Encephalitis is an acute inflammatory disease of the brain due to direct viral invasion or to hypersensitivity initiated by a virus or other foreign protein. If the same disorder affects the spinal cord structures as well as the brain, it is now called an encephalomyelitis.
Virus infection may cause encephalitis as a primary manifestation or as a secondary complication. Viruses causing primary encephalitis may be epidemic (arbo-, polio-, echo-, and coxsackie viruses) or sporadic (herpes simplex, herpes zoster).
Most cases of encephalitis occur as a complication of viral infection and are considered to have an immunologic mechanism. Very rarely, encephalitis or other encephalopathies occur as a late consequence of viral infections.
Viral central nervous system (CNS) infections must be differentiated from nonviral and noninfectious causes, but the major diagnostic problem is differentiation from acute or partially treated bacterial meningitis. Diagnosis is usually based on the cerebrospinal fluid (CSF) characteristics, including normal glucose and failure to grow bacteria on culture. Even under ideal circumstances, viruses causing aseptic meningitis and encephalitis are identified in fewer than half the cases.
Viruses are occasionally isolated directly from the CSF or from other tissues. A precise diagnosis, however, usually requires the use of paired serums documenting the rise in antibodies. Since many forms of encephalitis and aseptic meningitis have important public health implications, serum should be drawn and preserved whenever the diagnosis of encephalitis or aseptic meningitis of uncertain etiology is first suspected.
Physical examination is not very helpful, as the findings do not usually point to a specific etiology. Focality, in particular, is almost always-although not uniformly–present in herpes simplex infections, but also can suggest other diseases (2006).
Although herpes simplex encephalitis is clinically similar to other viral encephalitides, repeated seizures occurring early in the course, and localizing signs indicating temporal or frontal lobe involvement, strongly suggest herpes simplex as the cause. The virus is rarely present in the CSF, and serologic tests are not sufficient to implicate herpes simplex virus since antibody levels normally fluctuate even in healthy persons. Diagnosis is certain only upon demonstration of the virus (by recovery of the virus or immunologic techniques) in cerebral tissue obtained by brain biopsy or at a postmortem examination.
The staged approach begins with first-line testing for the most likely causes. It is recommended that cerebrospinal fluid (CSF) polymerase chain reaction (PCR) be used for testing for herpes simplex virus and enterovirus (2006).
In first-line testing, it should also include evaluation of symptomatic body sites and, if suggested clinically or by epidemiologic history, tests for exposure-related pathogens requiring specific treatments, such as tuberculosis (2006).
If the first line testing does not produce a diagnosis, a second line of testing should be engaged. This would include Epstein-Barr serology; Mycoplasma pneumoniae CSF and throat PCR; testing for animal-related pathogens for which there have been relevant exposures; and tests for vectorborne pathogens, such as West Nile virus and other arborviruses, and for Lyme disease, if the epidemiology suggests possible exposures ( 2006).
As a third line, recommended tests for miscellaneous pathogens if they fit the clinical context, include tests such as parvovirus PCR and serology; human immunodeficiency virus PCR and serology; and tests for other specific exposure-related pathogens (2006).
In one study, researchers discovered that T-cells produce a protein, interferon-[gamma], which can clear the virus in neurons located in the spinal cord and brain stem, but not in neurons located in the cerebral cortex ( 2002).
During the experiments, researchers observed that, using interferon-[gamma], CD4 and CD8 T-cells both successfully cleared the virus in the neurons from the spinal cord and brain stem. The neurons in the brain cortex, however, did not react to the interferon-[gamma] in the same manner. This result indicated a site-specific response among neurons to the clearance mechanism. In addition, the researchers observed that another protein produced by the T-cells, tumor necrosis factor [alpha], was unable to clear the virus from the central nervous system.
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