Genomic characterization of Actinobacillus pleuropneumoniae serovars 5, 8, and 15 strains from diseased pigs in eastern Chinese provinces

Actinobacillus pleuropneumoniae causes porcine infectious pleuropneumonia in pigs. We aimed to characterize the phenotypic and genomic features of three A. pleuropneumoniae strains from clinical cases in eastern Chinese provinces. The serovar 5 strain ZJNH2023 was more pathogenic than strains AH2020 and ZJXS2022 in a murine model and was resistant to multiple antimicrobials. The core genome SNP (single nucleotide polymorphism) tree indicates that the three isolates are clustered with serovars 5, 8, and 15 strains of archived genomes. They harbor plasmids conferring resistance to florfenicol and are of substantial genome diversity, having more prophages, genomic islands (GIs) and antimicrobial resistance genes (ARGs) than the strains of corresponding serovars from other studies. The capsule-related gene clusters in strains AH2022 and ZJXS2022 are different from ZJNH2023 and contain an ISApl1 family transposase between the cps and cpx loci. The serovar 5 strain ZJNH2023 has a full set of ApxI genes, Apa1/Apa2, intact flp family genes related to Flp pilus assembly, and a full set tadABCD genes related to adherence, while strains ZJXS2022 and AH2022 carry ApxIII gene set, lack ApxIAC genes and Apa1/Apa2, and do not have intact flp family genes. Thus, we conclude that possession of the cytotoxic ApxI gene set and those involved in adhesion contributes to higher pathogenicity of the serovar 5 strain ZJNH2023. Distinct GIs and floR-containing plasmids in these strains might have been involved in multiple resistance and horizontal transfer of ARGs on the pig farms.