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News: Avian Influenza Backgrounder
Posted by: JimEdwards on Oct 16, 2005 - 12:51 PM
technical 
Source:


Causative agent
Avian influenza (AI) is caused by a type A Orthomyxovirus. Multiple serotypes (strains) of the AI virus exist and are classified based on relative numbers of hemagglutinin (H) and neuraminidase (N) surface antigens (e.g., H7N2, H5N1). Avian influenza viruses may be of low pathogenicity (LPAI) or high pathogenicity (HPAI) in birds. Most AI virus strains are LPAI and typically cause no to few clinical signs in infected birds. Low pathogenicity AI virus strains, however, are capable of mutating under field conditions into HPAI viruses, and some highly virulent strains of AI have evolved from milder strains after serial passage through poultry populations.

Natural distribution
Most domestic and wild bird species appear to be susceptible to AI. Waterfowl (including geese, ducks, swans, and sea and shore birds) throughout the world carry the virus, but clinical signs of disease are usually mild or not evident. Mortalities do occasionally occur. Infections in poultry may be more severe, and turkeys are more commonly infected than chickens. Pigs have been implicated in the epidemiology of infection in turkeys when production facilities are located in close proximity.

An avian source of the H5N1 strain has been associated with severe human disease and death in Asia.

Transmission
Waterfowl serve as a reservoir of AI virus and are likely the main source for original introduction of the disease into poultry flocks. Infected birds shed the virus in oculonasal discharges and feces, and contaminated drinking water is commonly implicated as the source of infection. Once introduced into a flock, infected birds, contaminated equipment, insects, rodents, and personnel have all been implicated in the spread of the virus within the flock and between flocks. When birds are in close proximity and air movement is conducive, airborne transmission can occur. Although virus can be recovered from the yolk, shell, and albumin of eggs, vertical transmission has not been demonstrated. Incubation period is usually 3 to 7 days.
Exposure of poultry to migratory waterfowl and international movement of poultry, farm equipment, and people increase risk for introducing HPAI into U.S. poultry flocks. Live-bird markets are a reservoir of infection because they serve as a focal point for gathering and housing many species of birds.

Clinical signs
The clinical course of AI ranges from mild disease to rapidly fatal, and depends on the age and species of the bird affected, husbandry practices, the pathogenicity of the virus strain, and environmental factors. In some flocks, the only evidence of infection is seroconversion (i.e., birds develop a detectable antibody titer to AI antigen).

Avian influenza can manifest as respiratory, enteric, reproductive, or neurologic disease. Associated clinical signs may include decreased egg production; soft-shelled or misshapen eggs; swelling of the head, eyelids, comb, wattles, and hocks; cyanosis of the wattles, combs, and legs; clear, mucopurulent, or blood-tinged nasal discharge; coughing; incoordination; diarrhea; ruffled feathers; depression; inappetence; petechiation (pinpoint hemorrhages) of the feet and shanks; and respiratory distress.

Because the clinical signs of AI are similar to those of other avian diseases, AI may be confused with infectious laryngotracheitis, infectious bronchitis, fowl cholera, E. coli and Newcastle disease.

Diagnosis
Whereas clinical signs may be suggestive of AI, diagnosis is confirmed through serologic testing and virus isolation and identification. Serum samples from several birds should be submitted for serologic testing. Avian influenza virus may be isolated from tissue samples (trachea, lung, spleen, cloaca, and brain), tracheal or cloacal swabs, or fecal samples. Multiple specimens from multiple birds should be submitted to a qualified laboratory because many samples fail to yield virus. Determination of virulence for a particular strain requires virus isolation and subsequent controlled laboratory challenge of healthy chickens. Strains determined to be highly pathogenic (HPAI), as well as H5 and H7 subtypes that are not HPAI, must be reported to the U.S. Department of Agriculture.

Findings on necropsy vary with age of bird, species, and pathogenicity of the virus; however, typical lesions include subcutaneous edema of the head and neck, congestion and petechiation of the conjunctivae, excess mucous or hemorrhage in the trachea, congestion and ureate deposits in the kidneys, and petechiation of the keel, proventriculus, gizzard, intestines, abdominal fat, and peritoneum. The ovaries of laying hens may be hemorrhagic or necrotic, and the peritoneal cavity may be filled with yolk from ruptured eggs. The latter may lead to peritonitis and air sacculitis in birds that survive for longer periods. Often only dehydration and severe muscular congestion are found in young birds or those that die of peracute disease.

Prevention and Control
Appropriate biosecurity practices are key to preventing infection with AI viruses. All-in, all-out flock management, with thorough cleaning and disinfection between flocks, can prevent spread of virus from one flock to another. Poultry flocks should not be allowed to come in contact with wild or migratory birds, and should be kept away from any source of water that may have been contaminated by wild birds. Personnel and equipment entering and leaving facilities must be appropriately disinfected on entry and exit, and should not be exchanged between facilities.

Producers and dealers utilizing live-bird markets must be especially cautious. Avian influenza can be introduced into these markets by infected birds or contaminated crates and trucks. Once the virus is established in the market, movement of birds, crates, or trucks from a contaminated market can spread the virus to other farms and markets. Protective measures that may prevent spread of AI include use of plastic, rather than wooden, crates; meticulous removal of manure, feathers and other debris from floors; appropriate cleaning and disinfection of equipment and vehicles; segregating birds by lots; and comprehensive cleaning and disinfection of premises after every day of sale. Birds not sold at the market should not be returned to the farm.

Mild forms of AI have been controlled in commercial chicken and turkey flocks through vaccination (autogenous) and strict quarantine. For HPAI, strict quarantine and rapid depopulation of infected flocks is the only approach found to be effective in stopping spread of the virus. Vaccination to control HPAI (H5N1) in Asia has been initiated.

Treatment
Treatment for AI has not been effective and prognosis for flocks infected with HPAI is poor. Morbidity and mortality rates approach 100% within 2 weeks of onset of illness. Good husbandry and nutrition may assist birds in mounting an appropriate immune response and antibiotics may prevent secondary infections. Laying hens that survive infection with AI may not return to normal production for several weeks. Recovered flocks continue to intermittently shed virus and appropriate precautions and surveillance should be undertaken. Once an infected flock has been removed, the facility and equipment should be thoroughly cleaned and disinfected.

Decontamination
Avian influenza viruses are sensitive to most detergents and disinfectants, and heating and drying will readily inactivate them. Organic material, such as feces, will protect AI virus from inactivation, and active virus may be recovered from these sources for up to 105 days. Facilities and equipment should be cleaned and disinfected after infected flocks are removed, and poultry litter or manure should be composted before further use.

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