Mycoplasma synoviae (MS) is an important pathogen of domestic poultry and is prevalent in commercial layers. Avian influenza (AI; H9N2) infections are emerging respiratory problems causing huge economic losses to the poultry industry, especially in the presence of other co-infecting pathogens. The possible role of MS vaccination and response to AI (H9N2) virus in commercial layers was evaluated during this study. Experimental commercial layers were divided into different groups which were identified as follows: non-vaccinated non-challenged (NVNC), non-vaccinated challenged (NVC), vaccinated non-challenged (VNC), and vaccinated challenged (VC). The titer of AI antibodies was measured pre- and post-challenge to confirm experimental infection. Infected layers showed clinical signs of differing severity, with the most prominent disease signs and mortality (25%) appearing in layers of the VC group. Moreover, the layers in VC group showed a significant decrease in weight and enhanced gross lesions. All infected layers showed positive results for virus shedding; however, the pattern of virus shedding was different, with layers of VC group showing more pronounced virus excretion than the layers in the NVC group. In addition, layers of VC group showed significantly reduced antibody responses and interferon gene expression when compared with the layers of NVC group. The present study revealed that MS vaccine could facilitate replication of avian influenza viruses and thus avian influenza virus infections can be worse after MS vaccination, especially in AIV-endemic areas.
Avian influenza (H9N2) virus infection is an emerging respiratory problem and its prevalence varies significantly among different species of birds. The current knowledge about virus shedding parameters in terrestrial birds is limited. With this in mind, the present study was conducted in different domestic and wild terrestrial birds to investigate species-related differences in infectivity and pattern of viral shedding associated with H9N2 AI virus. Groups of terrestrial birds (domestic Guinea Fowl Numida meleagridis, Japanese Quail Coturnix coturnix japonica, House Sparrows Passer domesticus, House Crows Corvus splendens and Bank Myna Acridotheres ginginianus) were inoculated intra-nasally with A/chicken/Pakistan/10RS3039-284-48/2010 (H9N2) AI virus (106 EID50) and then examined for infectivity and virus shedding patterns. With the exception of House Crows, all infected birds showed clinical signs of different severity, showing the most prominent disease signs in Japanese Quail. All infected birds showed positive results for virus shedding, however, the pattern of virus shedding was different among wild terrestrial birds. Japanese Quail showed the highest levels of virus shedding while samples collected from House Crows revealed only very low levels. Interestingly, virus shedding was observed predominantly via the gastrointestinal tract in House Sparrows and Bank Myna and via the buccal cavity route in Guinea Fowl and Japanese Quail. Here we investigated that the novel genotype of H9N2 AI virus circulating in Pakistan causes clinical disease signs in domestic and wild terrestrial birds. The results of this study suggest that virus shedding varies between different related avian species and highlights the potential role of Guinea Fowl, Japanese Quail, House Sparrows and Bank Myna as mixing bowls for the transmission and maintenance of H9N2 AI viruses between premises.
The study was designed to investigate the replication of a re-assortant H9N2 avian influenza virus (AIV) and induction of the interferon (IFNγ) response after aerosol or intranasal inoculation with the virus in guinea fowl. To determine virus shedding pattern, oropharyngeal and cloacal swabs and tissue specimens of trachea, lungs, spleen and caecal tonsils were collected post-inoculation (pi). Infected guinea fowl showed mild clinical signs, while negative control guinea fowl remained healthy and active throughout the experiment irrespective of the inoculation route. However, the clinical signs were more prominent in guinea fowl infected through the aerosol route. Virus was detected in all oropharyngeal and cloacal swabs up to 7 d pi in guinea fowl from both inoculation groups. However, virus was detected more frequently and in higher titres in oropharyngeal swabs and specimens of trachea and lungs from the group exposed to aerosols than in the group given intranasal drops. In accordance with viral replication findings, expression of IFNγ was up-regulated on 1, 2 and 4 d pi to a significantly higher level in lung tissue specimens from the group exposed to virus aerosol than from controls treated with PBS intranasally. On the other hand, IFNγ was up-regulated above that of controls in lung tissue specimens from the group treated with intranasal drops of virus only on 4 d pi. These findings indicate that virus administered in aerosols was more efficient in infecting the lower respiratory tract and in inducing activity of the IFNγ gene than virus administered as intranasal drops. The results of this study suggest that virus aerosols cause more intense respiratory infection and increase the shedding of the H9N2 AIV in guinea fowl, highlighting the potential role of guinea fowl as a mixing bowl for transmission and maintenance of H9N2 AIV between poultry premises.
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