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.