Location: Ruminant Diseases and Immunology Research
Title: Pasteurella multocida filamentous hemagglutinin B1 (fhaB1) gene is not involved with avian fowl cholera pathogenesis in turkey poultsAuthor
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Dassanayake, Rohana |
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Briggs, Robert |
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Kaplan, Bryan |
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MENGHWAR, HARISH - Oak Ridge Institute For Science And Education (ORISE) |
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Kanipe, Carly |
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Casas, Eduardo |
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Tatum, Fred |
Submitted to: BMC Veterinary Research
Publication Type: Peer Reviewed Journal Publication Acceptance Date: 3/13/2025 Publication Date: 3/26/2025 Citation: Dassanayake, R.P., Briggs, R.E., Kaplan, B.S., Menghwar, H., Kanipe, C.R., Casas, E., Tatum, F.M. 2025. Pasteurella multocida filamentous hemagglutinin B1 (fhaB1) gene is not involved with avian fowl cholera pathogenesis in turkey poults. BMC Veterinary Research. 21(1). Article 207. https://doi.org/10.1186/s12917-025-04668-1. DOI: https://doi.org/10.1186/s12917-025-04668-1 Interpretive Summary: Pasteurella multocida is the causative agent of fowl cholera (FC) in avian species including chickens and turkeys. P. multocida can cause both chronic and acute forms of infection in birds resulting in high morbidity rates and economic loss. The bacterium harbors several virulence factors and, therefore, understanding the molecular basis of pathogenesis will advance the development of safer and more efficacious vaccines against FC. Here we investigated the role of the filamentous hemagglutinin B1 protein of P. multocida. A mutant with an inactive filamentous hemagglutinin B1 protein was produced. This mutant strain did not show any attenuation in turkeys when administered intranasally and/or intramuscularly. These observations suggest that highly conserved filamentous hemagglutinin B1 protein is not necessary for the development of acute FC disease in turkeys. Technical Abstract: Pasteurella multocida is the causative agent of fowl cholera (FC) in avian species. It has been previously demonstrated that P. multocida fhaB2 (filamentous hemagglutinin B2 gene) is an important virulence factor in the development of FC disease. In the current study, we examined the potential role of fhaB1 in FC disease development. An fhaB1 deletion mutant was constructed in P. multocida avian strain P-1059 (A:3). The fhaB1 mutant and the wild-type parent strain were assessed for virulence in turkey poults. Inactivation of fhaB1 did not reduce virulence in either intranasal or intramuscular challenge routes indicating that this large highly conserved protein is not necessary for the development of acute FC disease in turkeys. |