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.
The etiology is complex and involves at least two organisms. Various infections (eg, inclusion body rhinitis and pseudorabies) and noninfectious agents (eg, dust or high ammonia levels) cause sneezing and tear-staining, usually without leading to atrophic rhinitis. Bordetella bronchiseptica has long been implicated as a major cause. This bacterium is not host-specific, although strains that cause atrophic rhinitis are generally isolated only from pigs. Dogs, cats, rodents, and other species may harbor B bronchiseptica for long periods, but their role in the spread of atrophic rhinitis in pigs is uncertain. Toxigenic strains of Pasteurella multocida (type D), often acting with B bronchiseptica, cause permanent turbinate atrophy and nasal distortion. Both organisms can cause clinical atrophic rhinitis.
The disease has been divided into two forms: nonprogressive atrophic rhinitis, due to B bronchiseptica, is mild and transient and probably does not greatly affect the animal’s 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, which usually appear at 3–8 wk 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 to the above clinical signs, 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, the level of management, 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 than do older multiparous sows.
The degree of atrophy and distortion is best assessed by examining a transverse section at the level of the second premolar tooth (the first cheek tooth, up to 7–9 mo 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; 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 (see Necrotic Rhinitis in Pigs).
It is rarely possible to keep herds entirely free from mild outbreaks of sneezing, and a low level of aberrant turbinates and nasal bones at necropsy is common, even in herds that show no clinical signs of rhinitis. When atrophic rhinitis rises to an unacceptable level in a herd, control measures are usually strategic: chemoprophylaxis, vaccination, temporary closure of the herd to introduction of new pigs, and improved management (eg, better ventilation and hygiene, less dusty feed). Chemoprophylaxis usually includes administration of antibacterial drugs to all sows, particularly before farrowing, as well as programs of repeated medications for newborn piglets and sometimes for newly weaned pigs. Medication of weaner and grower rations, and sometimes sow rations, is often helpful. Drugs commonly used are ceftiofur, sulfonamides, tylosin, and tetracyclines.
Bacterins against toxigenic P multocida and B bronchiseptica have been developed. Both toxoid vaccines and bacterin-toxoid mixtures are available against P multocida; although both give satisfactory results in most herds, infection can be best prevented with bacterin-toxoid mixtures. Typically, sows are vaccinated 4 and 2 wk before farrowing, and the young pigs at 1 and 4 wk 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.