# Pathogenicity and Genomic Characterization of Pasteurella multocida Serogroup F Isolate AH01 From Porcine Pneumonia in China

## TL;DR

This study characterizes a virulent strain of Pasteurella multocida from pigs in China, revealing its pathogenic effects and unique genomic features.

## Contribution

The study provides the first detailed genomic and pathogenic analysis of a porcine-derived P. multocida serogroup F isolate.

## Key findings

- Intratracheal challenge with AH01 caused rapid mortality and severe respiratory symptoms in pigs.
- Genomic analysis revealed 254 virulence genes, drug resistance traits, and a novel 16.7-kb region encoding Zot and GspD.
- Polymorphisms in LPS biosynthesis genes suggest host-specific adaptations in porcine P. multocida strains.

## Abstract

Pasteurella multocida (P. multocida), a significant animal pathogen, causes swine pneumonia and atrophic rhinitis, primarily associated with serogroups A, D, and F. Although serogroups A and D are prevalent in pigs and well-established causes of these diseases, the pathogenicity and genomic characteristics of porcine serogroup F remain poorly characterized. Here, we isolated a virulent P. multocida strain—AH01, from pigs with fatal acute respiratory disease in Anhui, China. It was characterized as a capsular Type F, lipopolysaccharide (LPS) antigen Type L3 isolate of sequence type (ST) 9. To evaluate the pathogenicity of this strain, pigs were challenged intratracheally with AH01 (6 × 109 CFU), inducing acute pyrexia, dyspnea, anorexia, and rapid mortality (≤12 h postinfection, hpi). PacBio SMRT (Single-Molecule Real Time) sequencing generated a complete 2.27-Mbp chromosome (40.3% GC content; 2058 CDSs). Annotation identified 254 potential virulence-associated genes, 47 different drug resistance phenotypes, and three genomic islands (GIs). Comparative genomics revealed a novel 16.7-kb specific region insertion encoding zonula occludens toxin (Zot) and general secretion pathway protein D (GspD), potentially facilitating epithelial barrier disruption. Furthermore, polymorphisms in LPS outer core biosynthesis genes natC and gatF were characterized across strains avian Pm70, porcine AH01, and HN07. Strain AH01 harbors a single-nucleotide deletion (natC position 760), causing a frameshift and premature stop. Both porcine strains AH01 and HN07 exhibited a 216-bp N-terminal extension in gatF compared to avian Pm70 strain, indicating host-specific or strain-dependent LPS biosynthetic divergence. Collectively, these findings provide critical insights into the pathogenicity and genomic basis of porcine-derived P. multocida serogroup F.