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

Low Pathogenicity Avian Influenza Viruses:LP 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. Sporadic infections by any subtype of LP AI viruses can occur, but H9N2 LP AI is common in poultry in Asia, the Middle East, and North Africa.

High Pathogenicity Avian Influenza Viruses:Even in the absence of secondary pathogens, HP AI viruses cause severe, systemic disease with high mortality in chickens, turkeys, and other gallinaceous poultry; mortality can be as high as 100% in a few days. 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.

a. A constant amount of hemagglutinating (HA) antigen is added to each well in a microtiter plate.

b. The test serum is then placed in the first well and serially diluted.

c.  The plates are incubated for one hour and then chicken RBCs are added to each well. If antibody is present in the test serum the RBCs will not agglutinate with the HA antigen.

d.  HI NEGATIVE wells will have a diffuse sheet of agglutinated RBCs covering       the bottom.

e.  HI POSITIVE wells will have a well circumscribed button of unagglutinated       RBCs



http://cal.vet.upenn.edu/projects/poultry/Syllabus/page20.htm

Coexistence of H7/H9, N9/N2, and H5/N1 in poultry markets determined by real-time RT-PCR.Poultry and environment specimens were collected from 12 poultry markets epidemiologically linked to 10 human H7N9 infection cases that occurred between 4 and 20 April 2013 in Hangzhou. Specimens positive for the H7 and N9 segments were found in all 12 of the poultry markets (Table 1; see also Table S1 in the supplemental material). Coexistence of H7N9 and H9N2, even with H5N1, was detected in chickens and ducks. Among 15 pharyngeal and rectal swabs from chickens in two live poultry markets, 6 were found positive for H7, N9, H9, N2, H5, and H1 and 4 positive for H7, N9, H9, and N2. In eight pharyngeal and rectal swabs from ducks in one live poultry market, two were positive for H7, N9, H9, and N2 and two positive for H7 and N9. In one pharyngeal swab from a quail, only H9N2 was detected. The environments of these poultry markets linked to H7N9 cases were heavily contaminated by influenza A H7N9 and H9N2 viruses, with or without H5N1 virus. A total of 46 of 86 specimens (53.5%) from the environment in all 12 markets were positive for H7, N9, H9, and N2. Thus, the novel H7N9 virus likely coexisted generally with at least an H9N2 virus in live poultry markets.