20/3/25, 8:51 a.m.

Viral meningitis in children: Epidemiology, pathogenesis, and etiology - UpToDate

Official reprint from UpToDate®

www.uptodate.com © 2025 UpToDate, Inc. and/or its affiliates. All Rights Reserved.

Viral meningitis in children: Epidemiology,

pathogenesis, and etiology
AUTHOR: Cecilia Di Pentima, MD
SECTION EDITOR: Sheldon L Kaplan, MD
DEPUTY EDITOR: Carrie Armsby, MD, MPH

All topics are updated as new evidence becomes available and our peer review process is complete.

Literature review current through: Feb 2025.

This topic last updated: Mar 12, 2025.

INTRODUCTION

Viral meningitis is defined as:

● A febrile illness with clinical signs and symptoms of meningeal irritation

● No associated neurologic dysfunction
● No evidence of bacterial pathogens in the cerebrospinal fluid (CSF) in a patient who has
not received prior antibiotics

The epidemiology, pathogenesis, and etiology of viral meningitis will be reviewed here. Other
related topics include:

● (See "Viral meningitis in children: Clinical features and diagnosis".)

● (See "Viral meningitis in children: Management, prognosis, and prevention".)
● (See "Bacterial meningitis in children older than one month: Clinical features and
diagnosis".)
● (See "Bacterial meningitis in children older than one month: Treatment and prognosis".)

EPIDEMIOLOGY

Reported incidence rates of viral meningitis range from 10 to 20 cases per 100,000 children
per year [1-3]. In the United States, viral meningitis accounts for approximately 26,000 to
42,000 hospitalizations each year [4]. The incidence is highest among infants <1 year old,
with a second peak occurring in children >5 years old [3,4]. In temperate climates, most

https://www.uptodate.com/contents/viral-meningitis-in-children-epidemiology-pathogenesis-and-etiology/print?search=meningitis+pediatria&source=search_re… 1/22
20/3/25, 8:51 a.m. Viral meningitis in children: Epidemiology, pathogenesis, and etiology - UpToDate

cases occur in the summer and autumn, reflecting the peak activity of enteroviral and
arthropod-borne infections ( table 1) [5,6].

PATHOGENESIS

Most viral pathogens affecting the central nervous system (CNS) initially infect mucosal
surfaces of the respiratory and gastrointestinal tract, followed by viral replication in regional
lymph nodes. This precedes a primary viremia that signals the onset of illness and
subsequent seeding of other organs. Except for neonatal herpes simplex virus (HSV)
infection, most viruses reach the CNS during a second viremia that follows viral replication in
other organs, particularly the liver and spleen [7].

The mechanisms involved in viral transport from the circulation to the brain are not clearly
understood. However, it is clear that trans endothelial passage of the virus occurs in vessels
of the choroid plexus, meninges, or cerebrum by one or more of the following mechanisms
[7]:

● Bridging the endothelium within migrating leukocytes

● Pinocytosis or colloidal transport
● Breaking through damaged endothelium
● Direct infection of endothelial cells

The pathogenesis of viral meningitis associated with specific viruses is discussed below.

ETIOLOGY

Enteroviruses (EVs) are the most common cause of viral meningitis [1,6]. Other important
causes of viral meningitis in children include human parechoviruses, herpesviruses,
arboviruses, lymphocytic choriomeningitis virus (LCMV), rabies, and influenza.

Enteroviruses

● Epidemiology – EVs are responsible for approximately 85 percent of cases of viral

meningitis [6,8]. Nonpolio-EV serotypes cycle from year to year; however, certain serotypes
have remained prevalent. Coxsackieviruses A6 and B3 and echoviruses 30, 18, 9, and 11
were the most common serotypes detected in the United States from 2014 to 2016 [9]. EV-
D68 was by far the most commonly detected EV during this time, but this was associated
with a large outbreak in the United States during 2014 [10]. The epidemiology of EV
infection is discussed in greater detail separately. (See "Enterovirus and parechovirus
infections: Epidemiology and pathogenesis", section on 'Epidemiology'.)

https://www.uptodate.com/contents/viral-meningitis-in-children-epidemiology-pathogenesis-and-etiology/print?search=meningitis+pediatria&source=search_re… 2/22
20/3/25, 8:51 a.m. Viral meningitis in children: Epidemiology, pathogenesis, and etiology - UpToDate

EVs are an important cause of meningitis in neonates and young infants (<3 months) [8].
Meningitis in infants under three months of age has been associated mainly with group B
coxsackieviruses and parechoviruses [11-14]. (See "Enterovirus and parechovirus
infections: Clinical features, laboratory diagnosis, treatment, and prevention", section on
'Neonates'.)

EV-71, closely related to coxsackievirus A16 and the viral agent of hand-foot-mouth
disease, has emerged as a significant cause of viral meningitis, encephalitis, and myelitis. It
has been responsible for major outbreaks in Asia and sporadic cases in the United States
and Europe [15-19]. (See "Enterovirus and parechovirus infections: Epidemiology and
pathogenesis", section on 'Periodicity and variability of disease by serotype'.)

Approximately 1 percent of wild poliovirus infections are associated with paralytic illness.
More common clinical presentations in susceptible individuals are asymptomatic
infections, minor illness or abortive poliomyelitis, and aseptic meningitis or nonparalytic
poliomyelitis. With successful vaccine eradication campaigns, polioviruses are no longer
recovered from patients with aseptic meningitis in resource-abundant countries and only
rarely in resource-limited countries where poliomyelitis still occurs. Vaccine strains from
the oral polio vaccine have rarely been recovered from the cerebrospinal fluid (CSF) of
patients with aseptic meningitis [20-22]. (See "Poliomyelitis and post-polio syndrome",
section on 'Poliomyelitis'.)

● Transmission – Humans are the only known reservoir for EVs, and transmission of EV
occurs most commonly by the fecal-oral route. A few members of the EV genus can be
acquired by inhalation of infected droplets. Transplacental transmission resulting in
stillbirth, abortion, or neonatal infection has been described with many different EVs,
including polioviruses, coxsackieviruses, and EV-71 [23,24].

● Seasonality, risk factors, and incubation – In temperate climates, most EV infections

occur in outbreaks during the warmest months; however, sporadic cases can develop
throughout the year. In the United States, infections are seen more frequently from June to
October [9]. In tropical and subtropical regions, the incidence of EV infections remains
stable throughout the year. Individual host factors, such as immunodeficiency and age,
can predispose to more severe nonpolio EV infections. Furthermore, children with a
deficient humoral immunodeficiency, especially X-linked agammaglobulinemia, are at risk
for developing chronic meningoencephalitis [25]. The incubation period for EV infection is
approximately three to six days.

● Pathogenesis – The pathogenesis of EV infections has been extensively studied; however,

many questions remain unsolved [26]. Following exposure, viral particles bind to specific
receptors on enterocytes and traverse the intestinal lining cells to reach the Peyer's
patches in the lamina propria, where they replicate [26]. Few viral particles may replicate in
https://www.uptodate.com/contents/viral-meningitis-in-children-epidemiology-pathogenesis-and-etiology/print?search=meningitis+pediatria&source=search_re… 3/22
20/3/25, 8:51 a.m. Viral meningitis in children: Epidemiology, pathogenesis, and etiology - UpToDate

the nasopharynx, with subsequent spread to the respiratory tract lymphatics. An initial
viremia spreads the virus to other organs such as the liver, spleen, and heart, where
further replication occurs, generating a second major viremia that is associated with signs
and symptoms of infection [26]. Seeding of the central nervous system (CNS) can occur
during the first or second viremia; however, the mechanisms by which the virus enters the
CNS remain unknown [26]. An alternative path involving neural spread has been proposed
[26,27]. The molecular determinants of neurotropism and neurovirulence have been
extensively studied for polioviruses and are now under investigation for nonpolio EVs.
Genomic differences among EV serotypes might explain the tendency of some strains to
cause aseptic meningitis and encephalitis [26].

Human parechoviruses — The parechoviruses share many biologic, clinical, and

epidemiologic characteristics with the enteroviruses but differ sufficiently in genomic
sequence to be classified as a separate genus. Four species (parechovirus A to D) and 14
parechovirus serotypes are now recognized. (See "Enterovirus and parechovirus infections:
Epidemiology and pathogenesis", section on 'Classification'.)

Human parechoviruses (HPeV) account for the second most common cause of viral
meningitis in children, especially under three months of age [8]. Most cases of severe disease
are in infants younger than three months and are caused by HPeV type 3 [28]. (See
"Enterovirus and parechovirus infections: Clinical features, laboratory diagnosis, treatment,
and prevention", section on 'Neonates'.)

Symptoms of CNS involvement, including neonatal sepsis, meningitis, encephalitis, and

paralysis, have been reported with HPeV types 1 and 3 [14,29-38].

HPeV have been identified in Asia [39-41], Australia [38], Europe [13,42-44], North America
[36,45-47], and South America [48]. The rate of isolation from the CSF is usually highest
between June and October but varies from region to region and year to year (eg, from 0.4 to
8.2 percent in the Netherlands and 0 to 17 percent in the United States) [13,36,37].

Herpesviruses — All members of the Herpesviridae family can cause viral meningitis;
however, herpes simplex viruses (HSVs) are classically associated with neurologic infection
[26]. Cytomegalovirus, varicella-zoster virus (VZV), human herpesvirus (HHV)-6 and HHV-7,
and Epstein-Barr virus (EBV) infections are only infrequently associated with meningitis. (See
"Human herpesvirus 6 infection in children: Clinical manifestations, diagnosis, and
treatment", section on 'Less common manifestations'.)

Members of the Herpesviridae family share similar features: The virion, roughly spherical and
encased by an envelope, measures 15 to 200 nm in diameter and contains a large double-
stranded DNA molecule. Primary infection is followed by lifelong infection, with the potential
risk for reactivation.

https://www.uptodate.com/contents/viral-meningitis-in-children-epidemiology-pathogenesis-and-etiology/print?search=meningitis+pediatria&source=search_re… 4/22
20/3/25, 8:51 a.m. Viral meningitis in children: Epidemiology, pathogenesis, and etiology - UpToDate

Herpesviridae have a worldwide distribution. Humans are the only reservoir for transmission
to susceptible individuals. Infections occur worldwide without seasonal prevalence.

Herpes simplex virus — CNS infections caused by HSV can have devastating sequelae,
particularly in neonates. In a retrospective cross-sectional study performed at 23 North
American emergency departments, the prevalence of HSV infection among infants <60
days old undergoing meningitis evaluation was 0.42 percent [49].

The postulated mechanisms involved in the spread of HSV-1 to the brain include
hematogenous dissemination, direct extension through the cribriform plate from infection
of nasopharyngeal mucosa, or via neurogenic pathways [50,51]. Whether HSV-2 reaches
the meninges by neuronal or hematogenous dissemination is under debate [52]. Humoral
immunity does not prevent recurrent infections [53].

● HSV-1 – HSV-1 is primarily transmitted by direct contact; therefore, the incidence of HSV-
1 infection is influenced by socioeconomic status, age, and geographic location [53]. In
resource-limited countries, 70 to 80 percent of adolescents have serologic evidence of
HSV-1 infection, while the age-specific prevalence of HSV-1 is decreasing in resource-
abundant countries [52,53]. HSV-1 is the most common etiologic agent of sporadic
necrotizing encephalitis, representing more than 85 percent of all cases, and is
infrequently associated with aseptic meningitis [52,54,55]. Neonatal infections due to
HSV-1 account for 25 percent of all cases of neonatal HSV infection, with an overall
incidence of HSV infection in newborns ranging from 1 case in 2000 to 5000 deliveries
per year [53]. (See "Neonatal herpes simplex virus (HSV) infection: Clinical features and
diagnosis", section on 'Epidemiology and transmission'.)

Infections with HSV-2 are acquired mainly by sexual contact; however, increasing
proportions of genital infections are due to HSV-1, acquired from orolabial lesions and
herpetic whitlow [53]. Aseptic meningitis syndrome is usually caused by HSV-2 primary
infection; it occurs mainly in adults but can occur in young children [56].

● HSV-2 – HSV-2 accounts for 75 percent of neonatal infections due to HSV. Infants
become colonized with HSV mainly by vertical transmission through the vaginal canal
and less frequently by ascending infection or during the postnatal period by horizontal
transmission. The rate of perinatal transmission is 30 to 50 percent with maternal
primary infection and 3 percent with recurrent infection [57]. (See "Genital herpes
simplex virus infection and pregnancy".)

Clinical symptoms of meningitis have been reported in 36 percent of women and 11

percent of men with primary HSV-2 infection, but only 25 to 33 percent of patients with
HSV meningitis ever report a history of genital lesions [52,54,58]. Furthermore, recurrent
meningitis has been reported in 25 percent of adult patients with HSV-2 meningitis and

https://www.uptodate.com/contents/viral-meningitis-in-children-epidemiology-pathogenesis-and-etiology/print?search=meningitis+pediatria&source=search_re… 5/22
20/3/25, 8:51 a.m. Viral meningitis in children: Epidemiology, pathogenesis, and etiology - UpToDate

can occur in young children (but rarely in neonates) [52,55,59-61]. Neonates, however,
can develop recurrent episodes of encephalitis.

Mollaret meningitis is characterized by recurrent episodes of aseptic meningitis. Using

polymerase chain reaction-based testing, HSV-2 has been strongly associated with
Mollaret meningitis, a form of benign recurrent aseptic meningitis [6,62,63]. An
additional few cases have been reported due to HSV-1 and EBV [6,64,65].

In the majority of patients, HSV mucosal lesions precede signs and symptoms of
meningeal inflammation, with a mean interval of one week [52]. In general, neonates
with disseminated and localized infections usually develop symptoms earlier than
neonates with CNS infections: on average, 9 to 11 days and 16 to 17 days, respectively
[66]. Beyond the neonatal period, the incubation period ranges from 2 days to 12 days,
with a mean of four days [53].

Varicella-zoster virus — Since the introduction of the varicella vaccine, the incidence of
VZV infection in children has declined substantially [67]. Furthermore, the overall incidence
of neurologic complications of VZV infection in healthy children is less than 1 percent (most
frequently, acute cerebellar ataxia and encephalitis). (See "Clinical features of varicella-
zoster virus infection: Chickenpox" and "Epidemiology of varicella-zoster virus infection:
Chickenpox".)

Aseptic meningitis is a rare complication of chickenpox and herpes zoster [26,68-70]. The
syndrome known as zoster sine herpete is characterized by the presence of CSF
pleocytosis, documented CNS infection with VZV by polymerase chain reaction, and
absence of typical skin lesions [26].

Cytomegalovirus and Epstein-Barr virus — Meningitis due to cytomegalovirus and EBV is

also rare; however, aseptic meningitis is the most common neurologic complication seen
in patients with primary EBV infection [71,72]. The prevalence of EBV infection in pediatric
patients has a direct correlation with socioeconomic status, with the highest incidence
seen in resource-limited countries. In the United States, approximately 50 percent of five-
year-old children are seropositive for EBV [71]. (See "Clinical manifestations and treatment
of Epstein-Barr virus infection".)

Human herpesvirus 6 and 7 — HHV-6, the etiologic agent of roseola, or exanthem

subitum, is a common cause of febrile seizures in infancy and has been associated with
meningitis in this age group [26,73] (see "Human herpesvirus 6 infection in children:
Clinical manifestations, diagnosis, and treatment", section on 'Less common
manifestations'). HHV-7, also associated with exanthem subitum and febrile seizures in
infancy, can also cause meningitis in children [74,75]. (See "Human herpesvirus 7
infection".)

https://www.uptodate.com/contents/viral-meningitis-in-children-epidemiology-pathogenesis-and-etiology/print?search=meningitis+pediatria&source=search_re… 6/22
20/3/25, 8:51 a.m. Viral meningitis in children: Epidemiology, pathogenesis, and etiology - UpToDate

Arboviruses — Arboviruses are a heterogeneous group of arthropod-borne RNA viruses

responsible for important epidemics of CNS infections worldwide; these infections have been
increasing in frequency [33]. Although encephalitis and meningoencephalitis are more
commonly recognized as hallmarks of CNS infection by most of these viruses, aseptic
meningitis is an important clinical manifestation of their disease spectrum [26].

Of the seven taxonomic families of arboviruses, three are more commonly involved in human
disease: Flaviviridae, Togaviridae, and Bunyaviridae ( table 2) [76]. Important arboviruses
endemic in the United States include:

● West Nile virus (WNV) (see "Clinical manifestations and diagnosis of West Nile virus
infection")
● Eastern equine encephalitis virus (see "Arthropod-borne encephalitides", section on
'Eastern equine encephalitis virus')
● Western equine encephalitis virus (see "Arthropod-borne encephalitides", section on
'Western equine encephalitis virus')
● La Cross virus (see "Arthropod-borne encephalitides", section on 'California serogroup
viruses')
● St. Louis encephalitis virus (see "Arthropod-borne encephalitides", section on 'Specific
viruses')

Other arboviruses are discussed separately. (See "Arthropod-borne encephalitides".)

The pathogenesis of arboviral CNS infection is relatively similar for all pathogens. Viruses are
inoculated subcutaneously or intravenously during the bite of an infected vector (most
commonly, mosquitoes) ( table 2). Replication in the skin or muscle precedes a primary
viremia that subsequently spreads the virus to the reticuloendothelial system or to the CNS.
(See "Arthropod-borne encephalitides".)

Arboviruses have a worldwide distribution, with the highest incidence in tropical and
resource-limited regions. In the United States, arboviruses constitute most of the cases of
viral meningitis that are not due to EV [77,78]. The incubation period for arboviral infections
ranges from 1 to 18 days ( table 2). (See "Arthropod-borne encephalitides".)

Most arboviruses are maintained in nature in a cycle involving a nonhuman primary

vertebrate host and a primary arthropod vector that determine their geographic and
seasonal distribution [79]. Human infections are seen most frequently at the peak of
mosquito and tick activity during summer and fall or sporadically when the virus is brought
into the peridomestic environment by a bridge vector [79]. The geographic distribution of
arboviral infections in the United States is shown in the table ( table 2).

The age distribution of infection varies according to the virus. Children are generally more
susceptible than adults to CNS infections, particularly with infections due to St. Louis
https://www.uptodate.com/contents/viral-meningitis-in-children-epidemiology-pathogenesis-and-etiology/print?search=meningitis+pediatria&source=search_re… 7/22
20/3/25, 8:51 a.m. Viral meningitis in children: Epidemiology, pathogenesis, and etiology - UpToDate

encephalitis, Eastern equine encephalitis, and Western equine encephalitis [76].

WNV has emerged as a major public health concern in the United States and Europe [80-84].
In a report from a national arboviral surveillance program in the United States from 2003
through 2012, the most common arboviral causes of meningitis in children were WNV and La
Crosse virus [80-84]. La Cross virus tends to cause infection in younger children than does
WNV [83]. WNV persists in nature as part of an enzootic cycle among wild birds, the primary
reservoir, and Culex spp, the main mosquito vector. In the United States, as well as in other
temperate climates, WNV infections coincide with maximal mosquito activity. In the United
States, outbreaks occur from July to October, with the highest incidence seen in August
[80,85]. (See "Epidemiology and pathogenesis of West Nile virus infection".)

Other viruses

Lymphocytic choriomeningitis virus — LCMV is an enveloped, single-stranded RNA virus

member of the Arenaviridae family. It is a rare cause of human CNS infections in developed
countries.

Rodents, including hamsters, rats, and mice, harbor and shed LCMV in nasal secretions,
saliva, urine, semen, milk, and feces. Children living in impoverished conditions are at
higher risk of acquiring the infection through ingestion of animal-urine-contaminated
food, exposure of open wounds to contaminated dirt, or inhalation of aerosolized virus
[86].

Transplacental infection with LCMV was first described in the United States in 1992,
although initially reported in England in 1955 [86]. Transmission to the fetus occurs
primarily during maternal viremia [86]. LCMV infections occur most commonly during the
winter months, when rodents seek food and shelter in human dwellings.

Rabies — Rabies is an enveloped, bullet-shaped RNA virus that causes fatal CNS infection
[68]. Transmission of rabies from animal to human occurs mainly through direct contact
with saliva from a rabid animal onto mucous membranes or into open wounds or by direct
inoculation through a bite, followed by local replication and subsequent spread to the CNS
[87]. Once the virus enters neuronal cells, it moves by passive neuronal transit, reaching
the CNS by retrograde axonal transport. After reaching the CNS, there is a subsequent
centrifugal spread back to peripheral sites, including the salivary and submaxillary glands.
Following inhalation of viral particles, rabies virus reaches the CNS by direct neuronal
transmission through the olfactory tract after initial replication in the olfactory epithelium
[87]. (See "Clinical manifestations and diagnosis of rabies".)

Not all humans bitten by a rabid animal develop infection [87]. The incubation period is
generally 20 to 60 days; however, it can be a short as five to six days and as long as six

https://www.uptodate.com/contents/viral-meningitis-in-children-epidemiology-pathogenesis-and-etiology/print?search=meningitis+pediatria&source=search_re… 8/22
20/3/25, 8:51 a.m. Viral meningitis in children: Epidemiology, pathogenesis, and etiology - UpToDate

months to seven years [68]. Travelers to hyperendemic areas, especially children, are at
increased risk.

Influenza — Influenza A and B viruses have been associated with different neurologic
syndromes in children, including aseptic meningitis and acute necrotizing encephalitis or
encephalopathy [26,88,89]. Influenza viruses are orthomyxoviruses of three antigenic
types: A, B, and C. Influenza viruses are subclassified according to two surface antigens,
neuraminidase and hemagglutinin, with shift and drifts accounting for pandemics and
outbreaks [68,88]. (See "Influenza: Epidemiology and pathogenesis".)

In temperate climates, the circulation of influenza viruses has a seasonal variation, with a
peak incidence in the United States during the months of January and February. Children
younger than five years are at increased risk for influenza A virus infection of the CNS,
mainly encephalitis. Although less frequent, influenza B virus can also be associated with
CNS infections, mainly in children and adolescents [68,90,91]. (See "Seasonal influenza in
children: Clinical features and diagnosis", section on 'Central nervous system'.)

Involvement of the CNS is a rare complication of influenza virus infection, mainly

presenting as encephalitis rather than aseptic meningitis [88,89]. Children younger than
five years are at higher risk for the development of neurologic complications independent
of the strain involved [68]. Of the 121 children with fatal Fujian influenza A (a drift strain) in
the United States in the 2003 to 2004 season, 60 percent were younger than five years (46
percent of these between 6 and 23 months of age) and a number of these patients had
encephalitis [92]. The pathogenesis of influenza viral infection of the CNS remains unclear
[68].

Severe acute respiratory syndrome coronavirus 2 — Although very rare, severe acute
respiratory syndrome coronavirus 2 (SARS-CoV-2) can present with neurologic
manifestations in the absence of respiratory symptoms, including meningitis [93,94]. SARS-
CoV-2 infection in children is discussed separately. (See "COVID-19: Clinical manifestations
and diagnosis in children".)

Less common viruses — Less common viral pathogens associated with aseptic meningitis
and their geographic distribution are listed in the table ( table 3).

Human metapneumovirus (hMPV) is a common cause of upper and lower respiratory tract
infections in children. The ability of hMPV to invade the CNS was demonstrated in an infant
with fatal encephalitis [95]. hMPV has been isolated from respiratory specimens in children
with neurologic manifestations, but who lacked evidence of hMPV in the CSF [96,97].

Adenoviruses are responsible for a wide range of clinical manifestations affecting the
respiratory tract, gastroenteritis, cystitis, and conjunctivitis. Life-threatening infections

https://www.uptodate.com/contents/viral-meningitis-in-children-epidemiology-pathogenesis-and-etiology/print?search=meningitis+pediatria&source=search_re… 9/22
20/3/25, 8:51 a.m. Viral meningitis in children: Epidemiology, pathogenesis, and etiology - UpToDate

such as myocarditis and meningoencephalitis are rare but increasingly recognized [98].
(See "Pathogenesis, epidemiology, and clinical manifestations of adenovirus infections".)

INFORMATION FOR PATIENTS

UpToDate offers two types of patient education materials, "The Basics" and "Beyond the
Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th
grade reading level, and they answer the four or five key questions a patient might have
about a given condition. These articles are best for patients who want a general overview
and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are
longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th
grade reading level and are best for patients who want in-depth information and are
comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to
print or email these topics to your patients. (You can also locate patient education articles on
a variety of subjects by searching on "patient info" and the keyword[s] of interest.)

● Basics topics (see "Patient education: Viral meningitis (The Basics)")

SUMMARY

● Epidemiology – In children, viral meningitis occurs most frequently in infants <1 year old,
with a second peak occurring in children >5 years old. In the United States, the peak
incidence occurs from late spring to autumn, reflecting the peak activity of enteroviral and
arthropod-borne infections ( table 1). (See 'Epidemiology' above.)

● Pathogenesis – Most viral pathogens affecting the central nervous system (CNS) initially
infect mucosal surfaces of the respiratory and gastrointestinal tract and reach the CNS
through viremia following viral replication. (See 'Pathogenesis' above.)

● Etiology – Enteroviruses (EVs) are the most common cause of viral meningitis. Other
important causes of viral meningitis in children include human parechoviruses,
herpesviruses, arboviruses, lymphocytic choriomeningitis virus (LCMV), rabies, and
influenza. (See 'Etiology' above.)

Use of UpToDate is subject to the Terms of Use.

REFERENCES

https://www.uptodate.com/contents/viral-meningitis-in-children-epidemiology-pathogenesis-and-etiology/print?search=meningitis+pediatria&source=search_r… 10/22
20/3/25, 8:51 a.m. Viral meningitis in children: Epidemiology, pathogenesis, and etiology - UpToDate

1. Michos AG, Syriopoulou VP, Hadjichristodoulou C, et al. Aseptic meningitis in children:

analysis of 506 cases. PLoS One 2007; 2:e674.

2. Martin NG, Iro MA, Sadarangani M, et al. Hospital admissions for viral meningitis in
children in England over five decades: a population-based observational study. Lancet
Infect Dis 2016; 16:1279.

3. Hviid A, Melbye M. The epidemiology of viral meningitis hospitalization in childhood.

Epidemiology 2007; 18:695.

4. Centers for Disease Control and Prevention (CDC). Outbreaks of aseptic meningitis
associated with echoviruses 9 and 30 and preliminary surveillance reports on
enterovirus activity--United States, 2003. MMWR Morb Mortal Wkly Rep 2003; 52:761.
5. Nigrovic LE. Aseptic meningitis. Handb Clin Neurol 2013; 112:1153.
6. Bronstein DE, Glaser CA. Aseptic meningitis and viral meningitis. In: Feigin and Cherry's t
extbook of pediatric infectious diseases, 8th, Cherry JD, Harrison GJ, Kaplan SL, Steinbac
h WJ, Hotes PJ (Eds), Elsevier, Philadelphia 2019. Vol 1, p.355.
7. Cassady K, Gnann JW, Whitley RJ. Viral infections of the central nervous system. In: Thera
py of Infectious Diseases, Baddour L, Gorbach S (Eds), WB Saunders, Philadelphia 2003.
p.237.
8. Kadambari S, Abdullahi F, Celma C, Ladhani S. Epidemiological trends in viral meningitis
in England: Prospective national surveillance, 2013-2023. J Infect 2024; 89:106223.
9. Khetsuriani N, Lamonte-Fowlkes A, Oberst S, et al. Enterovirus surveillance--United
States, 1970-2005. MMWR Surveill Summ 2006; 55:1.
10. Abedi GR, Watson JT, Nix WA, et al. Enterovirus and Parechovirus Surveillance - United
States, 2014-2016. MMWR Morb Mortal Wkly Rep 2018; 67:515.

11. Kaplan MH, Klein SW, McPhee J, Harper RG. Group B coxsackievirus infections in infants
younger than three months of age: a serious childhood illness. Rev Infect Dis 1983;
5:1019.

12. Khetsuriani N, Lamonte A, Oberste MS, Pallansch M. Neonatal enterovirus infections

reported to the national enterovirus surveillance system in the United States, 1983-2003.
Pediatr Infect Dis J 2006; 25:889.

13. Wolthers KC, Benschop KS, Schinkel J, et al. Human parechoviruses as an important viral
cause of sepsislike illness and meningitis in young children. Clin Infect Dis 2008; 47:358.
14. Evans AS, Singh S, Joshi C, et al. Examining Clinical Features and Severe Neurologic
Disease of Parechovirus Infection in Young Infants: A Multistate Cohort Study. Clin Infect
Dis 2024; 79:1479.
15. Li CC, Yang MY, Chen RF, et al. Clinical manifestations and laboratory assessment in an
enterovirus 71 outbreak in southern Taiwan. Scand J Infect Dis 2002; 34:104.

https://www.uptodate.com/contents/viral-meningitis-in-children-epidemiology-pathogenesis-and-etiology/print?search=meningitis+pediatria&source=search_r… 11/22
20/3/25, 8:51 a.m. Viral meningitis in children: Epidemiology, pathogenesis, and etiology - UpToDate

16. Herrero LJ, Lee CS, Hurrelbrink RJ, et al. Molecular epidemiology of enterovirus 71 in
peninsular Malaysia, 1997-2000. Arch Virol 2003; 148:1369.
17. Kehle J, Roth B, Metzger C, et al. Molecular characterization of an Enterovirus 71 causing
neurological disease in Germany. J Neurovirol 2003; 9:126.
18. Alexander JP Jr, Baden L, Pallansch MA, Anderson LJ. Enterovirus 71 infections and
neurologic disease--United States, 1977-1991. J Infect Dis 1994; 169:905.
19. Pérez-Vélez CM, Anderson MS, Robinson CC, et al. Outbreak of neurologic enterovirus
type 71 disease: a diagnostic challenge. Clin Infect Dis 2007; 45:950.
20. Gutierrez K, Abzug MJ. Vaccine-associated poliovirus meningitis in children with
ventriculoperitoneal shunts. J Pediatr 1990; 117:424.

21. Centers for Disease Control and Prevention (CDC). Acute flaccid paralysis associated with
circulating vaccine-derived poliovirus--Philippines, 2001. MMWR Morb Mortal Wkly Rep
2001; 50:874.

22. Inaba H, Hori H, Ito M, et al. Polio vaccine virus-associated meningoencephalitis in an

infant with transient hypogammaglobulinemia. Scand J Infect Dis 2001; 33:630.
23. Chow KC, Lee CC, Lin TY, et al. Congenital enterovirus 71 infection: a case study with
virology and immunohistochemistry. Clin Infect Dis 2000; 31:509.
24. Cherry, JD, Krogstad, P. Enterovirus and parechovirus infections. In: Infectious Diseases o
f the Fetus and Newborn Infant, 7th ed, Remington, JS, Klein, JO, Wilson, CB, et al (Eds), E
lsevier Saunders, Philadelphia 2011. p.756.

25. Minor P. Characteristics of poliovirus strains from long-term excretors with primary
immunodeficiencies. Dev Biol (Basel) 2001; 105:75.

26. Rotbart HA. Viral meningitis and the aseptic meningitis syndrome. In: Infections of the C
entral Nervous System, 2nd ed, Scheld MW, Durack WR (Eds), Lippincott Raven, Philadelp
hia 1997. p.23.

27. Wyatt HV. Provocation poliomyelitis and entry of poliovirus to the CNS. Med Hypotheses
1976; 2:269.
28. Kadambari S, Harvala H, Simmonds P, et al. Strategies to improve detection and
management of human parechovirus infection in young infants. Lancet Infect Dis 2019;
19:e51.
29. Levorson RE, Jantausch BA. Human parechoviruses. Pediatr Infect Dis J 2009; 28:831.
30. Boivin G, Abed Y, Boucher FD. Human parechovirus 3 and neonatal infections. Emerg
Infect Dis 2005; 11:103.
31. Benschop KS, Schinkel J, Minnaar RP, et al. Human parechovirus infections in Dutch
children and the association between serotype and disease severity. Clin Infect Dis 2006;
42:204.

https://www.uptodate.com/contents/viral-meningitis-in-children-epidemiology-pathogenesis-and-etiology/print?search=meningitis+pediatria&source=search_r… 12/22
20/3/25, 8:51 a.m. Viral meningitis in children: Epidemiology, pathogenesis, and etiology - UpToDate

32. Figueroa JP, Ashley D, King D, Hull B. An outbreak of acute flaccid paralysis in Jamaica
associated with echovirus type 22. J Med Virol 1989; 29:315.
33. Gubler DJ. The global resurgence of arboviral diseases. Trans R Soc Trop Med Hyg 1996;
90:449.
34. Verboon-Maciolek MA, Groenendaal F, Hahn CD, et al. Human parechovirus causes
encephalitis with white matter injury in neonates. Ann Neurol 2008; 64:266.

35. Levorson RE, Jantausch BA, Wiedermann BL, et al. Human parechovirus-3 infection:
emerging pathogen in neonatal sepsis. Pediatr Infect Dis J 2009; 28:545.
36. Selvarangan R, Nzabi M, Selvaraju SB, et al. Human parechovirus 3 causing sepsis-like
illness in children from midwestern United States. Pediatr Infect Dis J 2011; 30:238.
37. Sharp J, Harrison CJ, Puckett K, et al. Characteristics of young infants in whom human
parechovirus, enterovirus or neither were detected in cerebrospinal fluid during sepsis
evaluations. Pediatr Infect Dis J 2013; 32:213.
38. Khatami A, McMullan BJ, Webber M, et al. Sepsis-like disease in infants due to human
parechovirus type 3 during an outbreak in Australia. Clin Infect Dis 2015; 60:228.

39. Ito M, Yamashita T, Tsuzuki H, et al. Isolation and identification of a novel human
parechovirus. J Gen Virol 2004; 85:391.
40. Watanabe K, Oie M, Higuchi M, et al. Isolation and characterization of novel human
parechovirus from clinical samples. Emerg Infect Dis 2007; 13:889.
41. Pham NT, Trinh QD, Khamrin P, et al. Diversity of human parechoviruses isolated from
stool samples collected from Thai children with acute gastroenteritis. J Clin Microbiol
2010; 48:115.
42. Harvala H, Robertson I, Chieochansin T, et al. Specific association of human
parechovirus type 3 with sepsis and fever in young infants, as identified by direct typing
of cerebrospinal fluid samples. J Infect Dis 2009; 199:1753.
43. Piñeiro L, Vicente D, Montes M, et al. Human parechoviruses in infants with systemic
infection. J Med Virol 2010; 82:1790.

44. van der Sanden S, de Bruin E, Vennema H, et al. Prevalence of human parechovirus in
the Netherlands in 2000 to 2007. J Clin Microbiol 2008; 46:2884.
45. Centers for Disease Control and Prevention (CDC). Nonpolio enterovirus and human
parechovirus surveillance --- United States, 2006-2008. MMWR Morb Mortal Wkly Rep
2010; 59:1577.

46. Abed Y, Boivin G. Human parechovirus types 1, 2 and 3 infections in Canada. Emerg
Infect Dis 2006; 12:969.
47. Felsenstein S, Yang S, Eubanks N, et al. Human parechovirus central nervous system
infections in southern California children. Pediatr Infect Dis J 2014; 33:e87.

https://www.uptodate.com/contents/viral-meningitis-in-children-epidemiology-pathogenesis-and-etiology/print?search=meningitis+pediatria&source=search_r… 13/22
20/3/25, 8:51 a.m. Viral meningitis in children: Epidemiology, pathogenesis, and etiology - UpToDate

48. Drexler JF, Grywna K, Stöcker A, et al. Novel human parechovirus from Brazil. Emerg
Infect Dis 2009; 15:310.
49. Cruz AT, Freedman SB, Kulik DM, et al. Herpes Simplex Virus Infection in Infants
Undergoing Meningitis Evaluation. Pediatrics 2018; 141.
50. Davis LE, Johnson RT. An explanation for the localization of herpes simplex encephalitis?
Ann Neurol 1979; 5:2.
51. Johnson RT, Mims CA. Pathogenesis of viral infections of the nervous system. N Engl J
Med 1968; 278:23.
52. Bergström T, Vahlne A, Alestig K, et al. Primary and recurrent herpes simplex virus type
2-induced meningitis. J Infect Dis 1990; 162:322.
53. Whitley RJ, Kimberlin DW, Roizman B. Herpes simplex viruses. Clin Infect Dis 1998;
26:541.
54. Simko JP, Caliendo AM, Hogle K, Versalovic J. Differences in laboratory findings for
cerebrospinal fluid specimens obtained from patients with meningitis or encephalitis
due to herpes simplex virus (HSV) documented by detection of HSV DNA. Clin Infect Dis
2002; 35:414.
55. Dupuis C, Despert V, Vigneron P. [Herpetic meningitis in the child]. Arch Pediatr 2002;
9:1153.
56. Do AN, Green PA, Demmler GJ. Herpes simplex virus type 2 meningitis and associated
genital lesions in a three-year-old child. Pediatr Infect Dis J 1994; 13:1014.

57. Brown ZA, Benedetti J, Ashley R, et al. Neonatal herpes simplex virus infection in relation
to asymptomatic maternal infection at the time of labor. N Engl J Med 1991; 324:1247.
58. Schlesinger Y, Tebas P, Gaudreault-Keener M, et al. Herpes simplex virus type 2
meningitis in the absence of genital lesions: improved recognition with use of the
polymerase chain reaction. Clin Infect Dis 1995; 20:842.
59. Opitz JC, Kettrick MA, Sullivan BJ. Recurrent neonatal herpes presenting initially with
hoarseness. Am J Perinatol 1989; 6:307.
60. Cohen BA, Rowley AH, Long CM. Herpes simplex type 2 in a patient with Mollaret's
meningitis: demonstration by polymerase chain reaction. Ann Neurol 1994; 35:112.
61. Conway JH, Weinberg A, Ashley RL, et al. Viral meningitis in a preadolescent child caused
by reactivation of latent herpes simplex (type 1). Pediatr Infect Dis J 1997; 16:627.
62. Tedder DG, Ashley R, Tyler KL, Levin MJ. Herpes simplex virus infection as a cause of
benign recurrent lymphocytic meningitis. Ann Intern Med 1994; 121:334.
63. Jensenius M, Myrvang B, Størvold G, et al. Herpes simplex virus type 2 DNA detected in
cerebrospinal fluid of 9 patients with Mollaret's meningitis. Acta Neurol Scand 1998;
98:209.

https://www.uptodate.com/contents/viral-meningitis-in-children-epidemiology-pathogenesis-and-etiology/print?search=meningitis+pediatria&source=search_r… 14/22
20/3/25, 8:51 a.m. Viral meningitis in children: Epidemiology, pathogenesis, and etiology - UpToDate

64. Steel JG, Dix RD, Baringer JR. Isolation of herpes simplex virus type I in recurrent
(Mollaret) meningitis. Ann Neurol 1982; 11:17.
65. Graman PS. Mollaret's meningitis associated with acute Epstein-Barr virus
mononucleosis. Arch Neurol 1987; 44:1204.
66. Gutierrez KM, Whitley RJ, Arvin AM. Herpes simplex virus infections. In: Infectious Diseas
es of the Fetus and Newborn Infant, 7th ed, Remington JS, Klein JO, Wilson CB, et al (Ed
s), Elsevier Saunders, Philadelphia 2011. p.813.

67. Centers for Disease Control and Prevention (CDC). Decline in annual incidence of
varicella--selected states, 1990-2001. MMWR Morb Mortal Wkly Rep 2003; 52:884.
68. Romero JR, Newland JG. Viral meningitis and encephalitis: traditional and emerging viral
agents. Semin Pediatr Infect Dis 2003; 14:72.
69. Gnann JW Jr. Varicella-zoster virus: atypical presentations and unusual complications. J
Infect Dis 2002; 186 Suppl 1:S91.

70. Kleinschmidt-DeMasters BK, Gilden DH. The expanding spectrum of herpesvirus

infections of the nervous system. Brain Pathol 2001; 11:440.
71. Ross JP, Choen JI. Epstein-Barr virus. In: Infections of the Central Nervous System, 2nd e
d, Scheld MW, Durack WR (Eds), Lippincott Raven, Philadelphia 1997. p.117.
72. Griffiths PD, McLaughlin JE. Cytomegalovirus. In: Infections of the Central Nervous Syste
m, 2nd ed, Scheld MW, Durack WR (Eds), Lippincott Raven, Philadelphia 1997. p.107.
73. Caserta MT, Hall CB. Human Herpes-6. In: Infections of the Central Nervous System, 2nd
ed, Scheld MW, Durack WR (Eds), Lippincott Raven, Philadelphia 1997. p.129.
74. Yoshikawa T, Ihira M, Suzuki K, et al. Invasion by human herpesvirus 6 and human
herpesvirus 7 of the central nervous system in patients with neurological signs and
symptoms. Arch Dis Child 2000; 83:170.
75. Pohl-Koppe A, Blay M, Jäger G, Weiss M. Human herpes virus type 7 DNA in the
cerebrospinal fluid of children with central nervous system diseases. Eur J Pediatr 2001;
160:351.
76. Calisher CH. Medically important arboviruses of the United States and Canada. Clin
Microbiol Rev 1994; 7:89.
77. Hammer SM, Connolly KJ. Viral aseptic meningitis in the United States: clinical features,
viral etiologies, and differential diagnosis. Curr Clin Top Infect Dis 1992; 12:1.
78. Sawyer MH. Enterovirus infections: diagnosis and treatment. Pediatr Infect Dis J 1999;
18:1033.
79. Gubler DJ. Arboviruses as imported disease agents: the need for increased awareness.
Arch Virol Suppl 1996; 11:21.

https://www.uptodate.com/contents/viral-meningitis-in-children-epidemiology-pathogenesis-and-etiology/print?search=meningitis+pediatria&source=search_r… 15/22
20/3/25, 8:51 a.m. Viral meningitis in children: Epidemiology, pathogenesis, and etiology - UpToDate

80. Petersen LR, Brault AC, Nasci RS. West Nile virus: review of the literature. JAMA 2013;
310:308.

81. Lindsey NP, Hayes EB, Staples JE, Fischer M. West Nile virus disease in children, United
States, 1999-2007. Pediatrics 2009; 123:e1084.
82. Lindsey NP, Lehman JA, Staples JE, et al. West nile virus and other arboviral diseases -
United States, 2013. MMWR Morb Mortal Wkly Rep 2014; 63:521.
83. Gaensbauer JT, Lindsey NP, Messacar K, et al. Neuroinvasive arboviral disease in the
United States: 2003 to 2012. Pediatrics 2014; 134:e642.
84. Lindsey NP, Lehman JA, Staples JE, Fischer M. West Nile Virus and Other Nationally
Notifiable Arboviral Diseases - United States, 2014. MMWR Morb Mortal Wkly Rep 2015;
64:929.
85. Horga MA, Fine A. West Nile virus. Pediatr Infect Dis J 2001; 20:801.

86. Barton LL, Mets MB. Congenital lymphocytic choriomeningitis virus infection: decade of
rediscovery. Clin Infect Dis 2001; 33:370.
87. Whitley RJ. Rabies. In: Infections of the Central Nervous System, 2nd ed, Scheld MW, Whi
tley RJ, Durack WR (Eds), Lippincott Williams & Wilkins, Philadelphia 1997. p.181.
88. Wang YH, Huang YC, Chang LY, et al. Clinical characteristics of children with influenza A
virus infection requiring hospitalization. J Microbiol Immunol Infect 2003; 36:111.
89. Fazal A, Reinhart K, Huang S, et al. Reports of Encephalopathy Among Children with
Influenza-Associated Mortality - United States, 2010-11 Through 2024-25 Influenza
Seasons. MMWR Morb Mortal Wkly Rep 2025; 74:91.

90. Newland JG, Romero JR, Varman M, et al. Encephalitis associated with influenza B virus
infection in 2 children and a review of the literature. Clin Infect Dis 2003; 36:e87.
91. Newland JG, Shah SS, Zaoutis TE. The child with aseptic meningitis. Pediatr Case Rev
2003; 3:218.
92. Centers for Disease Control and Prevention (CDC). Update: influenza activity--United
States, January 18-24, 2004. MMWR Morb Mortal Wkly Rep 2004; 53:63.
93. Yousefi K, Poorbarat S, Abasi Z, et al. Viral Meningitis Associated With COVID-19 in a 9-
year-old Child: A Case Report. Pediatr Infect Dis J 2021; 40:e87.
94. Naz S, Hanif M, Haider MA, et al. Meningitis as an Initial Presentation of COVID-19: A
Case Report. Front Public Health 2020; 8:474.
95. Schildgen O, Glatzel T, Geikowski T, et al. Human metapneumovirus RNA in encephalitis
patient. Emerg Infect Dis 2005; 11:467.
96. Arnold JC, Singh KK, Milder E, et al. Human metapneumovirus associated with central
nervous system infection in children. Pediatr Infect Dis J 2009; 28:1057.

https://www.uptodate.com/contents/viral-meningitis-in-children-epidemiology-pathogenesis-and-etiology/print?search=meningitis+pediatria&source=search_r… 16/22
20/3/25, 8:51 a.m. Viral meningitis in children: Epidemiology, pathogenesis, and etiology - UpToDate

97. Sánchez Fernández I, Rebollo Polo M, Muñoz-Almagro C, et al. Human

Metapneumovirus in the Cerebrospinal Fluid of a Patient With Acute Encephalitis. Arch
Neurol 2012; 69:649.
98. Zhang XF, Tan CB, Yao ZX, et al. Adenovirus Infection-associated Central Nervous System
Disease in Children. Pediatr Infect Dis J 2021; 40:205.
Topic 5980 Version 29.0

https://www.uptodate.com/contents/viral-meningitis-in-children-epidemiology-pathogenesis-and-etiology/print?search=meningitis+pediatria&source=search_r… 17/22
20/3/25, 8:51 a.m. Viral meningitis in children: Epidemiology, pathogenesis, and etiology - UpToDate

GRAPHICS

Epidemiologic, clinical data, and pathogenesis of common viruses causing

meningitis in children

Associated Pathw
Virus Transmission Age Season Frequency
syndromes to CN

Piconavirus- Person to All ages Summer Encephalitis Common Blood

enterovirus person:
More Fall Myocarditis
Oral-fecal common
Coxsackievirus Neonatal
Inhalation in
sepsis
Echovirus children
Poliomyelitis

Arboviruses Direct All ages Summer Encephalitis Common Blood

inoculation by
Fall
vectors:

Mosquitoes
Ticks

Rabies Direct All ages No Rare Neuron

population by seasonal
bite of a rabid pattern
animal,
transplant or
inhalation

Influenza Person to All ages Winter Encephalitis Infrequent Unknow

person:

Inhalation

Herpesviridae Person to No
person seasonal
pattern

Herpes simplex Vertical or More Meningo- Common Blood

horizontal common encephalitis
Neuron
in
neonates

Varicella-zoster Respiratory Any age Cerebellitus Infrequent

following
Encephalitis
primary
infection Myelitis

Epstein-Barr Encephalitis Rare

virus
Myelitis

https://www.uptodate.com/contents/viral-meningitis-in-children-epidemiology-pathogenesis-and-etiology/print?search=meningitis+pediatria&source=search_r… 18/22
20/3/25, 8:51 a.m. Viral meningitis in children: Epidemiology, pathogenesis, and etiology - UpToDate

Guillain-
Barre

Adenoviridae Human No Encephalitis Rare Blood

seasonal
Adenovirus pattern

CNS: central nervous system.

Graphic 59663 Version 3.0

https://www.uptodate.com/contents/viral-meningitis-in-children-epidemiology-pathogenesis-and-etiology/print?search=meningitis+pediatria&source=search_r… 19/22
20/3/25, 8:51 a.m. Viral meningitis in children: Epidemiology, pathogenesis, and etiology - UpToDate

Clinically significant arboviruses causing central nervous system infections

in humans

Incubation
Viral taxonomy Vectors Geographic distribution
period, days

Togaviridae

Eastern equine Mosquitoes 3 to 10 East United States and Canada,

encephalitis virus South America

Western equine Mosquitoes 2 to 10 West United States and Canada

encephalitis virus South America

Venezuelan equine Mosquitoes 1 to 4 Central and South America

encephalitis virus

Flaviviridae

St. Louis encephalitis virus Mosquitoes 4 to 14 United States

Powassan virus Ticks 4 to 18 North United States

West Nile virus Mosquitoes 5 to 15 United States, southern Europe

Asia, Africa

Japanese encephalitis Mosquitoes 4 to 14 Asia

virus

Murray Valley encephalitis Mosquitoes 4 to 14 Australia and New Guinea

virus

Tick-borne encephalitis Ticks 8 to 14 Europe

virus

Bunyaviridae

California encephalitis Mosquitoes 5 to 15 West United States, Europe,

viruses Asia

Snowshoe hare North United States

Jamestown Canyon United States

La Crosse Midwest, east, south United

States

Graphic 55340 Version 2.0

https://www.uptodate.com/contents/viral-meningitis-in-children-epidemiology-pathogenesis-and-etiology/print?search=meningitis+pediatria&source=search_r… 20/22
20/3/25, 8:51 a.m. Viral meningitis in children: Epidemiology, pathogenesis, and etiology - UpToDate

Viruses uncommonly associated with meningitis

Viruses Transmission Distribution

Mumps Human to human – Airborne Worldwide

Measles virus Human to human – Droplets Worldwide

Lymphocytic Animal to human – Aerosol or ingestion of Worldwide

choriomeningitis virus contaminated food or dust from urine, feces,
secretions of infected rodents

HIV Human to human Worldwide

Parainfluenza viruses Human to human – Airborne/droplets and fomites Worldwide

Rotavirus Human to human – Oral-fecal Worldwide

Parvovirus B19 Human to human – Airborne, percutaneous, and Worldwide

vertical transmission

Coronavirus Human to human – Airborne (probable animal to Worldwide

human)

Adenovirus Human to human – Airborne/droplets, oral-fecal, Worldwide

and fomites

Human Human to human – Likely direct contact with Worldwide

metapneumovirus contaminated secretions*

Vaccine associated

Vaccinia Limited to vaccine use

Measles Worldwide

* No formal studies have been performed.

Graphic 75752 Version 4.0

https://www.uptodate.com/contents/viral-meningitis-in-children-epidemiology-pathogenesis-and-etiology/print?search=meningitis+pediatria&source=search_r… 21/22
20/3/25, 8:51 a.m. Viral meningitis in children: Epidemiology, pathogenesis, and etiology - UpToDate

Contributor Disclosures
Cecilia Di Pentima, MD No relevant financial relationship(s) with ineligible companies to
disclose. Sheldon L Kaplan, MD Grant/Research/Clinical Trial Support: Pfizer [Streptococcus
pneumoniae]. Other Financial Interest: Elsevier [Textbook honoraria – Pediatric infectious diseases]. All
of the relevant financial relationships listed have been mitigated. Carrie Armsby, MD, MPH No
relevant financial relationship(s) with ineligible companies to disclose.

Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these
are addressed by vetting through a multi-level review process, and through requirements for
references to be provided to support the content. Appropriately referenced content is required of all
authors and must conform to UpToDate standards of evidence.

Conflict of interest policy

https://www.uptodate.com/contents/viral-meningitis-in-children-epidemiology-pathogenesis-and-etiology/print?search=meningitis+pediatria&source=search_r… 22/22