Dr Bhavesh Zapadia-avian Infflueza

AVIAN INFLUENZA

SUBMITTED TO: DR. K.S. PRAJAPATI PROFESSOR AND HEAD DEPTT. OF VETY . PATHOLOGY SUBMITTED BY :’ ANSHU JAIN MVSC. [II SEM]

AVIAN INFLUENZA NATURE OF THE DISEASE Virulent avian influenza (AI) – fowl plague – is highly contagious fatal disease of poultry. Infection with the virus is accompanied by respiratory, gastro-intestinal and /or nervous signs. Wild water birds such as waterfowl and seabirds are recognised as important reservoir of infection . CLASSIFICATION OIE List A disease

HISTORY • A highly pathogenic form of avian influenza was known as "fowl plague". It first appeared in Italy more than 100 years ago (around 1878). Pathogenic avian influenza was first recognized in the United States in 1924-25. It occurred again in 1929. It was eradicated both times. • A major epidemic of highly pathogenic avian influenza occurred in the northeastern United States in 1983-84. • The United States has not had a major outbreak of highly pathogenic avian influenza since 1986, although less pathogenic strains of avian influenza virus are present and have caused significant losses in the poultry industry. • In 1996-97 a number of table-egg farms in Lancaster and Lebanon Counties, PA tested positive for H7N2 avian influenza . Between the first week of December 1996 and June 6 1997 nine flocks were depopulated.

AETIOLOGY Classification of the causative agent Virus family Orthomyxoviridae, genus Influenzavirus A, B. To date, all highly pathogenic isolates have been influenza A viruses of subtypes H5 and H7 Resistance to physical and chemical action Temperature: Inactivation by 56°C/3 hours; 60°C/30 min pH: Inactivated by acid pH Chemicals: Inactivated by oxidising agents, sodium dodecyl sulphate, lipid solvents, ß-propiolactone Disinfectants: Inactivated by formalin and iodine compounds Survival: Remains viable for long periods in tissues, faeces and also in water

Structure of virus

SEROTYPES Avian influenza viruses are subdivided into serotypes based on their hemagglutinin (H) and neuraminidase (N) surface antigens.There are 15 HA antigen and 9 NA antigen types.The virus is subject to high mutation due to genetic shift. The highly pathogenic serotype of avian influenza responsible for the 1983-84 outbreak in the United States and the 1994 outbreak in Mexico was H5N2. Historically, serotypes including H5 and H7 are associated with disease in poultry.

TRANSMISSION •Direct contact with secretions from infected birds, especially faeces •Contaminated feed, water, equipment and clothing •Clinically normal waterfowl and sea birds may introduce the virus into flocks •Broken contaminated eggs may infect chicks in the incubator SOURCES OF VIRUS •Faeces, respiratory secretions •Highly pathogenic viruses may remain viable for long periods of time in infected faeces, but also in tissues and water

OCCURRENCE Apathogenic and mildly pathogenic influenza A viruses occur worldwide. Highly pathogenic avian influenza A (HPAI) viruses of the H5 and H7 HA subtypes have been isolated occasionally from free-living birds in Europe and elsewhere. Outbreaks due to HPAI were recorded in the Pennsylvania area, USA, in the years 1983-84. More recently outbreaks have occurred in Australia, Pakistan and Mexico. There is evidence that H5 viruses of low pathogenicity may mutate and become highly pathogenic. HPAI infections are very rarely seen, and should not be confused with viruses of low pathogenicity, which may also be of H5 or H7 subtypes

SUSCEPTIBLE SPECIES AI infects almost all commercial, domestic and wild bird species. •chickens and turkeys are highly susceptible to infection and clinical disease •ducks and geese are susceptible but only very virulent strains produce disease •guinea fowl, quail, pheasant and partridges are susceptible to infection and clinical disease •wild birds: viruses can be recovered from a wide range of species but no significant disease problems are known to occur. • Generally, humans are not affected, but an outbreak of influenza in humans was associated with an avian source in Hong Kong (January 1998).

CLINICAL SIGNS Clinical signs are variable and influenced by the virulence of the virus strain, the species affected, age, environmental conditions and presence of pre-existing bacterial infections.  Low pathogenicity strains • mild to severe respiratory symptoms (may be confused with infectious laryngotracheitis). • egg production may drop by up to 45% and take 2—4 weeks to recover. • mortality from 3% in caged layers up to 15% in broilers.

High pathogenicity strains • severe respiratory distress • watery eyes and sinuses • cyanosis of the combs, wattle and shanks • swelling of the head • diarrhoea • nervous signs • sudden death - deaths may commence 24 hours after first signs and can approach 100%

Pathogenic H5 avian influenza infected chicken

Cyanosis of The Unfeathered Areas on the Head

POST-MORTEM FINDINGS • Lesions vary greatly depending on pathogenicity of the virus, age of the bird, type of poultry, etc. Lesions may include swelling of the face and area below the beak. Removing skin from the carcass will show a clear straw-colored fluid in the subcutaneous tissues. • Blood vessels are usually engorged. Hemorrhage may be seen in the trachea, proventriculus, beneath the lining of the gizzard, and throughout the intestines. The lining of the gizzard may be easily removed. • Other areas likely to show swelling and hemorrhages include the muscle along the breast bone as well as in the heart, gizzard fat, and abdominal fat. • Young broilers may show signs of severe dehydration with other lesions less pronounced or absent entirely.

Watery eyes and sinuses and swelling of the head.

Cyanosis of the shanks.

Bloody cloaca and dark coloured skin of a chicken that died of AI.

Haemorrhage in the small intestine, between two dark coloured caeca

Haemorrhages of the trachea

Haemorrhages of the intestine.

DIFFERENTIAL DIAGNOSIS •Newcastle disease •Fowl cholera •Infectious laryngotracheitis •Duck viral enteritis

SPECIMENS REQUIRED FOR DIAGNOSIS Samples should be taken from live, clinically affected birds and recently dead birds. Samples should be collected from at least six birds. Live birds Cloacal and tracheal swabs, fresh faeces and serum. Swabs should be mixed with transport media. Blood samples from several birds should be collected for serum. Dead birds  Alimentary tissue samples (proventriculus, intestine, caecal tonsil) and respiratory tissues (lung, trachea) should be collected fresh (not preserved). Impression smears of internal organs can be made. If delays of more than 48 hours in transit are expected, samples should be frozen.

LABORATORY DIAGNOSIS Procedures Identification of the agent •Inoculation of 9-11-day-old embryonated chicken eggs followed by: • Demonstration of haemagglutination • Immunodiffusion test to confirm the presence of influenza A virus • subtype determination with monospecific antisera • strain virulence evaluation: evaluation of the intravenous pathogenicity index (IVPI) in 4-8-week-old chickens

Serological tests •Haemagglutination and haemagglutination inhibition tests •Agar gel immunodiffusion Samples Identification of the agent •Tracheal and cloacal swabs (or faeces) from live birds or from pools of organs and faeces from dead birds Serological tests Clotted blood samples or serum

TREATMENT There is no effective treatment for avian influenza. However, good husbandry, proper nutrition, and broad spectrum antibiotics may reduce losses from secondary infections. It must be remembered that recovered flocks continue to intermittently shed the virus. All buildings should be cleaned and disinfected after an infected flock is removed. The poultry litter or manure should be composted before application to cultivated lands

BIOSECURITY MEASURES ON THE FARM Poultry producers should strengthen biosecurity practices to prevent the introduction of AI into their flocks. The following are some sound biosecurity practices: • Keep an “all-in, all-out” philosophy of flock management. • Protect poultry flocks from coming into contact with wild or migratory birds. Keep poultry away from any source of water that may have been contaminated by wild birds. • Permit only essential workers and vehicles to enter the farm. • Provide clean clothing and disinfection facilities for employees.

•Thoroughly clean and disinfect equipment and vehicles (including tires and undercarriage) entering and leaving the farm. • Do not loan to, or borrow equipment or vehicles from, other farms. Avoid visiting other poultry farms. If you do visit another farm or live-bird market, change footwear and clothing before working with your own flock. • Do not bring birds from slaughter channels, especially live-bird markets, back to the farm.

PREVENTION AND CONTROL Sanitary prophylaxis •Avoidance of contact between poultry and wild birds, in particular waterfowl •Avoidance of the introduction of birds of unknown disease status into flock •Control of human traffic •Proper cleaning and disinfection procedures •One age group per farm ('all in-all out') breeding is recommended

In outbreaks •Slaughtering of all birds •Disposal of carcasses and all animal products •Cleaning and disinfection •Allow at least 21 days before restocking Medical prophylaxis •In the past, it has been considered counterproductive to vaccinate against HPAI as some vaccinated individuals may, nonetheless, become infected and shed virulent virus. However, in the recent outbreaks in Pakistan and Mexico, inactivated vaccines have been employed to combat rapidly spreading disease

VACCINATION Vaccines have been used in the past but have not proven very effective. Because of the risk of producing pathogenic strains, live virus vaccines are not appropriate. In the USA inactivated commercial vaccines have been developed. When vaccine is used in an outbreak, the risk that vaccination teams may spread the disease is a concern. For eradicating the disease, a slaughter policy is preferable to a vaccination policy. Affected flocks should be slaughtered and the carcases buried or burned and the premises cleansed and disinfected.