- B. bronchiseptica causes Atrophic rhinitis of pigs in association with Pasteurella multocida
- Colonises nasopharynx
- Infection must occur during first few weeks of life
- Produces dermonecrotic toxin which damages osteoblasts, preventing bone formation
- Leads to turbinate atrophy without distortion of the snout in uncomplicated infections
- Atrophic rhinitis results when Pasteurella multocida colonises and produces osteolytic toxin, leading to bone resorption
- Malformation of snout in growing pigs as well as poor growth
- increases with high stocking density and poor ventilation
- Vaccine available
Severe atrophic rhinitis (Image sourced from Bristol Biomed Image Archive with permission) - Atrophy of nasal turbinates and distortion and shortening of the snout
- Caused by co-infection of the nasal mucosa with
- Bordetella bronchiseptica
- Appears to facilitate colonisation of nasal epithelium by the toxigenic Pasteurella
- Toxin-producing strain of Pasteurella multocida capsular type D (or sometimes A)
- Experimental evidence shows that the toxin acts directly on bone cells of the nasal turbinates to cause bone loss, each pathogen can cause atrophy itself but greater damage when together
- Exacerbated by adverse dietary and managemental factors
- In rapidly growing young pigs (4-12 weeks old)
- Clinical signs
- Progressive facial deformity with rhinitis, catarrhal nasal discharge
- Sneezing, coughing, can progress to dyspnoea and anorexia
- Gross pathology
- Overlying skin on shortened snout is thrown into folds
- Deviation of the snout to most affected side
- Various loss of turbinate bone, ventral usually more affected
- Deviation of nasal septum away from affected chamber
- Inflammatory, haemorrhagic and ulcerative lesions in the nasal mucosa
- Micro pathology
- Reduction in the amount of bone in the turbinates
- No osteoid laid down between osteoblasts and existing bone
- Increased fibrous tissue
- Non-specific mucosal inflammation
- 2 forms of the disease
- 'Progressive' atrophic rhinitis
- Due to infection of the nasal turbinates by P.multocida strains carrying the toxA gene that encodes for an osteolytic toxin. P.multocida adheres poorly to mucous membranes, and therefore requires a predisposing nasal insult to assist colonisation eg: co-infection with B.bronchiseptica or Porcine cytomegalovirus (inclusion body rhinitis)
- Turbinate bone atrophy is permanent and progressive
- 'Non-progressive' atrophic rhinitis
- Due to infection of the nasal turbinates by Bordetella bronchiseptica strains alone, that carry a gene that encodes for a dermonecrotic toxin.
- Turbinate bone can regenerate by the time of slaughter
