Viral encephalitis

Viral encephalitis

Viral encephalitis– acute infectious inflammation of the brain caused by the direct action of the pathogen (primary encephalitis) or an inflammatory reaction that develops in response to the penetration of the virus into the body (secondary encephalitis). The disease is accompanied by lesions of the meninges, spinal cord and peripheral nerves. In the bulk of cases, primary viral encephalitis is an infrequent complication of a generalized viral infection (herpetic, enteroviral, mumps). Secondary encephalitis is traditionally caused by immunological mechanisms (hypersensitivity reaction) and develops 2-12 days after primary viral infection. Etiology. Causative agents – HSV types 1 and 2, Epstein-Barr virus, Herpes zoster virus, influenza virus, adenoviruses, mumps virus, enteroviruses (usually group B Coxsackie viruses), cytomegalovirus, measles virus, rubella virus, BICH, Denge virus, Californian encephalitis virus, Japanese encephalitis B virus, tick-borne encephalitis virus (togavirus), Murray Valley encephalitis virus, arboviruses, rabies virus. Epidemiology. Depending on the biology of the pathogen, the reservoir and carriers are sick people, all kinds of arthropods. The epidemiology of vector-borne infections includes an additional reservoir – animals and birds. Infection of a person occurs by airborne, contact, fecal-oral, sexual routes, transmissively or by eating contaminated milk. The peak of transmissible encephalitis is spring, summer; the peak of enterovirus infections is the second half of summer. Encephalitis caused by mumps and chicken pox viruses is most often observed in the spring. In most other viral encephalitis, seasonality is not pronounced. Pathomorphology

• • Perivascular inflammation predominates
  • Swelling and degenerative changes in nerve elements
  • Pathological findings vary by etiology
  • In herpetic encephalitis, Cowdry bodies type A are detected.
  • With the defeat of HSV-2, necrosis in the gray and white matter of the brain, mainly in the cortex of the temporal lobes
  • With cytomegalovirus etiology, inflammation and focal necrosis first appear, then fibrosis and calcification. Areas of localization in the brain – ependyma and subependymal zone of the ventricles. Sometimes pathognomonic giant cells with nuclear inclusions (owl’s eye cell) are detected, more often they are found in the epithelial tissue
  • With rabies in the brain, conjunctiva, skin of the base of the neck, Negri bodies are found.

Clinical picture

• • Nonspecific symptoms (malaise, fever, runny nose) may precede the onset of neurological symptoms.
  • Then headache, nausea and vomiting, photophobia, disorders of consciousness (coma), convulsions, focal neurological symptoms join.
  • The progression of the disease is variable (from fulminant to rather slow). Involvement of the meninges is manifested by headache and meningeal symptoms (stiff neck, positive Koernig’s and Brudzynski’s signs).
  • With intrauterine infection, other organs (lungs, liver, kidneys) are not often involved.
  • Symptoms vary depending on the etiology
  • With varicella encephalitis, cerebellar and vestibular disorders are typical: unsteady gait, head trembling, nystagmus, chanted speech, intentional tremor, difficulty performing coordination tests; Symptoms can be unilateral or bilateral
  • In tick-borne, epidemic and HSV-1 encephalitis, the cranial nerves are often involved. Laboratory research
  • In general and biochemical blood tests, no specific changes are detected.
  • CSF examination (lumbar puncture)
  • The number of leukocytes is traditionally increased (0.01-0.1 x 109 / l), but may be normal, especially with impaired immunity; neutrophils predominate in the early stages, then lymphocytes
  • An increase in the number of red blood cells is noted with herpetic encephalitis
  • Protein content is normal or moderately elevated
  • Glucose levels are normal or moderately low
  • Possible CSF opalescence
  • Therapy with glucocorticoid hormones may distort the results of the study of CSF 4 In patients with a decrease in immunity, the results of the CSF study may be within the normal range.

Special Studies

• • EEG
  • Inhibition of the a-rhythm, the presence of slow & and 5-waves, sharp peak-waves of the fast range
  • Long periods of winding are unfavorable
  • Periodic epileptiform discharges in the temporal lobes – an indirect sign of herpetic encephalitis
  • Specific diagnosis of most viral encephalitis is the determination of the level of AT in serum to a specific Ag. The study is carried out in the acute period and the period of convalescence (after 2-3 weeks). An increase in AT titer by 4 times or more has diagnostic value.
  • Determination of the AT index in

CSF is performed to confirm the infectious etiology of encephalitis. The content of immunoglobulins and albumin in CSF and blood serum is determined. The infectious genesis of the disease is indicated by a higher globulin/albumin ratio in CSF than in serum.

• • Identification of specific antigens in the CSF by PCR is likely in enterovirus and herpes infections
  • In 60% of cases, enterovirus infection is diagnosed by the results of CSF culture. For other etiologies, the pathogen is present in the CSF at such a low concentration that this method is not suitable for diagnosis.
  • In the early stages of the disease, the results of x-ray studies, CG, MRI and brain scans may be within the normal range, later nonspecific abnormalities are detected. In herpetic encephalitis, a decrease in tissue density in the temporal lobes, expansion of the ventricles, and a shift in the central structures of the brain towards a larger lesion are recorded. Differential Diagnosis
  • Bacterial meningitis
  • brain abscess
  • Tuberculosis
  • cat scratch disease
  • Rocky Mountain Spotted Fever
  • erlichiosis
  • Syphilis
  • Lyme disease
  • Leptospirosis
  • Amoebic encephalitis (caused by Naegleria and Acanthamoeba species)
  • Toxoplasmosis
  • Stroke
  • subarachnoid hemorrhage
  • CNS tumor
  • brain injury
  • SLE
  • Poisoning
  • Hypoglycemia.

Treatment:

Tactics of conducting

• • Maintaining respiratory and circulatory functions
  • Relief of cerebral edema during its development (hyperventilation, osmotic diuretics)
  • Anticonvulsants – according to indications
  • Timely detection of a probable syndrome of inadequate ADH secretion. Drug therapy
  • Drugs of choice
  • Acyclovir (intravenous drip for adults at 10 mg/kg every 8 hours, for children from 3 months to 12 years at 5 mg/kg/day [250 mg/m2 of the body plane/day]) for at least 10 days – with herpetic infections. Treatment should be started in the early stages of the disease.
  • Ribavirin (ribamidil) IV 2 g, then 1 g every 6 hours for 4 days, then 0.5 g every 8 hours for 6 days – with arboviruses.
  • For encephalitis of other etiologies, specific antiviral treatment has not been developed.
  • supportive therapy.
  • Precautions
  • Aciclovir can cause liver dysfunction, bone marrow hematopoiesis suppression, renal failure, phlebitis at the injection site, skin rash
  • To prevent nephrotoxicity, acyclovir should be administered by intravenous infusion over 1 hour. In case of impaired renal function, the dose of acyclovir is reduced
  • The main side effect of ribavirin is hemolysis of red blood cells.
  • drug interaction. The combination of acyclovir with drugs that have a nephrotoxic effect increases the risk of kidney damage.

Complications vary depending on the etiology. Among all viral encephalitis, the highest morbidity and mortality is recorded in herpetic encephalitis (without treatment, mortality is 70%, less than 5% of surviving patients have no deviations in the neurological status). The prognosis of the disease is often difficult to predict, depends on the etiological agent more favorable for varicella encephalitis). With herpes infection, the prognosis depends on the time of initiation of treatment (therapy is more effective if started before the development of coma).

Age features

• • Children
  • In children with arbovirus encephalitis, clinical symptoms are more pronounced than in adults.
  • Newborns are at high risk of developing severe forms of diseases caused by HSV or enteroviruses.
  • Elderly. There is also a high risk of developing severe forms of encephalitis. Pregnancy. The risk of infection of a newborn during childbirth through natural routes with a primary lesion of a pregnant woman with HSV-2 is 40%; the risk is reduced to 3-5% with recurrence of genital herpes. Possible intrauterine infection of the fetus with enteroviruses.

Prevention. Use of appropriate repellents. Providing information about diseases and how they are transmitted to people traveling to endemic areas. See also Adenovirus infection, Herpes simplex, Bacterial meningitis

ICD

• • A83 Mosquito-borne viral encephalitis
  • A84 Tick-borne viral encephalitis
  • A85 Other viral encephalitis, not elsewhere classified
  • A87 Viral meningitis, unspecified Literature. 129:300-303