology and Pathogenesis of Avian Influenza Type a Virus Infection Copyright© Blate ME.
in Poultry, A Review. J Vet Sci Res 2023, 8(1): 000233.
8
Open Access Journal of Veterinary Science & Research

9. Perdue ML, Suazer DL, Swayne DE (2000) Avian influenza basic cleavage site is activated by furin, a subtilisin-like
in the 1990s. Poultry and Avian Biology Reviews 11(1): endoprotease. EMBO 11(7): 2407-2414.
1-20.
24. Murphy F, Gibbs E, Horiznek M, Studdert M (1999)
10. Sfakianos JN, Alcamo IE, Heyman D (2006) Avian Flu: Veterinary Virology. 3rd (Edn.), Academic press, USA, pp:
Deadly Disease epidemics. Info Base, USA, pp: 50. 460-468.
11. Swayne DE (2008) Avian Influenza. 1st(Edn.), John Wiley 25. Kahn CM (2005) The Merck Veterinary Manual. 9th
& Sons, Inc, pp: 287-298. (Edn.), Merck & Co, USA, pp: 2712.
12. Pommerville JC (2010) Alcamo’s Fundamentals of 26. DACA (Drug Administration and Control Authority of
Microbiology. 9th (Edn.), In: Jomes and Bartlett (Eds.), Ethiopia) (2006) Standard Treatment Guide lines for
Iowa State University Press, pp: 915. Veterinary Practice. 1st(Edn.), Addis Ababa university,
Ethiopia, pp: 265-266.
13. Hampson AW (2002) Influenza Virus Antigens and
Antigenic drift. In: Potter CW, et al. (Eds.), Influenza. 27. Atlas RM (1997) Principles of Microbiology. 2nd (Edn.),
1st(Edn.), Elsevier science Ltd., pp: 49-86. McGraw-Hill, New York, pp: 1298.
14. Sandrock C (2009) Ecology and epidemiology of 28. Peiris JSM, Jong MDD, Guan Y (2007) Avian Influenza
influenza viruses. In: Arch GM, et al. (Eds.), Management Virus (H5N1): a Threat of Human Health. Clin Microbiol
of Infectious Diseases: Impact of antibiotic resistance. Rev 20(2): 243-267.
2nd (Edn.), Claire pomery, UK, pp: 112-148.
29. Krauss H, Weber A, Appel M, Enders B, Isenberg HD, et al.
15. Kawaoka Y, Chambers TM, Sladen WL, Webster RG (2003) Zoonoses: Infectious disease transmission from
(1988) Is the gene pool of influenza viruses in shorebirds Animal to Humans. 3rd(Edn.), ASM press, pp: 456.
and gulls different from that in wild ducks? Virol 163(1):
247-250. 30. Taubenberger JK (2005) The virulence of the 1918
Pandemic influenza virus: unraveling the enigma. Arch
16. Radostits OM, Gay CC, Hinchclifft KW, Constable PD Virol Suppl 19: 101-115.
(2007) Veterinary Medicine: A Text Book of the diseases
of cattle, horses, sheep, pigs and goats. 10th (Edn.), 31. FAO (2008) The Global Strategy for Prevention and
Saunders Elsevier Ltd., London, pp: 2162. Control of H5N1 Highly Pathogenic Avian Influenza
Virus. Food and Agricultural Organization of the United
17. Suazer DL, Schultz-Cherry S (2000) Immunology of avian Nations, pp: 1-60.
influenza virus: a review. Dev Comp immunol 24(2-3):
269-283. 32. Avian Influenza: Current H5N1 Situation.

18. Ardans AA (1999) Orthomyzoviridae. In: Hirsh DC, Zee 33. CDC (2021) Prevention-Avian Influenza (Flu).
YC (Eds.), Veterinary Microbiology. 1st(Edn.), Black well 34. Gauthier CM, Lebarbenchon C, Thomas F (2007) Recent
Science, USA, pp: 396-402. expansion of highly pathogenic avian influenza H5N1: a
19. Davorak G, Spickler AR, Roth JA (2008) Hand Book for critical review. Wiley Online Library 149(2): 202-214.
Zoonotic Diseases of Companion Animals. 1st(Edn.), 35. Klenk HD, Keil W, Neimann H, Geyer R, Schwarz RT
Iowa State University Press, USA, pp: 76-145. (2008) Influenza. In: Thomas C, et al. (Eds.), Animal
20. Easterday BC, Hinshaw VS (1991) Influenza. In: Calnek viruses molecular Biology. Caister Academic Press, Great
BW, et al. (Eds.), Diseases of Poultry. 9th(Edn.), Iowa state Britain, pp: 254-262.
University Press, USA, pp: 532-551. 36. (2011) Pathogenesis and Immunology of Influenza.
21. Faquet CM, Mayo MA, Desselberger U, Ball LA (2005) 37. Webster RG, Bean WJ, Gorman OT, Chambers TM,
Virus Taxonomy: Classification and nomenclature. Iowa Kawaoka Y (1992) Evolution and ecology of influenza A
State University Press, USA, pp: 92-131. viruses. Microbiol Rev 56(1): 152-179.
22. Gorman OT, Bean WJ, Kawaoka Y, Webster RG (1990)
Evolution of the nucleoprotein gene of Influenza A virus.
J Virol 64(4): 1487-1497.
23. Stenek GA, Vey M, Angliker H, Shaw E, Thomas G, et
al. (1992) Influenza virus hemagglutinin with multi

Blate ME. Epidemiology and Pathogenesis of Avian Influenza Type a Virus Infection Copyright© Blate ME.
in Poultry, A Review. J Vet Sci Res 2023, 8(1): 000233.

View publication stats