Atrophic Rhinitis (Progressive Atrophic Rhinitis, PAR)

Occurrence: Worldwide, some herds free
Age affected: Piglets pre-weaning, weaners (all ages)
Causes: Strains of a bacterium, Pasteurella multocida, which produce a powerful toxin, the dermonecrotoxin. Poor ventilation and overcrowding increase its effects.
Effects: Sneezing, snuffling, nasal discharge in piglets, with tear staining and followed by twisting/shortening of the snout, poor growth.


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 cultivate and recognised by the colony produced, but strains involve din 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 colonise 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 P. multocida to grow in numbers sufficient to cause disease and for its toxin to gain access to the bloodstream. Once toxin has been produced and absorbed, it affects the production and remodelling 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, cause the distorted snout by which PAR is recognised.

An employee of Dutch Animal Health Service takes a nose swab for testing on AR.
Photo credit: Hans Prinsen. 

Mode of transmission

Toxigenic P. multocida capable of causing PAR are spread from pig to pig by snout contact, by drinking water previously contaminated by infected pigs and by breathing in the organism in air. It survives for days in cool moist conditions and can be spread from farm to farm in carrier pigs and breeding stock and also in contaminated clothing and implements.

Clinical signs

Outbreaks of sneezing occur in piglets aged between 1 and 8 weeks of age and are accompanied by tear staining or even nose bleeds. These are suggestive of PAR but do not confirm its presence.The sneezing and snuffling gradually becomes milder, but after 14 days, bony changes begin to appear in the snout. As the disease progresses, the upper jaw become displaced from the mid-line and grows more slowly than the covering skin or lower jaw so that the skin over the snout appears corrugated and the lower jaw sticks out further. Bending of the snout is difficult to detect in young piglets, but an early indication of PAR can be obtained by looking at the incisor teeth. They normally meet, but in PAR the lower incisors stick out further. The bony changes are usually confirmed by routine monitoring at slaughter or during farm post-mortem examination.

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 although turbinate atrophy may be found at slaughter. This form is most common where infection does not occur until after weaning and or where immunity is present. Severely 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. Effects on growth rate associated with the bony changes have been estimated at 0.5% (growth depression of 25-40 g/day) or nil, depending upon the study. The presence of the organism is confirmed by demonstrating its presence in nasal swabs from early cases or from carrier animals using a combination of bacterial culture and polymerase chain reaction (PCR) methods in the laboratory.

Retarded growth in the upper jaw is a clinical sign for progressive AR.
Photo credit: DAP Deurne.

Postmortem lesions

The external changes in PAR can be seen at post-mortem and protrusion of the incisor teeth of the lower jaw can be seen more easily. The bony changes are usually seen by routine monitoring at slaughter or during farm post-mortem examination. In affected pigs, the fine scroll bones (conchae) which occupy the nasal chamber are missing and the nasal septum which divides the two nasal chambers if often bent. These changes can be seen best when the snout is sawn across at the level of premolar tooth 2 (level with the corner of the mouth). The changes can be graded 1-5 to give an idea of the severity of the condition. Culture of the toxigenic P. multocida from nasal swabs and demonstration of the toxin confirms that the changes seen are those of PAR and is the method used in monitoring schemes. Antibody to the toxin can be demonstrated in serum or recovered and vaccinated pigs.

Treatment and prevention

Elimination of infection with toxigenic P. multocida 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 doser as appropriate. Animals should be supported with additional food and electrolyte 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 an airspace in an all-in, all-out system is the most efficient method. Vaccination of sows with the toxoid (inactivated toxin) to give colostral 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 and confirming the absence of the toxin gene, coupled with routine screening of a sample of snouts at slaughter. These techniques have been used to identify carrier pigs in an affected herd and they can be eliminated to give a PAR-free herd.

Nose deformation as a result of Atrophic Rhinitis. 
Photo credit: DAP Deurne - Marten de Jong.