Avian Influenza Training
| This course provides the information and resources needed to recognize clinical signs and gross lesions that could be suggestive of Avian Influenza. To view larger images, follow the jpeg links. |
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Welcome |
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Purpose The purpose of this training course is to provide the inplant inspection team with the information and additional resources needed to recognize clinical signs and gross lesions that could be suggestive of Avian Influenza. |
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Objectives
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Avian Influenza |
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Etiology Avian Influenza viruses are members of the family Orthomyxoviridae. The influenza viruses that belong to this family are classified into types A, B or C. These types are based on differences between their nucleoprotein and matrix protein antigens. The Avian Influenza viruses belong to Type A. Influenza viruses are further classified into subtypes according to the antigens of the Haemagglutinin (H) and Neuraminidase (N) projections on their surfaces. There are 16 Haemagglutinin subtypes and 9 Neuraminidase subtypes of the Influenza A viruses. The subtypes that are of concern are the H5 and H7 because of their potential to mutate into highly pathogenic strains. AI viruses can also be classified into low-pathogenicity (LPAI) and high-pathogenicity (HPAI) based on the severity of the illness they cause. The Low Pathogenic form may go undetected and usually causes only mild symptoms such as ruffled feathers and a drop in egg production. However, some LPAI virus strains are capable of mutating under field conditions into HPAI viruses. The High Pathogenic form causes severe, systemic disease with high mortality in chickens, turkeys, and other gallinaceous birds. The HPAI virus is extremely infectious and once established, can spread rapidly from flock to flock. The strain that is currently causing worldwide concern is the HPAI H5N1 due to the millions of birds that have died in Asia, Africa and Europe. This strain has also infected humans, most of whom have had direct contact with infected birds. |
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Transmission Avian Influenza Type A viruses are distributed worldwide, with wild shorebirds and migrating waterfowl, serving as the natural reservoir. Many of the strains in wild birds are either non-pathogenic or mildly pathogenic for poultry. However, through mutation or reassortment of less virulent strains, virulent strains can emerge. These viruses infect the gastrointestinal and respiratory tracts of these birds. Even though they are infected with the virus, the birds usually do not show signs of disease. The viruses are shed in the feces and respiratory secretions. The virus can survive in water and at low temperatures for weeks. Susceptible birds become infected by contact with contaminated secretions or excretions by either direct or indirect contact. Domesticated birds may become infected through direct contact with infected waterfowl, other infected poultry or indirectly by dirt, cages, water or feed that is contaminated with the Avian Influenza Type A virus. Airborne transmission is possible if birds are in close proximity. The virus can be introduced into the nares, conjunctival sac and the trachea. Once avian influenza is established in a domestic poultry flock, it is a highly contagious disease. Infected birds excrete high concentrations of virus in their feces and nasal and ocular discharges. After the virus is introduced into a flock, the virus is spread from farm to farm by the movement of infected birds, contaminated equipment and people. |
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Clinical Signs |
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Common Signs The clinical signs and course of Avian Influenza Type A are variable and are influenced by the virulence of the infecting virus, species affected, age, sex, concurrent diseases and environment. In some flocks, seroconversion may be the only evidence of infection. Avian Influenza can manifest as respiratory, enteric, or neurological disease with mild signs to a rapidly fatal fulminating disease. With HPAI, the disease may appear suddenly and birds die either without clinical signs or with minimal signs of depression, inappetence, and ruffled feathers. Other birds may show ataxia and torticollis. |
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The combs and wattles can be cyanotic and edematous, with petechial or ecchymotic hemorrhages at the tips Per orbital edema is often associated with the swollen combs and wattles. Hemorrhages and subcutaneous edema may occur on the hocks of the birds. The birds can also be excessively thirsty and have a watery white to green diarrhea. |
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Layers In layers, with HPAI, the disease may appear suddenly and birds die either without clinical signs or with minimal signs of depression and inappetence. The sick birds typically sit or stand, in a semi-comatose state. The hens at first may lay soft-shelled or misshapen eggs, but then stop laying. The mortality rate varies from 50 to 100%. Birds that do survive are usually in poor condition and may resume laying after several weeks |
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Broilers In broilers with HPAI, like layers, the disease may appear suddenly and birds die acutely or with minimal clinical signs. Common clinical signs seen are severe depression, ruffled feathers, inappetence, and a marked increase in mortality. Respiratory signs include clear, mucopurulent or blood-tinged nasal discharge, coughing and respiratory distress. |
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Turkeys In turkeys, the clinical signs are similar to that seen in layers and broilers. However, the course of the disease generally lasts 2 to 3 days longer in turkeys. This poult exhibits swollen sinuses which is a common clinical sign in turkeys. |
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Gross Post Mortem Lesions |
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Common Lesions In the less acute form, significant gross lesions are frequently observed. Fluid may exit the nares and oral cavity as the bird is positioned for postmortem examination. The birds may have subcutaneous edema of the head and neck area, which is evident as the skin is reflected. The trachea may appear relatively normal except that the lumen contains excessive mucous exudates. There may also be hemorrhagic tracheitis similar to the lesions seen with Infectious Laryngotracheitis. |
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When the bird is opened, pinpoint petechial hemorrhages are frequently observed on the inside of the keel as it is bent back. Petechia may cover the abdominal fat, serosal surfaces, and peritoneum. Kidneys are severely congested and may occasionally be grossly plugged with white urate deposits in the tubules. |
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Hemorrhages may be present on the mucosal surface of the proventriculus particularly at the juncture with the gizzard. The lining of the gizzard peels easily and exposes hemorrhages and erosions underneath. The intestinal mucosa may also have hemorrhagic areas which can be seen on the serosal surface. These hemorrhagic areas are usually associated with the Peyer's Patches and in the cecal tonsils. |
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Layers In laying hens, the ovary may be hemorrhagic or degenerated with darkened areas of necrosis. In birds that survive for 7 to 10 days, the peritoneal cavity is filled with yolk from ruptured ova, causing severe airsacculitis and peritonitis. |
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Broilers and Turkeys Broilers and turkeys that die peracutely may not have significant gross lesions other than severe congestion of the musculature and dehydration. If the birds do not die peracutely, there can be petechial and ecchymotic hemorrhages in the trachea, epicardial fat, serosal surfaces and intestines. The spleen, liver, kidneys and lungs may have grey or yellow necrotic foci. |
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Differential Diagnosis
However, in an area where AI is prevalent, such as during an outbreak, a sound presumptive diagnosis can be made by flock history, signs, and gross lesions. |
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Slide Show
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Regulatory ActionsIf you see something unusual, it is most important that you contact the District Office as soon as possible. FSIS Directive 6000.1, Rev. 1 provides specific instructions when you observe symptoms of Foreign Animal Diseases or other reportable conditions.
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ScenariosEducating the media and the public about the complexities of avian influenza as a disease among birds is one of USDA primary communications objectives. |
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Resources and Links |
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Glossary |
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