IntroductionDespite the advancements in the field, there is a lack of data when it comes to co-infections in poultry. Therefore, this study was designed to address this issue.Material and MethodsBroiler birds were experimentally infected with E. coli (O78) and low pathogenic avian influenza (LPAI) strain, alone or in combination. The experimental groups were negative control.ResultsThe infected birds showed most severe clinical signs in E. coli+LPAI group along with a significant decrease in weight and enhanced macroscopic and microscopic pathological lesions. The survival rate was 60%, 84%, and 100% in birds inoculated with E. coli+LPAI, E. coli, and LPAI virus alone, respectively. The results showed that experimental co-infection with E. coli and H9N2 strain of LPAI virus increased the severity of clinical signs, mortality rate, and gross lesions. The HI titre against LPAI virus infection in the co-infected group was significantly higher than the HI titre of LPAI group, which may indicate that E. coli may promote propagation of H9N2 LPAI virus by alteration of immune response.ConclusionThe present study revealed that co-infection with E. coli and H9N2 LPAI virus caused more serious synergistic pathogenic effects and indicates the role of both pathogens as complicating factors in poultry infections.
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.
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