Encephalitis
Encephalitis is an inflammation of the brain.
Encephalopathy is suggested when the patient demonstrates the clinical manifestations of encephalitis but inflammation of the brain has not occurred (eg, Reye syndrome, hepatic encephalopathy).
Most cases occur in the late summer or early fall and can be epidemic in pattern.
This pattern reflects the etiologic agents most often responsible for encephalitis, namely, arboviruses and enteroviruses.
Core Knowledge Points - Viral Agents
Spread by man to manMumpsMeaslesEnterovirusRubellaHerpesvirus (herpes simplex 1 and 2)Varicella zosterCytomegalovirusEpstein-Barr
Arthropod-borne agentsEastern equineCaliforniaJapanese BWestern equinePowassan West NileSt. LouisVenezuelan equineDengue
Spread by warm-blooded animalsRabiesHerpesvirus simiaeLymphocytic choriomeningitis (rodent excreta)
Critical Actions - Encephalitis
Management is supportive.
CSF should be sent for special testing (call pediatric infectious disease specialist if possible).
ABCs, ECG and pulse oximetry monitoring
Increased ICP might need to be aggressively treated with endotracheal intubation, hyperventilation, and mannitol (0.5 to 1 g/kg).
Corticosteroids are controversial in this setting.
Antiviral therapy should be initiated.
Administer acyclovir at an initial dose of 20 mg/kg IV.
Pediatric ICU care is indicated, so patient might require transfer.
Core Knowledge Points - West Nile Virus
West Nile virus (WNV) first appeared in the Americas in summer 1999, when it became a New York City epidemic. It is an arbovirus in the Flaviviridae family, which was first isolated in 1937 in a woman with a febrile illness in Uganda. It is transmitted by mosquitoes of the Culex family with birds as natural hosts. Humans become infected but they are dead-end hosts, ie, if a mosquito bites an infected person, that human will not directly transmit the disease.
Most WNV infections are generally asymptomatic, with approximately 120 to 160 asymptomatic infections per one symptomatic patient. Significant WNV infections are rare in children.
Severe neurologic disease due to WNV infection has occurred in patients of all ages, although older patients are at higher risk. WNV should be considered in all persons with unexplained encephalitis and meningitis.
Most WNV infections are mild and often clinically unapparent
Approximately 20% of those infected develop a mild illness (West Nile fever).
The incubation period is thought to range from 3 to 14 days.
Symptoms generally last 3 to 6 days.
Nonspecific signs and symptoms initially; usually fever and abrupt onset of symptoms, as follows:
Malaise
Periocular pain
Lymphadenopathy
Myalgia
Headache
Nausea
Vomiting
Some patients with severe disease have developed a maculopapular or morbilliform rash involving the neck, trunk, arms, or legs.
Neurologic presentations include altered mental status, ataxia and extrapyramidal signs, cranial nerve abnormalities, myelitis, optic neuritis, polyradiculitis, and seizures.
Several patients have experienced severe muscle weakness and flaccid paralysis.
Rare symptoms include myocarditis, pancreatitis, and hepatitis.
Treatment at this time is supportive.
Critical Actions - West Nile Virus
Total leukocyte counts in peripheral blood are often normal or elevated, with lymphopenia and anemia also occurring.
Hyponatremia is sometimes present, particularly among patients with encephalitis.
CSF shows a pleocytosis with a predominance of lymphocytes and moderately elevated protein.
CSF glucose is generally normal.
Test of choice is WNV ELISA (blood or CSF). There can be false-positives with other viral infections.
WNV testing for patients with encephalitis or meningitis can be obtained through local or state health departments:http://www.cdc.gov/ncidod/dvbid/westnile/city_states.htm
The most efficient diagnostic method is detection of IgM antibody to WNV in serum or CSF collected within 8 days of illness onset using the IgM antibody capture enzyme-linked immunosorbent assay (MAC-ELISA).
Since IgM antibody does not cross the blood-brain barrier, IgM antibody in CSF strongly suggests CNS infection.
Patients who have been recently vaccinated against or recently infected with related flaviviruses (eg, yellow fever, Japanese encephalitis, dengue) can have positive WNV MAC-ELISA results.
Management – West Nile Virus
Supportive care includes monitoring, intravenous fluid resuscitation, and control of secondary infection.
Ribavirin in high doses and interferon alpha-2b have been found to have some activity against WNV in vitro, but no controlled studies have been completed on the use of these or other medications, including steroids, antiseizure drugs, or osmotic agents, in the management of WNV encephalitis (CDC WNV fact sheet).
Core Knowledge Points - Reporting Suspected WNV Infection
Refer to local and state health department reporting requirements: www.cdc.gov/ncidod/dvbid/westnile/city_states.htm
WNV encephalitis is on the list of designated nationally notifiable arboviral encephalitides.
Aseptic meningitis is reportable in some jurisdictions.
The timely identification of persons with acute WNV or other arboviral infection can have significant public health implications and will likely augment the public health response to reduce the risk of additional human infections.
Case Development
PCR of CSF for herpes simplex infection was negative.
West Nile Virus ELISA was positive.
Patient was discharged 14 days after admission with mild neurologic sequelae.
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