Discussion
Borreliosis is a tick-borne infection caused by Spirochetes of Borrelia species. Depending upon the geographical location, the most common causative agents for Lyme disease includes B. burgdorferi andB. garinii . This spirochetal infection occurs as a result of a tick bite. However, in disseminated or late infection, many patients do not recall the insect bite [4, 5]. Neurological manifestations of Lyme disease, known as neuroborreliosis, occur in up to 50% of borreliosis cases. Neurological involvement of Lyme disease can present in various forms, ranging from simple neuropathy, neuritis or facial palsy to seizures, psychosis, paraplegia, meningoencephalitis, radiculomyelitis, and stroke [6-9]. Convulsion was our patient’s main manifestation, resulting from meningoencephalitis.
Diagnosis of Lyme disease is suspected in individuals with compatible manifestations like characteristic cutaneous features (erythema migrans, acrodermatitis chronica atrophicans, malar rash), musculoskeletal presentations (migratory pain in the joints and muscles, arthritis, panniculitis), neurologic symptoms (meningitis, ataxia, neuritis, radiculopathy), cardiac complications (myopericarditis, AV block, cardiomegaly) and ophthalmic abnormalities (iritis, keratitis, conjunctivitis). However, paraclinical evaluation should confirm the diagnosis [10-12]. CSF changes in Lyme disease with CNS involvement are expected to include a pleocytosis, usually with lymphocyte dominance, elevated protein, and normal glucose levels [13, 14]. Microbiological tests (e.g., culture) and molecular tests (e.g., PCR) yield low conclusive results in neurologic involvement of Lyme. Hence, the definite diagnosis is based on serologic tests and a demonstration of the patient’s immune response [15]. Our patient was suspected of neuroborreliosis due to aseptic meningitis with lymphocyte dominance. Hence, we requested serum anti-Borrelia antibodies (IgM and IgG) tests, both positive in high titers.
Nevertheless, the Western blot test should have been used as a secondary test to exclude reactive IgG false positivity. However, due to our inaccessibility to this confirmatory test, we started the patient on Lyme treatment based on the initial ELISA positivity. Increased oligoclonal bands in the CSF have also been reported to suggest neuroborreliosis [16], but it was not performed due to resource shortage. On the other hand, some authorities only accept intrathecal anti-Borrelia antibody production (ITAb) as the confirmatory diagnostic test for neuroborreliosis [17]. Unfortunately, serological evaluation of Borreliosis was not performed on our patient’s CSF. Recently, an increase in CXCL13 levels in the CSF and positive Borrelia C6 peptide reaction have been suggested to be beneficial diagnostic markers for neuroborreliosis [18, 19]. It should be acknowledged that CSF pleocytosis, with lymphocytes dominance, also known as aseptic meningitis, has several other differential diagnoses, including viral CNS infections, late stages of tuberculosis meningitis, neurobrucellosis, neurosyphilis, HIV infection, listeriosis, convulsion, subarachnoid hemorrhage (SAH), neuroimmunogic and neurodegenerative disorders, neoplasms, and vasculitis [20]. Nevertheless, most of these diagnoses were excluded with corresponding laboratory tests in our patient.
The treatment response of neuroborreliosis is more satisfactory with intravenous antimicrobials. Ceftriaxone or penicillin G, alternatively, are the most appropriate options, but oral doxycycline could also be used [21]. Our patient responded favorably to antibiotics, improving his condition within two weeks.