Atrophic Rhinitis (AR) and Progressive Atrophic Rhinitis (PAR)

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Atrophic Rhinitis (AR) and Progressive Atrophic Rhinitis (PAR)

pig nose - atrophic rhinitis - moderate conchae atrophia

Atrophic rhinitis: moderate conchae atrophia

"Progressive Atrophic Rhinitis (PAR) describes a specific disease where the nose tissues permanently atrophy."

Rhinitis in pigs is very common and can be caused by a variety of bacteria and irritant substances. Rhinitis may result in damage of the nasal turbinates.

Non-Progressive Atrophic Rhinitis (NPAR) is caused by Bordetella bronchiseptica and is a reversible form of atrophic rhinitis. Progressive Atrophic Rhinitis (PAR) describes a specific disease where the nose tissues permanently atrophy. It is caused by specific toxin-producing strains of Pasteurella multocida.

About AR and PAR


Etiology

Bordetella bronchiseptica is a widespread commensal organism in the respiratory tract of pigs. It is an aerobic Gram-negative rod and typically causes disease in 1 - 6 week old piglets, leading to mild lesions and possible atrophy of the nasal turbinates. However, destruction by this pathogen is mostly healed by the host and does not cause progressive atrophic rhinitis. (Swine Disease Manual, 4th Ed) Pasteurella multocida is a normal commensal organism in the respiratory tract of pigs but is less widespread across pig populations. The strains causing Progressive Atrophic Rhinitis (PAR) produce a powerful toxin, the dermonecrotizing toxin, which is responsible for the lesions found in the disease. Pasteurella multocida can easily be cultivated and recognized by the colony produced in the laboratory, but strains involved in PAR can only be distinguished by demonstrating their ability to produce toxin.

Pasteurella multocida will only colonize the nasal passages in sufficient numbers to cause disease if the mucosa is already damaged. The damaging agent is usually the bacterium, B. bronchiseptica, which causes inflammation in the nasal cavity and allows P. multocida to grow, produce toxins, and cause disease.

The toxins produced are absorbed by the host and affect bone production and remodeling. In young, fast-growing piglets, the nasal and facial bones become distorted. piglets the nasal bones become distorted.

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Contributing factors to Atrophic Rhinitis and Progressive Atrophic Rhinitis

  • More common in young herds, particularly those containing large numbers of gilts
  • Large, permanently populated farrowing houses
  • Poor environmental conditions - poor ventilation, low humidity, dust
  • The presence of other diseases such as Enzootic Pneumonia, PRRS, Glasser Disease and Aujeszky's disease in the herd

Milder rhinitis, termed non-progressive disease, in which the turbinate bones heal and regenerate, may be caused by the following.

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

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Pathogenesis

The pathogens responsible for Atrophic Rhinitis can be spread from carrier sows to newborn piglets. Piglets may become infected later due to waning maternal immunity as they grow older. Although the sow normally passes along some maternal immunity to her piglets, older sows may pass more antibodies, and possibly lower infectious doses of pathogen, to their piglets when compared to low parity gilts, which more frequently pass on disease. Pasteurella multocida can colonize the nasal passages after rhinitis has occurred, which is usually the result of B. bronchiseptica or other environmental agents. The P. multocida toxin causes disease of the bones that leads to Progressive Atrophic Rhinitis.

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Clinical Signs of Progressive Atrophic Rhinitis

In piglets between 1 and 8 weeks of age, sneezing, sniffling, nasal discharge, tear staining, and sometimes nosebleeds may be observed. The sneezing gradually reduces, but after 14 days, bony changes become visible. Signs of P. multocida infection most likely occur in piglets that are 4 - 8 weeks old. As the disease progresses, the upper jaw becomes displaced and grows slower than the soft tissue and lower jaw. The skin over the snout appears corrugated, and the lower jaw protrudes. Some pigs will develop a deviated snout. Signs of pneumonia or stunting may also be seen. Severally affected animals may have difficulty eating and the nasal changes may be found in pigs of all ages in affected herds. Daily weight gain is reduced.

In some animals, sneezing may be transitory with few other clinical signs, but 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.

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Diagnosis

Diagnosis is based on clinical signs. 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 appear as the piglets age.

The disease is easily identified by post-mortem examinations of the nose and culture of the organism from nasal swabs. At slaughter the snout is sectioned at the 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.

Grading of snouts at slaughter
Grade Explanation
Grade 0 Normal snout
Grade 1 Slight loss of symmetry of the nose
Grade 2 A slight loss of turbinate tissue
Grade 3 A moderate amount of loss of turbinate tissue
Grade 4 and 5 Severe progressive loss of tissue, PAR suspected


pig snout not affected - intact conchae

Grade 0 - snout not affected, intact conchae


Pig snout - moderate Atrophic rhinitis

Grade 3 - moderate loss of turbinate tissue

Culture of the toxigenic P. multocida from nasal swabs and demonstration of the toxin confirms the diagnosis of PAR.

Antibody to the toxin can be demonstrated in serum from recovered and vaccinated pigs.

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Treatment and control

  • Elimination of infection with toxigenic P. multocida prevents the development of the bony lesions and negative production effects. Acute disease in piglets can be treated with potentiated sulphonamides, ampicillin, tetracyclines, ceftiofur or enrofloxacin. Supportive therapy such as additional feed and electrolytes may be necessary.
  • Weaned pigs at risk may be treated with an antimicrobial at therapeutic levels in feed or water. Medication of groups of animals entering airspace in an all-in, all-out system is the most efficient method
  • Improving the environment of the pigs can reduce the risk of infection by P. multocida. Changes to improve husbandry practices and the quality of housing should be taken into consideration.
  • Vaccination of sows with the toxoid (inactivated toxin) to give protection via the colostrum to piglets. See Vaccines.
  • 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 done by culture of nasal swabs for toxigenic P. multocida.

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