TICK BORNE ENCEPHALITIES

SYNONYMS:1.TICK BORNE MENINGO ENCEPHALITIES

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.

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.

TBEV has 3 subtypes:

1. European or Western tick-borne encephalitis virus

2. Siberian tick-borne encephalitis virus3. 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.

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

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.

• 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.

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.

•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.

•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%.

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

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

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.

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

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