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The group A beta-haemolytic streptococcus is known to be the aetiologic agent in acute rheumatic fever, but the exact pathogenesis remains obscure. A review of the histopathology of the Aschoff body suggests that the cardiac pathology is a granulomatous hypersensitivity reaction. However the strepto...
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| Format: | Thesis |
| Language: | English |
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Department of Paediatrics and Child Health
2018
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| _version_ | 1867613202938855424 |
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| access_status_str | Open Access |
| author | Sprenger, Kenneth John |
| author2 | Beatty, David William |
| author_browse | Beatty, David William Sprenger, Kenneth John |
| author_facet | Beatty, David William Sprenger, Kenneth John |
| author_sort | Sprenger, Kenneth John |
| collection | Thesis |
| description | The group A beta-haemolytic streptococcus is known to be the aetiologic agent in acute rheumatic fever, but the exact pathogenesis remains obscure. A review of the histopathology of the Aschoff body suggests that the cardiac pathology is a granulomatous hypersensitivity reaction. However the streptococcus has not been found in the lesions, and the agent responsible for the granuloma has not yet been identified. Circulating immune complexes have previously been measured in some children with acute rheumatic fever. The normal or raised complement components measured by some workers in acute rheumatic fever suggests that the immune complexes may not be complement fixing. Considering that the usual assays for measuring immune complexes depend on complement fixation, the failure of the immune complexes to fix complement might produce false negative results. A physical, non-complement fixing assay (polyethylene glycol precipitation - PEG), was therefore used to measure circulating immune complexes. Results were expressed as total IgG precipitated (g/L), or as a percentage of serum IgG. Immune complexes were also measured by two complement dependent assays, a Clq binding assay (ClqBA), and conglutinin binding assay (CBA). Complexes were assayed in 15 children with acute rheumatic carditis (ARC), 11 with non-active, chronic rheumatic heart disease (CRHD), 13 with acute poststreptococcal glomerulonephritis (APSGN), and 15 normal children and adults (NORMAL). Total haemolytic complement, complement components as well as the complement breakdown product C3d, were measured. |
| format | Thesis |
| id | oai:open.uct.ac.za:11427/27055 |
| institution | University of Cape Town (South Africa) |
| language | eng |
| last_indexed | 2026-06-10T12:32:24.523Z |
| license_str | Not specified — see source repository |
| provenance_str_mv | Harvested via OAI-PMH from UCTD — University of Cape Town Open Access Repository |
| publishDate | 2018 |
| publishDateRange | 2018 |
| publishDateSort | 2018 |
| publisher | Department of Paediatrics and Child Health |
| publisherStr | Department of Paediatrics and Child Health |
| record_format | dspace |
| source_str | UCTD — University of Cape Town Open Access Repository |
| spelling | oai:open.uct.ac.za:11427/27055 Circulating immune complexes in acute rheumatic carditis Sprenger, Kenneth John Beatty, David William Antigen-Antibody Complex - immunology - in infancy and childhood Rheumatic Fever - etiology - in infancy and childhood Rheumatic Heart Disease - immunology - in infancy and childhood Immune Complex Di The group A beta-haemolytic streptococcus is known to be the aetiologic agent in acute rheumatic fever, but the exact pathogenesis remains obscure. A review of the histopathology of the Aschoff body suggests that the cardiac pathology is a granulomatous hypersensitivity reaction. However the streptococcus has not been found in the lesions, and the agent responsible for the granuloma has not yet been identified. Circulating immune complexes have previously been measured in some children with acute rheumatic fever. The normal or raised complement components measured by some workers in acute rheumatic fever suggests that the immune complexes may not be complement fixing. Considering that the usual assays for measuring immune complexes depend on complement fixation, the failure of the immune complexes to fix complement might produce false negative results. A physical, non-complement fixing assay (polyethylene glycol precipitation - PEG), was therefore used to measure circulating immune complexes. Results were expressed as total IgG precipitated (g/L), or as a percentage of serum IgG. Immune complexes were also measured by two complement dependent assays, a Clq binding assay (ClqBA), and conglutinin binding assay (CBA). Complexes were assayed in 15 children with acute rheumatic carditis (ARC), 11 with non-active, chronic rheumatic heart disease (CRHD), 13 with acute poststreptococcal glomerulonephritis (APSGN), and 15 normal children and adults (NORMAL). Total haemolytic complement, complement components as well as the complement breakdown product C3d, were measured. 2018-01-29T07:15:15Z 2018-01-29T07:15:15Z 1995 Doctoral Thesis Doctoral MD http://hdl.handle.net/11427/27055 eng application/pdf Department of Paediatrics and Child Health Faculty of Health Sciences University of Cape Town |
| spellingShingle | Antigen-Antibody Complex - immunology - in infancy and childhood Rheumatic Fever - etiology - in infancy and childhood Rheumatic Heart Disease - immunology - in infancy and childhood Immune Complex Di Sprenger, Kenneth John Circulating immune complexes in acute rheumatic carditis |
| thesis_degree_str | Doctoral |
| title | Circulating immune complexes in acute rheumatic carditis |
| title_full | Circulating immune complexes in acute rheumatic carditis |
| title_fullStr | Circulating immune complexes in acute rheumatic carditis |
| title_full_unstemmed | Circulating immune complexes in acute rheumatic carditis |
| title_short | Circulating immune complexes in acute rheumatic carditis |
| title_sort | circulating immune complexes in acute rheumatic carditis |
| topic | Antigen-Antibody Complex - immunology - in infancy and childhood Rheumatic Fever - etiology - in infancy and childhood Rheumatic Heart Disease - immunology - in infancy and childhood Immune Complex Di |
| url | http://hdl.handle.net/11427/27055 |
| work_keys_str_mv | AT sprengerkennethjohn circulatingimmunecomplexesinacuterheumaticcarditis |