Graduate Thesis Or Dissertation
 

Pasteurella multocida infection in turkeys : pathogenesis and immunity

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  • Pathogenesis and immunity involved in fowl cholera were studied with the turkey, one of the most susceptible natural hosts. The causative agent, Pasteurella multocida, was analyzed in terms of its virulence and immunogenic factors, using a highly virulent, encapsulated strain P-1059. Protective immunity was induced by lipopolysaccharide (LPS)- protein complex antigens prepared by two different methods. The LPS prepared by Westphal's phenol-water method, in contrast, did not induce immunity. High titers of anti-LPS antibody were induced by LPS-protein complexes, but not by LPS. Immunogenicity of the LPS-protein complex was lost upon the treatment with periodate, but not with protease. The results suggest that immunoprotective determinants probably reside in the LPS moiety of the complex, and that the protein(s) may function as the carrier of LPS. Virulence of the organism was closely associated with its capsule-producibility, since a non-encapsulated mutant derived from the strain P-1059 was significantly less virulent than the parent strain. The capsule was removable by hyaluronidase, but the decapsulation did not cause the loss of virulence. When the encapsulated or decapsulated form of organism, as well as the non-encapsulated mutant was intravenously inoculated into susceptible turkeys, the majority of bacteria were rapidly removed from the bloodstream, and trapped in the liver and spleen. The presence or absence of capsule did not influence the clearance of bacteria from the blood. Thus, the capsule appeared not to act as an anti-phagocytic factor to the phagocytes responsible for the intravascular clearance of bacteria. The non-encapsulated mutant was readily inactivated in the liver (but not in the spleen), while the encapsulated organisms multiplied freely in the liver and spleen. Hence, the capsule seemed to be important for the bacteria to resist the bactericidal activity of hepatic phagocytes. Similar experiments with immune turkeys showed that specific immunity did not enhance the clearance of bacteria from the blood, but that immunity was essential for inactivation of the encapsulated bacteria entrapped in the liver. Immunity, however, did not facilitate the killing of bacteria in the spleen. Involvement of humoral and cellular defense factors in the bactericidal activity in the liver was investigated by the passive transfer of immune serum or by the treatment with macrophage activating agents. The results indicated that specific antibody has a primary role, and that activation of macrophages may also contribute to enhancing the bactericidal activity.
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