Eur J Pediatr (2012) 171:795–800

DOI 10.1007/s00431-011-1626-z

ORIGINAL PAPER

Characteristics of pediatric patients with enterovirus

meningitis and no cerebral fluid pleocytosis
Stephanie C. M. de Crom & Marceline A. M. van Furth &
Marcel F. Peeters & John W. A. Rossen &
Charles C. Obihara

Received: 3 October 2011 / Accepted: 8 November 2011 / Published online: 22 November 2011
# Springer-Verlag 2011

Abstract Human non-polio enterovirus (EV) is the most
important cause of aseptic meningitis in children. Only a few
studies report the lack of cerobrospinal fluid (CSF) pleocy-
tosis in children with confirmed EV meningitis; however, the
characteristics of these children have not been well defined.
This paper describes the clinical and laboratory features of EV
meningitis in children with no CSF pleocytosis. Clinical,
laboratory, and virological data of Dutch patients <16 years
diagnosed with EV meningitis, between 2003 and 2008, were
analyzed retrospectively. Data of children with and without
CSF pleocytosis were compared. A total of 149 children were
infected with EV. Patients presented mainly with fever
(n=113), malaise (n=43), abdominal pain (n=47), and
irritability (n=61). Of the 60 patients with EV meningitis,
23 had no pleocytosis. Those who lacked CSF pleocytosis
were younger [odds ratio (OR) 1.00; 95% confidence
interval (CI) 1.000–1.002; p=0.001], had experienced
S. C. M. de Crom (*) : C. C. Obihara
Department of Pediatrics, St. Elisabeth Hospital,
Hilvarenbeekseweg 60,
5022 LC Tilburg, The Netherlands
e-mail: stephanie_de_crom@hotmail.com
M. A. M. van Furth : C. C. Obihara
Department of Pediatric Infectious Disease,
Immunology and Rheumatology, VU Medical Centre,
Amsterdam, The Netherlands
M. F. Peeters : J. W. A. Rossen
Laboratory of Medical Microbiology and Immunology, St.
Elisabeth Hospital,
Tilburg, The Netherlands
J. W. A. Rossen
Laboratory of Experimental Virology, Department of Medical
Microbiology, Center for Infection and Immunity Amsterdam
(CINIMA), Academic Medical Center, University of Amsterdam,
Amsterdam, The Netherlands
drowsiness more (OR 9.60; 95% CI 2.24–41.15; p=0.002),
had lower white blood cell counts (OR 0.73; 95% CI 0.61–
0.89; p=0.001), and had higher C-reactive protein (OR 1.13;
95% CI 1.03–1.23; p=0.006) than those with pleocytosis.
Conclusion. These findings show that EV meningitis occurs
in the absence of CSF pleocytosis, particularly in young
infants, meaning that EV meningitis in this age group cannot
be solely excluded by the absence of CSF pleocytosis. They
also confirm the importance of genome detection in the
diagnosis of EV meningitis in young infants.
Keywords Enterovirus . Children . Meningitis .
Pleocytosis . Cerebrospinal fluid
Introduction
Human non-polio enterovirus (EV) is a major cause of aseptic
meningitis in children, especially in neonates and young infants
[13, 21, 23]. The clinical spectrum of EV infections varies
from fever to severe systemic disease, including septicemia
and meningoencephalitis. EV infection has also been associ-
ated with severe neurodevelopmental sequelae [7, 10, 13, 16,
21]. Reverse-transcriptase real-time polymerase chain reaction
(RT-PCR) is presently considered as the gold standard for the
diagnosis of EV infections [2, 19, 21, 23]. EV meningitis is
defined clinically as the presence of pleocytosis and detection
of enteroviral genome in the cerebrospinal fluid (CSF) by RT-
PCR or detection of EV with viral culture [2, 5, 14, 21, 23].
Only a few studies have reported the lack of CSF pleocytosis
in children with EV meningitis [8, 9, 17, 20]. The character-
istics of these children have, thus far, not been well
documented. The aim of this paper is to describe the clinical
and laboratory features of pediatric patients with EV
meningitis and no CSF pleocytosis.
796
Methods
Study setting and population
We screened the hospital records of Dutch pediatric
patients <16 years of age with viral infection and
analyzed the data of those with EV infection, in two major
general pediatric units in the Netherlands. The study was
carried out between the 1 January 2003 and 31 of January
2008. The pediatric units involved are in St. Elisabeth Hospital,
Tilburg (EZ) and in Franciscus Hospital, Roosendaal. These
units belong to the largest non-university pediatric units in the
country. The emergency and out-patient clinics of both
hospitals are attended by more than 20,000 children per
annum. The Laboratory of Medical Microbiology and Immu-
nology (LMMI) located in EZ is responsible for viral
diagnostics in both hospitals.
Inclusion criteria
All pediatric patients (<16 years of age) with virologically
confirmed EV infection were included. In order not to miss
any eligible study patient, clinical records of patients were
cross-checked with the database of the LMMI.
Exclusion criteria
Patients were excluded if they were ≥16 years or if their
clinical condition had another (infectious) etiology.
Definitions
EV infection was defined as the detection of an EV (viral
culture or RT-qPCR) in feces, throat swab, or CSF of a
symptomatic patient.
EV meningitis was defined as the detection of EV in the
CSF
Pleocytosis was defined as the presence of elevated leukocyte
count for age in the CSF [4, 5, 21, 25, 26]. The age-specific
reference values used were: CSF white blood cell (WBC)
count >22/μL for infants ≤4 weeks of age, >15/μL for
infants 4–6 weeks of age, and >7/μL for children >6 weeks
of age.
Virological tests
EV RT-quantitative (q)PCR. An aliquot of the collected
sample of feces, throat swab, or CSF was used to extract
viral nucleic acids using the MagNA Pure LC total nucleic
acid detection kit (Roche Diagnostics, Basel, Switzerland)
as described previously [27]. Subsequently, cDNA was
synthesized using MultiScribe reverse transcriptase and
random hexamers (Applied Biosystems, Foster City, CA,
Eur J Pediatr (2012) 171:795–800
USA). Detection of viral genome was performed using an
EV-specific RT-qPCR [19], which has been used in the
hospital since 2006.
EV culture. An aliquot of the collected sample of feces,
throat swab, and/or CSF was used for immediate viral
culture. Virus detection was done systematically in tertiary
Cynomolgus monkey kidney cells, human embryonic lung
fibroblast cells, and HEp-2 Cincinatti and Vero cell lines.
Cultures were examined every other day for 14 days for the
development of a cytopathologic effect, and positive
cultures were confirmed by a direct immunofluorescence
assay with monoclonal antibodies specific for EV (DaKo,
Glostrup, Denmark).
Data collection and statistical methods
Relevant data from the medical records of included children
were extracted using standardized case record forms and
captured in a Microsoft Access database (version 2007).
Subject data collected included demographics, history of
illness, symptoms and their duration, findings on physical
examination, results of blood and CSF chemistry, results of
virological testing of feces, throat swab and/or CSF,
antibiotic prescription, and hospitalization.
Statistical analysis was performed with SPSS 15.0
(Windows Inc, Chicago, IL, USA). Chi-squared test or the
Fisher’s exact test was used for the analysis of categorical
data and the Student’s t test for continuous variables with
normal distribution. Mann–Whitney test was used for
continuous variables without a normal distribution. An
odds ratio (OR) with a 95% confidence interval (CI) was
used to test differences within groups. Continuous param-
eters are presented as median and range. Spearman
correlation coefficients were used to assess the relationship
between age and CSF WBC count. A p value <0.05 was set
as the level of significance. Regression analyses were
performed using a logistic regression analysis model. In this
model, meningitis without pleocytosis was used as the
dependent variable and the patient features (including
history, signs and symptoms, and laboratory parameters)
as the independent variables. Adjustment was made for
age and sex as potential confounders. The study was
approved by the medical ethics committee of the involved
hospitals.
Results
Demographic and clinical data
An EV infection was found in 149 pediatric patients. Their
characteristics are summarized in Table 1. Their age
Eur J Pediatr (2012) 171:795–800 797

Table 1 Characteristics of children with positive EV infection The presenting symptoms in the patients were fever in
EV-positive 113 (89%), malaise in 43 (86%), abdominal pain in 47
children (80%), and irritability in 61 (76%) patients (Table 2). The
(n=149) median duration of symptoms before presentation was 24 h
(range 0 hour–14 days). Patients <3 months of age were
Median age in days (range) 133 (0–5320)
significantly more irritable than older ones (OR 7.4, 95%
Male/female ratio 1.4 (87/62)
CI 1.3–123.5). Patients >1 year of age vomited more
Diagnosis (%): meningitis 60 (40%)
frequently (OR 3.2, 95% CI 1.4–7.4), had more feeding
Gastroenteritis 50 (34%)
problems (OR 2.7, 95% CI 1.3–6.0), nuchal rigidity (OR
Respiratory infection 8 (6%) 5.1, 95% CI 1.4–18.8), earache (OR 6.7, 95% CI 1.7–26.3),
Bornholm disease 5 (3%) and less rash (OR 0.31, 95% CI 0.1–0.8) than those <1 year
Lymphadenitis mesenterica 2 (1.3%) of age. The following EV serotypes were detected in the
Acute disseminated encephalomyelitis 1 (0.7%) patients: coxsackie B1–B6 virus (n=68), coxsackie A9
Encephalitis 1 (0.7%) virus (n = 3), echovirus 3 (n = 5), echovirus 5 (n = 2),
Myeloradiculitis 1 (0.7%) echovirus 6 (n=4), echovirus 7 (n=3), echovirus 9 (n=11),
Cardiomyopathy 1 (0.7%) echovirus 11 (n=10), echovirus 18 (n=1), echovirus 21
Coxitis fugax 1 (0.7%) (n=2), echovirus 25 (n=4), echovirus 27 (n=1), and
Fever of unknown origin 14 (9%) echovirus 30 (n=8).
No specific organ involvement 5 (3%)
No. of hospitalized children (%) 121 (81%) Meningitis and pleocytosis
Median duration of hospitalization in days (range) 4 (1–57)
No. children who received antibiotic treatment (%) 84 (56%) There were 60 patients diagnosed with EV meningitis.
Mortality (%) 0 (0%) Enteroviral genome was not detected in the CSF of two
patients, despite CSF pleocytosis and EV RT-qPCR-
No. number, EV enterovirus
positive test of the feces sample and/or throat swab. These
two patients were excluded from the analysis. There was no
distribution is shown in Fig. 1. The median age was 133 other viral or bacterial coinfection found in any of the
(range 0–5320) days and 58.4% was male. Sixty-eight patients. Twenty-three patients with EV meningitis had no
patients were <1 year of age. The most important clinical CSF pleocytosis. These patients were significantly younger
diagnoses at presentation were meningitis in 60 (40%) and (p=0.001), had more often a history of drowsiness (p=
gastroenteritis in 50 (34%). Other less frequent diagnoses 0.002), lower WBC counts (p=0.001), and higher C-
are shown in Table 1. A total of 121 (81%) patients were reactive protein (CRP) levels (p=0.006) than those with
hospitalized, for a median of 4 (range 1–57) days. EV meningitis and CSF pleocytosis (Table 3). The findings
Hospitalized patients were significantly younger than non- remained significant in a logistic regression model after
hospitalized ones (mean age 1.4 versus 4.1 years; p<0.01). adjustment for age and sex (Table 3). Presenting symptoms

Fig. 1 Age distribution of

patients
Number of patients

Age
798 Eur J Pediatr (2012) 171:795–800

Table 2 Presenting signs and symptoms of pediatric patients with EV infection, EV meningitis and CSF pleocytosis, and EV meningitis and no
CSF pleocytosis

Symptom EV-positive EV meningitis and no EV meningitis and CSF OR (EV meningitis without 95% CI
children (n=149) CSF pleocytosis (n=23) pleocytosis (n=35) versus with CSF pleocytosis) (lower–upper)

Fever 113/127 23/23 32/34 NA

Malaise 43/50 12/12 13/14 NA
Feeding problems 55/120 11/22 13/32 1.30 0.42–4.05
Vomiting 40/103 7/20 9/31 1.32 0.40–4.38
Nausea 7/19 0/0 2/8 NA
Abdominal pain 47/59 12/15 11/16 1.82 0.35–9.46
Diarrhea 69/130 13/23 13/33 2.00 0.68–5.89
Coughing 19/73 2/12 5/22 0.68 0.11–4.18
Rhinitis 33/90 6/18 9/22 0.72 0.20–2.64
Dyspnea 6/69 3/15 0/23 NA
Irritability 61/80 19/20 23/25 1.65 0.14–19.65
Drowsiness 44/98 16/19 10/28 9.60 2.24–41.15*
Nuchal rigidity 17/53 2/8 13/20 0.18 0.03–1.14
Photophobia 1/7 0/0 1/3 NA
Sore throat 3/65 0/13 0/19 NA
Earache 13/91 1/15 2/26 0.86 0.07–10.33
Aphtha 0/67 0/16 0/22 NA
Conjunctivitis 4/48 1/11 2/15 0.65 0.05–8.23
Rash 30/92 12/21 9/28 2.82 0.87–9.10
Paralysis 1/83 0/17 0/24 NA

The denominator is the case number of data available, and the numerator is the case number with the symptoms or signs
EV enterovirus, NA not applicable, CSF cerebrospinal fluid
*
P =0.002, statistically significant

did not differ between patients with meningitis and CSF
pleocytosis and those with meningitis and no CSF
pleocytosis.
Significantly more patients with EV meningitis and
no CSF pleocytosis received antibiotic treatment than
those with meningitis and CSF pleocytosis (100%
versus 82%; p=0.012). The duration of symptoms (33.7
versus 32.7 hours, p=0.226), rate (33% versus 23%, p=0.160),
and length of hospitalization (6.0 versus 7.5 days, p=0.500)
did not significantly differ between patients with EV
meningitis and CSF pleocytosis and those with EV meningitis
and no CSF pleocytosis. The frequency of using the RT-qPCR

Table 3 Unadjusted and adjusted comparison of characteristics of patients with EV meningitis and CSF pleocytosis and those with no CSF
pleocytosis (n=58)

Characteristic EV meningitis and CSF EV meningitis and no Unadjusted 95% CI Adjusted 95% CI
pleocytosis (n=35) CSF pleocytosis (n=23) OR odds ratioa

Mean age [months] (range) 26.1 (0.1–139.1) 4.2 (0.1–48.2) 1.00 1.00–1.00 NA NA
Gender: male/female ratio 1.7 (22/13) 0.9 (11/12) 1,85 0.64–5.37 NA NA
History of drowsiness 33% (9/27) 83% (15/18) 9.60 2.24–41.15 9.10 1.96–42.39
Blood WBC count 12.3 (4.9–23.7) 8.1 (4.2–14.6) 0.73 0.61–0.89 0.70 0.57–0.87
[×109 per liter] (range)
C-reactive protein level 6.1 (0–24) 17.1 (3–62) 1.13 1.03–1.23 1.17 1.05–1.30
[mg/l] (range)

Only parameters which achieved statistical significance in the univariate model were included in the logistic regression analysis model. Only the
significant variables are depicted in the table
EV enterovirus, CSF cerebrospinal fluid, NA not applicable
a
Adjusted for age and sex
Eur J Pediatr (2012) 171:795–800
and/or viral culture in the detection of EV in CSF did not
differ between patients with meningitis and CSF pleocytosis
and those with meningitis and no CSF pleocytosis (p=0.15).
Discussion
This study shows that pediatric patients with EV meningitis
and no CSF pleocytosis (40%) were younger and drowsier
at presentation, had lower WBC counts, and higher CRP
than patients with EV meningitis and CSF pleocytosis. This
observation is relevant because detection of CSF pleocy-
tosis is an important biochemical marker of meningitis in
the clinical practice. Although there have been a few reports
of young infants and children with no CSF pleocytosis
during EV meningitis, the clinical and laboratory character-
istics of these children have not been well documented,
especially not in those beyond the neonatal age [1, 3, 6, 8,
9, 11, 12, 17, 18, 20, 24, 28].
The mechanism to explain the lack of pleocytosis in
some patients during EV meningitis is still unclear. Sato et
al. suggested that young infants with EV meningitis and no
CSF pleocytosis may be at an initial stage of illness when,
though production of (pro) inflammatory cytokines has
been stimulated, the blood leukocytes have not yet
infiltrated the cerebrospinal cavity [22]. Kawashima et al.
observed that only 4 out of 21 patients with EV meningitis
had CSF pleocytosis, despite high levels of the inflamma-
tory cytokine, interleukin IL-6, in the CSF at presentation
[12]. This may explain the significantly lower WBC count
and higher CRP levels in patients with no CSF pleocytosis
in this study. The finding that patients with EV meningitis
and no CSF pleocytosis did not have a shorter duration of
symptoms does not support Sato’s hypothesis [22]. This
may partly be explained by recollection bias of parents.
That patients with EV meningitis and no CSF pleocy-
tosis were younger than those with CSF pleocytosis is in
support of previous studies [15, 17, 26]. Though it has been
suggested that age-related immaturity of specific immunity
against EV may explain the lack of CSF pleocytosis in
infants and young children with EV meningitis, prospective
and experimental studies are needed to clarify the temporal
relationship and mechanism involved.
Surprisingly, patients with EV meningitis and no CSF
pleocytosis had a higher rate of antibiotic prescription than
those with CSF pleocytosis. This can only be explained by
their younger age, as clinicians tend to prescribe antibiotics
more rapidly in younger patients because of the higher risk
of serious bacterial infection.
Among the strengths of this study is the availability of
both clinical and laboratory data of patients, which enabled
us to compare these features between pediatric patients with
EV meningitis and CSF pleocytosis and those with EV
799
meningitis and no CSF pleocytosis. The fact that the study
was conducted in general pediatric units implies that results
could easily be extrapolated to similar settings elsewhere.
Limitations of this study, next to those inherent to its
retrospective design, include selection bias resulting from
the loss of patients with very mild symptoms because they
were not sick enough to be referred to the pediatric units
involved. In addition, it is possible that the introduction of
EV RT-qPCR may have caused an underestimation of the
prevalence of EV meningitis in the afore period (2003–
2006), resulting in bias in the prevalence figures before and
after its introduction. However, as the aim of this study was
not to determine the prevalence of EV infection, any
eventual difference could not have created a major bias of
the findings.
In conclusion, this study confirms results of a number of
earlier studies that EV meningitis may occur in the absence
of CSF pleocytosis, particularly in young infants. These
findings mean that EV meningitis in this age group cannot
be solely excluded by the absence of CSF pleocytosis and
stress the importance of detecting viral genome with
molecular techniques, such as RT-PCR.
Acknowledgments We thank Dr. A.J.C.M. van der Velden, Pedia-
trician, Franciscus Hospital Roosendaal, for providing the clinical
charts of patients from his hospital. We thank M.A. Verboon-Maciolek
for critical reading of the manuscript.
Statement of competing interest The authors declare that they have
no competing interests.
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