Evaluation of the effect of simultaneous infection with E. coli O2 and H9N2 influenza virus on inflammatory factors in broiler chickens

Abstract

This study was conducted to evaluate the effect of experimental infection with Escherichia coli O2 and H9N2 influenza virus on inflammatory factors in broiler chickens. A total of 120 oneday-old Cobb broiler chicks were divided randomly to 6 groups. Inoculation program with 10 9 EID50/bird of the A/Chicken/Iran/772/1998 (H9N2) virus and 10 9 CFU/mL/bird of E. coli O2 was carried out as follows: the chicks in group 1 were inoculated with virus and bacteria simultaneously on day 26, group 2 received virus on day 26 and then bacteria 3 days later, group 3 were inoculated with bacteria on day 23 and then virus on day 26, group 4 received only bacteria on day 26, group 5 were inoculated with only virus on day 26 and group 6 served as control. Serum samples were collected from wing vein at days 20, 30, and 40. Sera were examined for inflammatory mediators (TNF-a and INF-γ), acute phase reactants (haptoglobin and serum amyloid A) and gangliosides (total, lipid-bound and protein-bound sialic acids) using validated standard procedures. Among the measured parameters, serum gangliosides showed significant differences between the challenged and control groups in different days post inoculation (P<0.05). Significant increase in serum concentrations of serum sialic acids was observed on the 30 th day in challenged groups. Elevations were found in the concentrations of serum gangliosides on day 40 compared to their first concentrations. The most obvious increase in serum sialic acids was observed in group 1 challenged with avian influenza virus and E. coli O2 simultaneously. Bacterial infected group showed more significant changes in comparison with viral infected one. These findings suggest that serum sialic acids may be a useful indicator of H9N2 avian influenza virus and avian pathogenic E. coli O2 co-infection.

Molecular survey and interaction of common respiratory pathogens in chicken flocks (field perspective)

“…Our observation in both backyard and commercial broiler flocks confirms a bidirectional synergistic effect between these concurrently interacting respiratory pathogens in which each pathogen augment pathogenesis of the other one. These bidirectional interactions explain the resulting severe clinical outcomes and higher MR, which coincide with the results of Dadras et al and Mosleh et al [15,30]. E. coli infection before, after, or concurrently with LPAIV (H9N2) infection could exacerbate the adverse effects of the LPAIV (H9N2).…”

“…AIV of H9N2 subtype has been endemic in poultry in Asia and the Middle East [13,14]. It is clear that IBV infection maximized the pathogenicity and extended the period of H9N2 AIV shedding in chickens [15,16], increasing MR and economic losses, possibly due to mixed infection, and interaction with other respiratory pathogens [2,12,[15][16][17].…”

“…E. coli infection before, after, or concurrently with H9N2 virus infection could exacerbate the adverse effects of the H9N2 virus. E. coli and H9N2 together can mutually exacerbate the condition of either disease as compared to single infected birds [15,30].…”

Minor differences in body condition and immune status between avian influenza virus‐infected and noninfected mallards: a sign of coevolution?

“…Complement is thought to be involved in host defense of AIV; however, the extent of complement activation may depend on AIV subtype (O'Brien et al 2011). Markers of acute phase responses (e.g., Hp) increase with LPAIV infection in chickens (Sylte and Suarez 2012;Dadras et al 2014). Lymphocytes are essential in controlling LPAIV infection in birds (e.g., reduce viral shedding; Suarez and Schultz-Cherry 2000), whereas heterophils play important roles in the initial replication and dissemination of HPAIV (Pantin-Jackwood and Swayne 2009).…”

Enhanced pathogenicity of low-pathogenic H9N2 avian influenza virus after vaccination with infectious bronchitis live attenuated vaccine

“…It is almost one decade that the Middle East and Asian countries are facing frequent outbreaks of H9N2 infection [ 4 , 5 ]. Mixed infection or coinfection of H9N2 AIV with other respiratory pathogens is one of the possible explanations for increasing the economic losses of H9N2 infection in commercial broiler chickens[ 6 , 7 ]. It was reported that infectious bronchitis virus (IBV) infection increased the pathogenicity and extended the period of H9N2 AIV shedding in broiler chickens [ 6 - 8 ].…”