Avian Influenza (Fowl Plague)

Avian Influenza or AI (Fowl Plague) is an infection of domestic poultry as well as pet, zoo, and wild birds caused by influenza A virus of the H5 or H7 subtypes.

These viruses are divided into high pathogenicity avian influenza (HPAI) viruses and low pathogenicity avian influenza (LPAI) viruses based on intravenous pathogenicity index (IVPI).

High pathogenicity avian influenza (HPAI) viruses have an intravenous pathogenicity index (IVPI) in six-week-old chickens were greater than 1.2 or, as an alternative, cause at least 75% mortality in four-to eight-week-old chickens infected intravenously.

Low pathogenicity avian influenza (LPAI) viruses are all influenza A viruses of H5 and H7 subtypes that are not have high pathogenicity.

Etiology

•  Avian Influenza (Fowl Plague) is caused by Type A Influenza virus, genus Orthomyxoviruses of family Orthomyxoviridae. It is a single stranded , segmented  RNA virus.
• AI viruses are further divided into 16 hemagglutinin (H1-16) and 9 neuraminidase (N1-9) subtypes based on hemagglutinin inhibition and neuraminidase inhibition tests respectively.
• Most AI viruses (H1-16 subtypes) are of low pathogenicity, but some of the H5 and H7 AI viruses are highly pathogenic for chickens, turkeys, and related gallinaceous domestic poultry.
• New subtype of  influenza A virus emerge periodically as a result of point mutation (antigenic drift) and genetic reassortment.
• The virus is labile in the environment  and are sensitive to heat, pH Changes, lipid solvents and oxidizing agents.

 Epidemiology

• Avian Influenza (AI) viruses have been circulating worldwide for centuries with four known outbreaks recorded in the last century. The present wave of highly pathogenic avian influenza (HPAI) emerged in Hong Kong in 1997
• In India first outbreak of avian influenza reported on 18.02.2006 in states of  Maharastra, Gurajarat and followed by second outbreak in Madhya Pradesh in March-April-2006, subsequent outbreaks have been recorded in Manipur, West Bengal, Tripura, Assam, Sikkim, Odisha, Meghalaya, Karnataka, Bihar, Chhattisgarh, Kerala and Chandigarh and Kerala since 2007-2015.
• LPAI viruses are distributed worldwide and are frequently recovered from apparently normal ducks, shorebirds and migrating waterfowl. HPAI viruses arise from mutation of some H5 and H7 low pathogenic viruses and cause devastating epidemics.
• In most wild birds, AI viral infections are subclinical except for the recent H5N1.

Host affected

• Chicken, ducks, turkeys, guinea-fowl, goose, quail , pet, zoo, and wild birds.

Source of infection

• The ducks and migratory water fowl are source of infection; these birds excrete the virus through faeces.
• Faeces and nasal discharge of infected chicken.

Transmission

• Ingestion of food and water contaminated with the faeces and respiratory secretion of infected birds.
• Through contaminated equipments and clothing.
• Air borne transmission may be important over limited distance.

Pathogenesis

• Spread of influenza virus in tissue is depends on type of protease in host tissue and structure of haemagglutininin molecule.
• In the majority of influenza A virus subtype haemagglutinin is cleaved by host protease such as trypsin like enzymes found only in  the epithelial cells of the respiratory and digestive tracts.
• This is facilitating the development of generalized infection.

Clinical manifestation

Highly pathogenic avian influenza (HPAI)

• Sudden onset of unusual mortality.
• In acute cases, respiratory distress, sinusitis, lacrimation, cyanosis and edema of the head, comb, wattle, and snood (turkey); edema and red discoloration of the shanks and feet due to subcutaneous ecchymotic hemorrhages; petechial hemorrhages on visceral organs and in muscles, and blood-tinged oral and nasal discharges.
• In severely affected birds, greenish diarrhoea is common. Birds that survive the peracute infection may develop CNS involvement evident as torticollis opisthotonos, incoordination, paralysis, and drooping wings.

Low pathogenic avian influenza (LPAI)

• LPAI viruses typically produce respiratory signs such as sneezing, coughing, ocular and nasal discharge and swollen infraorbital sinuses.
• Sinusitis is common in domestic ducks, quail, and turkeys.
• Decreased egg production and fertility in layers.
• A few layer and breeder chickens may have acute renal failure and visceral urate deposition (visceral gout).
• Lesions in the respiratory tract typically include congestion and inflammation of the trachea and lungs.
• The morbidity and mortality is usually low unless accompanied by secondary bacterial or viral infections or aggravated by environmental stressors.

Zoonotic risk

• Human get infection through direct contact with live or dead infected poultry, but a few cases have resulted from consumption of uncooked poultry products, defeathering of infected wild swans.
• Respiratory infection has been the most frequent presentation of human H5N1 cases.

Sample collection

• Oropharyngeal, tracheal and cloacal swabs and faeces (approximately 1g) preserved in viral transport medium or tissue culture medium for virus isolation.

Diagnosis

• Based on clinical signs and lesions.
• Isolation of virus from clinical samples by allantoic route of  inoculation at 9-11 days of embryonated egg.
• Haemagglutination test for detection of virus in clinical sample.
• Intravenous pathogenicity test should be done in chicken at 4-8 weeks of age to assess pathogenicity of the virus.
• Genome sequencing can be used to determine the amino acid composition at the cleavage site of haemagglutinin molecule to assess pathogenicity .
• Detection of antibody in serum by haemagglutination inhibition test.
• Agar gel immunodiffusion test (AGID) and competitive ELISA can also be used for antibody detection.
• Reverse transcriptase- polymerase chain reaction (RT-PCR) and real time polymerase chain reaction techniques are commonly used for rapid detection of virus in clinical sample.

Differential diagnosis

• New castle disease
• Septicaemic pasteurollosis
• Water deprivation syndrome

Prevention and control

• Currently, only inactivated whole AI virus, recombinant fowlpox-AI-H5, and recombinant herpesvirus-turkey-AI-H5 (rHVT-AI-H5) vaccines are licensed in the USA.
• The use of any licensed AI vaccine requires approval of the state veterinarian. In addition, use of H5 and H7 AI vaccines in the USA requires USDA approval.
• Treating of birds infected with LPAI with broad-spectrum antibiotics to control secondary pathogens and increasing house temperatures may reduce morbidity and mortality
• Treatment with antiviral compounds is not approved or recommended.
• Suspected outbreaks should be reported to appropriate regulatory authorities.

Biosecurity measures

• Restriction of entry of vehicles inside the farm.
• Restriction of movement of people inside the farm and other birds in the farm.
• The personnel working inside the farm should wear protective clothing all the time inside the farm, including face-masks and gloves, gumboots.
• The infected farm premises area should be invariably disinfected by spraying disinfectants like 2% Sodium hypochlorite or 4% Formalin to reduce the virus load.
• Treating all the equipment with 2% sodium-hypochlorite solution for 48 hrs.
• Use 2% NaOH or Kmno4  solution at the entrance of the premises.
• White-washing of concrete areas with lime .
• Cages and other large metal structures may be decontaminated by heat treatment (flame gun) 
• Water-reservoirs must also be emptied, washed and disinfected.
• Feed tanks (silos) need to be emptied, washed with a hot water-pressure pump and subsequently fumigated.
• Wash hands and feet of farm workers and the visiting officials with soap and disinfectant with approved detergent or rectified spirit.
• Use virucidal agent Vircon-S®, D-125, Trilocid concentrate for cleaning of floor.