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Background Hemorrhagic septicemia is a highly fatal disease of cattle caused by the bacteria; Pasteurella multocida serotypes B and E in Asia and Africa respectively. Even though the capsular serotype E is considered to be the common cause of Hemorrhagic septicemia in Africa, there is not enough evidence that other serotypes are not involved. Furthermore, the serotypes currently circulating in South West Ethiopia have not been identified. This study was carried out to identify circulating capsular serotypes of Pasteurella multocida and assess its antimicrobial resistance on hemorrhagic Septicemic cattle through bacterial isolation, molecular identifications, and antimicrobial susceptibility tests in Keffa and Bench Sheko Zones of South West Ethiopia Peoples’ Regional State. Results The bacteriological analysis from 45 purposively collected nasopharyngeal swab samples of hemorrhagic Septicemic cattle revealed that 12 (26.7%) isolates were identified as Pasteurella multocida. Similarly, the molecular analysis of these isolates revealed all twelve (12) isolates were confirmed to be Pasteurella multocida. On further capsular typing, serotype B ( n  = 5, 41.6%) and E ( n  = 5, 41.6%) were the confirmed circulating strains in the area while two ( n  = 2, 16.6%) isolates formed non-specific bands. All the Pasteurella multocida isolates were susceptible to Gentamicin (100%), Chloramphenicol (100%), Oxytetracycline (91.7%), and Streptomycin (75%). However, all the isolates showed multidrug resistance (100%), to four antibiotics “Ampicillin, Clindamycin, Penicillin-G, and Vancomycin”. Conclusions Molecular analysis of the study isolates confirmed serotypes B and E as the etiology for Hemorrhagic septicemia in cattle in the study area. A multivalent vaccine comprising serotypes B and E is recommended to prevent outbreaks along with early treatment of suspected cases during the pyretic stage using antibiotics that are effective against the strains.

Pasteurella multocida is incriminated in fowl cholera in poultry and snuffles in rabbits, causing significant economic losses in the poultry industry worldwide. This study investigated the prevalence, kmt 1 gene sequencing, antibiogram, pathogenicity, and PCR detection of the virulence and resistance genes of P. multocida recovered from chickens, ducks, and rabbits. Approximately 150 samples were collected from diseased chickens, ducks, and rabbits (50 for each) from commercial farms in Ismailia government, Egypt. The collected samples were bacteriologically examined, and the recovered isolates were subsequently subjected to kmt 1 gene sequencing, antibiogram, pathogenicity test, and PCR-based detection of virulence and antibiotic resistance genes. The overall prevalence of P. multocida was 20% (30/150). The highest prevalence was recorded in rabbits (24%; 12/50), followed by ducks (20%; 10/50) and chickens (16%; 8/50). The lung was the most predominant infected organ. Moreover, the kmt 1 phylogenetic analysis emphasized that the tested P. multocida strains presented remarkable genetic identity with other P. multocida strains from the USA, Denmark, China, India, and Iran. Chloramphenicol and ciprofloxacin exhibited promising results in treating P. multocida . Moreover, the prevalence of oma 87, ptf A, lux S, tad G, and nan B virulence genes was 100%, 86.7%, 76.6%, 73.3%, and 56.7% respectively. Herein, 13.3% of the tested strains were multidrug-resistant (MDR) to 5 antibiotic classes and carried bla ROB−1 and tet H genes. Besides, 10% of the tested P. multocida strains were extensively drug resistant (XDR) to 7 antibiotic classes and harbored the bla ROB−1 , tet H, and erm X genes. Moreover, 10% of the recovered P. multocida strains were MDR to 5 antibiotic classes and had tet H and erm X genes. Pathogenicity test revealed that the mortality rate was 20% at 1 day post-infection, reaching its highest point (100%) at 2 days post-infection. Briefly, this study highlights the occurrence of MDR and XDR P. multocida in domestic birds and rabbits, revealing a public health threat. The oma 87, ptf A, luxS , and tad G virulence genes and the bla ROB−1 , tet H, and erm X antibiotic resistance genes are usually associated with emerging MDR P . multocida strains.

Pasteurella multocida is an important multihost animal and zoonotic pathogen that is capable of causing respiratory and multisystemic diseases, bacteremia, and bite wound infections. The glycosaminoglycan capsule of P. multocida is an essential virulence factor that protects the bacterium from host defenses. However, chronic infections (such as swine atrophic rhinitis and the carrier state in birds and other animals) may be associated with biofilm formation, which has not been characterized in P. multocida . Biofilm formation by clinical isolates was inversely related to capsule production and was confirmed with capsule-deficient mutants of highly encapsulated strains. Capsule-deficient mutants formed biofilms with a larger biomass that was thicker and smoother than the biofilm of encapsulated strains. Passage of a highly encapsulated, poor-biofilm-forming strain under conditions that favored biofilm formation resulted in the production of less capsular polysaccharide and a more robust biofilm, as did addition of hyaluronidase to the growth medium of all of the strains tested. The matrix material of the biofilm was composed predominately of a glycogen exopolysaccharide (EPS), as determined by gas chromatography-mass spectrometry, nuclear magnetic resonance, and enzymatic digestion. However, a putative glycogen synthesis locus was not differentially regulated when the bacteria were grown as a biofilm or planktonically, as determined by quantitative reverse transcriptase PCR. Therefore, the negatively charged capsule may interfere with biofilm formation by blocking adherence to a surface or by preventing the EPS matrix from encasing large numbers of bacterial cells. This is the first detailed description of biofilm formation and a glycogen EPS by P. multocida . IMPORTANCE Pasteurella multocida is an important pathogen responsible for severe infections in food animals, domestic and wild birds, pet animals, and humans. P. multocida was first isolated by Louis Pasteur in 1880 and has been studied for over 130 years. However, aspects of its lifecycle have remained unknown. Although formation of a biofilm by P. multocida has been proposed, this report is the first to characterize biofilm formation by P. multocida . Of particular interest is that the biofilm matrix material contained a newly reported amylose-like glycogen as the exopolysaccharide component and that production of capsular polysaccharide (CPS) was inversely related to biofilm formation. However, even highly mucoid, poor-biofilm-forming strains could form abundant biofilms by loss of CPS or following in vitro passage under biofilm growth conditions. Therefore, the carrier state or subclinical chronic infections with P. multocida may result from CPS downregulation with concomitant enhanced biofilm formation. Pasteurella multocida is an important pathogen responsible for severe infections in food animals, domestic and wild birds, pet animals, and humans. P. multocida was first isolated by Louis Pasteur in 1880 and has been studied for over 130 years. However, aspects of its lifecycle have remained unknown. Although formation of a biofilm by P. multocida has been proposed, this report is the first to characterize biofilm formation by P. multocida . Of particular interest is that the biofilm matrix material contained a newly reported amylose-like glycogen as the exopolysaccharide component and that production of capsular polysaccharide (CPS) was inversely related to biofilm formation. However, even highly mucoid, poor-biofilm-forming strains could form abundant biofilms by loss of CPS or following in vitro passage under biofilm growth conditions. Therefore, the carrier state or subclinical chronic infections with P. multocida may result from CPS downregulation with concomitant enhanced biofilm formation.

The zoonotic bacterium Pasteurella multocida infects a wide range of animals worldwide. While the genetic diversity of this pathogen is well described in production animals, it remains underexplored in companion animals. In Australia, most P. multocida genomes come from commercial poultry. Here, 59 P. multocida clinical isolates obtained from Australian pets, (cats, dogs, rabbits), farm animals (birds, ruminants, porcine) and captive wildlife (Quolls, Serval) between 2006 and 2023 were sequenced and compared to 523 representative RefSeq genomes. Clustering and phylogenomic analyses placed 24/25 Australian pet isolates in a long-branched clade containing several MLST profiles (ST36, ST37, ST171, ST359, ST451 and ST527) also found in human isolates. Genotypes associated with Australian production animals (e.g., ST8, ST9 and ST20 from poultry, ST79 and ST394 from cattle) fell in the main branch of the tree. Minimum spanning tree and SNP analyses suggested several occurrences of cross-species transmission. Mobile genetic elements were found across the P. multocida population, without clustering into any specific phylogenetic, host, or geographic group. However, a 1.8 kb cryptic plasmid (Acc. U51470), previously described in Pasteurella canis strains from South Korea, was detected in 99/289 (34.3%) Australian P. multocida isolates from various hosts, while being largely absent from the rest of the world. Antimicrobial resistance was not detected in the isolates from Australian companion animals and captive wildlife. However, resistances to tetracyclines in bovine isolates (2/10) and ampicillin in avian (1/17) isolates were identified. This study greatly expands our insights on the diversity of P. multocida genomes from Australian companion animals and provides the basis for wider investigations on the molecular epidemiology and diversity of this pathogen, with potential applications to better understand the zoonotic risks associated with this pathogen.

Background Pasteurella multocida causes progressive atrophic rhinitis and suppurative bronchopneumonia in pigs, which results in severe economic losses in swine industry. This study aimed to determine the serovar, genotype and prevalence of toxA virulence gene of Pasteurella multocida isolates collected in Taiwan. A total of 164 Pasteurella multocida isolates from 161 diseased pigs were characterized by serotyping, multilocus sequence typing (MLST), antimicrobial susceptibility testing, and the presence of virulence gene ( toxA ) and antibiotic resistance gene ( floR ). Results The majority of Pasteurella multocida strains were serovar D:L6 (48.2%; 79/164) followed by A:L6 (28.7%; 47/164) and A:L3 (19.5%; 32/164). More than 80% of strains carrying toxA gene belonged to serovar A:L6 (82.6%; 19/23). The MLST data showed five sequence types (STs), where multi-host ST10 was the most dominant. Most Pasteurella multocida strains of multi-host ST10 were serovar A:L6 (93.9%; 31/33), which suggested that STs were highly associated with specific serovars. Most of the floR -carrying Pasteurella multocida strains belonged to serovar D:L6 with significantly high resistance to some antimicrobial agents, especially florfenicol. Conclusions This study demonstrated that serovar D:L6 and multi-host ST10 was the most prevalent Pasteurella multocida strain in Taiwan. A:L6 accounted for the majority of tox A-positive strains and the presence of  floR gene may be responsible for the antimicrobial resistance to florfenicol.

Pasteurella multocida (P. multocida), a pathogenic bacterium known to induce duck cholera, stands as a significant contributor to bacterial diseases afflicting the duck industry, causing substantial annual economic losses on a global scale. In this study, the genes encoding the lipoproteins PlpE of P. multocida strain PMWSG-4 was cloned, inserted into the pBAD-ClyA vector, and the recombinant outer membrane vesicles (OMVs) fused with PlpE antigen of P. multocida was expressed by Escherichia coli (E. coli). Ducks immunized with OMV-PlpE had significantly (P < 0.001) increased production of antigen-specific antibodies. Moreover, at 28 days post-immunization, the expression of genes associated with immune response, including interleukin (IL)-2, IL-4, IL-10, and interferon (IFN)-γ in the spleen tissue of immunized ducks were significantly (P < 0.001) up-regulated compared to unimmunized ducks in the control group. And the active serum had significant bactericidal effects against the PMWSG-4 strain (P < 0.001). The protective efficacy of the vaccines was evaluated by leg muscle challenge with 20 LD50 doses of P. multocida, with the recombinant OMV-PlpE conferring 100 % protection. Histopathological examination and tissue bacterial load detection revealed that OMV-PlpE mitigated tissue damage and bacterial colonization to a statistically significant extent (P < 0.001). These findings serve as a valuable reference for the development of vaccines against P. multocida.

Pasteurella multocida is a leading cause of respiratory disease in pigs worldwide. In this study, we determined the genetic characteristics of 115 P. multocida isolates from the lungs of pigs with respiratory disease in China in 2015 using capsular typing, lipopolysaccharide (LPS) genotyping, and virulence genotyping based on the detection of virulence-associated genes. The results showed that the isolates belonged to three capsular types: A (49.6%), D (46.1%), and nontypable (4.3%); and two LPS genotypes: L3 (22.6%) and L6 (77.4%). When combining the capsular types with the LPS genotypes, a genotype group D: L6 (46.1%) was the most prevalent among the strains. Among the 23 virulence-associated genes detected in this study, a small number of them displayed a certain level of “genotype-preference”. We found that pfhA, hgbA, and hgbB had a close association with P. multocida LPS genotypes, while tadD was more associated with P. multocida capsular types. In addition, multilocus sequence typing (MLST) on 40 P. multocida isolates identified four sequence types: ST3, ST10, ST11, and ST16, and the distribution of ST11 was significantly higher than the other MLST genotypes. Interestingly, all of the ST11 isolates detected in this study were genotype D: L6 strains and they were 100% positive for hgbB. Our data suggest that a capsule/LPS/MLST genotype D/L6/ST11 is likely to be strongly associated with respiratory clinical manifestation of the disease in pigs.

Pasteurella multocida infects a wide range of animals, causing hemorrhagic septicemia or infectious pneumonia. Iron is an essential nutrient for growth, colonization, and proliferation of P. multocida during infection of the host, and competition for iron ions in the host is a critical link in the pathogenesis of this pathogen. In recent years, there has been significant progress in the study of the iron uptake system of P. multocida , including its occurrence and regulatory mechanisms. In order to provide a systematic theoretical basis for the study of the molecular pathogenesis of the P. multocida iron uptake system, and generate new ideas for the investigation and development of molecular-targeted drugs and subunit vaccines against P. multocida , the mechanisms of iron uptake by transferrin receptors, heme receptors, and siderophores, and the mechanism of expression and regulation of the P. multocida iron uptake system are all described.

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 × 10 9 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.

Pasteurella multocida is the leading cause of wound infections in humans following animals’ bites or scratches. This bacterium is also commonly found in the respiratory tract of many mammals and can cause serious diseases resulting in the rapid death of infected animals, especially cattle. To prevent these infections in cattle, a subunit-based vaccine utilizing the surface lipoprotein PmSLP was developed and showed remarkable protection with a single dose administration. Here, we report that PmSLP binds host complement factor I (FI) and facilitates cleavage of complement components C3b and C4b independently of any cofactors (e.g., FH, C4BP), thereby allowing the pathogen to evade host defence. Cryo-EM structure of PmSLP bound to FI reveals that PmSLP stimulates FI enzymatic activity by stabilizing the catalytic domain. This is the first time that a bacterial protein has been shown to directly activate FI independent of complement cofactors and target all arms of the complement cascade.