Lyme-Like Disease Presenting With Myelitis in an Immunocompetent Patient

Lyme disease is a bacterial zoonosis caused by spirochetes of the Borrelia burgdorferi sensu lato complex, transmitted to humans by ticks, and is endemic in the Northern Hemisphere, particularly in North America. In contrast, Lyme-like syndrome is an entity attributed to atypical spirochetes that mimic the classic form. In Brazil, reports exist in the Northeast, Center-West, Southeast, South, and Amazon regions. However, Borrelia burgdorferi has never been isolated in Brazil, generating debate about etiology and diagnostic criteria. A 29-year-old man, previously healthy, a cook, living in Encruzilhada do Sul/RS, with a history of contact with livestock and handling of leather, developed low back pain after running, with partial improvement on anti-inflammatories, followed by paresthesias in the lower limbs and urinary retention at the end of the day. Paresthesias progressed with difficulty walking, although muscle strength remained preserved. He denied fever, travel, vaccination, or recent infections. He sought emergency care due to suspected spinal cord compression, which was ruled out by MRI that showed a diffuse intramedullary hyperintense lesion from T7–T8 to the conus medullaris. CSF analysis showed 157 cells (lymphomononuclear), protein 57, glucose 78 (serum: 124). CSF PCR was negative for infectious agents. Electroneuromyography was normal. Pulse therapy with methylprednisolone was introduced, considering infectious or immune-mediated myelitis, with marked improvement: recovery of spontaneous urination, regression of sensory symptoms, and radiological improvement. Serology for infectious agents was obtained, showing reactive IgM and IgG for Borrelia burgdorferi; Western blot confirmation was unavailable. Although he did not have typical manifestations (erythema migrans, febrile illness, arthralgias), he was treated for neuroborreliosis with ceftriaxone for 14 days. He was discharged with follow-up in a neuroimmunology clinic and maintained on prednisone for three months with gradual tapering, with preserved strength and symptom-free status on follow-up. Repeat pulse therapy was planned for the following three months. The marked response to corticosteroid therapy, suggesting an immune-mediated basis, even with positive serology for Borrelia burgdorferi but without Western blot confirmation, underscores diagnostic challenges in regions where the agent has not been isolated and highlights the need for critical analysis of possible false-positive results in inflammatory myelitis of unclear etiology.