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Aseptic Meningitis

Aseptic meningitis is a benign, self-limiting illness, and severe illness and death are uncommon. The treatment is symptomatic and the majority of patients recover in approximately 1 week. Enteroviruses typically are spread person to person through the fecal-oral or oral-oral routes and through respiratory droplets and fomites. Adherence to good hygienic practices, such as frequent and thorough hand washing (especially after diaper changes), disinfection of contaminated surfaces by household cleaners (e.g., diluted bleach solution), and avoidance of shared utensils and drinking containers, are recommended to help interrupt transmission.

Aseptic meningitis is a central nervous system infection characterized by fever and meningeal symptoms with moderate, predominantly lymphocytic CSF pleocytosis and the absence of bacterial pathogens in CSF. The disease occurs both sporadically and in outbreaks, and >90% of cases with an identified cause are associated with enteroviruses (2). Many aseptic meningitis outbreaks occurring during the current enterovirus season reflect high levels of E9 and E30 activity. In 2003, E9 has been involved predominantly in the outbreaks in the East, and E30 has been linked exclusively with outbreaks in the West.

During 1970–2001, both E9 and E30 were among the 15 enteroviruses reported most commonly each year, accounting for 10.2% and 8.2% of all enterovirus isolates reported to CDC, respectively (CDC, unpublished data, 2003). However, these enteroviruses have been relatively quiescent in recent years; E9 has not been the predominant enterovirus isolated from clinical specimens since 1995, and E30 has not been widespread since 1998 (7,8). This probably has resulted in an accumulation of cohorts of susceptible persons who have not been exposed previously to these agents. The increase in aseptic meningitis cases associated with high activity of E9 and E30 is consistent with the historic data; during 1988–1999, peak years for viral meningitis hospitalizations in the United States coincided with periods of high activity of either E9 or E30 (1).

Although the majority of cases of enterovirus infections are asymptomatic or result in mild febrile illnesses, aseptic meningitis is the predominant diagnosis reported with the current E9 and E30 activity in the United States because patients with meningitis are more likely to be tested for enteroviruses than those with less severe manifestations. In a small proportion of cases, more severe, life-threatening diseases (e.g., encephalitis, paralysis, myopericarditis, and neonatal enteroviral sepsis) might occur.

Enteroviruses typically demonstrate a marked seasonality in temperate climates, with a typical enterovirus season in the United States occurring during June – October (9). In 2003, the enterovirus season appears to have started early, with the first isolations of E9 reported in January (in Louisiana), the first outbreaks of E9-associated aseptic meningitis reported in March, and the first isolations of E30 reported in April (in Arizona).

WNV has the same seasonal pattern as enteroviruses, and is associated with neurologic signs and symptoms of aseptic meningitis. However, WNV-associated meningitis tends to occur among older persons (median age: 46 years) (10), whereas children and young adults (median age: 13 years) are at highest risk for enteroviral meningitis (1). The investigation of an aseptic meningitis outbreak in an area of high WNV epizootic activity in 2001 indicated that enteroviruses were the leading cause of aseptic meningitis in this area, and no evidence of WNV infection was detected (10). For this reason, diagnostic testing of specimens from younger patients with aseptic meningitis should include testing for enteroviruses, even during a documented WNV outbreak (10).

Early etiologic diagnosis of aseptic meningitis helps to avoid unnecessary antibiotic treatment and additional testing. Although virus culture is the standard technique for enterovirus detection, it consumes time and resources and has limited clinical use. Molecular methods of enterovirus detection (e.g., PCR and typing based on genomic sequences) are increasingly becoming available. Serotype-specific PCR primers have been developed by CDC for several enteroviruses, including E30 (5). These serotype-specific primers are useful for rapid differentiation of cases in patients infected with the outbreak strain from sporadic infections with other enteroviruses.

No specific prevention or control measures are available for nonpolio enteroviruses including E9 and E30. Adherence to good hygienic practices, such as frequent and thorough hand washing (especially after diaper changes), disinfection of contaminated surfaces by household cleaners (e.g., diluted bleach solution), and avoidance of shared utensils and drinking containers, are recommended to help interrupt transmission.

1. Rotbart HA. Viral meningitis. Semin Neurol 2000;20:277-92.
2. Oberste MS, Nix WA, Maher K, Pallansch MA. Improved molecular identification of enteroviruses by RT-PCR and amplicon sequencing. J Clin Virol 2003;26:375-7.
3. CDC. Healthy swimming. Your disinfection team: chlorine and pH. Atlanta, Georgia: U.S. Department of Health and Human Services, CDC, 2004. Available at
meningitis associated with echoviruses 9 and 30 and preliminary surveillance reports on enterovirus activity-United States, 2003. MMWR 2003;52:761-4.
5. American Academy of Pediatrics. Enterovirus (nonpoliovirus) infections. In: Pickering LK, ed. Red Book: 2003 report of the Committee on Infectious Diseases, 26th ed. Elk Grove Village, Illinois: American Academy of Pediatrics, 2003:269-70.
6. Kee F, McElroy G, Stewart D, Coyle P, Watson J. A community outbreak of echovirus infection associated with an outdoor swimming pool. J Pub Health Med 1994;16:145-8.
7. Lenaway DD, Brockmann R, Dolan GJ, Cruz-Uribe F. An outbreak of an enterovirus-like illness at a community wading pool: implications for public health inspection programs. Am J Public Health 1989; 79:889-90.
8. Hawley HB, Morin DP, Geraghty ME, Tomkow J, Phillips CA. Coxsackievirus B epidemic at a boys' summer camp: isolation of virus from swimming water. JAMA 1973;226:33-6.
9. CDC. Surveillance for waterborne-disease outbreaks-United States, 1999-2000. In: CDC Surveillance Summaries (November 22). MMWR 2002;51(No. SS-8).
10. CDC. Surveillance data from swimming pool inspections-selected states and counties, United States, May-September 2002. MMWR 2003;52:513-6.

Disease Reporting

See Also
CDC's viral (aseptic) meningitis fact sheet
Additional references for clinicians:

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