Objective: Infectious myelopathy of any stage and etiology carries the potential for significant morbidity and mortality. This article details the clinical presentation, risk factors, and key diagnostic components of infectious myelopathies with the goal of improving the recognition of these disorders and guiding subsequent management.
Latest Developments: Despite our era of advanced multimodal imaging and laboratory diagnostic technology, a causative organism often remains unidentified in suspected infectious and parainfectious myelopathy cases. To improve diagnostic capability, newer technologies such as metagenomics are being harnessed to develop diagnostic assays with a greater breadth of data from each specimen and improvements in infection identification. Conventional assays have been optimized for improved sensitivity and specificity.
Essential Points: Prompt recognition and treatment of infectious myelopathy decreases morbidity and mortality. The key diagnostic tools include serologies, CSF analysis, and imaging; however clinical presentation, epidemiologic risk factors, and history of recent illness are all vital to making the proper diagnosis because current laboratory and imaging modalities are often inconclusive. The cornerstone of recommended treatment is targeted antimicrobials with appropriate immune modulation, surgical intervention, supportive care, and interdisciplinary involvement, all of which further improve outcomes for patients with infectious myelopathy.
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http://dx.doi.org/10.1212/CON.0000000000001393 | DOI Listing |
Nat Immunol
January 2025
Institute for Immunity, Transplantation and Infection, School of Medicine, Stanford University, Stanford, CA, USA.
We performed a systems vaccinology analysis to investigate immune responses in humans to an H5N1 influenza vaccine, with and without the AS03 adjuvant, to identify factors influencing antibody response magnitude and durability. Our findings revealed a platelet and adhesion-related blood transcriptional signature on day 7 that predicted the longevity of the antibody response, suggesting a potential role for platelets in modulating antibody response durability. As platelets originate from megakaryocytes, we explored the effect of thrombopoietin (TPO)-mediated megakaryocyte activation on antibody response longevity.
View Article and Find Full Text PDFNat Immunol
January 2025
Jill Roberts Institute for Research in Inflammatory Bowel Disease, Weill Cornell Medicine, Cornell University, New York, NY, USA.
The inflammasome plays multifaceted roles in cancer, but less is known about its function during premalignancy upon initial cell transformation. We report a homeostatic function of the inflammasome in suppressing malignant transformation through Ras inhibition. We identified increased hematopoietic stem cell (HSC) proliferation within the bone marrow of inflammasome-deficient mice.
View Article and Find Full Text PDFPLoS Comput Biol
January 2025
Department of Hematology, Rheumatology and Infectious Disease, Faculty of Life Sciences, Kumamoto University, Kumamoto, Japan.
Human T-cell leukemia virus type 1 (HTLV-1) causes adult T-cell leukemia (ATL) and HTLV-1-associated myelopathy (HAM) after a long latent period in a fraction of infected individuals. These HTLV-1-infected cells typically have phenotypes similar to that of CD4+T cells, but the cell status is not well understood. To extract the inherent information of HTLV-1-infected CD4+ cells, we integratively analyzed the ATAC-seq and RNA-seq data of the infected cells.
View Article and Find Full Text PDFJ Clin Neurosci
December 2024
Department of Infectious Diseases, Okayama University Hospital, Okayama, Japan. Electronic address:
EBioMedicine
December 2024
Department of Hematology and Cell Therapy, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang province, PR China. Electronic address:
Background: Bronchiolitis obliterans syndrome (BOS) is one of the most devastating outcomes of chronic graft-versus-host disease (cGVHD) after allogeneic hematopoietic stem cell transplantation (allo-HSCT). This remains an area of unmet clinical need for optimal therapy for BOS patients partly due to the limited understanding of pathogenic mechanisms.
Methods: We collected blood samples from 22 patients with cGVHD and 11 patients without cGVHD following allo-HSCT.
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