The pathogenesis of colibacillosis in broilers infected with virulent or vaccine strains of infectious bronchitis virus

Abstract

Colibacillosis is caused by E. coli bacteria and occurs predominantly in broilers in the second half of the growing period. The disease is of economic importance worldwide due to growth retardation, increased feed conversion, mortality and high condemnation rate at slaughter. Moreover, colibacillosis results in impaired welfare. Infections of the respiratory tract, amongst others infection with infectious bronchitis virus (IBV), increase the susceptibility for colibacillosis of broilers significantly. From recently made field observations it was hypothesised that not only virulent IBV but also live IBV vaccine strains, which are commonly used in the field to prevent birds from clinical signs of infectious bronchitis (IB), are able to increase colibacillosis susceptibility in broilers substantially. This hypothesis was tested experimentally. The experiments showed that IBV vaccines H120 and H52 increased colibacillosis susceptibility in four-weeks-old broilers to the same level as virulent IBV strains (M41 and D387) did. It was also demonstrated that the IBV H120 vaccine spread extensively between broilers. From the latter data it seems obvious that IBV H120 vaccine also might spread between flocks. In case not IB vaccinated flocks are infected with IB vaccine virus by that route, especially in the second half of the growing period, serious colibacillosis might occur. The significance of IBV vaccine strains in the occurrence of colibacillosis in broilers in the field has to be elucidated. The underlying mechanism of E. coli superinfections (E. coli infection after triggering by a previous viral infection) in IBV infected broilers was studied based on morphological and functional immunology. The results strongly suggest that preceding infection with vaccine or virulent IBV does not seem to impair the clearance of the E. coli in the respiratory tract of broilers, but rather induces an exaggerated inflammatory response. It also seems that infection with virulent or vaccine strains of IBV altered the innate systemical immunity rather than the phagocytic cell function.