Virulence mechanisms of avian fimbriated Escherichia coli in experimentally inoculated chickens.

Virulence mechanisms of avian pathogenic Escherichia coli were investigated by inoculating commercial broiler chickens via the left caudal thoracic air sac with three highly pathogenic and three less pathogenic E. coli isolates. At 6 h postinoculation, all isolates had colonized the respiratory tract (trachea, lungs, and air sacs) and internal organs (liver, spleen, and kidney) of inoculated birds, but bacteria were recovered from pericardial fluid and blood only of birds inoculated with the more pathogenic isolates.

Localization of the in vivo expression of P and F1 fimbriae in chickens experimentally inoculated with pathogenic Escherichia coli.

Escherichia coli causing septicemia in poultry often possess F1 (type 1) and/or P fimbriae which may be involved in bacterial colonization and infection. To investigate the expression of these fimbriae in vivo, two pathogenic E. coli strains with different fimbrial profiles, TK3 (fim+/pap+) and MT78 (fim+/pap-), were administered to 2-week-old chickens by either the intratracheal or caudal thoracic air sac inoculation route.

Dynamics of Escherichia coil infection in experimentally inoculated chickens.

In order to study the dynamics of avian colibacillosis, commercial broiler chickens were inoculated with a pathogenic Escherichia coli strain (01:K1:H7) into the left caudal thoracic air sac. Chickens were euthanatized at different times from 3 to 48 hr postinoculation and examined for bacterial counts and macroscopic and microscopic lesions. The E.

Ultrastructural characterization of the nasal respiratory epithelium in the piglet.

Background: Very little information is available on the ultrastructure of the nasal cavity epithelium of the piglet. However, the nasal respiratory epithelium plays an important role in the pathology of atrophic rhintis of the piglet. Indeed, ciliated cells and mucus play a co-ordinate role in the colonization of the nasal cavity by the etiological agents of the disease.