Avian influenza virus causes domestic poultry as well as wild birds and pets. Avian influenza in birds is caused by type A influenza viruses. Orthomyxo viruses causes significant numbers of natural infections and diseases, mostly of the lower and upper respiratory tract in humans, horses, pigs, dogs and various bird species.
Infection with avian influenza viruses typically produces asymptomatic infection to respiratory disease, drop in egg production, systemic diseases with nearly 100% mortality. Disease severity depends on the virus strain as well as age, species, and immune status of the bird. Wild water fowl and many other aquatic birds are the primary reservoir of all influenza A viral gene.
Commonly avian influenza is known as bird flu infection in humans, poultry and other mammals. Office International des Epizooties (OIE) classify avian influenza as highly pathogenic avian influenza (HPAI) and low pathogenic avian influenza (LPAI).
The World Organization for Animal Health (Office International des Epizooties (OIE) uses the designation of notifiable AI (HP notifiable AI (HPNAI) and LP notifiable AI (LPNAI) for international animal health regulatory purposes.
Avian influenza viruses are classified in the family Orthomyxoviridae, genus Influenza virus A. Morphologically Virions are spherical to pleomorphic (120 nm) but can be filamentous with lengths up to several hundred nm. The surface is covered by two types of glycoprotein projections rod-shaped trimers of hemagglutinin (HA) and mushroom-shaped tetramers of neuraminidase (NA).
AI viruses are further divided into 16 hemagglutinin and 9 neuraminidase subtypes. The nucleocapsid is helical. The viral genome is composed of eight segments. Virus is negative sense single-stranded RNA that code for 10 or 11 proteins depending on strain. Eight proteins are constituents of the virus (HA, NA, nucleoprotein (NP), M1, M2, PB1, PB2, and PA, and minor amount of NS2), and a non- structural protein (NS1) is present in the host cell cytoplasm.
Economic losses from AI depends on the strain of virus, age and species of infected bird, number of farms involved, control strategies, control implementation speed or eradication method used. Many outbreaks and economic losses occur from epidemics of HPAI or LPAI in commercially raised poultry, mostly chicken and turkeys.
Direct losses in HPAI outbreaks includes high morbidity and mortality, disinfection and cleaning, depopulation and disposal cost, surveillance and quarantine costs and indemnities paid for the birds. However, Indirect losses due to HPAI includes temporary or permanent loss in poultry exports, loss of income during production down time. The cost for eradication of HPAI is very high and appear to be proportional to the number of birds that died or culled.
Low pathogenic AI also cause significant economic losses for producers of chickens, ducks and turkeys especially when accompanied with secondary infection. Losses from LPAI epidemics include mortality loss, medication cost against secondary bacterial infection, increase condemnation at slaughter, cleaning and disinfection, delayed placement of new birds, restriction in trade of poultry bird.
In LPAI, losses are less than HPAI outbreak because infected flock is eliminated through a controlled marketing program, low mortality rate, no federal eradication cost and no national and international trade have been disrupted although bans are placed on imports by some countries.
Epidemiology and Transmission
AI virus is distributed worldwide. AI virus may be present in village or backyard flocks that sold through live poultry market but most commonly raised poultry in many developed countries are free from avian influenza virus. The incubation period is highly variable depends upon dose of virus, route of exposure, species effected but it ranges from few hours to 3 days in natural infection and upto 14 days in flock.
While OIE recognizes incubation period upto 21 days. AI virus shed from mouth nares, cloaca, conjunctiva of infected birds because of virus replication in respiratory, intestinal, reproductive and renal organs. Transmission between birds is through ingestion or inhalation, direct contact, virus contaminated fomites. infected premises and equipment used.
Clinical Findings and Lesions
Clinical signs, mortality rate and severity of disease spends upon viral strain and host specie.
Low Pathogenicity Avian Influenza Viruses
Most infection by LPAI in wild birds produces no clinical signs. LPAI viruses mainly produce respiratory signs such as sneezing, coughing, oculo-nasal discharge, excessive lacrimation, swollen infra orbital sinuses. In ducks, quails and turkeys, sinusitis is very common.
Lesions in the respiratory tract typically include congestion and hemorrhages of tracheal mucosa, fibrinous and muco-purulent inflammation of sinuses, plug formation that lead to asphyxia, airsacculitis. In layer and breeders, there may be decrease egg production or fertility, egg yolk peritonitis, inflammatory exudate in the lumen of oviduct and visceral gout lesion may present in kidneys with urates deposit. Morbidity and mortality is low unless there is no secondary infection. H9N2 LPAI is common in Asia, Middle East and North America.
High pathogenic Avian Influenza Viruses
In domestic and wild water fowl, produces few clinical signs but recently isolated H5N1 produces clinical disease showing neurological signs, depression, anorexia, diarrhea and sudden death. Even in the absence of secondary pathogen, it causes severe systemic disease with high mortality. In per-acute cases, there may be no clinical signs or gross lesion before death.
In acute cases, lesions include cyanosis and edema in visceral organs and skin, edema and red discoloration of shanks and feet due to hemorrhages, blood tinged oro-nasal discharge. Swelling of head, face, upper neck and feet may be observed as a result of subcutaneous edema.
In severely affected bird, greenish diarrhea is common. Hemorrhages on heart and pectoral muscles, congestion of lungs is also seen. In per-acute infection, there may be involvement of CNS as torticollis, opisthotonos, paralysis, incoordination and dropping of wings. Microscopic lesions may consist of edema, hemorrhages and necrosis in parenchymal cells of skin, visceral organs and CNS.
Disease is diagnosed by;
- Clinical signs
- Gross lesions
- Direct detection of AIV viral proteins in the tissues, swabs, cell culture or by embryonated eggs.
- Isolation and identification of AIV
- Direct detection of AIV by RT-PCR
- HA-HI test
Prevention and Treatment
Vaccination can prevent clinical signs and death. Viral replication and shedding is reduced in vaccinated birds. Specific protection can be achieved through autogenous vaccine or from vaccine prepared from AIV of the same hemagglutinin sub type. Currently, inactivated whole AIV is used. Killed vaccines are also available for H9, H7and H5. There is no specific treatment for AIV infection.
Although, amantadine experimentally shows reduce mortality but this drug is not used in food animals. Supportive care, immune stimulants and antibiotics are used to reduce secondary bacterial infection and to boost up immune system. Treatment with antiviral drug is not approved or recommended. Suspected outbreaks should be reported to appropriate regulatory authorities.
Public Health significance
Influenza virus transmission occur most frequently between individuals of the same species. Occasionally inter species to closely related species transmission occurs. Although, AI viruses or their genes have been transferred to humans rarely.
The primary risk factor for the humans is direct contact with live or dead tissue, few cases reported with consumption of uncooked poultry products. H5N1 HPAI and recently Chinese H7N9 LPAI virus cause infection in humans. Total accumulated cases of H5N1 from 2003-2013 is 648 out of which 60% are died.
For H7N9 LPAI, total reported cases are 137 with 30% mortality. Conjuctivitis was the most common symptom with HPAI virus. Other HPAI and LPAI viruses produce very rare or no human infection.
Article is collectively written by Muhammad Hunain Ahmed, Muhammad Usman Naseer, Yabaiz Tahir