Construction and immunization with double mutant Δ apxIBD Δ pnp forms of Actinobacillus pleuropneumoniae serotypes 1 and 5

• Published in: Journal of veterinary science (Suwŏn-si, Korea) Vol. 21; no. 2; p. e20
• Main Authors: Dao, Hoai Thu, Truong, Quang Lam, Do, Van Tan, Hahn, Tae-Wook
• Format: Journal Article
• Language: English
• Published: Korea (South) The Korean Society of Veterinary Science 01.03.2020; 대한수의학회
• Subjects: Original; 수의학; pnp gene; apxIBD gene; deletion mutation; virulence; Actinobacillus pleuropneumoniae
• ISSN: 1229-845X; 1976-555X; 1976-555X
• DOI: 10.4142/jvs.2020.21.e20

(APP) causes a form of porcine pleuropneumonia that leads to significant economic losses in the swine industry worldwide. The gene is responsible for the secretion of the ApxI and ApxII toxins and the gene is responsible for the adaptation of bacteria to cold temperature and a virulence factor. The and genes were deleted successfully from APP serotype 1 and 5 by transconjugation and sucrose counter-selection. The APP1Δ Δ and APP5Δ Δ mutants lost hemolytic activity and could not secrete ApxI and ApxII toxins outside the bacteria because both mutants lost the ApxI- and ApxII-secreting proteins by deletion of the gene. Besides, the growth of these mutants was defective at low temperatures resulting from the deletion of . The APP1Δ Δ and APP5Δ Δ mutants were significantly attenuated compared with wild-type ones. However, mice vaccinated intraperitoneally with APP5Δ Δ did not provide any protection when challenged with a 10-times 50% lethal dose of virulent homologous (APP5) and heterologous (APP1) bacterial strains, while mice vaccinated with APP1Δ Δ offered 75% protection against a homologous challenge. The Δ Δ mutants were significantly attenuated and gave different protection rate against homologous virulent wild-type APP challenging.