Background and history

Rhinitis implies inflammation of the nose and it can be caused by a variety of bacteria and irritant substances. During the process of infection the delicate structures or turbinate bones in the nose become damaged and atrophy or disappear. Progressive atrophic rhinitis describes a specific disease where the nose tissues permanently atrophy. It is caused by specific toxin producing strains of Pasteurella multocidia (PMt). There are two types A and D.

Bleeding from nose caused by atrophic rhinitis Typical signs of atrophic rhinitis Section through nose - grade 3 atrophic rhiniits

Spread of disease between herds is almost invariably by the carrier pig, the organism being found in the respiratory tract and the tonsils. Spread within herds is by droplet infection between pigs or by direct pig to pig (nose to nose) contact. It can also be spread indirectly on equipment, clothes etc. When first infected pigs can carry the infection for many months. Infection is usually picked up during the second half of the sucking period or after weaning and clinical disease may be evident from three weeks of age onwards. The toxin is absorbed into the system where it damages other tissues including the liver, kidneys and lung, resulting in reduced daily gain and depressed feed efficiency. Similar organisms may also be found in the cat, dog, rabbit, poultry, goat, sheep, turkey but it is thought that these are host adapted strains and are unlikely to cause serious disease in the pig. The human may carry PMt in the tonsils for a very short period of time, although the evidence for this is limited and there are no reports of transmission by people to pigs. Experience indicates that the main and probably only method of introduction into the herd is by carrier pigs, although occasionally unexplained outbreaks of disease may occur.

Similar diseases

Rhinitis may be caused by the following but the distinction is less evident, fewer pigs are obviously affected and the turbinate bones will heal and regenerate.

• Air containing high bacterial counts.
• Aujeszky's disease.
• Bordetella bronchiseptica infection.
• Chronic respiratory disease.
• Dust.
• Glässers disease.
• High levels of ammonia.
• Porcine cytomegalovirus infection (PCMV) (inclusion body rhinitis).
• PRRS.

Clinical signs

In sucking pigs sneezing, snuffling and a nasal discharge are the first symptoms, but in acute outbreaks where there is little maternal antibody, the rhinitis may be so severe to the extent that there is haemorrhage from the nose. By three to four weeks of age and from weaning onwards, there is evidence of tear staining and malformation of the nose associated with twisting and shortening.

Severely affected pigs may have problems eating. There is considerably reduced daily gain. In severe outbreaks pigs may not grow to market weight.

Diagnosis

This is based on clinical signs. However do not assume if sneezing is occurring in young pigs that automatically it will be progressive atrophic rhinitis. The disease is easily identified by post-mortem examinations of the nose and culture of the organism from nasal swabs. The snout is sectioned at slaughter at a level of the second premolar tooth and an assessment of the degree of atrophy of the turbinate bones made. The snouts are graded from 0 to 5, 0 to being a perfect snout. Grade 1 would show a slight loss of symmetry of the nose, grade 2 a slight loss of turbinate tissue and grade 3 a moderate amount. It is only when grades 4 and 5 are present, when there is severe progressive loss of tissue that PAR will be suspected. (Fig.9-21).

The five grades of Rhinitis

Prevention

• Keep disease out by purchasing pigs only from known negative sources.
• Monitor snout sections regularly.
• If the herd is infected do not breed from home bred gilts.
• Vaccinate sows.
• Maintain an old herd to produce good colostral immunity.
• Avoid continuously populated housing which may allow organisms to build up to a threshold level and initiate a disease outbreak.
• Adopt all-in all-out procedures from weaning to slaughter.
• Avoid high stocking levels.
• Avoid more than ten sows per farrowing room.
• Damp humid farrowing houses increase the risk of spread.
• Use solid divisions between farrowing crates to reduce droplet infection
• Keep weaners to less than 120 per group.
• Poor ventilation and high humidity post-weaning predispose.
• Do not re-circulate air in flat decks.
• Avoid fluctuating temperatures in flat decks.

Eradication

PAR may be eradicated from the herd after a 12 month period of sow vaccination provided all clinical evidence of disease has subsided. Piglets from vaccinated sows are weaned and segregated from disease carrying pigs until the weaning finishing accommodation has been depopulated and cleaned. The segregated pigs are then returned to the buildings. In the meantime the other finishing pigs are gradually sold to slaughter. The vaccinated "clean" pigs are not allowed contact with infected pigs and separate personnel are used between groups. PAR is only spread by close droplet contamination. An alternate and more successful method is to market all growing pigs over a 6 to 8 week period before bringing the segregated pigs back into the system.

Treatment

• The moment PAR is diagnosed all adult stock should be vaccinated twice with a toxin derived vaccine 4 to 6 weeks apart. Vaccination usually gives excellent control.
• Sows should then be vaccinated four to six weeks prior to each subsequent farrowing or as per the data sheet.
• All weaned pigs should be medicated in-feed until the clinical outbreak has subsided.
• At the same time and until a good immunity has developed, antibiotic treatment should be given to the piglets. Consider using the following routines:
• - Day three of age. Inject with either long-acting OTC or amoxycillin.
• - Day ten. Inject with either long-acting OTC or amoxycillin.
• - Inject again at weaning time with OTC or amoxycillin
• Other antibiotics could be used depending on the bacterial sensitivity, such as penicillin, trimethoprim sulphas, tylosin and enrofloxacin.
• The sows feed could be top-dressed with either OTC or trimethoprim/sulpha (TMS) commencing five to seven days prior to farrowing and throughout the farrowing period, or the lactating ration medicated with trimethoprim/sulpha (500g).
• At weaning time the creep feed should be medicated with OTC or CTC at dose levels of 500-800g/tonne or TMS for three weeks post-weaning.

In acute outbreaks PAR is evident clinically in up to 25% of pigs by the time they have reached 16 weeks of age. Four months after vaccination this should have dropped to around 10% and after six months down to less than 1%. Vaccination will usually prevent the establishment of infection up to approximately eight to twelve weeks of age until the pigs move into finishing houses. Here, unless the houses have been depopulated, the pigs will become infected but with few clinical signs. Infection however increases the predisposition to other respiratory diseases and depresses feed intake and performance.