Posted December 2, 2016 in Swine
Progressive atrophic rhinitis (PAR) is caused by particular strains of a bacterium Pasteurella multocida which live in the respiratory tract of the pig. The strains causing PAR produce a powerful toxin the dermonecrotoxin which is responsible for the changes seen in the disease. The organism can easily be cultivated and recognized by the colony produced, but strains involving PAR can only be distinguished by demonstrating their ability to produce toxin. PAR can be reproduced experimentally in injecting young pigs with the toxin alone in tiny amounts. In natural disease the organism cannot colonize the nose in sufficient numbers to cause the disease unless the lining has been damaged by some other agent. The damaging agent is usually the bacterium Bordetella Bronchiseptica which causes inflammation in the nasal cavity and allows toxins to gain access to the bloodstream. Once the toxin has been produced and absorbed it affects the production and remodeling of bone and produces permanent effects which are seen most obviously in the rapidly-growing nasal bones of the young piglet. These are damaged and do not recover; hence the distorted snout caused by PAR is recognized.
Outbreaks of sneezing occur in piglets aged between 1 and 8 weeks of age and are accompanied by tear staining or even nose bleeds. The sneezing and snuffling gradually becomes milder but after 14 days the bony changes begin to appear. As the disease progresses the upper jaw become displaced from the mid-line and grows more slowly than the covered skin or lower jaw so that the skin over the snout appears corrugated and the lower jaw sticks out further.
Signs of pneumonia or stunting may also be noted. In some animals or affected farms sneezing may be transitory and little outward effect may be seen. This form is most common where infection does not occur until after weaning and or where immunity is present. Severally affected animals may have difficulty in eating and the nasal changes may be seen in pigs of all ages in affected herds. Rates of daily live weight gain may be depressed and there may be some mortality amongst piglets.
Progressive atrophic rhinitis should be considered when outbreaks of severe sneezing occur in piglets and further evidence is provided by the changes in the snout which appears as the piglets age. As bending of the snout is difficult to detect in young piglets, an early indication of PAR can be obtained by looking at the incisor teeth. They normally meet but with PAR the lower incisors stick out further. The bony changes are usually seen by routine monitoring at slaughter or during farm post-mortem examination. Antibody to the toxin can be demonstrated in serum or recovered and vaccinated pigs.
Treatment and control
Elimination of infection prevents the development of the bony lesions and prevents production effects so acute disease in sucking piglets should be treated with trimethoprim sulphonamide, ampicillin, tetracyclines, ceftiofur or enrofloxacin given by injection or oral dosing as appropriate. Animals should be supported with additional food and electrolyte supplements if they cannot suck. Disease in weaned pigs can be treated by injection or by water medication. Initial control measures depend upon given the antimicrobial to piglets at 3 days 10 days and 21 days of age. Weaned pigs at risk may be given a course of antimicrobial treatment in feed or water at therapeutic levels.
Medication of groups of animals entering airspace in an all-in all-out system is the most efficient method. Vaccination of sows with the toxoid (inactivated toxin) to give colostrum protection is the preferred method of control in infected herds but for best effects all piglets must receive colostrum. Infection can be eradicated by depopulation and restocking and clean herds may be maintained free from PAR by isolation and the use of clean breeding stock. Monitoring for infection is carried out by culture of nasal swabs for the organism.