Submitted to: Microbial Pathogenesis
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: April 12, 2005
Publication Date: August 2, 2005
Citation: Tatum, F.M., Yersin, A.G., Briggs, R.E. 2005. Construction and virulence of a Pasteurella multocida fhaB2 mutant in turkeys. Microbial Pathogenesis. 39:9-17.
Interpretive Summary: Pasteurella multocida is the causative agent of fowl cholera in wild birds and poultry. P. multocida can cause both chronic and acute forms of infection in fowl resulting in high morbidity rates and economic loss. Few virulence factors have been characterized for this bacterium and better understanding of the molecular basis of pathogenesis of P. multocida will advance the development of safer and more efficacious vaccines against FC factors. Here we investigated the role of the filamentous hemagglutinin protein of P. multocida. A mutant with an inactive filamentous hemagglutinin protein was produced and it was shown to be highly attenuated in turkeys when administered intranasally and to a lesser degree when administered intravenously. The reduction in virulence of the P. multocida FHA mutant may therefore be linked to impaired ability of the mutant to cross the nasal mucosa of turkeys and establish septicemia or to reduced adherence resulting in poor colonization of the respiratory mucosa. Further studies are needed to discern the precise mechanism for reduced virulence of the mutant.
Pasteurella multocida is the causative agent of fowl cholera. The organism can occur as a commensal in the naso-pharyngeal region of apparently healthy animals and it can be a primary or secondary pathogen in the disease process of birds. The complete genome of an avian strain of P. multocida has been sequenced and was shown to possess two filamentous hemagglutanin genes designated fhaB1 and fhaB2. Filamentous hemagglutanin transposon mutants of a bovine strain of P. multocida are attenuated in mice. Here we report construction of an fhaB2 P. multocida mutant in an avian strain 1059 (A:3). The fhaB2 mutant and the parent were assessed for virulence in turkeys by intranasal and intravenous challenge. Inactivation of fhaB2 resulted in significant attenuation when turkeys were challenged intranasally and to a lesser degree when i.v. administered. Resistance of the fhaB2 mutant and parent strain to killing by the antibody dependent pathway of complement was similar.