Pathogenesis Of Atrophic Rhinitis Research Articles

Clinical Features and Pathogenesis of Atrophic Rhinitis in a Sharp Continental Climate: A Literature Review

Clinical Features and Pathogenesis of Atrophic Rhinitis in a Sharp Continental Climate: A Literature Review

Clinical and pathological effects of the dermonecrotic toxin of Bordetella bronchiseptica and Pasteurella multocida in specific-pathogen-free piglets.

The role of dermonecrotic toxin (DNT) of Bordetella bronchiseptica and Pasteurella multocida, purified by repeated chromatography in Sephacryl S-200 gel, in the pathogenesis of atrophic rhinitis (AR) of swine was studied bacteriologically, clinically and pathologically. Two-week-old specific pathogen-free (SPF) piglets were parenterally treated with 30 micrograms of DNT 3 times at 2-day interval and 7-week-old piglets were treated with 15 micrograms of DNT twice a week for 5 weeks. In 2- to 3-week-old piglets, both B. bronchiseptica DNT and P. multocida DNT produced nasal turbinate lesions with similar severity, characterized by damage of the cilia, epithelial metaplasia, intensive proliferation of osteoblasts, regressive changes, and diffuse osteocytic osteolysis. In 7- to 12-week-old piglets, treatment with B. bronchiseptica DNT failed to produce progressive changes in the nasal turbinates. Histopathological examination revealed osteogenic processes and osteoid synthesis besides the proliferation of osteoblasts and mild osteocytic osteolysis. Moreover, severe gross pathological lesions developed in the stomach, liver, kidneys, and lymphoid organs. The piglets' appetite and body weight gain gradually decreased during the DNT treatment and in the last week when the toxic signs appeared. Treatment of 7- to 12-week-old piglets with P. multocida DNT resulted in progressive AR. Histopathologically, diffuse osteocytic osteolysis was observed in the nasal turbinates. Neither clinical signs nor pathological lesions of the visceral organs developed in these piglets. The authors emphasize that the DNT of B. bronchiseptica basically differs from that of P. multocida in biological properties, though there are certain similarities between the DNTs.

Stimulation of bone resorption by inflamed nasal mucosa, dermonecrotic toxin-containing conditioned medium from Pasteurella multocida, and purified dermonecrotic toxin from P. multocida.

The effects of inflamed nasal mucosa from pigs with atrophic rhinitis (AR), cell extract from Bordetella bronchiseptica, conditioned medium from Pasteurella multocida, and purified dermonecrotic toxin (DNT) from P. multocida on mouse fetal long bones in organ culture were studied. Inflamed nasal "AR mucosa" stimulated the release of 45Ca from prelabeled cultures, while histologically the formation of calcified matrix was impaired as well. B. bronchiseptica cell extract only transiently increased 45Ca release, but also impaired the formation of matrix. 45Ca release was also stimulated by DNT-containing conditioned medium from P. multocida and by purified DNT. The effect of DNT was biphasic: low doses (1 to 25 ng/ml) slightly stimulated bone resorption, higher doses were inhibitory. The stimulatory action of DNT on 45Ca release was accompanied by an increase in numbers of preosteoclasts and osteoclasts. The significance of these findings for the pathogenesis of AR is discussed.

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.

Investigation into the pathogenesis of atrophic rhinitis in pigs. II. AR induction and protection after intramuscular injections cell-free filtrates and emulsions containing AR toxin of Pasteurella multocida.

The intramuscular administration of the cell-free culture filtrates of two AR pathogenic Pasteurella multocida (PM) isolates caused Atrophic Rhinitis (AR) in piglets. The culture filtrate of a non-AR-pathogenic PM isolate did not cause AR lesions after intramuscular injection. The severity of the AR lesions appeared to be correlated with the quantity of injected toxin. As the quantity of administered toxin increased, the piglets showed clinical growth retardation, icterus and mortality. Besides lesions typical of AR, severe liver degeneration was observed at necropsy; this liver degeneration was sometimes accompanied by fibrosis. After emulgation of the cell-free culture filtrates in incomplete Freunds adjuvant, AR was caused by administration of the toxin-containing emulsions in piglets of 3 and 6 weeks of age. An experimental water-in-oil emulsion containing the AR toxin of Pasteurella multocida caused AR when intramuscularly injected in 1- to 4-week-old piglets. A PM-AR toxin challenge method is described. After injection of the toxin into piglets born from sows vaccinated against AR, protection was demonstrated. Ten of the 12 piglets (83%) challenged at the age of 3 weeks showed protection. Six animals of the 12 pigs (50%) injected with the toxin at the age of 6 weeks, showed no protection. Differences in protection were noted between and within the litters. After injection with the toxin, all piglets of 3 and 6 weeks of age born from non-vaccinated sows showed deviations typical of AR.

The pathogenesis of atrophic rhinitis in pigs induced by toxigenic Pasteurella multocida

The pathogenesis of atrophic rhinitis was studied in an experiment in which piglets were infected with a toxigenic type D Pasteurella multocida strain in the right half of the nasal cavity. Two days before inoculation the nasal mucosa on the right side had been subjected to mild irritation by intranasal instillation of a weak solution of acetic acid. The untreated (left) half of the nasal cavity served as an intrinsic control. Macroscopically, changes in the turbinates were already appreciable at 3 days p.i., and pronounced turbinate atrophy was noted at 7 days p.i. At 14 days p.i. deviation of the snout and almost complete turbinate atrophy was observed. The turbinates in the untreated half of the nasal cavity developed normally. Histologically, the changes were initially characterized by bone resorption mediated by an increased number of osteoclasts. Later osteoclasts were sparse, and there was an apparent disruption of osteoid synthesis. Ultrastructurally, the osteoblasts showed nuclear indentations and dilatation of the endoplasmic reticulum. Since no inflammatory reaction was observed, the hypothesis is advanced that atrophic rhinitis in pigs is caused by a P. multocida-produced factor which will stimulate bone resorption and suppress osteoid synthesis.

Pathogenesis of atrophic rhinitis in pigs: a new perspective.

Pathogenesis of atrophic rhinitis in pigs: a new perspective.

Ultrastructural Evaluation of Thyroid Parafollicular Cells of Pigs with Naturally Occurring Atrophic Rhinitis

The thyroid parafollicular cells of 4-month-old control pigs and pigs with naturally occurring atrophic rhinitis were evaluated ultrastructurally. Significant difference was not observed in populations of parafollicular cells between the 2 groups of pigs. Parafollicular cells occurred in actively synthesizing and storage phases of the secretory cycle in both groups. Actively synthesizing cells had a well-developed endoplasmic reticulum, aggregated ribosomes, and prominent Golgi apparatuses with prosecretory granules. The cytoplasm of parafollicular cells in the storage phase was packed with electron-dense secretory granules. The Golgi apparatus and ergastoplasm were less prominent. There was no evidence to suggest that an interference in the synthesis or release of thyrocalcitonin by parafollicular cells was of criologic importance in the pathogenesis of atrophic rhinitis.