2. INFECTIOUS AGENT
• Tick-borne encephalitis, or TBE, is a human
viral infectious disease involving the central
nervous system.
• TBE is caused by the tick-borne encephalitis
virus (TBEV), a member of the family
Flaviviridae (single-stranded RNA virus), and
was initially isolated in 1937.
3. Family Flaviviridae also includes
• Omsk hemorrhagic fever virus in Siberia,
• Kyasanur Forest disease virus in India
• Alkhurma virus in Saudi Arabia.
• Louping ill virus (United Kingdom) it causes
disease primarily in
• In the USA and Russia, another tick-borne
flavivirus, Powassan virus, is responsible of
encephalitis in human.
• Yellow fever, dengue fever, West Nile encephalitis,
Japanese encephalitis and Powassan fever.
4. TBEV has 3 subtypes:
1. European or Western tick-borne encephalitis
virus
2. Siberian tick-borne encephalitis virus
3. Far Eastern Tick-borne encephalitis virus
(formerly known as Russian Spring Summer
encephalitis virus, RSSEV)
European TBE is mainly transmitted by Ixodes
ricinus,
Siberian and Far Eastern viruses are
transmitted mainly by I. persulcatus.
5. EPIDEMIOLOGY
• TBE is endemic in focal areas of Europe and Asia
(from eastern France to northern Japan and
from northern Russia to Albania).
• From 1990 through 2009, an average of 8,500
cases per year (range, 5,352–12,733 cases) were
reported from 19 European countries,
• Russia has the largest number of reported TBE
cases, and western Siberia has the highest
incidence of TBE in the world.
• Most cases occur from April through November
• incidence and severity of disease are highest in
people aged ≥50 years
6.
7. Transmission
• Ticks, specifically hard ticks of the family Ixodidae,
act as both the vector and reservoir for TBEV.
• The main hosts are small rodents, with humans
being accidental hosts.
• Large animals serve as feeding hosts for the ticks,
but do not play a role in maintenance of the virus.
• The virus can chronically infect ticks and is
transmitted both transtadially and transovarially.
8. • TBE cases occur in humans most frequently in rural
areas and during the highest period of tick activity
(between April and November).
• Infection also may follow consumption of raw milk
from infected goats, sheep, or cows.
• Laboratory infections were common before the use
of vaccines and availability of biosafety precautions to
prevent exposure to infectious aerosols.
• Person-to-person transmission has not been reported
with the exception of vertical transmission, from an
infected mother to fetus.
• people with recreational or occupational exposure
to rural or outdoor settings (e.g., hunters, campers,
forest workers, farmers)
• Tourism expands, travel to areas of endemicity
broadens the definition of who is at risk for TBE
infection.
9.
10. Signs and Symptoms
• The incubation period of TBE is usually between
7 and 14 days and 2/3rd is asymptomatic.
• Shorter incubation times have been reported
after milk-borne exposure.
11. • First phase: nonspecific febrile illness with
headache, myalgia, and fatigue.
▫ Usually lasts for several days and may be followed
by an afebrile and relatively asymptomatic period.
▫ two-thirds of patients may recover without any
further illness.
• Second phase: central nervous system
involvement resulting in aseptic meningitis,
encephalitis, or myelitis. Findings include
meningeal signs, altered mental status, cognitive
dysfunction, ataxia, tremors, cranial nerve
palsies, and limb paresis.
12.
13. • Disease severity increases with age.
• European subtype is associated with milder
disease, a case-fatality ratio of <2%, and
neurologic sequelae in up to 30% of patients.
• Far Eastern subtype is often associated with a
more severe disease course, including a case-
fatality ratio of 20%–40% and higher rates of
severe neurologic sequelae.
• Siberian subtype is more frequently associated
with chronic or progressive disease and has a
case-fatality ratio of 2%–3%.
14. DIAGNOSIS
• first phase low white blood cell count
(leukopenia), low platelet count
(thrombocytopenia). Liver enzymes in the serum
may also be mildly elevated.
• second phase onset of neurologic disease increase
in the number of white blood cells in the blood and
the cerebrospinal fluid (CSF)
• Virus isolation from the blood during the first phase
of the disease and CSF from second phase.
• Moderate pleocytosis and increased cerebrospinal
fluid albumin
15. Laboratory diagnosis
• Serology is typically used for laboratory
diagnosis. IgM-capture ELISA performed on
serum or cerebrospinal fluid
• virus isolation or RT-PCR
• MRI images reveal abnormalities in 15-20% of
patients
• EEG will be abnormal in 75% of all patients
16. TREATMENT
• There is no specific antiviral treatment for TBE
• therapy consists of supportive care and
management of complications.
• Intubation and corticosteroids are generally
used
• CNS depressants, analgesics.
17. PREVENTION
• Travelers should avoid consuming unpasteurized
dairy products
• using insect repellents and protective clothing to
prevent tick bites.
• The chemical DEET (diethyltoluamide) is often used
in insect repellents
• Wear light-coloured clothes so ticks are easier to
spot and brush off
• Clothing and camping gear can be impregnated with
compounds containing permethrin, which have an
acaricidal and repellent effect
18. Vaccine
• No TBE vaccines are licensed or available in the
United States.
• Two inactivated cell culture-derived TBE
vaccines are available in Europe, in adult and
pediatric formulation
• Two other inactivated TBE vaccines are available
in Russia