An infectious disease characterized in early stages by snuffling, sneezing, snorting, and perhaps nosebleed which may progress to atrophy and distortion of the turbinates, nasal and facial bones of some affected pigs.
Atrophic rhinitis (AR) is restricted only to swine although a similar disease has been described in dogs and goats. Signs and/or lesions can occur in any age group of swine more than one week old. In the United States, AR is becoming a rare disease as prevalence has been decreasing in most areas as a result of early weaning, age segregation and/or vaccination. AR occurs in all major swine-raising countries.
Atrophic rhinitis (AR) was described first in 1830. AR was reported in the US in 1944. It rapidly increased in frequency with expansion and intensification of swine production and stimulated a great amount of research. AR has a complex etiology.
Toxigenic strains of Bordetella bronchiseptica and Pasteurella multocida (primarily type D) may cause AR. Bordetella bronchiseptica is an aerobic, Gram-negative rod. The organism readily colonizes the nasal passages of swine and is widely distributed in the swine population. It often is non-pathogenic but can sometimes cause severe losses from septicemia and suppurative bronchopneumonia in pigs up to 12 weeks old. Bordetella bronchiseptica has been isolated from many species other than swine (dogs, cats, rodents, rabbits, wildlife). Those strains are not believed to play a role in causing AR in swine. However, toxigenic porcine strains can cause atrophy of turbinates, particularly in pigs one to six weeks old. Lesions tend to be mild and can be largely repaired by the host, therefore may not lead to progressive AR.
Toxigenic Pasteurella multocida is less widespread in the swine population. Colonization of the nasal passages is enhanced following prior insult to nasal mucous membranes. It often can be isolated from tonsils and lungs of swine with or without the usual signs and lesions of AR. It sometimes is found together with B. bronchiseptica in outbreaks of AR. ToxigenicP. multocida produces a potent dermonecrotizing toxin that causes marked turbinate atrophy as well as bony alterations in nasal and facial bones. Turbinate lesions usually are initiated in pigs less than 16 weeks old but older pigs can be affected if immunologically naïve. The lesions can persist for a lifetime.
Management and husbandry factors have long been suspected of being important predisposing or contributing factors to AR. Research on dust in confinement houses suggests the incidence of AR may be increased by three toxic agents; endotoxin from Gram-negative bacteria; beta 1, 3-glycan, a cell wall component of molds; and possibly peptidoglycans from cell wall components of all bacteria. More research is needed in this area.
Numerous factors assure survival of toxigenic B. bronchiseptica and P. multocida among swine. Atrophic rhinitis results in the establishment of inapparent carriers. Swine introduced into a clean herd from an outside source can be carriers and disseminate the agents that cause AR. Also, carrier sows expose their piglets. When their infected piglets are mingled with others, the agents can be transmitted. Although immune sows provide their piglets with some colostral immunity against the agents that cause AR, waning colostral immunity and weaning soon leave young pigs susceptible to infection. Older sows may provide more colostral immunity (and perhaps less infective dose) than do gilts. Several microbiologic agents, other than B. bronchiseptica and P. multocida are known to cause or be associated with rhinitis (see Diagnosis). The rhinitis they cause may predispose to colonization by the bacteria that cause AR. Management or environmental factors, when slighted or ignored, increase the susceptibility of pigs to AR. Ventilation is an especially important factor. Irritating dust or ammonia from urine and feces may contribute to the severity of rhinitis. The irritants make nasal mucous membranes more susceptible to colonization by the primary agents of AR. Other contributing factors include overstocking, substandard housing or sanitation, continuous use of facilities, and failure to use all in/all out production methods.
There is colonization of the nasal passages by toxigenic strains of Bordetella bronchisepticaand/or Pasteurella multocida, perhaps augmented by environmental or other microbial irritation of turbinates. Bordetella bronchiseptica adhere to the nasal mucosa, probably by attaching to the ciliated epithelial cells. The toxin elaborated by the organisms diffuses into the turbinates and is responsible for an osteopathy and hypoplastic rhinitis. Later, after the disease becomes more quiescent, some degree of regeneration and repair can occur. The term “regressive atrophic rhinitis” sometimes is used for this form of AR.
Toxigenic P. multocida colonizes the nasal mucosa, probably after a rhinitis has been established by B. bronchiseptica, other agents or environmental irritants. Toxigenic P. multocida produce a potent toxin that causes a rhinitis with progressive osteopathy of facial and turbinate bones. The term “progressive atrophic rhinitis” sometimes is used to indicate this form of AR.
Signs may appear in pigs as young as one week old but more often appear shortly after weaning. Sneezing, snorting and a serous or mucopurulent nasal discharge are early signs of AR. Rhinitis obstructs the flow of tears through the infraorbital ducts and tears flow from the medial canthus of the eyes causing “dirty” or discolored hair and skin below the canthus. Signs caused by B. bronchiseptica alone tend to peak in a few weeks, and then diminish. Signs related to toxigenic P. multocida often appear in four to eight week old pigs and may persist for weeks or months. Signs occasionally include nosebleed in more acute outbreaks in weaned, growing pigs. Growth retardation may become apparent. Occasional pigs develop secondary bronchitis, bronchiolitis or pneumonia as an indirect effect of AR.
A variable number of pigs develop lateral or dorsal deviation of the snout. Dorsal deviation often results in shortening of the snout or wrinkling of the skin over the snout. Marked snout deviation in many pigs usually is associated with toxigenic P. multocida.
Lesions are usually restricted to turbinates, nasal septum and nasal and facial bones and can be observed by sawing transversely across the snout at the commissure of the lips (2nd premolar or 1st cheek tooth in pigs less than 6 months of age). Lesions vary in severity and are usually graded on a scale of 0-5. Minor lesions must be differentiated from normal variations in anatomy and breed character.
Mild lesions usually result in atrophy of the ventral scroll of the ventral turbinates; severe cases are more likely to involve the dorsal turbinate scrolls. In extreme cases the dorsal and ventral turbinates may be almost completely destroyed and there may be atrophy of ethmoid turbinates. Deviation of the nasal septum is more common in severe cases. Nasal and facial bones may be thinned or distorted. Mucoid or mucopurulent exudate often is present on blanched mucous membranes and in adjacent sinuses. Microscopic study usually reveals fibrous replacement of the bony plates of conchae that remain.
History, signs and lesions often are adequate for a clinical diagnosis of AR, with confirmation by isolation and identification of the etiologic agent(s). Bacterial cultures made from nasal swabs from live or sacrificed pigs are most rewarding early in the course of infection (nursery).
Differential diagnosis should exclude other diseases or irritants that can cause rhinitis such as porcine reproductive and respiratory syndrome virus (PRRS), pseudorabies virus (PRV), inclusion body rhinitis (cytomegalovirus), or excessive dust or ammonia.
After the specific cause(s) of AR have been accurately determined and the extent of loss considered, a decision should be made to either attempt to control the disease, or to depopulate and restock with swine known to be free of AR. If the decision is made to control rather than eradicate AR, control measures fall into three major categories. The first control measure is improvement of husbandry, management and housing, including ventilation. The second measure is initiation of a vaccination program for the breeding stock, pigs, or both. Vaccination of the sows may be most cost effective. Sows often are vaccinated twice at about four and two weeks prior to parturition. Bacterin-toxoid vaccines provide some protection and historically were widely used. The third control measure involves administration of antibiotics to sows and piglets around the time of farrowing/weaning in an effort to limit the extent of colonization in the young pigs. The value of antibiotic therapy to control AR in growing swine is questionable.
Progress of controlling AR should be evaluated repeatedly by examining the nasal passages of a substantial number of swine submitted for slaughter. Several systems for scoring the severity of lesions are available.
Eradication of toxigenic P. multocida from a herd or system has been successful. The method first combined medication and prefarrowing vaccination of sows. Later, their litters were medicated and early weaned at 8-10 or 12-14 days. Finally, nasal swabs were used on maturing animals, toxigenic P. multocida isolates were identified by polymerase chain reaction (PCR) testing, and infected animals were identified and eliminated.