Tick-borne encephalitis
Tick-borne encephalitis (TBE) is a disease caused by a virus of the genus Flavivirus
Primarily transmitted by tick bite and also widespread in large parts of Europe, including Italy.
The virus responsible, a single-stranded RNA Flavivirus related to those that cause serious diseases such as yellow fever, survives and is transmitted by ticks, particularly Ixodes ricinus and Ixodes persulcatus, which become infected by feeding on the blood of animals carrying the virus and in turn retransmit it.
Two types of TBE (subtype 1 and subtype 2) are known in the European region that are extremely similar to each other, having 94.4 percent of their amino acid sequence in common.
The virus is transmitted by the bite of larvae, nymphs or adult ticks, typically (but not only) of the genus Ixodes ricinus (subtype 1) or Ixodes persulcatus (subtype 2), inoculated into the host via saliva. Far rarer is transmission by intake of unpasteurized dairy products (milk and cheese) from infected goats, sheep, or cows.
Although the possibility of interhuman passage of the virus has never been described, it cannot be completely ruled out by blood transfusion from one infected person in the viremic stage to another susceptible person.
In 2/3 of cases, the patient is asymptomatic and shows no obvious clinical signs.
In the remaining 1/3, after an incubation of 7-14 days, a nonspecific febrile illness begins, lasting 1-8 days corresponding to the viremic phase with fatigue, headache, lower back pain, nausea, and general malaise.
After an interval ranging from 1 to 20 days, during which patients are symptomless, up to one-third of cases abruptly take on the characteristics of meningitis or meningoencephalitis, with fever, headache, muscle aches, malaise, photophobia, and vomiting. This phase may last about a week and may be accompanied by paralysis that progresses for two weeks and then partially recedes.
Age, neurological signs at onset and a low IgM response (Immunoglobins: glycoproteins that appear first in the human body's immune response to an antigen) are risk factors for severe forms of tick-borne encephalitis. Cases in which the disease progresses from a febrile syndrome to CNS (Central Nervous System) disorders without the intermediate asymptomatic period, or a two-stage course with a short asymptomatic interval have been associated with severe forms of TBE.
The disease is generally milder in children.
Etiologic diagnosis is obtained by analyzing serum collected in the acute early phase of the disease for the presence of specific IgM antibodies. Serologic diagnosis may involve cross-reactivity due to other vaccinations or previous flavivirus infections, but TBE virus can also be identified by PCR (C Reactive Protein, produced by the liver, which appears in higher concentrations in case of an inflammatory state).
There is no specific treatment for tick-borne encephalitis. Patient care is mainly delegated to supportive therapies for symptom management, including intensive care interventions in severe cases.
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The information presented is general in nature, is published for general audiences, and is not a substitute for the relationship between patient and physician.