Course of infection and immune responses in the respiratory tract of IBV infected broilers after superinfection with E. coli

Abstract

Colibacillosis results from infection with avian pathogenic Escherichia coli bacteria. Healthy broilers are resistant to inhaled E. coli, but previous infection with vaccine or virulent strains of Infectious Bronchitis Virus (IBV) predisposes birds for severe colibacillosis. The aim of this study was to investigate how IBV affects the course of events upon infection with E. coli. Broilers were inoculated with IBV H120 vaccine virus or virulent M41 and challenged 5 days later with E. coli 506. A PBS and E. coli group without previous virus inoculation were included. Sections of trachea, lung and airsacs were stained for CD4, CD8, gammadelta-TCR, alphabeta1-TCR, and for macrophages (KUL-01) and both pathogens. Changes in the mucociliary barrier of trachea, lung and airsacs did not predispose for bacterial superinfection. The disease in the lungs of the E. coli group and both IBV/E. coli groups was similar. Lesions in the airsacs were more pronounced and of longer duration in the IBV/E. coli groups. The immunocytological changes differed substantially between the E. coli group and both IBV/E. coli groups. In trachea, lungs and airsacs the CD4+ and CD8+ populations were significantly larger than in the E. coli and PBS groups. In the lungs and the airsacs the macrophages were more numerous in the IBV/E. coli and the E. coli groups than in the PBS group. The presence of high numbers of T cells and macrophages in IBV infected birds most likely induced an altered immune response, which is responsible for the enhanced clinical signs of colibacillosis.

Progression of lesions in the respiratory tract of broilers after single infection with Escherichia coli compared to superinfection with E. coli after infection with infectious bronchitis virus

“…It appears that from the three compartments of the respiratory tract: trachea, lungs (bronchi and parabronchi) and the airsacs, the airsacs are the only site which may harbour both IBV and E. coli during a maximum of 2 dpi. A plausible explanation for the longer persistence of airsac lesions compared to trachea and lungs upon successive infection of broilers with both IBV and E. coli was given previously by Matthijs et al (Matthijs et al, 2008), who demonstrated the occurrence of a reduction in the number of macrophages a week after inoculation with E. coli, whereas these cells were still present in high numbers at this stage in the airsacs of IBV-E. coli infected broilers. Possibly, upon the influence of both pathogens the high concentrations of macrophages will be prompted to overproduce pro-inflammatory cytokines, favouring the occurrence of the persistent airsacculitis.…”

“…From 2 to 5 days following IBV inoculation the number of birds with nasal discharge in the M41 group was significantly higher in comparison with the H120 group (for detailed information see Matthijs et al, 2008).…”

Uptake of Particulate Antigens in a Nonmammalian Lung: Phenotypic and Functional Characterization of Avian Respiratory Phagocytes Using Bacterial or Viral Antigens

“…Slides were washed in PBS and incubated for 1 h with optimally diluted primary Ab or isotype controls (Table I) in staining buffer. Sections were washed three times and blocked with normal horse serum diluted in PBS followed by incubation with biotinylated horse anti-mouse IgG and avidinbiotinylated enzyme complex (VECTASTAIN Elite) as described previously (27). Color development was done using 3,3-diaminobenzidine tetrahydrochloride (Sigma-Aldrich).…”

Induction of respiratory immune responses in the chicken; implications for development of mucosal avian influenza virus vaccines

“…However, the tracheal mucosa is highly responsive to infection and reacts with extensive lymphocyte infiltration followed by proliferation (Gaunson et al 2000;Gaunson et al 2006;Matthijs et al 2009). Tracheal lesions characteristic for Mycoplasma infections predominantly consist of proliferating B cells (Gaunson et al 2006) and this is similar to IBV infection (Kotani et al 2000).…”