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![Pigeon breeder's disease: A study of the clinical, immunological and pulmonary function abnormalities in the pulmonary extrinsic allergic alveolitis which occurs amongst pigeon fanciers için kapak resmi Pigeon breeder's disease: A study of the clinical, immunological and pulmonary function abnormalities in the pulmonary extrinsic allergic alveolitis which occurs amongst pigeon fanciers için kapak resmi](/client/assets/d79c3e4af2b6d196/ctx/images/no_image.png)
Pigeon breeder's disease: A study of the clinical, immunological and pulmonary function abnormalities in the pulmonary extrinsic allergic alveolitis which occurs amongst pigeon fanciers
Başlık:
Pigeon breeder's disease: A study of the clinical, immunological and pulmonary function abnormalities in the pulmonary extrinsic allergic alveolitis which occurs amongst pigeon fanciers
Yazar:
Boyd, Gavin, author.
ISBN:
9780438058170
Yazar Ek Girişi:
Fiziksel Tanımlama:
1 electronic resource (239 pages)
Genel Not:
Source: Dissertation Abstracts International, Volume: 76-08C.
Advisors: Francis Moran.
Özet:
This thesis examines the relationship between immunological and clinical evidence of hypersensitivity lung disease in Pigeon Breeders. Clinical material was collected in a field study of a representative sample of pigeon breeders and supplemented by acute cases which presented at the Glasgow Royal Infirmary. A sensitive radioimmunoassay technique was developed to enable immunological responses following exposure to pigeon protein to be quantified and to avoid the occurrence of non-specific reactions encountered with precipitin tests. This was applied to sera from the field study, pulmonary function studies in symptomatic cases, serial investigations of patients during recovery and during the planned challenge in a known sensitised individual. The field study clarified the frequency with which clinical symptoms occurred and the relationship between these and exposure to antigen. A personal interview technique in conjunction with questionnaires on respiratory symptoms was more effective than questionnaires used alone for eliciting minor but relevant allergic symptoms following exposure to pigeons and their incidence was higher than has been reported elsewhere. In addition to the characteristic acute presentation, symptoms of a more insidious nature occurred frequently so that the clinician must be aware of this alternative syndrome in subjects who are exposed to organic antigens. Most individuals regularly handling pigeons were sensitised to pigeon protein and the antibody levels extended over a wide range. Those with higher levels were at greater risk of developing symptoms than those with lower levels. Positive precipitin reactions occurred in those with the greater amounts of antibody but symptoms of Pigeon Breeder's Disease were present in some individuals whose antibody levels were not high enough to be detected with precipitin tests. Smokers were found to have significantly lower levels of antibody. The level of circulating antibody appeared to be determined by the individual's own immunological responsiveness rather than by the duration or intensity of exposure to antigen. Those who responded to inhalation of pigeon protein by the production of large amounts of antibody, probably possess immunological systems capable of responding more vigorously to antigen in general. The classification of Pigeon Breeder's Disease into 3 Grades of severity of symptoms established the relationship between symptoms, functional changes and antibody levels which did not emerge from previous reports. Severe symptoms were associated with the highest levels of antibody and marked impairment of pulmonary function. When they were less intense, antibody was significantly lower and pulmonary function, although abnormal, was significantly less so than in those incapacitated by the disease. Patients with acute symptoms had restrictive ventilatory defects with hypoxaemia, chronic hyperventilation and abnormalities of gas exchange. The Alveolar-arterial oxygen tension difference and the physiological dead space/tidal volume ratio were shown to be the most sensitive indicators of abnormal function. Antibody levels were shown to fall following challenge with antigen indicating that antibody was utilised during the initial phase of the immunological reaction although no concomitant utilisation of complement was detected. This, together with the relationships demonstrated between antibody levels and clinical symptoms, offered further support to the importance of Type III allergic reactions in this condition. The study of a patient with acute pulmonary disease who developed a transient pericarditis and a renal lesion consistent with an immune disorder, suggested that circulating immune complexes are present in this disease and that, occasionally, extra-pulmonary pathology may occur. Antibody levels are constant in individuals regularly exposed to pigeons. The soluble protein antigen produced a poorly sustained antibody response and removal from antigen resulted in a rapid decline in circulating levels. When exposure continued in previously symptomatic subjects antibody remained elevated despite satisfactory clinical response to steroid therapy. Other workers have demonstrated abnormal complement activity and increased T-cell sensitivity in symptomatic subjects. It is likely that these factors may modulate the humoral antibody response to produce the high levels of antibody that are recorded in the acute disease. The amount of antibody will influence the number of immune complexes that are formed. This will affect the extent of the pulmonary damage which results and, therefore, the degree of pulmonary dysfunction. This study of Pigeon Breeder's Disease strongly suggests that no single example of "extrinsic allergic alveolitis" is a valid model for all such conditions. It has been demonstrated that the dynamics of the immunological responses are complex and that several different mechanisms are involved. However, situations of antigen exposure can be clearly identified in a large number of individuals and the investigation of Pigeon Breeder's Disease provides an appropriate basis for the further elucidation of other syndromes of this general type.
Notlar:
School code: 0547
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Yer Numarası | Demirbaş Numarası | Shelf Location | Lokasyon / Statüsü / İade Tarihi |
---|---|---|---|
XX(684655.1) | 684655-1001 | Proquest E-Tez Koleksiyonu | Arıyor... |
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