Section: Livestock Bacteria

Pasteurella multocida Toxigenic Strains and Progressive Atrophic Rhinitis in Pigs

Etiology

Progressive atrophic rhinitis (PAR) in pigs is a chronic, infectious disease of the upper respiratory tract caused by toxigenic strains of Pasteurella multocida. P. multocida is a Gram-negative, non-motile, facultatively anaerobic coccobacillus belonging to the family Pasteurellaceae. The species is classified into five capsular serogroups (A, B, D, E, F) and 16 somatic serotypes based on lipopolysaccharide antigens. In swine, the vast majority of toxigenic isolates associated with PAR belong to capsular serogroups A and D, with serogroup D being historically predominant in many regions.

The critical virulence determinant distinguishing toxigenic from non-toxigenic strains is the production of a 146 kDa dermonecrotic toxin (DNT). This toxin is encoded by the toxA gene, which is located on a mobile genetic element, often a temperate bacteriophage integrated into the bacterial chromosome. The presence of the toxA gene is the defining molecular feature of a toxigenic P. multocida strain. Non-toxigenic strains of P. multocida can colonize the nasal cavity but do not induce the progressive, irreversible turbinate atrophy characteristic of PAR.

The pathogenesis of PAR is often multifactorial. Primary infection with Bordetella bronchiseptica is a well-established predisposing factor. B. bronchiseptica colonizes the nasal epithelium, causing ciliostasis and epithelial damage, which facilitates the subsequent colonization and proliferation of toxigenic P. multocida. Co-infection with other respiratory pathogens, such as Mycoplasma hyopneumoniae or porcine reproductive and respiratory syndrome virus (PRRSV), can exacerbate clinical disease. Poor environmental conditions, including high stocking density, poor ventilation, and elevated ammonia levels, further compromise mucosal defenses and increase disease severity.

Epidemiology

Toxigenic P. multocida is distributed globally in swine-producing regions. The prevalence of infection at the herd level can be high, particularly in intensive production systems. Transmission occurs primarily via direct contact between pigs through nasal secretions and aerosols. Indirect transmission via contaminated fomites, feed, and water is also possible. Carrier sows are a major reservoir for transmission to piglets during the suckling period. Infection typically occurs in young pigs, with clinical signs most commonly observed between 3 and 8 weeks of age. The severity of disease is influenced by the age at infection, the dose of the toxigenic strain, the presence of co-infections, and environmental stressors.

Clinical Signs

The hallmark clinical sign of PAR is progressive nasal distortion and shortening of the snout. The disease is divided into two forms: non-progressive atrophic rhinitis (NPAR), which is mild and often self-limiting, and progressive atrophic rhinitis (PAR), which is severe and irreversible. PAR is exclusively associated with toxigenic P. multocida.

Clinical signs of PAR include:

  • Sneezing and nasal discharge, initially serous and later mucopurulent.
  • Epistaxis (nosebleeds), particularly in younger pigs.
  • Tearing and periocular staining due to obstruction of the nasolacrimal duct.
  • Snout deviation (twisting) to one side, resulting from asymmetric turbinate atrophy.
  • Shortening or wrinkling of the snout.
  • Reduced growth rate and feed conversion efficiency due to impaired respiration and olfactory function.
  • Increased susceptibility to secondary bacterial pneumonias.

In severe cases, the nasal turbinates are completely destroyed, leading to a characteristic "bulldog" or "snuffler" appearance. Clinical scoring systems, such as the snout score (0 to 5), are used to grade the severity of external snout distortion.

Pathology

The primary pathological lesion in PAR is bilateral, progressive atrophy of the nasal turbinates, particularly the ventral and dorsal turbinates. Gross examination of a transverse section of the snout at the level of the first premolar tooth reveals loss of the normal scroll-like architecture of the turbinates. In advanced cases, the turbinates may be completely absent, leaving an empty nasal cavity.

Histologically, the initial lesion is a neutrophilic and mononuclear inflammatory infiltrate in the nasal mucosa. The dermonecrotic toxin (DNT) produced by toxigenic P. multocida is the direct cause of turbinate atrophy. DNT acts by constitutively activating the Rho GTPases (RhoA, Rac1, and Cdc42) within osteoblasts and osteoclasts. This activation disrupts the normal balance of bone remodeling. Specifically, DNT stimulates osteoclast activity and inhibits osteoblast differentiation and function, leading to net bone resorption. The toxin also induces apoptosis of osteoblasts. The result is a profound and irreversible loss of bone matrix in the turbinates. The nasal mucosa may show hyperplasia, metaplasia, and fibrosis in chronic cases.

Diagnostics

Accurate diagnosis of PAR requires differentiation from NPAR and other causes of rhinitis. A combination of clinical examination, gross pathology, and laboratory testing is recommended.

Clinical and Gross Examination

  • Snout scoring based on external deformation.
  • Postmortem examination of a transverse section of the snout at the level of the first premolar tooth. Turbinate atrophy is scored on a scale of 0 (normal) to 5 (complete atrophy).

Bacteriological Culture

  • Nasal swabs or turbinate tissue samples are cultured on selective media, such as blood agar or MacConkey agar. P. multocida appears as small, gray, non-hemolytic colonies. Identification is confirmed by Gram stain, oxidase positivity, and catalase positivity.

Toxigenicity Testing

  • In vivo mouse lethality test: Historically used but now largely replaced by in vitro methods.
  • Cell culture assay: Detection of cytotoxic effects on Vero or embryonic bovine lung cells. DNT causes characteristic cell rounding and multinucleation.
  • Enzyme-linked immunosorbent assay (ELISA): Detection of DNT antigen in culture supernatants or directly from nasal swabs. Commercial ELISA kits are available for this purpose.
  • Polymerase chain reaction (PCR): Detection of the toxA gene directly from clinical samples or bacterial isolates. PCR is highly sensitive and specific and is the preferred method for molecular confirmation of toxigenic strains. Multiplex PCR assays can simultaneously detect P. multocida and differentiate toxigenic from non-toxigenic strains.

Serological Testing

  • Detection of antibodies against DNT in serum or colostrum can be used for herd-level surveillance. ELISA-based serological assays are available.

Differential Diagnosis

  • Non-progressive atrophic rhinitis (NPAR) caused by B. bronchiseptica alone.
  • Inclusion body rhinitis caused by porcine cytomegalovirus.
  • Foreign body rhinitis.
  • Nasal trauma.
  • Neoplasia.

Treatment

Treatment of PAR is challenging because the turbinate atrophy is irreversible once established. Therapeutic intervention is most effective when initiated early in the course of infection.

Antimicrobial Therapy

  • Administration of antimicrobials effective against P. multocida can reduce bacterial load and limit the progression of disease. Commonly used antimicrobials include tetracyclines, sulfonamides, penicillins, and fluoroquinolones. Antimicrobial susceptibility testing is recommended to guide therapy due to the emergence of resistant strains.
  • In-feed or in-water medication is often used for group treatment. Injectable antimicrobials may be used for individual pigs with severe clinical signs.

Supportive Care

  • Improving environmental conditions, including ventilation, reducing ammonia levels, and decreasing stocking density.
  • Ensuring adequate nutrition and water intake.

Control and Prevention

Control of PAR relies on a comprehensive herd health management program that addresses both the primary pathogen and predisposing factors.

Vaccination

  • Commercial bacterin-toxoid vaccines containing inactivated toxigenic P. multocida and B. bronchiseptica are widely used. These vaccines are administered to sows prior to farrowing to provide passive immunity to piglets via colostrum. Vaccination of piglets directly is also practiced in some herds.
  • Autogenous vaccines prepared from the specific toxigenic P. multocida strain(s) circulating in a herd can be used when commercial vaccines are ineffective.

Management Practices

  • All-in/all-out production: Reduces the continuous cycling of pathogens between age groups.
  • Early weaning: Can reduce the transmission of B. bronchiseptica and P. multocida from sows to piglets.
  • Biosecurity: Strict protocols for the introduction of new animals, quarantine, and sanitation.
  • Environmental control: Optimizing ventilation, humidity, and temperature to minimize respiratory irritants like ammonia.
  • Elimination of carrier animals: Culling of sows with severe clinical signs or confirmed infection can reduce the reservoir of toxigenic strains.

Eradication

  • Eradication of PAR from a herd is possible but difficult. It typically involves depopulation of the breeding herd, thorough cleaning and disinfection, and repopulation with specific-pathogen-free (SPF) stock. Partial depopulation strategies combined with intensive medication and vaccination have also been described.

Diagnostic Decision Workflow

The following Mermaid diagram outlines a diagnostic workflow for investigating suspected cases of progressive atrophic rhinitis in pigs.

flowchart TD
    A[Clinical Signs: Sneezing, Nasal Discharge, Snout Deformation], > B{Postmortem Snout Section}
    B, > C[Gross Turbinate Atrophy Present]
    B, > D[No Gross Atrophy]
    C, > E[Collect Nasal Swab or Turbinate Tissue]
    E, > F[Bacterial Culture for P. multocida]
    F, > G[P. multocida Isolated]
    F, > H[No P. multocida Isolated]
    G, > I[PCR for toxA Gene]
    I, > J[toxA Positive: Toxigenic Strain Confirmed]
    I, > K[toxA Negative: Non-Toxigenic Strain]
    J, > L[Diagnosis: Progressive Atrophic Rhinitis]
    K, > M[Consider NPAR or Other Etiology]
    D, > N[Consider NPAR, Viral Rhinitis, or Other Causes]
    H, > O[Consider Alternative Pathogens or Sample Error]

Conclusion

Progressive atrophic rhinitis remains a significant economic concern for the swine industry due to its negative impact on growth performance and increased susceptibility to secondary respiratory infections. The disease is caused exclusively by toxigenic strains of Pasteurella multocida that carry the toxA gene and produce dermonecrotic toxin. Effective control requires a multifaceted approach combining vaccination, biosecurity, environmental management, and antimicrobial stewardship. Molecular diagnostics, particularly PCR for the toxA gene, provide the most reliable means of confirming the presence of toxigenic strains and guiding intervention strategies.

References

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  2. Lax AJ, Chanter N. Cloning of the toxin gene from Pasteurella multocida and its role in atrophic rhinitis. Journal of General Microbiology. 1990;136(1):81-87.
  3. Foged NT. Pasteurella multocida toxin: the characterisation of the toxin and its significance in the diagnosis and prevention of progressive atrophic rhinitis in pigs. APMIS Supplementum. 1992;25:1-56.
  4. Register KB, Brockmeier SL. Pasteurella multocida: toxigenic strains and their role in atrophic rhinitis. Animal Health Research Reviews. 2001;2(2):137-148.
  5. Magyar T, Lax AJ. Atrophic rhinitis. In: Zimmerman JJ, Karriker LA, Ramirez A, Schwartz KJ, Stevenson GW, editors. Diseases of Swine. 10th ed. Ames: Wiley-Blackwell; 2012. p. 769-782.