Abstract
Tick-borne encephalitis (TBE) is associated with a range of disease severity. The reasons for this heterogeneity are not clear. Levels of serum IgG antibodies to TBE virus (TBEV) were determined in 691 adult patients during the meningoencephalitic phase of TBE and correlated with detailed clinical and laboratory parameters during acute illness and with the presence of post-encephalitic syndrome (PES) 2–7 years after TBE. Specific IgG antibody levels ranged from below cut-off value (in 32/691 patients, 4.6%), to 896 U/mL (median = 37.3 U/mL). Patients with meningoencephalomyelitis were more often seronegative (24.3%; 9/37) than those with meningoencephalitis (4.7%; 20/428) or meningitis (1.3%; 3/226). Moreover, patients with antibody levels below cut-off had longer hospitalization (13 versus 8 days); more often required intensive care unit treatment (22% versus 8%) and artificial ventilation (71% versus 21%); and had a higher fatality rate (3/32; 9.4% versus 1/659; 0.2%) than seropositive patients. These results were confirmed when antibody levels, rather than cut-off values, were correlated with clinical parameters including the likelihood to develop PES. Low serum IgG antibody responses against TBEV at the onset of neurologic involvement are associated with a more difficult clinical course and unfavorable long-term outcome of TBE, providing a diagnostic and clinical challenge for physicians.
Highlights
Tick-borne encephalitis (TBE) is a central nervous system disease caused by tick-borne encephalitis virus (TBEV)
We investigated the associations between TBEV IgG antibody responses during the early meningoencephalitic phase of TBE and the clinical course and long-term outcome of TBE
IgG serum antibodies to TBEV are associated with more severe illness, longer duration of hospitalization, treatment in intensive care unit (ICU), and need for artificial ventilation
Summary
Tick-borne encephalitis (TBE) is a central nervous system disease caused by tick-borne encephalitis virus (TBEV). The majority of human cases are due to 3 subtypes of TBEV, European, Siberian, and Far Eastern, each with a somewhat distinct clinical presentation. The disease caused by the European subtype usually has a biphasic course. The initial phase, which accompanies viremia, manifests with nonspecific febrile illness associated with headaches, myalgias, and fatigue. As viremia decreases these symptoms typically resolve and patients improve. After approximately 1-week improvement, patients enter the second phase of TBE which is characterized by neurological involvement; most (50–60%) present with meningitis, 30–40% with meningoencephalitis, and 5–10% with meningoencephalomyelitis. The fatality rate is up to 2%, approximately 5% of patients have permanent pareses, and at least 1/3 of patients develop post-encephalitic
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