Study On The Synergistic Pathogenesis Between Mildly Pathogenic Avian Influenza Virus And Avian Escherichia. Coli

Mildly pathogenic avian influenza virus H9N2 (MPAIV) is widely distributed andrecently has resulted in considerable economic losses to poultry industry in China. Clinically, mildly pathogenic avian influenza virus infection is often complicated with avian colibacciilosis. But there are few reports about the synergism between these two agents currently. We investigated their synergistic pathogenesis from the following four aspects in the synergism model: (1) the mortality rate in the synergism; (2) the dynamic distribution of Escherichia coli (E.coli) in the synergism; (3) the pathologic abnormalities in the synergism; (4) MPAIV isolation in the synergism.10-day-old specific pathogen free (SPF) chickens were inoculated intratracheally with virulent E.coli (026) and /or mildly pathogenic avian influenza virus (MPAIV). The mortality rate of chickens inoculated with 10 8 colony-forming units (CPU) E.coli and 2× 104.3 ELD50 MPAIV simultaneously was 32%. Chickens inoculated first with 2 × 1043 ELD50 MPAIV and then 10 8 CPU E.coli at an interval of 48 hours experienced the mortality rate of 24%, whereas those inoculated with 10 8 CPU E.coli and 2× 10 4.3 ELD50 MPAIV at the same interval exhibited the mortality rate of 16%. the groupinfected with MPAIV alone experienced the mortality rate of 12% while the group infected with E.coli alone had no death.10-day-old SPF chickens inoculated intratracheally with 108 CPU virulent E.coli (026) and /or 2 × 1043 ELD50 mildly pathogenic avian influenza virus (MPAIV), respectively, were euthanatized at different times from 1 to 96 h post-inoculation and examined for bacterial counts, macroscopic and microscopic lesions, and ultrastructural pathologic abnormalities. The challenging strain E.coli could be reisolated from trachea, lung of the chickens during the experiments. The distribution of E.coli isolated from blood and the other tissues correlated with the time of postinoculation. Chickens inoculated with E.coli and MPAIV had more severe and persistent respiratory lesions than those inoculated with E. coll or MPAIV alone.the group inoculated with MPAIV and E.coli was more severe inflammation of the trachea, lung, and air sac and dispersion necrosis of parenchyma organs than that of groups inoculated with MPAIV or E.coli alone. Chickens inoculated with MPAIV and E.coli simultaneously had the most severe and persistent lesions than the other experimental groups. The most severe pathological changes that ciliated cells were deciliated totally and the type II alveolar cells were vacuolated completely were taken place in trachea 4-48h and in lung 6h postinoculation. There were moderate pathological changes in lung and trachea at 6h post inoculation with E.coli alone. The pathological changes that ciliated cells were deciliated partly and the lamellar bodies were vanished in the type II alveolar cell appeared in trachea 3-48h and in lung 12h postinoculation with MPAIV alone.Samples of tracheas, lungs and cloacal swabs were taken from 3 chickens each group at different intervals postinoculation for isolating challenged MPAIV in 9-day-old embryonating chicken eggs. The results showed that there was no difference for the persistence of MPAIV in the tracheas and lungs between the group infected with MPAIV and E.coli and the group infected with MPAIV alone, while the duration ofvirus shedding from intestine for the group infected with both MPAIV and E.coli seemed to be slightly longer than that infected with MPAIV alone.These results suggest that E.coli colonized mainly the trachea and lung, MPAIV might maintain the time that E.coli colonized the trachea and lung of chickens, and it might facilitate E.coli invasion into the respiratory tract of the chickens resulting in more severe pathologic abnormalities. There was a pathogenic synergism between E. coli and MPAIV.