Is Borrelia Associated with Post-Infectious Autoimmune-Mediated Acute and Chronic Inflammatory Demyelinating Polyneuropathy? A Case Series

A variety of neurological syndromes—occurring more frequently in Europe because of the greater neurotropism of Borrelia garinii—have been described in neuroborreliosis. Recent case reports and two cohort studies describe the probable association between Lyme disease and inflammatory demyelinating polyneuropathy. Our case series reports on 3 patients with Guillain-Barre syndrome (GBS), and 2 patients with chronic inflammatory demyelinating polyneuropathy (CIDP) which are most probably linked to neuroborreliosis as antecedent infection. These cases originate from a series of n = 53 with Lyme neuroborreliosis diagnosed in the period 2011-2017. Cerebrospinal fluid analysis and serological and chemokine testing suggest GBS and CIDP are part of late neuroborreliosis rather than acute neuroborreliosis. We discuss if Lyme disease, known for its neurotropism, is a mimicker of Guillain-Barre syndrome or its variants due to active infection of the nervous system or if Borrelia sp. is only one of the many pathogens known to induce these syndromes as a consequence of its immunogenic capacity. Our case series and earlier reported cases suggest that among other infections, Lyme disease could trigger autoimmune response with anti-neuronal reactivity leading to neurologic injury. Such post-infectious autoimmune-mediated acute and chronic inflammatory demyelinating polyneuropathy could be more frequent/important than radiculoneuropathies occurring in the acute stadium of neuroborreliosis.