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At least 163 records · Page 9Linked to original sources
PubMed1980

Experimental atrophic rhinitis in gnotobiotic pigs.

Twenty-nine caesarian derived colostrum deprived germfree pigs were reared in isolators in groups of three to four per isolator. At seven days of age each group was inoculated intranasally with one of four strains of Bordetella bronchiseptica (designated B, J, L and 55B), or Pseudomonas aeruginosa or a mucoid strain of Escherichia coli, all previously isolated from nasal mucus of pigs affected with clinical atrophic rhinitis. Another group was inoculated simultaneously with B. bronchiseptica B and Pasteurella multocida. The animals were observed for clinical signs of atrophic rhinitis and monitored bacteriologically at weekly intervals for seven weeks. Then they were bled for serology and killed and their respiratory organs examined for gross and histopathological lesions. All of the pigs inoculated with the Bordetellae had inflammation of the nasal mucosa and developed positive serum antibody titers against all four of the Bordetella strains used in this study. Strain J caused sneezing and turbinate atrophy in three of four pigs. One of the three pigs inoculated with strain L died in ten days from bronchopneumonia and pericarditis and had turbinate atrophy. Strains B and B55 caused no turbinate atrophy, but two out of three pigs inoculated with both B. bronchiseptica B and P. multocida had turbinate atrophy. No nasal lesions were observed in the pigs inoculated with E. coli or P. aeruginosa or in the noninoculated germfree controls. The results indicate a variation in the ability of different strains of B. bronchiseptica to cause turbinate atrophy in pigs and demonstrate that nasal infections by these organisms stimulate serum antibody response. Presence of P. multocida appears to increase the severity of the lesions. As the E. coli and Pseudomonas failed to produce atrophic rhinitis, they are probably of no significance as primary etiological agents in the atrophic rhinitis syndrome in swine.

Animals↗
PubMed1992

Radiological and endoscopic study of the maxillary sinus in primary atrophic rhinitis.

The maxillary sinuses of 40 patients suffering from primary atrophic rhinitis (ozaena) were studied radiologically, antroscopically and histopathologically. Sixty per cent of the patients showed thick bony walls and a small cavity of the maxillary sinus on X-ray and on antroscopy. On the other hand, 25 per cent of the cases revealed signs of infection including mucopurulent secretion on antroscopy associated with corresponding histopathological changes. It is concluded that poor pneumatization of the antrum plays a more important role in the pathogenesis of ozaena than infection.

Endoscopy↗
PubMed1989

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.

Animals↗
PubMed1985

Effect of atrophic rhinitis on growth rate in Illinois swine herds.

Influence of atrophic rhinitis (AR) on mean daily weight gain (MDG) was studied in hogs randomly selected from 7 farrow-to-finish herds in Illinois. Herds were selected to obtain a wide range of clinical signs and lesions of the disease; thus, prevalence of clinical signs of AR in finishing hogs ranged from 0% to 20% among herds, and in hogs examined at slaughter the proportion of hogs with turbinate lesions ranged from 5% to 92%. None of the herds investigated had any obvious problems with pneumonia; nevertheless, hogs with moderate to severe pneumonic lesions were excluded from the study, to minimize any combined effect of AR and pneumonia. In 3 herds, MDG in AR-free pigs was 15% to 18% better than in pigs with severe AR lesions. Prevalence of clinical signs ranged from 5% to 20%, and of turbinate lesions, from 66% to 92%. In 4 herds in which MDG appeared to be unaffected by AR, prevalence of clinical signs of the disease ranged from 0% to 5%, and of turbinate lesions, from 5% to 74%. No consistent pattern of influence on AR lesions was found for bacterial infections, as determined by culturing of nasal swab specimens on MacConkey agar and blood agar.

Animals↗
PubMedDate not supplied

Light and electron microscopic study of primary atrophic rhinitis mucosa.

BACKGROUND: This study examined the light and the electron microscopic changes in the mucosa of primary atrophic rhinitis and compared them with the normal nasal mucosa to establish the changes in the surfactant system. A prospective original study was performed. METHODS: Twenty cases of primary atrophic rhinitis were randomly selected in the outpatient clinic of Sohag University Ear, Nose, and Throat Department. Ten volunteers with no history of chronic nasal disease and with normal rhinopharyngeal picture were selected as control cases. A small punch biopsy was performed with a small forceps under local anesthesia from the medial edge of the inferior turbinate. After histological laboratory preparations, semithin sections (0.5-1 microm) were prepared by using an LKB ultramicrotome. The sections were stained by toluidine blue, examined by light microscope, and photographed. Ultrathin sections (500-800) from selected areas of the trimmed blocks were made and collected on copper grids. The ultrathin sections were then contrasted in uranyl acetate for 10 minutes and examined by electron microscope Jeol JEM-1010. RESULTS: Light microscopy of primary atrophic epithelium revealed typical nonkeratinized stratified squamous epithelium to keratinized squamous epithelium with a thin layer of keratin on the surface. Well-developed desmosomes appeared between the epithelial cells. In the lamina propria, no submucosal glands could be seen. Electron microscopy of it revealed that the stratification of the epithelium increased. Sloughing of the superficial cells was observed in some regions of the proliferating epithelium. Epithelial penetration with neutrophils (mainly) and lymphocytes (some) could be seen. No numerous multilamellar bodies (MLBs) could be detected in these cases. An increased amount of collagenous fibers was observed in the basement membrane. CONCLUSION: In primary atrophic rhinitis, the epithelial cells revealed that desmosomes are characteristic of the metaplastic squamous epithelium and had no MLB in their cytoplasm, and cells in which occasional MLBs had been established showed interdigitations between them and the surrounding cells, suggesting an association between the surfactant deficiency and the development of desmosomes.

Biopsy↗
PubMed1999

Contributory and exacerbating roles of gaseous ammonia and organic dust in the etiology of atrophic rhinitis.

Pigs reared commercially indoors are exposed to air heavily contaminated with particulate and gaseous pollutants. Epidemiological surveys have shown an association between the levels of these pollutants and the severity of lesions associated with the upper respiratory tract disease of swine atrophic rhinitis. This study investigated the role of aerial pollutants in the etiology of atrophic rhinitis induced by Pasteurella multocida. Forty, 1-week-old Large White piglets were weaned and divided into eight groups designated A to H. The groups were housed in Rochester exposure chambers and continuously exposed to the following pollutants: ovalbumin (groups A and B), ammonia (groups C and D), ovalbumin plus ammonia (groups E and F), and unpolluted air (groups G and H). The concentrations of pollutants used were 20 mg m-3 total mass and 5 mg m-3 respirable mass for ovalbumin dust and 50 ppm for ammonia. One week after exposure commenced, the pigs in groups A, C, E, and G were infected with P. multocida type D by intranasal inoculation. After 4 weeks of exposure to pollutants, the pigs were killed and the extent of turbinate atrophy was assessed with a morphometric index (MI). Control pigs kept in clean air and not inoculated with P. multocida (group H) had normal turbinate morphology with a mean MI of 41.12% (standard deviation [SD], +/- 1. 59%). In contrast, exposure to pollutants in the absence of P. multocida (groups B, D, and F) induced mild turbinate atrophy with mean MIs of 49.65% (SD, +/-1.96%), 51.04% (SD, +/-2.06%), and 49.88% (SD, +/-3.51%), respectively. A similar level of atrophy was also evoked by inoculation with P. multocida in the absence of pollutants (group G), giving a mean MI of 50.77% (SD, +/-2.07%). However, when P. multocida inoculation was combined with pollutant exposure (groups A, C, and E) moderate to severe turbinate atrophy occurred with mean MIs of 64.93% (SD, +/-4.64%), 59.18% (SD, +/-2.79%), and 73.30% (SD, +/-3.19%), respectively. The severity of atrophy was greatest in pigs exposed simultaneously to dust and ammonia. At the end of the exposure period, higher numbers of P. multocida bacteria were isolated from the tonsils than from the nasal membrane, per gram of tissue. The severity of turbinate atrophy in inoculated pigs was proportional to the number of P. multocida bacteria isolated from tonsils (r2 = 0.909, P < 0.05) and nasal membrane (r2 = 0.628, P < 0.05). These findings indicate that aerial pollutants contribute to the severity of lesions associated with atrophic rhinitis by facilitating colonization of the pig's upper respiratory tract by P. multocida and also by directly evoking mild atrophy.

Air Pollution, Indoor↗
PubMed1993

Comparison of three biological assays for the detection of toxigenic properties of Bordetella bronchiseptica associated with atrophic rhinitis.

The toxigenic properties of Bordetella bronchiseptica strains associated with clinical atrophic rhinitis were compared using three biological assays: the guinea pig skin test, the mouse spleen atrophy and the suckling mice mortality assay. Forty one sick pigs were cultured and, in 20 of them B. bronchiseptica strains were isolated. Eighteen of the strains were toxigenic by at least one test. However, positivity did not always coincide amongst assays. This discrepancy raises the possibility of either differences in sensitivity between assays or the existence of more than one toxin.

Animals↗
PubMed1978

[Attempt at restoring the health of pigs suffering from atrophic rhinitis].

A group of 24 sows selected from herds affected by atrophic rhinitis was subjected to the study of the therapeutic effect of the administration of wide-spectrum antibiotics combined with an improvement of the zoohygienic conditions and with full-value nutrition in the pre-partal period and during lactation. It was found that the mentioned measures in sows before parturition and their housing in a sanitized farrowing house during treatment generally improved the health of the sows and enabled the rearing of healthy piglets. The mortality rate during rearing up to the age of 28 days was 12.5%. In the control group of piglets and sows the losses amounted to 29%; the clinical symptoms of rhinitis were found in 11% of the piglets already at the age of 28 days.

Animals↗
PubMed1977

Vaccination with Bordetella bronchiseptica vaccine on a farm with atrophic rhinitis: an evaluation of a field experiment.

On a farm where Atrophic rhinitis (AR) occurred the animals were vaccinated with a Bordetella bronchiseptica vaccine. The immune state of the sows was checked and also the effect of this vaccination on the antibody titre of the piglets. Groups of pregnant sows were vaccinated once or twice before the partus, another group of sows only had their piglets vaccinated and a third group were used as control. The serum titres of the sows were low, not higher than 1:100 before vaccination. A double vaccination of the pregnant sows induced the piglets to produce antibodies in a sufficiently high titre during the first 7 weeks of life. Vaccination only against Bordetella bronchiseptica did not protect the piglets against AR. Piglets of the vaccinated sows showed two types of titre progress. It is not recommended to vaccinate the piglets only. The rapid plate agglutination was found extremely useful for the early diagnosis of Bordetella bronchiseptica infection.

Agglutination Tests↗