1. VIRAL ENCEPHALITIS

2. Encephalitis is defined as an inflammation of parenchymal brain tissue clinically expressed by fever, consciousness impairment, seizures, focal neurologic deficits.

3. Definitions
Acute encephalitis is the brain inflammation that occurs over a relatively short period of time.
Chronic encephalitis presents over weeks to months.
Slow viral infections of the CNS (kuru, Bovine spongiforme encephalopathie)
Classification upon the mechanism of the disease:
Primary encephalitis-
Postinfectious encephalitis -.

4. Etiology
Togaviridae-Alphavirus (arbovirus): Western, Eastern, Venezuelean encephalitis virus
Flaviviridae-Flavivirus (arbovirus):
-West Nile fever virus,
-Japanese encephalitis virus
-St. Louis encephalitis virus,
-Tickborne encephalitis virus (TBE complex: louping ill, Powassan, TBE Western and Eastern subtype, Omsk hemorrhagic fever),
-Murray Valley virus.

5. Bunyaviridae (arbovirus)
Herpesviridae:
-Herpes simplex virus type 1 and 2
-Cytomegalovirus
-Epstein –barr virus
-Varicella –zoster virus
-human herpes virus -6
Picornaviridae: echovirus
Paramyxoviridae: mesles virus, mumps virus
Orthomyxoviridae: influenza viruses
Rhabdoviridae: rabies virus
Retroviridae: HIV-1
Arenaviridae: lymphocytic choriomeningitis virus
Adenoviridae: Adenovirus.

6. Pathogenesis
Enteroviruses and arboviruses have a viremic spread to the CNS.
Rabies and HSV infection are prototypes of viral CNS infection.
Poliovirus and reovirus infect CNS by viremia and neuronal spread.

7. Clinical manifestations
General symptoms: fever, headache chills;
Symptoms of cortical involvement: trouble of consciousness (obtundation, somnolence, delirium, confusion, coma), seizures, motor deficit, sleepness, dysphasia.
Symptoms of cerebral peduncles involvement: paresis of cranial nerves, respiratory and cardiovascular dysfunction, hemiparesis.
Spinal symptoms: paraparesis and tetraparesis
Meningeal signs and symptoms

8. Laboratory features CSF: Glucose level is normal/slightly elevated
Protein level is moderately raised
Pleocytosis: usually <500/mm3, with a predominance of mononuclear cells (early in the disease could be as high as 1000/mm3, with a predominance of neutrophils); persists for 3-6 weeks (may lasts for as long as 3-4 months).

9. Specific diagnosis Viral culture or antigen detection in brain
Serologic titers: hemagglutination inhibition (HI), complement fixation (CF), neutralizing antibody titer (NA), immunofluorescent antibody (IFA), counterimmunoelectrophoresis (CIE),
CSF IgM (ELISA)
PCR

10. Tick-borne encephalitis

11. The Western subtype virus produces a biphasic febrile illness:
First phase lasts 2-7 days without signs/symptoms of meningoencephalitis.
An afebrile and relatively asymptomatic period lasts 2-10 days
Second phase (in 1/3 of patients): fever and symptoms of meningitis and meningoencephalitis.

12. The Eastern subtype virus is characterized by a monophasic course: flushing of the face and neck, conjunctival injection, headache, somnolence, nausea, vomiting, dizziness, myalgia, hyperestesia.
The main clinical neurological syndromes associated with TBE are:
Febrile headache, with myalgia,.
Aseptic meningitis
Meningoencephalitis
Meningoencephalomyelitis

13. Differential diagnosis
Infection with other tick-borne pathogens: tularemia, spotted fever group of rickettsioses, babesiosis;
Other febrile headache: infectious mononucleosis, influenza, typhoid fever, shigellosis, legionellosis, relapsing fever, erlichiosis, brucellosis;
Infections causing meningitis meningoencephalitis or encephalomyelitis:
Syndromes mediated by bacterial toxins: botulism, tetanus, Bordetella pertussis infection
Noninfectious encephalopathies:
Neoplastic lesions
Guillain – Barre syndrome is an acute inflammatory demyelinating polyneuropathy
Behcet’s disease
Vogt-Koyanagi-Harada syndrome is an autoimmune disease:
-Meningitis: -
Severe anterior and posterior uveitis
-Vitiligo, alopecia
-Dysacousia and tinnitus

14. Treatment
There is no curative therapy for TBE. Treatment is supportive (antiedematous drugs, parenteral hydration, symptomatics).
Bed rest for up to 2 weeks improves outcome.
In severe cases corticosteroids could be administrated.

15. Herpes Simplex virus encephalitis
Decreasing level of consciousness with focal neurologic findings
Sometimes presence of skin vesicles
CSF pleocytosis and proteinosis
The absence of bacterial and fungal pathogens in CSF
Focal electroencephalographic (focal slowing, spiking, and paroxysmal lateralizing epileptiform discharges), CT and MRI findings.
Treatment
Acyclovir - at a dose of 10mg/kg every 8 hours (30mg/kg/day), for a period of days.

16. West Nile encephalitis
The disease incidence was 12.4 per inhabitants.
Epidemiology
The virus multiplies in various species of birds, some of which get severely sick, like humans, whereas others harbor the virus without signs of disease.
Humans, and occasionally cats and horses, get infected

17. Clinical manifestations
After an incubation period of 3 to 6 days, disease starts without any prodromal stage with:
-fever, joint pains and headache;
- temporary skin rash
lymph node swelling.
-a typical biphasic fever progression is observed with West Nile virus: after a few days of normal body temperature, fever increases again strongly.
The diagnosis detection of specific antibodies and/or the detection of viral RNA by PCR.
The lethality of this form of disease is between 3 and 15%.