Haemolytic Streptococcal Infections and Acute Rheumatism

Green, Cecil A.

doi:10.1136/ard.3.1.4

Cited by 22 publications

(7 citation statements)

References 56 publications

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“…Epidemiological and clinical studies have clearly established that antecedent streptococcal infection is a prerequisite to rheumatic fever (92,165,205,206,248). Widespread involvement of connective tissue structures, including endocardium, heart valves, myocardium, pericardium, lung and pleura, tendons, joints, subcutaneous tissue, and finally brain function, is supported by the clinical picture of the disease, as well as by numerous pathological studies.…”

Section: Possible Role Of Immunological Mechanisms In the Diseasementioning

confidence: 99%

Streptococcal Rheumatic Carditis.

Unny¹,

Middlebrooks²

1983

The Pediatric Infectious Disease Journal

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Section: Possible Role Of Immunological Mechanisms In the Diseasementioning

confidence: 99%

Streptococcal Rheumatic Carditis.

Unny¹,

Middlebrooks²

1983

The Pediatric Infectious Disease Journal

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“…Experiments similar to those described in animals were also carried out in man by several investigators (7)(8)(9). In using skin tests as an index of delayed sensitivity to streptococcal products, the general consensus of the workers was that hypersensitivity to streptococci and their products was a common occurrence in man and increased in intensity, depending on the age of the individual tested.…”

Section: The Journal Of Clinical Investigation Volume 54 August 1974*mentioning

confidence: 99%

“…In using skin tests as an index of delayed sensitivity to streptococcal products, the general consensus of the workers was that hypersensitivity to streptococci and their products was a common occurrence in man and increased in intensity, depending on the age of the individual tested. In general, these reactions were more intense in rheumatic subjects than in nonrheumatic controls (7,8), the reactivity was particularly intense with extracts of hemolytic streptococci as compared to nonhemolytic streptococcal strains (8), and the greatest number of positive reactions were obtained with autogenous streptococci, suggesting some type specificity to the reaction (10). In this connection, Beachey, Alberti, and Stollerman (11) and Pachman and Fox (12) have recently observed that immunization of guinea pigs with partially purified preparations of different M proteins resulted in specific delayed hypersensitivity (skin tests and macrophage inhibition tests) to the immunizing antigen.…”

Section: The Journal Of Clinical Investigation Volume 54 August 1974*mentioning

confidence: 99%

Cellular Reactivity Studies to Streptococcal Antigens MIGRATION INHIBITION STUDIES IN PATIENTS WITH STREPTOCOCCAL INFECTIONS AND REHEUMATIC FEVER

Read¹,

Fischetti²,

Utermohlen³

et al. 1974

J. Clin. Invest.

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A B S T R A C T The question of whether hypersensitivity to streptococcal antigens plays a role in the pathogenesis of the nonsuppurative sequelae of streptococcal infections remains at present unclear. As a first step in the approach to this question, the degree of cellular reactivity of peripheral blood leucocytes to streptococcal antigens was investigated in a number of rheumatic fever patients, patients with uncomplicated streptococcal infections, as well as normal healthy subjects.Using the in vitro technique for the inhibition of capillary migration of peripheral blood leucocytes as an index of the degree of sensitivity to streptococcal antigens, the results indicate that patients with acute rheumatic fever exhibit an exaggerated cellular reactivity to these antigens and in particular to streptococcal cell membrane antigens. This abnormal response to streptococcal membrane antigens appears to persist in rheumatic subjects for at least 5 yr after the initial 'attack of rheumatic fever. Only Group A streptococcal membrane antigens elicited this unusual response in rheumatic subjects, since the cellular reactivity to Group C and D streptococcal membranes was the same in all groups. Patients with evidence of valvular disease exhibited the same degree of cellular reactivity to these antigens as did patients without clinical evidence of rheumatic heart disease.The nature of the antigens responsible for the observed cellular response remains unknown. Enzymatic treatment of streptococcal cell walls and membranes designed to remove type-specific M proteins did not alter the observed cellular reactivity to the streptococcal antigens. The finding that an abnormal cellular response to certain streptococcal antigens is present only in rheuReceived for publication 17 July 1972 and in revised form 14 January 1974. matic patients suggests that cell-mediated factors may play an important role in the disease process. INTRODUCTICNThe question of whether hypersensitivity to hemolytic streptococci and their products might play a role in the pathogenesis of the nonsuppurative sequelae of streptococcal infections has been the subject of investigation for many years. Starting with the early work of Swift and Derick and Derick, Hitchcock, and Swift in animals (1-3), it was apparent that delayed hypersensitivity to streptococci behaved in a manner similar to that observed for tuberculin sensitivity (4). Initiation of sensitivity by prolonged focal contact between the intact bacteria and tissues of the host, inability to passively transfer streptococcal-delayed hypersensitivity with serum alone, and the lack of correlation between circulating antibodies to streptococcal products and delayed allergy were all characteristics of the streptococcal hypersensitive state (5). Apropos of these studies, several intriguing observations concerning the streptococcal hypersensitive state were made. First, repeated small inoculations of heat-killed streptococci were more effective in inducing the hypersensitive state than a single inoculation of ...

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“…Indeed, the basic cellular constituents of rheumatic subcutaneous nodules, cardiac Aschoff bodies, or acute valvular lesions are often characterized by a predomiReceived for publication 1 November 1974 and in revised form 13 January 1975. nance of lymphoid elements. The present study was designed to examine possible alterations in peripheral blood lymphocytes during the course of active rheumatic fever.…”

Section: Introductionmentioning

confidence: 99%

“…Particular attention was directed at acute and serial studies of lymphocyte cell surface markers in this disorder. For some time it has been held as an established clinical principle that acute rheumatic fever is somehow related to the host immune response to the streptococcus (1)(2)(3)(4)(5)(6)(7). Whether this response is principally mediated by humoral immunity and thus the products of bone marrow-derived lymphocytes (Bcells)1 (8,9) or whether cell-mediated mechanisms operating through thymus-derived lymphocytes (T-cells) (10)(11)(12) constitute the most significant aspect of the rheumatic inflammatory response still remains to be determined.…”

Section: Introductionmentioning

confidence: 99%