The Haemolytic Streptococcus as a Factor in the Causation of Acute Rheumatism

Gibson, H. J.; Thomson, William; Stewart, D. F.

doi:10.1136/adc.8.43.57

Cited by 14 publications

(5 citation statements)

References 4 publications

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“…Possibly an even higher figure would have resulted from the autogenous endotoxin had it been possible to use it throughout. The occurrence of negative reactors was to some extent corroborative of the conclusion reached by Gibson, Thomson and Stewart (1933) that skin sensitivity could not be regarded as an indication of a special reactivity necessary for the production of rheumatic infection, but it did not detract from the possibility that part of the rheumatic syndrome is due to hypersensitivity. As an analogy, cases of tuberculosis, in both the human and bovine species, may occasionally fail to react to tuberculin despite the recognised part played by allergy in this condition.…”

supporting

confidence: 75%

“…Coburn (1931) has been able, however, to utilise this method in associating rheumatism particularly with nasopharyngeal infection due to haemolytic streptococci. Collis (1931) has corroborated this work, but Gibson, Thomson and Stewart (1933) concluded that, although positive reactors to haemolytic streptococcal endotoxin were more common in rheumatic than in control cases, skin sensitivity could not be regarded as an indication of a special reactivity necessary for the production of acute rheumatic infection. On the assumption that hypersensitivity was an important factor in the production of the rheumatic state, treatment by desensitisation has been attempted.…”

mentioning

confidence: 80%

“…Coburn (1940) has emphasised that the low antistreptolysin S response was the only exception in a number of tests which revealed streptococcal activity in rheumatism. 36 HA-MOLYTIC STREPTOCOCCAL INFECTIONS PART XI.-TiHE FORMOL-GEL REACTION AND ERYTHROUYTE SEDIMENTATION RATE iN AcUTE RHEUMATISM This part, based on the paper published in ANNALS OF THE RHEUMATIC DISEASES, 1939, 1, 180, was included as a recognition of the valuable assistance which this non-specific test afforded when attempting correlation of clinical activity with serological findings. The insidious onset of cardiac complications in certain cases of acute rheumatism may baffle the most careful observer, but the above tests served to date the recurrence of activity with few exceptions.…”

Section: Hmemolytic Streptococcal Infectionsmentioning

confidence: 99%

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Haemolytic Streptococcal Infections and Acute Rheumatism

Green¹

1942

Annals of the Rheumatic Diseases

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supporting

confidence: 75%

mentioning

confidence: 80%

Section: Hmemolytic Streptococcal Infectionsmentioning

confidence: 99%

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Haemolytic Streptococcal Infections and Acute Rheumatism

Green¹

1942

Annals of the Rheumatic Diseases

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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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