{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,14]],"date-time":"2026-09-14T06:03:59Z","timestamp":1789365839245,"version":"build-2803163510"},"reference-count":19,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,9,14]],"date-time":"2026-09-14T00:00:00Z","timestamp":1789344000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Active central nervous system (CNS) infection can resemble acute immune polyradiculoneuropathy, and the two processes may coexist. We describe a patient with neurosyphilis, rapidly progressive paraparetic weakness, and anti-GT1a IgG detected in cerebrospinal fluid (CSF) but not serum by a qualitative line immunoblot.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Case presentation<\/jats:title>\n                    <jats:p>\n                      A 41-year-old man developed rapidly progressive paraparesis, urinary retention, and left abducens palsy. On hospital day 2, CSF opening pressure was 260 mmH\n                      <jats:sub>2<\/jats:sub>\n                      O, protein 1.56 g\/L, white-cell count 272 \u00d7 10\n                      <jats:sup>6<\/jats:sup>\n                      \/L, CSF TPPA was reactive, and CSF RPR was 1:8. Penicillin and methylprednisolone were started after the first lumbar puncture. By day 8, CSF white-cell count and protein had fallen during overlapping antimicrobial and corticosteroid treatment, but opening pressure remained 260 mmH\n                      <jats:sub>2<\/jats:sub>\n                      O and neurological deficits persisted. Paired serum-CSF testing showed marked blood-CSF barrier dysfunction (QAlb 17.4 \u00d7 10\n                      <jats:sup>-3<\/jats:sup>\n                      ), a type IV oligoclonal-band pattern, a Reiber-derived intrathecal IgM fraction of 35%, and anti-GT1a IgG detected in CSF but not serum. Day-11 electrodiagnostic testing showed reduced lower-limb motor amplitudes, preserved sensory responses, and absent F waves; a stable GBS electrophysiological subtype could not be assigned. Initial spinal MRI was normal; repeat lumbar MRI about 20 days later showed smooth enhancement along the ventral conus and cauda equina roots. IVIG was given on days 11-15; improvement was documented by day 30, and at 2 years the patient reported return to normal life and work.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Neurosyphilis can present with a paraparetic GBS-spectrum phenotype, making it difficult to determine whether syphilitic meningoradiculitis alone explains the syndrome or whether a concurrent immune polyradiculoneuropathy is also present. In this setting, blood-CSF barrier dysfunction, CSF-detected anti-GT1a IgG, and improvement after IVIG should be viewed as hypothesis-generating observations rather than proof of antibody compartmentalization, dual pathology, or treatment causality. In similar cases, longitudinal clinical follow-up, electrophysiology, imaging, and quantitatively validated paired serum-CSF immune testing are needed to distinguish a single infectious process, a concurrent immune neuropathy, and a biologically linked infection-autoimmunity process.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.3389\/fimmu.2026.1936622","type":"journal-article","created":{"date-parts":[[2026,9,14]],"date-time":"2026-09-14T05:39:09Z","timestamp":1789364349000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Case Report: Neurosyphilis with a paraparetic Guillain-Barr\u00e9-spectrum phenotype and CSF-detected anti-GT1a IgG: an infection-autoimmunity diagnostic challenge"],"prefix":"10.3389","volume":"17","author":[{"given":"Xing","family":"Zhao","sequence":"first","affiliation":[{"name":"Department of Neurology, The Second Hospital of Jilin University","place":["Changchun, 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