Atrophic rhinitis is characterized by sneezing, followed by atrophy of the turbinate bones, which may be accompanied by distortion of the nasal septum and shortening or twisting of the upper jaw. Its significance has declined substantially, and it is no longer considered a major health risk to swine herds.
Atrophic rhinitis has been divided into two forms: nonprogressive atrophic rhinitis, due to B bronchiseptica, is mild and transient and generally has little effect on growth and performance. Progressive atrophic rhinitis, due to toxigenic P multocida, is severe, permanent, and usually accompanied by poor growth.
Outbreaks of disease usually follow either the introduction of infected pigs or mixing of pigs from different sources. Piglets may be affected at any age, especially with P multocida, which also may infect mature animals. Crowding, inadequate ventilation, mixing and moving, and other concurrent diseases are important contributory factors in intensification of the disease.
Acute signs of atrophic rhinitis, which usually appear at 3–8 weeks of age, include sneezing, coughing, and inflammation of the lacrimal duct. In more severe cases, nasal hemorrhage may occur. The lacrimal ducts may become occluded, and tear stains then appear below the medial canthi of the eyes. Some severely affected pigs may develop lateral deviation or shortening of the upper jaw, whereas others may suffer some degree of turbinate atrophy with no apparent outward distortion. The degree of distortion can be judged from the relationship of the upper and lower incisors if breed variations are considered. In addition, outbreaks frequently impair growth rate and feed conversion.
The severity of atrophic rhinitis in a herd depends largely on the presence of toxigenic strains of P multocida, management practices, and the immune status of the herd. The latter is related to both vaccination status and the parity distribution of the sow herd, because younger sows tend to shed more organisms and produce less lactogenic immunity for their nursing piglets versus older multiparous sows.
The degree of atrophy and distortion is best assessed by post-mortem examination of a transverse section of the nasal cavity at the level of the second premolar tooth (the first cheek tooth, up to 7–9 months of age); some recommend additional parallel sections. In the active stages of inflammation, the mucosa has a blanched appearance, and purulent material may be present on the surface. In later stages, the nasal cavities may be clear, but there may be variable degrees of softening, atrophy, or grooving of the turbinates; deviation of the nasal septum; and asymmetric distortion of the surrounding bone structure.
The signs and lesions are commonly the basis for diagnosis of atrophic rhinitis; however, the presence of toxigenic strains of P multocida should be confirmed. Routine monitoring is done in some breeding herds by measuring the degree of turbinate atrophy and giving the herd an atrophy score. Atrophic rhinitis must be differentiated from necrotic rhinitis Necrotic Rhinitis in Pigs Necrotic rhinitis follows injury to the oral or nasal mucosa and is often accompanied by infection with Fusobacterium necrophorum. Signs include facial swelling, sneezing, nasal discharge, loss... read more .
Bacterins against toxigenic P multocida and B bronchiseptica have been developed. Both toxoid vaccines and bacterin-toxoid mixtures against P multocidaare available. Although both provide satisfactory results in most herds, infection is best prevented with bacterin-toxoid mixtures. Typically, sows are vaccinated 4 and 2 weeks before farrowing, and the young pigs at 1 and 4 weeks of age. However, vaccination schedules recommended by the manufacturer should be followed. A high level of colostral immunity is acquired by piglets nursing vaccinated sows. An intranasal vaccine using modified-live strains of B bronchiseptica is also available for young pigs.