Pathological Studies of A / Chicken / Tehran / ZMT - 173/99 (H9N2) Influenza Virus in Commercial Broiler Chickens of Iran

Variation in Viral Shedding Patterns between Domestic and Wild Terrestrial Birds Infected Experimentally with Reassortant Avian Influenza Virus (H9N2)

“…In the past, it was strongly believed that higher morbidity and mortality are due to co-infections with other pathogens and are not only due to the H9N2 virus (Nili et al, 2002;Bano et al, 2003;Haghighat-Jahromi et al, 2008;Umar et al, 2015b). Previously, other experimental studies on H9N2 infections in poultry showed clinical disease signs similar to our study (Nili et al, 2002;Pazani et al, 2008). Nevertheless, the concurrent infections of other co-infecting pathogens have been reported to exacerbate the H9N2 infection in chickens (Banani et al, 2002;Pazani et al, 2008).…”

Pathogenicity and amino acid sequences of hemagglutinin cleavage site and neuraminidase stalk of differently passaged H9N2-avian influenza virus in broilers

“…The high frequency of challenged birds showing tracheitis ( Table 2) could be a result of the efficient viral dissemination in an infection site that is rich in trypsinlike proteases. These enzymes enable the virus to replicate easily in the epithelial tracheal cells causing deciliaion, destruction of Goblet cells through cytolysis and t release of virions [14,15,17,24], and mucus accumulation in necrotic areas [14,15,17]. There was significant increase of tracheal heterophils following viral passaging from 15 heterophils/tissue section in P1, to 21, and 23 heterophils/tissue section in P2, and P3, respectively ( Table 3, Figure 2, P < 0.05).…”

“…A change in AI viruses from a low to high pathogenicity nature results in an increase in chicken mortality percent, from 5% by LPAI infection to 20% -100% in HPAI infections [5,8,13]; in addition, the frequency of morbidity signs are increased among birds, including a decrease in feed intake, a decrease in weight and egg production, and a higher frequency of huddling, coughing, sneezing, rales, ocular discharge, and swelling of infraorbital sinuses [5,8,14]. This increase in mortality and morbidity frequency is the result of viral dissemination and spreading from the nasal cavity, which is the primary site of infection, to the lower part of the respiratory tract, kidneys, intestines, heart and other visceral organs [5,8,14,15].…”

“…A modification in tissue tropism could lead into a higher pathogenicity and more prominent disease signs. Upon mutation of LPAI to HPAI, such viruses acquire pneumotropism, nephrotropism, neurotropism, enterotropism and even exert tropism toward lymphoid tissues [5,14,15]. The HPAI viruses replicate within epithelial and endothelial cells of the respiratory organs causing major macroscopic or gross lesions such as tracheitis, lung congestion, airsacculitis, and sinusitis; these replicating viruses could spread through the vascular and lymphoid system to visceral organs causing enteritis, nephritis, splenomegaly, vascular and myocardial damage [5,9,[14][15][16].…”

“…Upon mutation of LPAI to HPAI, such viruses acquire pneumotropism, nephrotropism, neurotropism, enterotropism and even exert tropism toward lymphoid tissues [5,14,15]. The HPAI viruses replicate within epithelial and endothelial cells of the respiratory organs causing major macroscopic or gross lesions such as tracheitis, lung congestion, airsacculitis, and sinusitis; these replicating viruses could spread through the vascular and lymphoid system to visceral organs causing enteritis, nephritis, splenomegaly, vascular and myocardial damage [5,9,[14][15][16]. The frequency of microscopic lesions are also increased, specifically in the respiratory system, causing deciliation and Goblet cells degeneration in the trachea, mucus accumulation and heterophils infiltration in the trachea, lung, and airsacs [5,16,17].…”