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tickborne encephalitis

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Datasheet

tickborne encephalitis

Summary

  • Last modified
  • 14 July 2018
  • Datasheet Type(s)
  • Animal Disease
  • Preferred Scientific Name
  • tickborne encephalitis
  • Overview
  • Many mammals are subclinically infected with tickborne encephalitis virus, whereas clinical disease is mostly observed in dogs, leading to neurological signs and frequently death. Humans can be infected directly by tick...

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Identity

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Preferred Scientific Name

  • tickborne encephalitis

International Common Names

  • English: spanish sheep encephalomyelitis, encephalitis- exotic; turkish sheep encephalomyelitis, encephalitis- exotic

English acronym

  • TBE

Overview

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Many mammals are subclinically infected with tickborne encephalitis virus, whereas clinical disease is mostly observed in dogs, leading to neurological signs and frequently death. Humans can be infected directly by ticks, or by contaminated unpasteurised milk from infected cattle.

Hosts/Species Affected

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Tickborne encephalitis infections occur in many mammals, but ruminants (cattle, sheep and goats) and dogs are thought to be the main source of infections for man (Anon., 1999c). TBEV has also been isolated from many wild rodents, bats, and birds. Many laboratory animals such as mice, rats, guinea pigs and monkeys can experimentally be infected by TBEV. Humans should be regarded as accidental hosts (Traavik, 1994).

Distribution

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Tickborne encephalitis is recognised in most parts of Europe, coinciding with the distribution of the principal tick vectors Ixodes ricinus in the west and Ixodes persulcatus in the east. TBEV-related disease has been recognised in Russia, Scandinavian countries, Germany, France, Austria, and Switzerland (Traavik, 1994). Interestingly, the key to the focal distribution of western-type tickborne encephalitis virus infection in Europe seems to be the geographically variable degree of synchrony in the seasonal activity of larval and nymphal Ixodes ricinus ticks, as determined from analysis of tick infestation patterns on rodents in Slovakia (Randolph et al., 2000).

Distribution Table

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The distribution in this summary table is based on all the information available. When several references are cited, they may give conflicting information on the status. Further details may be available for individual references in the Distribution Table Details section which can be selected by going to Generate Report.

Continent/Country/RegionDistributionLast ReportedOriginFirst ReportedInvasiveReferenceNotes

Asia

Russian Federation
-Russia (Asia)PresentTraavik, 1994

Europe

AustriaPresentLabuda et al., 1993; Traavik, 1994
Czech RepublicPresentKlimes et al., 2001
FinlandPresentTraavik, 1994
FrancePresentTraavik, 1994
GermanyPresentTraavik, 1994; Reiner and Fischer, 1998; Suss et al., 1999
NorwayPresentTraavik, 1994
PolandPresentMatuszczyk et al., 1997
Russian FederationPresentPresent based on regional distribution.
-Russia (Europe)PresentTraavik, 1994
SlovakiaPresentRandolph et al., 2000
SwedenPresentTraavik, 1994
SwitzerlandPresentTraavik, 1994

Pathology

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Neuropathological changes have been observed in dogs with confirmed TBEV infection. Lymphohystiocytic meningitis, neuronal necrosis, karyorrhexis of glial cells, and proliferation of microglial cells in the molecular layer of the cerebellum may occur. Numerous perivascular cuffs, comprising lymphocytes, macrophages and plasma cells may be present in all brain regions. Moderate lesions may be present in the grey matter of the cerebrum, hippocampus and the molecular and Purkinje cell layer of the cerebellum. TBEV antigen can be detected at low concentrations in the perikarya and neuronal processes, extracellular in the centres of neurophaghic nodules and in the cytoplasm of macrophages. Antigen is most consistently found in the neuroparenchyma surrounding the 4th ventricle and less frequently in the cerebellum, mesencephalon, thalamus, hippocampus and neocortex (Weissenbock, 1999).

Diagnosis

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Tickborne encephalitis virus (TBEV) antigen can be detected postmortem in the brain tissue of infected dogs by immunohistology (Weissenbock, 1999). TBEV may also be diagnosed by antigen detection of cerebrospinal fluid (CSF). CSF examination may show elevated protein concentration and mononuclear pleocytosis. TBE antibody concentrations for diagnosis may be detected in serum and CSF by ELISA (Reiner and Fischer, 1998).

In man, classical diagnosis involves inoculation of mice. Other techniques involve specific antibody detection, and antigen detection by virus isolation, or RT-PCR (Kreil et al., 1997).

List of Symptoms/Signs

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SignLife StagesType
Digestive Signs / Anorexia, loss or decreased appetite, not nursing, off feed Sign
Digestive Signs / Anorexia, loss or decreased appetite, not nursing, off feed Sign
Digestive Signs / Excessive salivation, frothing at the mouth, ptyalism Sign
Digestive Signs / Excessive salivation, frothing at the mouth, ptyalism Sign
Digestive Signs / Grinding teeth, bruxism, odontoprisis Sign
Digestive Signs / Grinding teeth, bruxism, odontoprisis Sign
Digestive Signs / Tongue protrusion Sign
Digestive Signs / Tongue protrusion Sign
General Signs / Abnormal proprioceptive positioning, knuckling Sign
General Signs / Abnormal proprioceptive positioning, knuckling Sign
General Signs / Ataxia, incoordination, staggering, falling Other:All Stages Sign
General Signs / Bunny hopping Sign
General Signs / Bunny hopping Sign
General Signs / Dysmetria, hypermetria, hypometria Sign
General Signs / Dysmetria, hypermetria, hypometria Sign
General Signs / Fever, pyrexia, hyperthermia Sign
General Signs / Fever, pyrexia, hyperthermia Sign
General Signs / Forelimb weakness, paresis, paralysis front leg Other:All Stages Sign
General Signs / Generalized lameness or stiffness, limping Sign
General Signs / Generalized lameness or stiffness, limping Sign
General Signs / Generalized weakness, paresis, paralysis Other:All Stages Sign
General Signs / Inability to stand, downer, prostration Sign
General Signs / Inability to stand, downer, prostration Sign
General Signs / Opisthotonus Sign
General Signs / Opisthotonus Sign
General Signs / Paraparesis, weakness, paralysis both hind limbs Sign
General Signs / Paraparesis, weakness, paralysis both hind limbs Sign
General Signs / Reluctant to move, refusal to move Sign
General Signs / Reluctant to move, refusal to move Sign
General Signs / Tetraparesis, weakness, paralysis all four limbs Other:All Stages Sign
General Signs / Trembling, shivering, fasciculations, chilling Sign
General Signs / Trembling, shivering, fasciculations, chilling Sign
General Signs / Underweight, poor condition, thin, emaciated, unthriftiness, ill thrift Sign
General Signs / Underweight, poor condition, thin, emaciated, unthriftiness, ill thrift Sign
General Signs / Weakness of one hindlimb, paresis paralysis rear leg Other:All Stages Sign
General Signs / Weight loss Sign
General Signs / Weight loss Sign
Musculoskeletal Signs / Forelimb spasms, myoclonus Sign
Musculoskeletal Signs / Forelimb spasms, myoclonus Sign
Nervous Signs / Abnormal behavior, aggression, changing habits Sign
Nervous Signs / Abnormal behavior, aggression, changing habits Sign
Nervous Signs / Circling Sign
Nervous Signs / Circling Sign
Nervous Signs / Coma, stupor Sign
Nervous Signs / Coma, stupor Sign
Nervous Signs / Dullness, depression, lethargy, depressed, lethargic, listless Sign
Nervous Signs / Dullness, depression, lethargy, depressed, lethargic, listless Sign
Nervous Signs / Excitement, delirium, mania Sign
Nervous Signs / Excitement, delirium, mania Sign
Nervous Signs / Head pressing Sign
Nervous Signs / Head pressing Sign
Nervous Signs / Hyperesthesia, irritable, hyperactive Sign
Nervous Signs / Hyperesthesia, irritable, hyperactive Sign
Nervous Signs / Propulsion, aimless wandering Sign
Nervous Signs / Propulsion, aimless wandering Sign
Nervous Signs / Seizures or syncope, convulsions, fits, collapse Other:All Stages Sign
Nervous Signs / Tremor Sign
Nervous Signs / Tremor Sign
Ophthalmology Signs / Blindness Sign
Ophthalmology Signs / Blindness Sign
Ophthalmology Signs / Lacrimation, tearing, serous ocular discharge, watery eyes Sign
Ophthalmology Signs / Lacrimation, tearing, serous ocular discharge, watery eyes Sign
Respiratory Signs / Dyspnea, difficult, open mouth breathing, grunt, gasping Sign
Respiratory Signs / Dyspnea, difficult, open mouth breathing, grunt, gasping Sign
Respiratory Signs / Increased respiratory rate, polypnea, tachypnea, hyperpnea Sign
Respiratory Signs / Mucoid nasal discharge, serous, watery Sign
Respiratory Signs / Mucoid nasal discharge, serous, watery Sign

Disease Course

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TBEV infections run mostly a subclinical course in animals. However, in dogs a neurological disease may follow after an infecting tick bite (Weissenbock, 1999; Klimes et al., 2001). Dogs may exhibit elevated body temperature and acute neurologic disease with depressed mentation, tetraparesis, seizures, vestibular strabism and facial sensory deficits pointing towards cervical spinal cord, brainstem and forebrain disease. Furthermore, lower motor neuron paresis and cervical muscle weakness may occur. Affected animals may recover, but usually suffer from neurological sequelae (Reiner and Fischer, 1998).

Epidemiology

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Tickborne encephalitis virus is transmitted by Ixodes ricinus and Ixodes persulcatus ticks (Traavik, 1994). Ixodes ricinus is mostly active in spring and early autumn in Europe, while Ixodes persulcatus ticks are mainly active in early spring and summer, with peak incidence of human disease in May and June. Other ticks that may be infected with TBEV are Dermacentor spp. and Haemophysalis spp. (Traavik, 1994). Cattle, sheep, goats and dogs often serve as amplifying hosts for ticks, but cattle may also transmit virus directly to humans via contaminated unpasteurised milk (Matuszczyk et al., 1997). In 1995 an outbreak of TBE in Poland resulted in 48 people exhibiting disease, of which 27 had to be hospitalised. Ticks serve as reservoirs of infection as well as vectors. Both male and female ticks are involved in transmission. Ticks may live for several years, and require throughout their life-stages (larva-nymph-adult) several blood meals, during which virus transmission can occur (transstadial transmission; from one developmental stage to another). Vertical (transovarial) transmission can also occur in ticks (Anon., 1999c). Studies on the prevalence of TBEV among ticks are scarce, but seem overall to be low. From 3404 Ixodes ricinus ticks collected in 12 localities in Styria, Austria, in 1990, 15 tickborne encephalitis virus isolates were recovered (Labuda et al., 1993). In Germany, the estimated virus prevalence of the tick population studied was less than 2%. Annual fluctuations in virus prevalence in ticks have been noted (Suss et al., 1999).

Zoonoses and Food Safety

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TBE is a serious cause of acute central nervous system disease in humans, which may result in death or long-term neurological sequelae (occurring in 30-60% of survivors of the eastern form, and in 10-20% of survivors of the western form) (Traavik, 1994; Dumpis et al., 1999). The onset of the disease is usually gradual with fever, headache and signs of meningal irritation followed by convulsions as well as abdominal pain and diarrhoea in children (Traavik, 1994). The mortality rate varies between <1% (western form) to 20% (eastern form).

Prevention and Control

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Palliative but no curative treatments are available for affected animals that show neurological signs. Humans are protected by vaccines. In Austria a mass vaccination campaign has been set up in humans due to the high perceived risk for tickborne encephalitis (TBE) (Dumpis et al., 1999). Inactivated, partly purified vaccines produced in Russia and Austria from TBEV propagated in primary chicken embryo cells have provided safe protection against the disease (Traavik, 1994). By adoptive transfer of sera or immunoglobulin preparations, vaccine-induced protection against TBEV has been demonstrated to be mediated by antibodies to the surface protein of TBE virus, glycoprotein E. Nevertheless, the mechanism of vaccine-induced protection against TBE virus remains unclear. Neutralising antibodies play a role in protection, but protection without correlation with neutralising antibodies has also been observed (Kreil et al., 1998). Recombinant vaccines will probably be available in the future. New strategies based on DNA immunisation are under study (Schmaljohm et al., 1999).

The antiviral activity of phosprenyl has been shown in BALB/c mice infected with tickborne encephalitis virus. Up to 60% of animals infected with TBE virus survived after 1-3 intramuscular injections of phosprenyl (Ozherelkov et al., 2000).

References

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Allison SL; Stiasny K; Stadler K; Mandl CW; Heinz FX, 1999. Maing of functional elements in the stem-anchor region of tick-borne encephalitis virus envelope protein. E. J. Vir., 73:5605-5612.

Anon., 1999c. Flaviviridae. In: Murphy FA, Gibbs EPJ, Horzinek MC, Studdert MJ, eds. Veterinary Virology. San Diego, USA: Academic Press, 556-569.

Dumpis U; Crook D; Oksi J, 1999. Tick-borne encephalitis. Clinical Infectious Diseases, 28(4):882-890; 98 ref.

Klimes J; Juricova Z; Literak I; Schanilec P; Trachta-e-Silva E, 2001. Prevalence of antibodies to tickborne encephalitis and West Nile flaviviruses and the clinical signs of tickborne encephalitis in dogs in the Czech Republic. Vet. Rec., 148:17-20.

Kreil TR; Maier E; Fraiss S; Attakpah E; Burger I; Mannhalter JW; Eibl MM, 1998. Vaccination against tick-borne encephalitis virus, a flavivirus, prevents disease but not infection, although viremia is undetectable. Vaccine, 16(11/12):1083-1086; 20 ref.

Kreil TR; Zimmermann K; Burger I; Attakpah E; Mannhalter JW; Eibl MM, 1997. Detection of tick-borne encephalitis virus by sample transfer, plaque assay and strand-specific reverse transcriptase polymerase chain reaction: what do we detect?. Journal of Virological Methods, 68(1):1-8; 19 ref.

Labuda M; Stünzner D; Kozuch O; Sixl W; Kocianová E; Schäffler R; Vyrosteková V, 1993. Tick-borne encephalitis virus activity in Styria, Austria. Acta Virologica, 37(2/3):187-190; 14 ref.

Matuszczyk I; Tarnowska H; Zabicka J; Gut W, 1997. An outbreak of milky epidemic of encephalitis caused by tick-borne encephalitis virus in Kielce Province. Przeglad Epidemiologiczny, 51(4):381-388; 9 ref.

Ozherelkov SV; Timofeev AV; Novikova GP; Deeva AV; Narovlyansky AN; Sanin AV; Pronin AV, 2000. Protective effect of phosprenyl, a new antiviral drug, in experimental tick-borne encephalitis. Voprosy-Virusologii, 45:33-37.

Randolph SE; Green RM; Peacey MF; Rogers DJ, 2000. Seasonal synchrony:the key to tick-borne encephalitis foci identified by satellite data. Parasitology, 121:15-23.

Reiner B; Fischer A, 1998. European tickborne meningoencephalitis in dogs in Germany: two case reports. Kleintierpraxis, 43(4):255-268; 29 ref.

Schmaljohn C; Custer D; VanderZanden L; Spik K; Rossi C; Bray M, 1999. Evaluation of tick-borne encephalitis DNA vaccines in monkeys. Virology (New York), 263(1):166-174; 24 ref.

Suss J; Schrader C; Abel U; Voigt WP; Schosser R, 1999. Annual and seasonal variation of tick-borne encephalitis virus (TBEV) prevalence in ticks in selected hot spot areas in Germany using a nRT-PCR: results from 1997 and 1998. Zentralblatt fur Bakteriologie, 289:564-578.

Traavik T, 1994. Tick-borne encephalitis, Wesselbron and Simian hemorrhagic fever viruses. In: Webster RG, Granoff A, eds. Encyclopedia of virology. London, UK: Academic Press, 367-372.

Weissenböck H, 1999. Post-mortem diagnosis of tick-borne encephalitis in dogs. Tierärztliche Umschau, 54(5):249-255; 15 ref.

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