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Early migration pattern of Avibacterium paragallinarum in the nasal passage of experimentally infected chicken and Japanese quail by immunohistochemistry
- Balouria, Aadish, Deshmukh, Sidhartha, Banga, H. S., Ahmad, Ajaz, Brar, R. S., Sodhi, Sandeep
- Avian pathology 2019 v.48 no.2 pp. 168-177
- Avibacterium paragallinarum, Coturnix japonica, antiserum, bacterial antigens, chickens, farmers, immunoelectrophoresis, immunohistochemistry, microorganisms, nasal cavity, pathogens, polyclonal antibodies, respiratory mucosa, swollen head syndrome, vaccines, virulence
- Infectious coryza (IC) is often a curse for poultry farmers when it occurs concurrently with several pathogens causing swollen head syndrome. The disease is caused by Avibacterium paragallinarum, which inflicts initial damage to the nasal and respiratory epithelium. This facilitates the progression of disease pathology across the nasal cavity, thereby providing a platform for multiplication of opportunistic microbes. In this study, we attempted to investigate the early entrance and migration pattern of A. paragallinarum in chicken and Japanese quail following experimental infection, by employing an in-house developed polyclonal antiserum against this pathogen. Antigenic-specificity of the raised antiserum was subsequently evaluated through immune-dot blot techniques and counter-current immunoelectrophoresis (CIE). The resultant antiserum characterized the antigen localization within formalin-fixed and partially decalcified nasal tissue sections though immunohistochemistry (IHC). Japanese quail showed prominent localization of the bacterial antigen at 12 h post-infection in anterior turbinates. However, the chicken exhibited a higher level of the bacterial pathogen with intense immuno-reactivity at 24 and 48 h post-inoculation. The decline in immunostaining intensity in the nasal tissue of chicken as well as Japanese quail by 72 h post-infection signifies either an attempt to resolve the infection by the resident immune cells across the nasal passage of the host, or its dissipation by certain inherent innate immune factors present across the nasal passage that are still unknown to us. In the present study, we used a moderately virulent pathogen (A. paragallinarum) that inflicted a mild to moderate degree of damage to histo-architecture of the nasal passage and provided a discernible migratory pattern with fewer alterations, along with provision toward unravelling basics of the immuno-pathogenetic mechanism. This knowledge will support efforts towards the development of a future mucosal nasal vaccine in birds affected with IC.