Atrophic Rhinitis in Swine

RICHARD D. SHUMAN, JOHN S. ANDREWS, AND F. L. EARL.

ATROPHIC rhinitis affects mainly the upper respiratory tract of the pig. It causes atrophy or shrinkage of the turbinates and distortion of the nasal septum. The disease process also can involve the bones of the face.

Atrophic rhinitis was first reported in the United States in 1944 by L. P. Doyle, C. R. Donham, and L. M. Hutchings, of Purdue University. Records indicate that it may have been present before then.

It has been encountered throughout the swine-raising areas of the United States and Canada. Rhinitis has been observed in the Scandinavian countries, England, Germany, and France.

It may be identical to a condition known as "sneezing sickness," which has been recognized in Europe for more than 100 years.

This disease caused alarm among swine producers and veterinarians in the United States in the late 1940's and early 1950's and has come to be considered a major disease of swine.

Atrophic rhinitis alone does not seem to kill pigs. But litters farrowed by affected darns tend to have greater losses than litters farrowed by dams that do not have the disease.

F. K. Kristjansson and R. Gwatkins, in Canada, reported that pigs affected with rhinitis were significantly lighter at 56, 84, 112, 140, and 168 days of age than their normal litter mates. Work at the Agricultural Research Center at Beltsville has shown that under Record-of-Performance conditions, the average weight of normal pigs at 56 and 140 days of age exceeded that of affected pigs by 3.9 and 6.4 percent, respectively. The normal pigs also exceeded affected ones in daily gain by 5.2 percent.

R. S. Smiley, of the Division of Animal Industry in Columbus, Ohio, summed up the effect of this disease on farm herds as follows: In some farm herds there is a 30-percent mortality rate after weaning. Some of the affected pigs stop growing after they attain a weight of 40 to 50 pounds. Some of the hogs take 3 to 5 months longer to reach market weight than others. Other animals belonging to the same herd show no apparent ill effects from the disease.

It is possible, however, that the damage attributed to the disease may be caused mainly by secondary conditions, such as pneumonia: Severe upper respiratory disturbance that causes a complete or partial loss of the turbinates when accompanied by a suppurative process could easily result in a type of pneumonia caused by mechanical inhalation of bacteria and debris.

On the other hand, while pneumonia and atrophic rhinitis can be seen in the same pig, the two conditions can also exist separately. In addition, malformation of the jaw, irritation of the nose when eating dry feed, and the lack of aggressiveness on the part of weakened pigs would have a cumulative effect and lead to an inadequate consumption of food. That in turn would be reflected by a deficiency in the normal rate of development.

HOW ATROPHIC RHINITIS is transmitted from animal to animal is not known exactly. The disease has been traced from one specific source of infection to 50 farms.

The disease may possibly be spread through contact with droplets of infective material blown from the noses of affected animals. W. P. Switzer, of Iowa State College, has observed that some of the baby pigs in a pen next to an infected litter became infected although separated from it by a solid tile partition more than 3 feet high.

Baby pigs can be infected experimentally through the intranasal instillation of fresh material from the noses of affected pigs. Experiments at Beltsville, Md., have shown that this type of material will produce the disease in baby pigs after being stored at the temperature of dry ice (-94 F.) for about 7 months. Some evidence also was found that the atrophy-producing factor may survive in the nose of the albino rat for about 3 weeks an indication that wild rodents may be able to transmit the disease to pigs.

F. W. Schofield, of the Ontario Veterinary College in Canada, reported in 1955 that the domestic cat can be a carrier of the disease.

Not all pigs in constant contact with affected pigs develop the characteristic lesions of the disease. This occurred in experiments at the Agricultural Research Center at Beltsville, when litter-mate pigs were inoculated with material from the noses of pigs affected with atrophic rhinitis. It also occurred naturally in litter-mate weanlings, on Record-of-Performance tests, which were in direct contact with pen littermates and pigs in adjacent pens that did have atrophic rhinitis. The findings indicate that pigs differ in their susceptibility to the disease or that affected pigs lose their infectiveness. In the same herd, contact with the soil seemed to have been important in the high incidence of atrophic rhinitis in the pigs on pasture (67 percent), compared with the incidence in the pigs kept on concrete floors (27 percent). The following year, however, the disease was distributed almost equally in both pasture-raised pigs and the pigs raised in concrete pens.

Atrophic rhinitis is not transmitted to the offspring at birth or through the milk of the dam. Hand-raised baby pigs have not become affected with the disease after having been fed or injected with pooled bacteriologically sterile swine sera obtained from two affected herds.

THE CAUSATIVE AGENT or agents of atrophic rhinitis also must be considered as unknown. Investigators have presented experimental evidence pointing to the identification of the etiological agents of the disease, but as of 1956 their findings await conformation.

"Sneezing sickness" has been attributed in Europe to a bacterium, Pseudomonas aeruginosa, as well as a particular localization of the cause of lung inflammation or pneumonia in influenza.

Dr. Switzer first found that species of Trichomonas, a microscopic parasitic organism, were present in a greater number of affected animals than in those not affected.

Observations at the Agricultural Research Center indicated that trichomonads may not be essential to turbinate atrophy. Attempts by other research workers to produce the condition experimentally, using pure cultures of trichomonads, were unsuccessful.

R. Gwatkins, L. Dzenis, and J. L. Byrne, of the Animal Disease Research Institute, Canada, and J. L. Flatla and M. Braend, of the Norwegian Veterinary College, Norway, reported that the disease could be transmitted experimentally by a bacterium, Pasteurella multocida.

K. A. McKay and G. R. Carter, of the Ontario Veterinary College, reported that they repeatedly produced rhinitis in young pigs by the nasal instillation of Pasteurella multocida and Spherophorus necrophorus.

Dr. Switzer found that filter-passing agent or agents could produce atrophy of the turbinates.

THE FIRST SYMPTOMS of atrophic rhinitis may be limited to persistent sneezing, which usually appears about 3 weeks after the farrowing. A clear mucous discharge may come from the nose. As the disease progresses, the discharge sometimes may become mucopurulent. The mucus from the nose is tinged at times with blood. Some mucopurulent debris may be passed from the nose following violent sneezing. Persistent bleeding also may occur following sneezing, vigorous exercise, or injury to the nose.

The irritation in the nose may become so severe that the pig will rub its snout on the ground or against some solid structure. The atrophy of the structures within the snout in some animals leads to visible distortion of the facial bones, and the snout may be turned to either side or upward and have an accordion-like appearance. Affected pigs with crooked noses have been found to be more the exception than the rule, however.

In light-colored ht-colored hogs, a blackish streak that extends from the inner corner of the eye and bulging of the facial bones also may be circumstantial evidence of atrophic rhinitis. Associated conditions, such as pneumonia, diarrhea, and unthriftiness, may occur in affected herds.

A postmortem examination of the normal animal reveals the turbinate bones as delicate, scroll-like structures of bone and tissue, which fill up the right and left nasal passages. They are separated by a relatively thick cartilaginous structure, called the nasal septum. The function of the turbinates is to warm the air before it passes into the lungs and assist in filtering out such foreign material as dust and bacteria. The mucous membrane that covers the structures inside the nose normally is pink and not excessively moist.