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Chapter 13 : Meningitis and Encephalitis

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Abstract:

This chapter reviews the two most common central nervous system (CNS) enterovirus (EV) infections, meningitis and encephalitis. Many patients exhibit less discrete signs and symptoms and are described as having ''meningoencephalitis.'' The EVs are the most common cause of aseptic meningitis in the United States as well as an important cause of encephalitis. Autoimmune diseases, malignancies, and reactions to certain drugs are occasionally manifested as aseptic meningitis as well. Children are the primary victims of CNS EV infections. Attack rates for aseptic meningitis among athletes have been higher than those among other students during EV outbreaks. A male-to-female incidence ratio for EV infections of 1.3 to 1.5:1 has been reported. EVs are acquired by fecal-oral contamination and, less commonly, by respiratory droplet. The benign nature of EV meningitis has made human pathologic data for this disease sparse. Disseminated intravascular coagulation and other findings of sepsis result in patients with illness indistinguishable from that due to overwhelming bacterial infection. One of these drugs, disoxaril, protects mice from developing meningoencephalitis due to echoviruses and cured mice of chronic EV meningitis in an experimental model. The most common CNS manifestations of the nonpolio EVs, meningitis and encephalitis, result in significant morbidity for tens of thousands of people in the United States each year.

Citation: Rotbart H. 1995. Meningitis and Encephalitis, p 271-289. In Rotbart H (ed), Human Enterovirus Infections. ASM Press, Washington, DC. doi: 10.1128/9781555818326.ch13

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Aseptic Meningitis
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Infectious Diseases
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Lymphocytic choriomeningitis virus
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Influenza B virus
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Image of FIGURE 1
FIGURE 1

Seasonal occurrence of aseptic meningitis in the United States from 1986 through 1992, as reported to the Centers for Disease Control and Prevention ( ). The striking predominance of cases during the summer months reflects the predominance of EVs as etiologic agents in aseptic meningitis.

Citation: Rotbart H. 1995. Meningitis and Encephalitis, p 271-289. In Rotbart H (ed), Human Enterovirus Infections. ASM Press, Washington, DC. doi: 10.1128/9781555818326.ch13
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Image of FIGURE 2
FIGURE 2

Clinical course of EV aseptic meningitis. Reprinted with permission ( ).

Citation: Rotbart H. 1995. Meningitis and Encephalitis, p 271-289. In Rotbart H (ed), Human Enterovirus Infections. ASM Press, Washington, DC. doi: 10.1128/9781555818326.ch13
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Image of FIGURE 3
FIGURE 3

Computerized tomography scan of the brain of a 9-month-old infant with focal EV encephalitis (case described in the text). An area of low density consistent in location with the child's left-sided focal seizures can be seen in the right parietal lobe. Minimal enhancement was seen with dye injection. (Case and photo courtesy of John Ogle.)

Citation: Rotbart H. 1995. Meningitis and Encephalitis, p 271-289. In Rotbart H (ed), Human Enterovirus Infections. ASM Press, Washington, DC. doi: 10.1128/9781555818326.ch13
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Image of FIGURE 4
FIGURE 4

Serial results of PCR testing for EVs in CSF specimens from a patient with X-linked agammaglobulinemia. Polyacrylamide gel electrophoresis (top) and confirmatory Southern hybridization (bottom) PCR findings are for specimens collected over 18 months from an indwelling Ommaya reservoir or from lumbar punctures in a single patient (lanes A through G). Lanes B, C, D, E, and G were positive; lanes A and F were negative. Negative (lane –) and positive (lane pv) PCR controls and size markers (lane m) are also shown. The arrow indicates a band length of 154 nucleotides, the predicted length of the EV PCR-amplified products when our standard primers are used.

Citation: Rotbart H. 1995. Meningitis and Encephalitis, p 271-289. In Rotbart H (ed), Human Enterovirus Infections. ASM Press, Washington, DC. doi: 10.1128/9781555818326.ch13
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Tables

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TABLE 1

Viral causes of aseptic meningitis in selected large series

Citation: Rotbart H. 1995. Meningitis and Encephalitis, p 271-289. In Rotbart H (ed), Human Enterovirus Infections. ASM Press, Washington, DC. doi: 10.1128/9781555818326.ch13
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TABLE 2

Most common EV isolates, 1984 through 1989

Citation: Rotbart H. 1995. Meningitis and Encephalitis, p 271-289. In Rotbart H (ed), Human Enterovirus Infections. ASM Press, Washington, DC. doi: 10.1128/9781555818326.ch13
Generic image for table
TABLE 3

Relative frequency of neurotropism and neurovirulence among nonpolio EVs

Citation: Rotbart H. 1995. Meningitis and Encephalitis, p 271-289. In Rotbart H (ed), Human Enterovirus Infections. ASM Press, Washington, DC. doi: 10.1128/9781555818326.ch13
Generic image for table
TABLE 4

Controlled long-term outcome studies of EV meningitis occurring in first year of life

Citation: Rotbart H. 1995. Meningitis and Encephalitis, p 271-289. In Rotbart H (ed), Human Enterovirus Infections. ASM Press, Washington, DC. doi: 10.1128/9781555818326.ch13
Generic image for table
TABLE 5

EV PCR: immunocompromised hosts

Citation: Rotbart H. 1995. Meningitis and Encephalitis, p 271-289. In Rotbart H (ed), Human Enterovirus Infections. ASM Press, Washington, DC. doi: 10.1128/9781555818326.ch13
Generic image for table
TABLE 6

EV PCR: clinical CSF specimens

Citation: Rotbart H. 1995. Meningitis and Encephalitis, p 271-289. In Rotbart H (ed), Human Enterovirus Infections. ASM Press, Washington, DC. doi: 10.1128/9781555818326.ch13

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