HERD HEALTH PIH-50 PURDUE UNIVERSITY. COOPERATIVE EXTENSION SERVICE. WEST LAFAYETTE, INDIANA Atrophic Rhinitis Authors Barbara Straw, University of Nebraska G. Michael Daniel, Sioux Center, Iowa Reviewers Peter and Brenda Blauwiekel, Fowler, Michigan David J. Ellis, Michigan State University Steven C. Henry, Abilene, Kansas Ralph A. Vinson, Oneida, Illinois Atrophic rhinitis (AR) is a widely prevalent, multifactorial disease of swine characterized by a degeneration and/or failure of growth of the nasal turbinate bones. Clinical signs include sneezing, nasal discharge or bleeding, and distortions of the snout. The milder, nonprogressive form of AR is caused by a toxin- producing bacterium, Bordetella bronchiseptica. The more severe and progressive form is caused by the toxin-producing Pasteurella multocida bacterium, alone or in combination with other bacteria such as Bordetella bronchiseptica. The severity of the disease may be related to the age of the pig when infected, the dose of infectious organisms, the amount of toxin produced by the bac- teria and environmental conditions. Although B. bronchiseptica and P. multocida have been demonstrated to cause AR, clinical disease cannot be attributed solely to infection with either one or both bacteria. Various environmental, management and husbandry factors contribute to the development of clinical disease. In some herds these bacteria are present, but outward signs of disease are not. In herds harboring B. bronchiseptica and P. mul- tocida, there are periods from 2 months to 2 years or longer when no clinical evidence of disease exists. Development of AR Caused by Bordetella bronchiseptica Infection Bordetella bronchiseptica readily colonizes the lining of the respiratory tract. It commonly locates in the nasal passages and the tonsils. The most severe disease occurs in piglets that are infected during the first week of life. Disease is less severe in pigs that are a few weeks older; and by 9 weeks of age, pigs show almost no clinical signs after infection. In some cases, damage from the initial infection persists until slaughter, but in many cases of pure B. bronchiseptica infection, damage to the nose begins to heal within 4 weeks after the onset of infection. Development of AR Caused by Pasteurella multocida Infection Toxin-producing strains of Pasteurella multocida have a poor capability for establishing themselves in a healthy nasal cavity. Experimentally, however, P. multocida readily colonize a nasal cavity that has been pretreated with chemical irritants or infected with B. bronchiseptica. Pasteurella multocida also infects tonsils and lungs. Similar to B. bronchiseptica infec- tion, pigs infected with P. multocida at an earlier age may show more severe clinical signs. However, in contrast to B. bron- chiseptica, P. multocida is capable of damaging the nasal cavity in pigs up to 16 weeks of age, and reversal of damage is less likely. In fact, the toxin produced by P. multocida has been shown to affect not only the structure of the nasal passages, but also to damage the liver, kidneys, ends of the long bones and certain components of the blood. Sources of Infectious Agents Infection in a herd most likely occurs after the introduc- tion of infected breeding stock or feeder pigs, although other animals such as rodents, dogs and cats also may be carriers. Bac- teria can be harbored in the nasal passages or tonsils of apparently healthy pigs. Bacteria are spread from one pig to another through droplets in expired air. Litters in the farrowing house may be infected by the sow, but generally the major spread occurs pig-to-pig after 2 to 3 weeks of age or after weaning. Bordetella bronchiseptica has been found in most domestic and wild animals; however, the strains of B. bronchiseptica iso- lated from non-swine species have only limited ability to produce disease in pigs. Toxin-producing strains of P. multocida have been found in cattle, rabbits, dogs, cats, poultry, sheep, goats and humans; however, the possible role of these other species in the spread of disease has not been determined. Other Factors that Contribute to Clinical Expression of AR Severity of infection is closely associated with intensive methods of swine production. The following factors all have been identified as contributing to the level of AR in infected herds: large herd size, additions of pigs from various sources, high proportion of gilt replacements in the breeding herd, large far- rowing units, large nurseries, frequent moving and mixing, high stocking density, poor ventilation and temperature control, poor hygiene, continuous flow of pigs, and excessive levels of gases and dust. On occasion it has been possible to control AR solely through improvement of housing and management practices. At one time it was thought that calcium:phosphorus imbalance led to AR, but this has been discounted. However, an existing imbalance would retard healing of lesions that might otherwise resolve. Clinical Signs of AR Clinical signs usually appear at about 4 to 12 weeks of age. Initially there is noticeable sneezing and snuffling and pigs may have a watery or thick mucous discharge from the nose. Tear staining appears as dirty brown streaks below the eyes. Some pigs have nose bleeding, which can be severe enough to be seen on the walls of the pen or on the backs of other pigs. As the condition progresses, damage to the interior bony structure of the nose may appear as a shortening or bending of the snout. Some pigs may have damage to their nasal turbinates without having obvious external signs. Pigs that are severely affected experience a reduction in growth rate and feed efficiency, which is compounded by the performance-depressing effects of poor environment and ventilation. Diagnosis of Infection When AR is moderate to severe, a diagnosis can be made clin- ically, based on the typical signs of disease. However, in milder cases additional testing may be necessary. Samples for bacterial culture are taken from the nasal passages and tonsils of affected pigs to check for toxin-producing strains of B. bronchiseptica and P. multocida. Specific laboratory tests are conducted to identify the two types of P. multocida (A and D) that are most commonly involved in AR. Subsequent testing is done to demon- strate the production of toxin. Frequently, examination of nasal structures is made at slaughter when a number of pigs can be examined to estimate the prevalence and severity of turbinate atrophy in the herd. See PIH-93, Slaughter Checks--An Aid To Better Herd Health. Control of AR Effective control of AR requires a combination of strategies involving management, environment, medication and vaccination. The main goals of control are to reduce the load of bacteria to which pigs are exposed, to treat pigs that are affected and to improve the environment which maximizes pig resistance and minim- izes bacterial spread. Vaccination. Vaccination of sows with a combination B. bronchiseptica/P. multocida vaccine helps reduce the prevalence of AR in their offspring, but does not eliminate the condition. For greater efficacy, it is important that the vaccine contain the specific P. multocida toxin so that the sow will produce antibodies to protect against the effects of the toxin. In some cases, piglets also should be vaccinated. However, immunity requires 2 weeks to develop, and often piglets are infected before they can develop a protective level of antibody. Proper timing of immunization is necessary to optimize the immune response. Medication. Medication may be used as a temporary measure to help bring severe cases to a controllable level, but it is not a long-term solution. To reduce shedding of bacteria, sows may be given feed containing sulfonamides or oxytetracycline during the last month of gestation. Nursing piglets are strategically medi- cated by injections of antibacterials up to 4 times during the first 3 to 4 weeks of life. Typically, oxytetracycline, penicillin/streptomycin, or potentiated sulfonamides (extra-label use requires veterinary/client relationship) are used. The choice of drug should be based on the results of drug sensitivity test- ing on bacteria recovered from infected pigs. Weaned pigs are sometimes medicated in the drinking water or feed. Management. Vaccination and medication efforts may fail unless combined with appropriate improvements in housing and management. It is important to employ all-in, all-out movement of pigs, minimize the number of gilts in the herd compared to older sows, reduce the stocking density, maintain strict hygiene, correct ventilation rates, and eliminate chilling drafts. Modifi- cations of medicated early weaning (MEW) and multiple site pro- duction help to reduce the prevalence and severity of disease. New animals brought into the herd should originate from herds of known status. Breeding companies and producers should know the AR status of their herds and work together to determine if health levels are comparable. Elimination of AR Once a herd is infected, it is impossible to eliminate the causative bacteria. However, good management practices can reduce the prevalence and severity of disease. Freedom from the severe detrimental effects of AR can be achieved through strict adherence to proper vaccination and/or management programs including all-in, all-out pig flow. Pigs free of AR may be pro- duced by SPF (Specific Pathogen Free) techniques or possibly through medicated early weaning. Breeding companies that adver- tise freedom from AR should be routinely monitoring to verify the absence of AR through periodic nasal cultures and slaughter exam- inations. Reference to products in this publication is not intended to be an endorsement to the exclusion of others which may be simi- lar. Persons using such products assume reesponsibility for their use in accordance with current directions of the manufacturer. REV 12/92 (7M) ______________________________________________ Cooperative Extension Work in Agriculture and Home Economics, State of Indiana, Purdue University and U.S. Department of Agri- culture Cooperating. H.A. Wadsworth, Director, West Lafayette, IN. Issued in furtherance of the Acts of May 8 and June 30, 1914. It is the policy of the Cooperative Extension Service of Purdue University that all persons shall have equal opportunity and access to our programs and facilities. .