Avian 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.
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.
LP and HP AI viruses can be readily isolated from tracheal and cloacal swabs, and HP AI viruses from many internal organs. AI viruses grow well in the allantoic sac of embryonating chicken eggs and agglutinate RBC. The hemagglutination is not inhibited by Newcastle disease or other paramyxoviral antiserum. AI viruses are identified by demonstrating the presence of 1) influenza A matrix or nucleoprotein antigens using AGID or other suitable immunoassays, or 2) viral RNA using an influenza A-specific reverse transcriptase-PCR test.
LP AI must be differentiated from other respiratory diseases or causes of decreased egg production including: 1) acute to subacute viral diseases such as infectious bronchitis, infectious laryngotracheitis, low virulent New-castle disease, and infections by other paramyxoviruses; 2) bacterial diseases such as mycoplasmosis, infectious coryza, ornithobacteriosis, turkey coryza, and the respiratory form of fowl cholera; and 3) fungal diseases such as aspergillosis. HP AI must be differentiated from other causes of high mortality such as virulent Newcastle disease, peracute septicemic fowl cholera, heat exhaustion, and severe water deprivation.
Prevention and Treatment
Vaccines can prevent clinical signs and death. Furthermore, viral replication and shedding from the respiratory and GI tracts may be reduced in vaccinated birds. Specific protection is achieved through autogenous virus vaccines or from vaccines prepared from AI virus of the same hemagglutinin subtype. Antibodies to the homologous viral neuraminidase antigens may provide partial protection. Currently, only inactivated whole AI virus and recombinant fowlpox-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 LP-affected flocks 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.
Avian influenza viruses exhibit host adaptation to birds. Human infections have occurred, usually as isolated, rare individual cases. Most human cases have originated from infection with Eurasian H5N1 HP AI virus. The first 18 cases occurred in Hong Kong during 1997, with total accumulative human cases in Asia and Africa by mid-2009 of 408 cases, of which 240 were fatal. The primary risk factor for human infection has been 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, or close contact with human cases. Respiratory infection has been the most frequent presentation of human H5N1 cases. Conjunctivitis was the most frequent symptom with human cases of H7N7 HP AI virus infection in the Netherlands during 2003.
Last full review/revision March 2012 by David E. Swayne, DVM, PhD, DACVP, DACPV