Septoplasty in unilateral atrophic rhinitis with deviated nasal septum.
Eight cases of atrophic rhinitis with DNS towards the opposite side were treated by septoplasty with reversal of the DNS. All the cases showed satisfactory results.
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Eight cases of atrophic rhinitis with DNS towards the opposite side were treated by septoplasty with reversal of the DNS. All the cases showed satisfactory results.
Atrophic rhinitis was diagnosed in a 10-month-old heifer with the assistance of computed tomography. The aetiology of the condition in cattle is uncertain and the clinical disease may be overlooked owing to the lack of signs such as the shortening or deformity of the snout observed in pigs.
Among many theories about the etiology of atrophic rhinitis with ozena, a reduced mucosal blood flow has been suggested, possibly caused by 'sympathetic spasm'. The nasal mucosal blood flow has been investigated in 6 patients with this disease before and after topical administration of a sympathomimetic drug. No difference in action compared to healthy subjects was found. Other pathophysiological mechanisms must be searched for.
Alterations in the nasal mucous layer of atrophic rhinitis "Ozaena" patients have been investigated. The vast majority (99%) of these patients were women. Morphological findings in healthy nasal mucosa demonstrated the different functional stages of the glandular tissue cells with the healthy epithelium. On the other hand, nasal mucosal material taken from the patients displayed prominent epithelial deterioration, decrease in and loss of cilia, increase in goblet cells with squamous epithelial metaplasia. A decrease in secretory granules and membrane deterioration in the apical region of the secretory cells was also clearly visible. It is possible to postulate that the ultrastructural changes seen in the secretory and storage cycles of glandular tissue of the nasal mucosa from patients seem to arise as a reaction to the superficial epithelial deterioration of the nasal mucosa together with the resulting deterioration of physiological conditions.
The aetiology of primary atrophic rhinitis (AR) is still unclear. Based on the sinus infection theories, endoscopic sinus surgery (ESS) was applied to treat AR. ESS was performed on 14 patients following Stammberger's techniques along with middle turbinectomy. Patients were evaluated using clinical symptoms, radiological sinus images, saccharine time tests, bacterial cultures and mucosal ultrastructures, before and 2 years after ESS. Three patients had good recoveries, 6 had partial recoveries and another 5 had persistent disease. Good recovery patients showed clear nasal cavities and mucociliary transport system normalisation. Patients possess in meagre infectious signs or crusting extending to their nasopharynx had poor outcomes. Patients with evidence of obvious infections (cloudy sinus images, mucopus presence in the sinuses and positive culture for Klebsiella ozaenae) had good recoveries following ESS. Candidate selection is critical for the success of ESS treatment in AR. Although further clinical trials are required to prove this strategy.
It is proposed that primary atrophic rhinitis belongs to a group of conditions under the heading 'Reflex Sympathetic Distrophy Syndrome'. This leads to decalcification of the turbinals, as in Sudeck's atrophy. Collapse of the decalcified turbinals is brought about by the impact of the inspiratory stream, and this is followed by atrophic changes. Based on this hypothesis, a new operation ('Vestibuloplasty') has been devised in order to direct the stream away from the turbinals and to dissipate the force of the stream so that its impact on the turbinals is minimized. Following this operation, 92 per cent of the cases have benefitted; this is comparable to the result following Young's or a modified Young's operation. After vestibuloplasty the patient can breathe through the nose and clean the nose as normal persons do; a second-stage procedure for reopening the nostril is not necessary and the chances of recurrence are negligible as compared to those following Young's operation.
Vaccination against progressive atrophic rhinitis using a purified recombinant derivative of the Pasteurella multocida toxin (PMT), was carried out. Ten pregnant gilts were vaccinated twice with the nontoxic derivative (dO) which apart from a lack of 121 amino acids had an amino acid sequence identical to PMT, while seven gilts were vaccinated with a purified, formaldehyde treated, native PMT and ten gilts served as non-vaccinated controls. The resulting piglets were inoculated intranasally with Bordetella bronchiseptica and toxigenic P. multocida. Among piglets from the nonvaccinated gilts all except one developed clinical atrophic rhinitis and 90% developed severe turbinate atrophy while only a few pigs in the vaccinated groups developed clinical or pathological signs of disease. Gilt colostra from the two vaccinated groups had similar mean anti-PMT titers and the mean titers in the offspring's sera from these groups were nearly identical throughout the study. No pigs born from unvaccinated gilts were seropositive until 8 wk of age (7 wk post-challenge) but 23% became seropositive at slaughter. The infection rate with toxigenic P. multocida in piglets and the total number of P. multocida colonies cultured from nasal swabs were significantly reduced at 5 wk and 8 wk of age in the vaccinated groups, when compared to controls. There was a significantly improved weight gain (greater than 9%) from birth to slaughter in offspring from vaccinated gilts. No significant differences in feed conversion rate or % lean meat were observed among the groups. The study showed the excellent immunoprotective properties of the nontoxic derivative of the PMT molecule.
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.
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 is a disease which manifests itself mainly by anosmia due to dryness and atrophy of the nasal mucosa. There is no specific therapy for the disease at present. In the past few years, 23 cases of atrophic rhinitis were treated mainly by deep puncture at three points in the nasal region with satisfactory results. In order to find out the functional changes of the nasal mucosa, the mucociliary transport rate (MTR), surface temperature of the conchal mucosa, acid-base scale of nasal secretion, and volume of nasal secretion were determined before and after the treatment.
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A field trial was carried out with Nobi-Vac AR vaccine in 11 swine breeding herds. One herd suffered from severe B. bronchiseptica (BB+) rhinitis in piglets, while no clinical Atrophic Rhinitis (AR) was observed. Ten herds were described as AR problem herds, because clinical AR was observed for at least 1 year in spite of the fact that medication of sows and piglets was carried out and adequate housing and management systems were available in most herds. BB+ was isolated in 9 of these 10 farms and the AR pathogenic P. multocida (PM+) in all these farms. The trial started when piglets were born of sows which had been vaccinated 3 times. All piglets between 7 and 10 weeks old were examined clinically for AR. Nasal swabs from 20 pigs on each farm were screened bacteriologically for BB+ and PM+ every other month. A severe reoccurrence of AR was found in 2 of the 10 AR problem farms. In these 2 herds the 'all in-all out' system was not applied in farrowing and weaning houses. In the 8 other AR problem herds the percentage of pigs with AR decreased significantly below the average level of 1% per year. The percentage of pigs infected with BB+ and PM+ also decreased significantly. PM+ was significantly related to the percentage of clinical AR piglets. Seasonal effects contributed to a minor extent to the percentage of AR piglets. After 2.5 years of this trial PM+ could not be isolated during the last 12 months in six of the remaining AR problems herds. The conclusion is that Nobi-Vac AR vaccination of the sow gave protection against clinical AR in piglets on those farms (80%) which provided adequate housing and management systems.
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