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At least 91 records · Page 5Linked to original sources
PubMed1990

Screening pig herds for toxigenic Pasteurella multocida and turbinate damage in a health scheme for atrophic rhinitis.

The Pig Health Control Association launched a health scheme for atrophic rhinitis in 1978. For several years pig herds were monitored by scoring the degree of turbinate damage and by clinical inspections. When laboratory facilities became available for detecting toxigenic Pasteurella multocida, nasal swabs were taken from pigs in Association herds during 1988 and 1989 to determine whether the organism was present. Sows were screened routinely and in the worst affected herds, sucklers and weaners were also swabbed. In 12 of 19 herds with consistently low snout scores toxigenic P multocida were not isolated, and in 15 herds which developed higher snout scores with time toxigenic P multocida were also not found. Eleven herds had never been listed by the Association, either because their snout scores were consistently high or because they had received importations of stock from herds with high snout scores; of six of these herds with the most persistently high snout scores five showed varying degrees of the clinical signs of atrophic rhinitis, but none of the six showed evidence of infection with toxigenic P multocida, and the organism was not found in the other five herds in the group. There seems to be an overlap between the clinical and gross pathological signs of atrophic rhinitis seen in some herds not infected with toxigenic P multocida and the mild and spasmodic signs of atrophic rhinitis seen in some herds which are substantially infected with the organism.

Animals↗
PubMed2000

Study of surfactant level in cases of primary atrophic rhinitis.

The surfactant system of the nose was examined biochemically in control cases and compared to cases of primary atrophic rhinitis. The study group included 25 cases with primary atrophic rhinitis compared to 10 normal volunteers. Biochemical analysis of the nasal aspirate in these cases revealed the presence of phospholipids constituting surfactant with phosphatidylcholine constituting 75.35 per cent of the total phospholipids. Biochemical analysis of the nasal aspirate in cases with primary atrophic rhinitis revealed a significant decrease in the total phospholipids compared to normal cases and also a significant change in the phospholipid profile. Thus significant biochemical changes in the surfactant system of the nose is an evident and early finding in cases of primary atrophic rhinitis. This suggests a possible role for surfactant deficiency in the aetiopathogenesis of cases of primary atrophic rhinitis.

Case-Control Studies↗
PubMed1988

Reopening of the closed nostril in atrophic rhinitis.

Closure of the nostril in atrophic rhinitis is a simple operation. Opening the obturated nose by excising the obturator membrane very often causes stenosis. A new and effective method for opening the nostrils, by means of flaps, is suggested.

Adult↗
PubMed1980

[Some aspects of the study of atrophic rhinitis in pigs (author's transl)].

Atrophic rhinitis is the most dreaded nasal inflammatory lesion described in pigs. Experimental studies showed that this form of rhinitis may be induced by inoculation of the bacterial species Bordetella bronchiseptica (BB) and/or Pasteurella multocida (PM). It is apparent from studies on AR in the Central Veterinary Institute during the past few years, that these species of bacterium may be classified into AR-pathogenic and AR-non-pathogenic micro-organisms. The significance of these findings in the prevention and control the disease is discussed. Investigations on the differences in pathogenicity between the strains of BB and PM isolate showed that 152 out of 157 BB isolates were AR-pathogenic (97%). Of 776 PM isolates studied, 396 were found to be AR-pathogenic. Thirty-six isolates were classified as doubtful.

Animals↗
PubMed1978

Porcine atrophic rhinitis: a model for studying nasal physiology and pathophysiology.

Porcine infectious atrophic rhinitis is a disease of swine which ought to be of considerable interest to rhinologists. We have reviewed some aspects of human atrophic rhinitis, and some aspects of etiology incidence, pathology and physiology of porcine infectious atrophic rhinitis. Swine with this nasal problem fail rather dramatically, to gain as much weight as unaffected animals. We have speculated on several reasons for this including altered nasal physiology and trigeminal reflexes and reduced olfaction. Photographs of infected pigs are included.

Animals↗
PubMed1984

[Methods of diagnosing infectious atrophic rhinitis].

Prevailing is the opinion that the infectious character of atrophic rhinitis is due to the causative agents isolated-- Bact . pseudomonas aeruginosa, Borditella bronchiseptica, and Mycoplasma. Using these either alone or in a mixed infection a successful reproduction of the disease was accomplished in 10-day-old pigs, which demonstrated its infectious character. It was found that most susceptible were pigs at the age of up to 30 days. The symptoms of the disease were dependent on the acute or chronic manifestation of atrophic rhinitis. The morphologic changes were mainly confined to the septum nasi, the conchae, and os cribriformis . Pathogenicity was tested on albino mice, guinea pigs, and rabbits, and diagnosing was effected with test animals through rentgenography and histologic and biochemical investigations. The diagnosis was based on the results of the above-mentioned investigations as well as on the clinical and morphologic manifestation of atrophic rhinitis.

Animals↗
PubMed1984

Pneumonia and atrophic rhinitis in pigs from a test station--a follow-up study.

Pneumonia and atrophic rhinitis were studied for the second consecutive year in pigs at the same test station. Pneumonia was found to reduce mean daily gain by 3.3% for every 10% of the pig's lungs that had lesions. Atrophic rhinitis did not affect mean daily gain. There was no association between the development of atrophic rhinitis and the development of pneumonia. Pigs that were vaccinated with a Bordetella bronchiseptica bacterin did not have turbinate atrophy scores or mean daily gains different from those in pigs that were not vaccinated. Yorkshire and Hampshire pigs had higher prevalences and severity of pneumonia and atrophic rhinitis, compared with pigs of other breeds.

Animals↗
PubMed1976

[Follow-up of occurrence of protozoa in the nasal cavity of pigs in relation to atrophic rhinitis].

Ninety-five pigs, twelve suffering from atrophic rhinitis, were examined for the presence of protozoans in their nasal cavity. Tritrichomonas suis was isolated only in a single case in a diseased boar representing 1.09% of the set. Amoebae of the Vahlkampfia genus were detected in two pigs (2.1%). The axenic cultures of the two protozoans isolated from the pigs were not pathogenic to laboratory animals. No etiological relation of Tritochomonas suis to atrophic rhinitis was demonstrated.

Animals↗
PubMed1980

Primary atrophic rhinitis: a scanning electron microscopic (SEM) study.

The surface features of atrophic rhinitis are shown and it is suggested that these explain the majority of symptoms. It seems clear that any lesion preventing the formation or maturation of large numbers of motile cilia, or the production of mucus capable of forming confluent sheets suitable for continuous propulsion, may cause atrophic rhinitis. In both familial and idiopathic forms of the disease, both abnormalities are present. It would be most interesting to know the ultrastructure of the cilia in transverse section of this condition. Transverse electron microscopic studies in Retinitis Pigmentosa, Usher's syndrome and Kartagener's syndrome now becoming known as the low cilia motility diseases show clearly the primary lesions in the micro-tubules and dynein arms of the cilia. A similar transmission electron microscopic study in atrophic rhinitis may show the fundamental cilial lesions. Surgical closure of the nasal passages has much to offer the patient with severe symptoms as the clinical features of the disease improve with the increasing normal micro-anatomical features demonstrated in this paper as a result of closure. This improvement in structure is not in all cases sufficient to fulfil the above criteria so a complete cure is improbable in the majority of cases.

Adolescent↗