Acute Encephalomyelitis: Extending the Neurological Manifestations of Acute Rheumatic Fever?

Munn, Robert; Farrell, Keith R.; Cimolai, Nevio

doi:10.1055/s-2008-1071340

Cited by 10 publications

(3 citation statements)

References 6 publications

(7 reference statements)

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“…1,2,22 Different species of the genus Streptococcus have been associated with meningitis, brain abscess, and encephalitis in humans. [26][27][28] In gerbils, recent experimental studies provide strong evidence of bacterial passage from the middle ear to the inner ear. Apart from direct infection (e.g., meningitis) or postinfectious, presumably immune-mediated reactions such as Sydenham's chorea and pediatric obsessive-compulsive disorders, 25 meningoencephalitis (or myeloencephalitis) complicating S. pyogenes infection has only been reported thrice in humans.…”

Section: Discussionmentioning

confidence: 99%

Encephalomyelitis-associated antimyelin autoreactivity induced by streptococcal exotoxins

Jorens¹,

VanderBorght²,

Ceulemans³

et al. 2000

Neurology

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Section: Discussionmentioning

confidence: 99%

Encephalomyelitis-associated antimyelin autoreactivity induced by streptococcal exotoxins

Jorens¹,

VanderBorght²,

Ceulemans³

et al. 2000

Neurology

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“…Various viral or bacterial pathogens have been associated with ADEM,4, 5 although frequently the preceding infection cannot be identified. Although Group A β hemolytic streptococcus (GABHS) is a recognized cause of autoimmune central nervous system (CNS) disease, ADEM has only rarely been reported after GABHS infection 1, 6, 7…”

mentioning

confidence: 99%

Poststreptococcal acute disseminated encephalomyelitis with basal ganglia involvement and auto‐reactive antibasal ganglia antibodies

Dale

Church

Cardoso

et al. 2001

Annals of Neurology

174

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Antibasal ganglia antibodies (ABGA) are associated with Sydenham's chorea and pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections. We present 10 patients with acute disseminated encephalomyelitis (ADEM) associated with Group A beta hemolytic streptococcal infection. The clinical phenotype was novel, with 50% having a dystonic extrapyramidal movement disorder, and 70% a behavioral syndrome. None of the patients had rheumatic fever or Sydenham's chorea. Enzyme-linked immunosorbent assay, Western immunoblotting, and immunohistochemistry were used to detect ABGA. Neurological (n = 40) and streptococcal (n = 40) controls were used for comparison. Enzyme-linked immunosorbent assay results showed significantly elevated ABGA in the patients with poststreptococcal ADEM. Western immunoblotting demonstrated ABGA reactivity to three dominant protein bands of 60, 67, or 80 kDa; a finding not reproduced in controls. Fluorescent immunohistochemistry demonstrated specific binding to large striatal neurones, which was not seen in controls. Streptococcal serology was also significantly elevated in the poststreptococcal ADEM group compared with neurological controls. Magnetic resonance imaging studies showed hyperintense basal ganglia in 80% of patients with poststreptococcal ADEM, compared to 18% of patients with nonstreptococcal ADEM. These findings support a new subgroup of postinfectious autoimmune inflammatory disorders associated with Group A beta hemolytic streptococcus, abnormal basal ganglia imaging, and elevated ABGA.

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“…Not all patients present with exactly the same manifestations or symptomatic degree of any such manifestations. If one were simply to acknowledge such autoimmune phenomena as originating post-S. pyogenes infection, there would be a better understanding of how such immune dysregulation could include variations on the theme such as acute encephalomyelitis or isolated post-infectious arthropathy [9,10]. An extension of this controversy is further exemplified by the broadening discoveries of other associated neurological diseases that extend beyond the scope of what was more formally diagnosed as Sydenham's chorea [11,12].…”

Section: The Perennial Problem With Syndromic Diagnosesmentioning

confidence: 99%

Mast Cell Biology and Linkages for Non-clonal Mast Cell Activation and Autoimmune/Inflammatory Syndrome Induced by Adjuvants

Cimolai

2020

SN Compr. Clin. Med.

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Non-clonal mast cell activation disorder (syndrome) (NC-MCAD) and autoimmune/inflammatory syndrome induced by adjuvants (ASIA) are complex syndromic and spectral clinical entities which have contemporaneously garnered considerable attention and rightfully so. NC-MCAD presents with a predominantly allergic profile, and causative clinical variables may or may not be identified. Manifest NC-MCAD illnesses can be complex and involve several organ systems. Such diversity may be in part explained by the ubiquity and plasticity of the mast cell. ASIA, due to its broad definition, continues to expand as a clinical entity, especially with the greater recognition of what might constitute adjuvancy. Such diversity has the potential to overly stretch the boundaries for scientific investigation. For both NC-MCAD and ASIA, the inciting molecular mechanisms require elucidation. Future research would benefit from greater precision for clinical diagnosis and risk factor identification, and the latter would be potentially facilitated by the discovery of reliable laboratory markers. Some patients with ASIA may present with clinical features that may be identified as NC-MCAD. This review examines the potential spectral nexus of NC-MCAD and ASIA and considers the role of the mast cell in such a possible interface.

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Acute Encephalomyelitis: Extending the Neurological Manifestations of Acute Rheumatic Fever?

Cited by 10 publications

References 6 publications

Encephalomyelitis-associated antimyelin autoreactivity induced by streptococcal exotoxins

Encephalomyelitis-associated antimyelin autoreactivity induced by streptococcal exotoxins

Poststreptococcal acute disseminated encephalomyelitis with basal ganglia involvement and auto‐reactive antibasal ganglia antibodies

Mast Cell Biology and Linkages for Non-clonal Mast Cell Activation and Autoimmune/Inflammatory Syndrome Induced by Adjuvants

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