On lyme neuroborreliosis
Lyme borreliosis is a tick-transmitted multisystem infection caused by Borrelia burgdorferi sensu lato. The spiro-chetes migrate early after the skin inoculation to various organ systems. The central and peripheral nervous sys-tem is frequently affected, and 10-20% of untreated cases develop neurological symptoms (neuroborreliosis), often with radiculoneuropathy, lymphocytic meningitis, and cranial neuritis, particularly facial nerve palsy. Another less common clinical pattern is focal or disseminated encephalomyelitis. Postinfectious sequelae are reported to occur in about 25% of the patients.To characterise the pattern of damage, biochemical markers in the cerebrospinal fluid (CSF) of patients with Lyme neuroborreliosis (LNB) were analysed before and after treatment. The astroglial protein markers glia fibrillary acidic protein (GFAp) and S-100 protein, and the neuronal markers neurofilament protein (light subunit) (NFL) and neuron-specific enolase (NSE), were quantified. The results indicate an astroglial reaction in early and late stages of LNB but no signs of glial tissue destruction. Both NFL and NSE levels were increased in CSF before treatment, reflecting axonal damage and neuronal tissue involvement. Increased pretreatment concentrations of CSF-GFAp and CSF-NFL were correlated to an unfavourable clinical outcome, and CSF-NFL was increased in patients with longer duration of neurological symptoms before treatment, reflecting progressive tissue injury.The myelin-associated glycolipid sulphatide was found to be increased in CSF of 90% of patients with LNB before compared with after treatment, but the levels were not correlated to clinical patterns or outcome. Antig-lycolipid antibodies have earlier been associated with the pathogenesis of various autoimmune processes with neuropathy, and the serum antisulphatide reaction was therefore analysed in patients with LNB. Serum IgG anti-sulphatide antibodies were found in 65% of the LNB patients, indicating infection-triggered autoimmune reac-tions in LNB.Antibiotic treatment of LNB is efficient, but current treatment regimens often recommend intravenous administration. To evaluate doxycycline therapy by the oral route, we studied 29 patients with LNB-associated facial palsy and meningitis in a prospective non-randomised treatment study. Oral doxycycline was given for a mean of 10.8 days. Twenty-six patients (90%) recovered without sequelae within six months. CSF showed a marked decrease of inflammatory cells and protein levels post-treatment in all patients. The favourable outcome agrees with fin-dings of reports on intravenous antibiotic treatment for LNB. In a pharmacokinetic study of doxycycline in pati-ents with suspected LNB, the CSF concentrations of doxycycline were found to exceed 0.6 mg/L (estimated mean of MIC for B. burgdorferi) in 3 out of 12 patients treated with 200 mg daily and in 9 out of 10 patients given 400 mg daily.
Göteborgs universitet/University of Gothenburg
Department of Infectious Diseases
Avdelningen för infektionssjukdomar
Date of defence
Dotevall, Leif 1956-
glia fibrillary acidic protein