AbstractPathogenesis of colibacillosis caused by avian pathogenic Escherichia coli (APEC) in poultry is not clear and experimental studies reveal substantial inconsistency. In this study, the impact of three infection routes that differ with respect to the site of deposition of inoculum in the respiratory tract, were investigated. Two-weeks old chickens were infected with a lux-tagged APEC strain via aerosol, intranasally or intratracheally and sequentially sampled along with uninfected birds. At 1 and 3 days post infection (dpi), liver or spleen to body-weight ratios in all infected groups were significantly higher than in negative control, while at 7 dpi, such differences were significant in both organs in the aerosol-infected group. The infection-strain colonized tracheas and lungs in infected birds at 1 dpi and persisted until 7 dpi. Among infected groups, in lungs, bacterial load at 1 dpi was significantly lower in intranasally inoculated birds. Histology revealed that independent of infection routes, lesions were mostly seen in the lower respiratory organs (lungs and air sacs) characterized by bronchitis/pneumonia and airsacculitis. Birds infected via aerosol showed the highest mean lesion score in lungs while intranasal application caused the mildest pathological changes, and the difference was significant at 1 dpi. In spleen, heterophilic infiltrations were prominent in affected birds. Interestingly, tracheas were pathologically unaffected. Altogether, the results demonstrated the importance of infection route with aerosol being the most suitable to induce pathological lesions of colibacillosis without predisposing factors. Furthermore, the lux-tagged APEC strain was discriminated from native isolates enabling exact differentiation and enumeration.
Keywords: APEC; aerosol; avian pathogenic Escherichia coli; chickens; colibacillosis; experimental infection; lux-tagged.