Atrophic rhinitis in goats in Norway

The spontaneous occurrence of atrophic rhinitis in 12 of 49 goat herds in one area of Norway is described. The clinical signs included nose bleeding, nasal discharge, sneezing and tender noses. Pathologically, the macroscopic and histological findings resembled those found in pigs with atrophic rhinitis. Bacteriological investigation of nasal swabs in five of the herds revealed toxigenic strains of Pasteurella multocida in three of them. In four of the herds the clinical signs were seen in two or more consecutive years. No specific source of the infection was discovered. Atrophic rhinitis was induced experimentally in kids by the nasal inoculation of toxigenic strains of P multocida and atrophic rhinitis toxin.     

Atrophic rhinitis in swine and other animal species

Evidence that cattle, goats and rabbits may suffer from natural diseases equivalent to porcine atrophic rhinitis is presented. Etiology and course of the progressive (enzootic) and non-progressive (sporadic) forms of atrophic rhinitis in pigs are discussed and compared with known data about similar diseases in other animals. It seems that atrophic rhinitis caused by toxigenic strains of Pasteurella multocida may be a disease of different animal species.     

Atrophic rhinitis in swine fattener herds. A field study of the spread of the disease with infected pigs bought at market

In three different fattener herds pigs primarily AR infected as baby piglets were mixed in the fattening units with healthy pigs at an age of 11--13 weeks. Snout alterations were registered on cut snouts at a slaughter weight of about 70 kg. Severe AR was registered in the groups of primarily infected pigs (Tables I--III). The incidence of snout alterations was lower in the groups of pigs infected at an age of 11--13 weeks, but was much higher than in the groups of healthy control pigs or in the normal pig population in the region (Table IV). The results indicate that pigs infected at a rather late age in the fattening units can develop severe atrophic rhinitis.     

Investigation into the pathogenesis of Atrophic Rhinitis in pigs

Summary

In two groups of swine herds, herds with and without clinical AR the presence of Atrophic Rhinitis (AR) correlated with the presence of toxinogenic Pasteurella multocida (PM) and not with the Bordetella bronchiseptica (BB) infection.

Six BB‐ and eighteen PM‐strains have been investigated for AR pathogenicity. Broth cultures were injected intradermally in guinea‐pigs (GPST) orintranasally in 3‐week‐old colostrum deprived specific pathogen free (SPF) piglets.

The average atrophy of the ventral conchae (A VC) correlated with the GPST in 4BB‐ and 7 PM‐strains. One BB‐ and 2 PM‐strains were qualified as doubtful, the others as non‐AR pathogenic. With AR pathogenic BB‐ and PM‐strains clinical AR could be induced in 3‐ and 6‐week‐old piglets. AVC lesions (gradation> 1) could be induced with BB in piglets of 6 and with pathogenic PM in 16‐week‐old piglets. Six of seven AR pathogenic PM‐strains resembled Carter‐type D and one resembled type A. No significance was found between AR pathogenicity and somatic serotypes.

Intranasal instillations of cell‐free broth culture filtrates of AR pathogenic PM‐strains also caused AR in piglets. These filtrates also caused lethality in piglets and in mice lethalitytest (MLT) and induced a positive GPST. After heating the pathogenic effects of the filtrates disappeared. The name AR toxin has been introduced for this thermolabile, haemorrhagic dermonecrotic (HDNT) fraction of the AR inducing filtrates. The severity of the AR lesions depended on the amount of the AR toxin intranasally instilled in pigs.

Cross protecting antibodies obtained in rabbits against the AR toxins of two PM strains could be demonstrated by a toxin neutralisation test in the MLT and the GPST.

Broth cultures were injected intradermally in guinea‐pigs (GPST) or intranasally in 3‐week‐old colostrum deprived specific pathogen free (SPF) piglets.     

Atrophic rhinitis of swine: neutralization of the toxin of Pasteurella multocida

The neutralization of the lethal as well as the growth-retarding action of the toxin on mice by an antitoxic serum is described.     

Atrophic rhinitis in New Zealand white rabbits infected with Pasteurella multocida

Atrophic rhinitis was detected in New Zealand White rabbits when upper respiratory tract disease was evaluated during a vaccine field trial for the prevention of pasteurellosis. Of 52 adult rabbits euthanatized and necropsied, 26 (50%) had evidence of turbinate atrophy. Atrophy was detected in 77% of rabbits with Pasteurella multocida infection only, 71% of rabbits with concurrent P multocida and Bordetella bronchiseptica infections, and 6% of rabbits with B bronchiseptica infection only. Grossly, turbinate atrophy was characterized by a mild to severe loss or diminution in the maxilloturbinates. Histologically, turbinate bones were small and irregular in thickness and had numerous osteoclasts and osteoblasts. A neutrophilic exudate filled the nasal passages, and infiltrates of neutrophils and lymphocytes were detected in the mucosa and submucosa of the nasal turbinates. Rhinitis was significantly (P less than 0.001) associated with turbinate atrophy. Isolates of P multocida from rabbits with turbinate atrophy were serotype A:12.     

Investigation into the pathogenesis of atrophic rhinitis in pigs. I. Atrophic rhinitis caused by Bordetella bronchiseptica and Pasteurella multocida and the meaning of a thermolabile toxin of P. multocida

In two groups of swine herds, herds with and without clinical AR the presence of Atrophic Rhinitis (AR) correlated with the presence of toxinogenic Pasteurella multocida (PM) and not with the Bordetella bronchiseptica (BB) infection. Six BB- and eighteen PM-strains have been investigated for AR pathogenicity. Broth cultures were injected intradermally in guinea-pigs (GPST) or intranasally in 3-week-old colostrum deprived specific pathogen free (SPF) piglets. The average atrophy of the ventral conchae (AVC) correlated with the GPST in 4 BB-and 7 PM-strains. One BB- and 2 PM-strains were qualified as doubtful, the others as non-AR pathogenic. With AR pathogenic BB-and PM-strains clinical AR could be induced in 3-and 6-week-old piglets. AVC lesions (gradation greater than 1) could be induced with BB in piglets of 6 and with pathogenic PM in 16-week-old piglets. Six of seven AR pathogenic PM-strains resembled Carter-type D and one resembled type A. No significance was found between AR pathogenicity and somatic serotypes. Intranasal instillations of cell-free broth culture filtrates of AR pathogenic PM-strains also caused AR in piglets. These filtrates also caused lethality in piglets and in mice lethalitytest (MLT) and induced a positive GPST. After heating the pathogenic effects of the filtrates disappeared. The name AR toxin has been introduced for this thermolabile, haemorrhagic dermonecrotic (HDNT) fraction of the AR inducing filtrates. The severity of the AR lesions depended on the amount of the AR toxin intranasally instilled in pigs. Cross protecting antibodies obtained in rabbits against the AR toxins of two PM strains could be demonstrated by a toxin neutralisation test in the MLT and the GPST. Broth cultures were injected intradermally in guinea-pigs (GPST) or intranasally in 3-week-old colostrum deprived specific pathogen free (SPF) piglets.     

Atrophic rhinitis caused by Pasteurella multocida type D: morphometric analysis.

In order to study the distribution and the extent of atrophy caused by Pasteurella multocida in the nasal conchae, experimental piglets were injected intramuscularly at seven days of age with either two or four 50% mouse lethal doses per kg body weight of P. multocida type D dermonecrotoxin. Experimental and control piglets were killed four, six and ten days postinjection. Serial transverse paraffin embedded sections of the noses were cut throughout the entire length of the nasal conchae. The area of the nasal ventral conchae was measured and the morphometric index of the nasal cavity was calculated. It was observed that P. multocida type D dermonecrotoxin induced severe atrophy of the nasal ventral conchae. This atrophy was present along the entire conchae. However, it was most severe at the level of the first and second premolar teeth.     

Growth hormone concentrations in plasma of healthy pigs and pigs with atrophic rhinitis.

Plasma concentrations of porcine growth hormone (PGH) were similar in healthy pigs and those with atrophic rhinitis (AR), therefore, observed reduced growth rates and feed efficiency in naturally infected pigs with AR were not attributed to low concentrations of plasma PGH. Also, pituitary glands in both groups of pigs were responsive to growth hormone-releasing hormone (GHRH) challenge by increasing PGH secretion. Administration of clonidine hydrochloride to pigs naturally infected with AR failed to elicit any significant change (5.3 +/- 1.4 ng/ml) in the plasma concentration of PGH within a 45-minute bleeding interval. The pretreatment concentrations of PGH were similar in specific-pathogen-free toxin-treated and specific-pathogen-free control groups, but they increased significantly in toxin-treated pigs (20.7 +/- 8.2 ng/ml) within 15 minutes after GHRH injection. Porcine growth hormone release in toxin-treated pigs was variable; however, all pigs did not respond to GHRH administration: 3 responded with an increase in PGH release (35.6 +/- 10.6 ng/ml), 2 did not respond (6.7 +/- 0.5 ng/ml), and 1 had a decrease in PGH release (3.9 ng/ml). Therefore, the observed reduced growth rates reported in the literature may be attributed to factors at the target level of PGH action, such as insufficient or down-regulation of PGH receptors, changes or impaired ability in the PGH receptor-binding characteristics, and inability of PGH receptor complex to transduce signal. Toxins are known to modulate signal transduction pathways. It has been speculated that serotype-D Pasteurella multocida toxin may influence growth by its effect on signal transduction from PGH receptor complex on the cell membrane to the interior of the cell.(ABSTRACT TRUNCATED AT 250 WORDS)