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Medline ® Abstracts for References 4,14-17

of 'Transverse myelitis'

4
TI
Diagnosis and management of acute myelopathies.
AU
Kaplin AI, Krishnan C, Deshpande DM, Pardo CA, Kerr DA
SO
Neurologist. 2005;11(1):2.
 
BACKGROUND: Acute myelopathies represent a heterogeneous group of disorders with distinct etiologies, clinical and radiologic features, and prognoses. Transverse myelitis (TM) is a prototype member of this group in which an immune-mediated process causes neural injury to the spinal cord, resulting in varying degrees of weakness, sensory alterations, and autonomic dysfunction. TM may exist as part of a multifocal CNS disease (eg, MS), multisystemic disease (eg, systemic lupus erythematosus), or as an isolated, idiopathic entity.
REVIEW SUMMARY: In this article, we summarize recent classification and diagnostic schemes, which provide a framework for the diagnosis and management of patients with acute myelopathy. Additionally, we review the state of current knowledge about the epidemiology, natural history, immunopathogenesis, and treatment strategies for patients with TM.
CONCLUSIONS: Our understanding of the classification, diagnosis, pathogenesis, and treatment of TM has recently begun to expand dramatically. With more rigorous criteria applied to distinguish acute myelopathies and with an emerging understanding of immunopathogenic events that underlie TM, it may now be possible to effectively initiate treatments in many of these disorders. Through the investigation of TM, we are also gaining a broader appreciation of the mechanisms that lead to autoimmune neurologic diseases in general.
AD
Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Osler 320, 600 N. Wolfe Street, Baltimore, MD 21287, USA. akaplin@jhmi.edu
PMID
14
TI
Staphylococcal enterotoxins B and C. Structural requirements for superantigenic and entertoxigenic activities.
AU
Bohach GA
SO
Prep Biochem Biotechnol. 1997;27(2-3):79.
 
AD
University of Idaho, Moscow, USA.
PMID
15
TI
Staphylococcal and streptococcal pyrogenic toxins involved in toxic shock syndrome and related illnesses.
AU
Bohach GA, Fast DJ, Nelson RD, Schlievert PM
SO
Crit Rev Microbiol. 1990;17(4):251.
 
Toxic-shock syndrome (TSS) is an acute onset, multiorgan illness which resembles severe scarlet fever. The illness is caused by Staphylococcus aureus strains that express TSS toxin-1 (TSST-1), enterotoxin B, or enterotoxin C. TSST-1 is associated with menstrual TSS and approximately one-half of nonmenstrual cases; the other two toxins cause nonmenstrual cases, 47% and 3%, respectively. The three toxins are expressed in culture media under similar environmental conditions. These conditions may explain the association of certain tampons with menstrual TSS. Biochemically, the toxins are all relatively low molecular weight and fairly heat and protease stable. Enterotoxins B and C, share nearly 50% sequence homology with streptococcal scarlet fever toxin A; they share no homology with TSST-1 despite sharing numerous biological properties. Numerous animal models for development of TSS have suggested mechanisms of toxin action, though the exact molecular action is not known. The toxins are all potent pyrogens, induce T lymphocyte proliferation, requiring interleukin 1 release from macrophages, suppress immunoglobulin production, enhance endotoxin shock, and enhance hypersensitivity skin reactions. The genetic control of the toxins has been studied and suggests the exotoxins are variable traits. Some additional properties of TSS S. aureus which facilitate disease causation have been clarified.
AD
Department of Microbiology, University of Minnesota, Minneapolis.
PMID
16
TI
Staphylococcal enterotoxins, toxic shock syndrome toxin and streptococcal pyrogenic exotoxins: a comparative study of their molecular biology.
AU
Betley MJ, Borst DW, Regassa LB
SO
Chem Immunol. 1992;55:1.
 
AD
Department of Bacteriology, University of Wisconsin-Madison.
PMID
17
TI
Activation and clonal expansion of human myelin basic protein-reactive T cells by bacterial superantigens.
AU
Zhang J, Vandevyver C, Stinissen P, Mertens N, van den Berg-Loonen E, Raus J
SO
J Autoimmun. 1995;8(4):615.
 
Autoreactive T cells specific for myelin basic protein (MBP) are part of the normal T cell repertoire and are present both in patients with multiple sclerosis (MS) and healthy individuals. There is evidence suggesting in vivo activation and persistent clonal expansion of MBP-reactive T cells in MS. This study was undertaken to investigate the potential role of bacterial superantigens (SA) in the activation of MBP-reactive T cells. Twenty-seven MBP-reactive T cell clones generated from 10 MS patients and one normal individual were examined for reactivity to SA, in association with their T cell receptor V beta gene usage. The majority of the clones responded to at least one of the SA tested, staphylococcal enterotoxins (SEA and SEB) and toxic shock syndrome toxin-1 (TSST-1). The clones reactive to SEA and SEB expressed various V beta genes while T cell reactivity to TSST-1 correlated with the V beta 2 expression. Furthermore, circulating MBP-reactive T cells could be expanded from lymphocyte cultures primarily exposed to respective SA in more than 50% of MS patients and normal individuals tested. However, activation and expansion of circulating MBP-reactive T cells by SA was not directly associated with the disease. This study lends support to the potential role of SA in the activation of MBP-reactive T cells and suggests that an altered regulatory mechanism may account for further expansion and persistence of MBP-reactive T cells in MS.
AD
Multiple Sclerosis Research and Immunology Unit, Dr. Willems Instituut, Diepenbeek, Belgium.
PMID