21 Sunday July 2019
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Overview of Avian InfluenzaAvian influenza (AI) viruses infect domestic poultry, and pet, zoo, and wild birds. In domestic poultry, AI viruses are typically of low pathogenicity (LP), causing subclinical infections, respiratory disease, or drops in egg production. However, a few AI viruses cause severe systemic infections with high mortality. This highly pathogenic (HP) form of the disease has historically been called fowl plague. In most wild birds, AI viral infections are subclinical except for the recent H5N1 HP AI viruses of Eurasian lineage.

Etiology

Avian influenza viruses are type A orthomyxoviruses characterized by antigenically homologous nucleoprotein and matrix internal proteins, which are identified by serology in agar gel immuno-diffusion (AGID) tests. AI viruses are further divided into 16 hemagglutinin (H1-16) and 9 neura-minidase (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.

Epidemiology and Transmission

LP AI viruses are distributed worldwide and are recovered frequently from clinically normal shorebirds and migrating waterfowl. Occasionally, LP viruses are recovered from imported pet birds and ratites. The viruses may be present in village or backyard flocks and other birds sold through live-poultry markets, but most commercially raised poultry in developed countries are free of AI viruses. The HP viruses arise from mutation of some H5 and H7 LP viruses and cause devastating epidemics. Stamping-out programs are used to quickly eliminate the HP viruses.

The incubation period is highly variable and ranges from a few days to 2 wk. Transmission between individual birds is by ingestion or inhalation. Naturally and experimentally, cats and dogs have been infected with one strain of H5N1 Eurasian HP AI virus. Experimental infections occurred following respiratory exposure, ingestion of infected chickens, or contact exposure, but cats were more susceptible than dogs. Potentially, domestic pets could serve as a transmission vector between farms, but the ability of other AI viruses, including other H5N1 strains, to infect pets is unknown. Other mammals that have been experimentally infected include pigs, ferrets, rats, rabbits, guinea pigs, mice, mink, and nonhuman primates. Transmission between farms is the result of breaches in biosecurity practices, principally by movement of infected poultry or contaminated feces and respiratory secretions on fomites such as equipment or clothing. Airborne dissemination may be important over limited distances. Limited spread by wild birds of the Eurasian H5N1 HP AI virus has been suggested but is not typical of other HP AI viruses.

Clinical Findings and Lesions

Clinical signs, severity of disease, and mortality rates vary depending on AI virus strain and host species.

Low Pathogenicity AI Viruses

These AI viruses typically produce respiratory signs such as sneezing, coughing, ocular and nasal discharge, and swollen infraorbital sinuses in poultry. Sinusitis is common in domestic ducks, quail, and turkeys. Lesions in the respiratory tract typically include congestion and inflammation of the trachea and lungs. In layers and breeders, there may be decreased egg production or fertility, ova rupture (evident as yolk in the abdominal cavity) or involution, or mucosal edema and inflammatory exudates in the lumen of the oviduct. A few layer and breeder chickens may have acute renal failure and visceral urate deposition (visceral gout). The morbidity and mortality is usually low unless accompanied by secondary bacterial or viral infections or aggravated by environmental stressors.
High Pathogenicity AI Viruses

Even in the absence of secondary pathogens, HP viruses cause severe, systemic disease with high mortality in chickens, turkeys, and other gallinaceous poultry. In peracute cases, clinical signs or gross lesions may be lacking before death. However, in acute cases, lesions may include 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 diarrhea is common. Birds that survive the peracute infection may develop CNS involvement evident as torticollis, opisthotonos, incoordination, paralysis, and drooping wings. The location and severity of microscopic lesions are highly variable and may consist of edema, hemorrhage, and necrosis in parenchymal cells of multiple visceral organs, skin, and CNS.