Progressive atrophic rhinitis

Progressive atrophic rhinitis



Progressive atrophic rhinitis (PAR) is an important disease of pigs characterized by turbinate atrophy with varying degrees of facial deformation. It is caused by infection with toxigenic strains of Pasteurella multocida. Clinical disease can cause production losses due to growth retardation in fattening pigs.17 Subclinical disease also occurs.

The aetiology of PAR was long disputed, as various causes of turbinate atrophy have been identified. Infection with Bordetella bronchiseptica can cause severe rhinitis with turbinate atrophy in piglets less than six weeks old. However, it is accepted that the progressive form of the disease, which can affect older pigs, is caused only by toxigenic strains of P. multocida,17, 22, 24, 67 although various factors including infection with B. bronchiseptica can predispose to PAR. The progressive nature of the disease probably depends upon chronic infection with toxigenic P. multocida, as turbinate atrophy experimentally induced by a single intraperitoneal administration of toxin resolved within approximately three months.57

Progressive atrophic rhinitis has probably been known since 1830, when it was described as ‘Schnüffelkrankheit’.17 It was reported from the USA in 194428 and the UK in 1954.8 It is widespread, occurring in most countries that produce pigs, including South Africa. It has recently been reported in Kenya.82 Lesions suggestive of PAR have been described in extensively kept pigs of local breed in Zimbabwe,36 although this was not confirmed by bacterial isolation.

The importance of PAR lies not only in its ability to cause production losses, but in the fact that subclinical disease is common. Herds that have never shown clinical signs of atrophic rhinitis may nevertheless harbour carriers that, introduced into herds under different management, may spread the infection. Detection of carriers is therefore of critical importance to prevent introduction into clean herds. Because even modern techniques may fail to identify infected individuals, continuous monitoring of herds is necessary to ensure freedom from PAR.

Although PAR is of importance only in pigs, toxigenic strains of P. multocida have been isolated from rabbits, humans, and calves, in which they produce similar effects of turbinate atrophy, as well as from dogs, cats, goats and poultry.44


A toxin produced by particular strains of P. multocida is the cause of progressive turbinate atrophy in pigs, either alone or in combination with B. bronchiseptica.17, 24, 74, 75 Pasteurella multocida is best cultured in broth media.17 Strains of both types A and D cultured from pigs, rabbits and humans have been identified that produce a thermolabile dermonecrotic protein toxin. An untypable strain was isolated from cattle with turbinate atrophy and found also to produce a dermonecrotic toxin.44 The majority of toxigenic strains isolated from pigs belong to type D, but occasionally toxigenic type A strains are reported.33, 85 Identification of the gene that encodes for the toxin indicated that it may be located in a bacteriophage, transfer of which may be able to cause non-toxigenic strains to produce toxin.7 This hypothesis was supported by the finding in another study that the toxin-encoding gene may have had a different origin from the rest of the genome of the organism studied.47


Clinical PAR usually occurs in young pigs. Experimental infection has succeeded in producing typical lesions of PAR in pigs up to 16 weeks old, although infection usually occurs in the farrowing unit before piglets are four weeks old.62 Lesions decrease in severity with age, and infection of adults may result in subclinical disease with subsequent infection of piglets by their dams, 10 to 15 per cent of which may be carriers.17 The highest prevalence of carriers was found in the 6- to 12-month age group.83

Introduction into clean herds is usually by means of carriers, which may shed organisms when stressed by transport and mixing with other pigs. Molecular fingerprinting of isolates in Australia suggested that importation of infected pigs from a single source was responsible for PAR in Australia.33

Transmission is usually by direct nose-to-nose contact or aerosol, but, since toxin administered by various routes can produce lesions of PAR, and it appears that toxin can be produced in sites other than the nasal mucosa, infection by other routes may be possible.1, 2, 85 Toxigenic P. multocida is usually carried in the pharyngeal tonsils1, 2 but may be isolated from the nasal mucosa and the lungs.60 It has also been isolated from the vaginas of sows.17 Transmission between species might occur, but it has been suggested that this may not always result in disease.45 However, piglets developed turbinate atrophy after inoculation with toxigenic P. multocida cultured from a human patient.59

Although toxin produced by P. multocida is capable of producing typical lesions of PAR, colonization of the nasal mucosa is enhanced by the presence of B. bronchiseptica.17, 29, 74, 75 However, vaccination with purified P. multocida toxin alone gave good protection against severe lesions of PAR.32 Damage induced by high levels of ammonia and dust also facilitates colonization.17, 38

The severity of PAR, and indeed...

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