MAJOR ARTICLE HIV/AIDS

Herpes Simplex Virus Type 2 as a Cause of Severe

Meningitis in Immunocompromised Adults
Herve Mommeja-Marin,1 Matthieu Lafaurie,1 Catherine Scieux,2 Lionel Galicier,3 Eric Oksenhendler,3
and Jean-Michel Molina1
1
Department of Infectious Diseases, and 2Laboratory of Virology and Department of Clinical Immunology, Hopital Saint-Louis, Assistance-Publique
Hopitaux de Paris, France

We reviewed the clinical and demographic characteristics and outcomes for 13 immunocompromised patients

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with herpes simplex virus (HSV)induced meningitis. Eleven patients were receiving chemotherapy for leu-
kemia or lymphoma, and 10 had acquired immunodeficiency syndrome. Patients presented with acute febrile
meningitis. The median white blood cell count at the onset of symptoms was 400 cells/mm3. Examination of
cerebrospinal fluid (CSF) specimens showed lymphocytic meningitis, but activated lymphocytes and low glucose
levels were both noted in 7 patients. HSV DNA was detected in all CSF specimens, and HSV type 2 was
identified in 7. Eight patients had suspected HSV-associated mucocutaneous lesions at the time of meningitis
onset. Six patients had initial radiculalgia, with sphincter involvement in 2. Eleven patients received intravenous
antiviral therapy, but treatment was delayed for 6 patients. Two of the 6 patients for whom treatment was
delayed developed encephalitis and died, whereas 2 others experienced persistent neurological symptoms. HSV-
2 can cause severe meningitis in immunocompromised patients. Early recognition and treatment might improve
the outcome of such infections.

After mucocutaneous primary infection, herpes simplex
virus types 1 (HSV-1) and 2 (HSV-2) establish latent
infections in sensory ganglia, the reactivation of which
result in a broad range of clinical manifestations [1].
The major CNS consequences of HSV reactivation are
encephalitis and meningitis [2, 3]. The diagnosis of
HSV-induced meningitis relies on the detection of HSV
DNA in the CSF by PCR. This method is extremely
sensitive and highly specific for the diagnosis of herpetic
infection involving the CNS [47]. Cases of herpetic
meningitis are mainly described in nonimmunosup-
pressed patients, and HSV-2 is usually identified as the
cause of herpetic meningitis. HSV-2associated men-
ingitis is usually observed in the context of primary
genital HSV-2 infection, but it can also be associated
with recurrent genital herpes and is a classical cause of
benign recurrent lymphocytic meningitis [3, 6, 8, 9].
Compared with HSV-1induced encephalitis, the out-
come of HSV-2induced meningitis in adults is usually
self-limited, with spontaneous recovery. Although HSV-
2 can cause fatal encephalitis in neonates, severe CNS
infections associated with this virus are rare in adults
[10]. We present here the clinical course, laboratory
findings, and outcomes for 13 immunocompromised
patients with HSV-induced meningitis.
PATIENTS AND METHODS

Patients. The study included 919 adult patients, who

Received 29 May 2003; accepted 20 July 2003; electronically published 6
were admitted to the Saint-Louis Hospital in Paris from
November 2003.
Reprints or correspondence: Dr. Jean-Michel Molina, Service des Maladies
January 1994 through June 2001, from whom CSF sam-
Infectieuses, Hopital Saint-Louis, 1 Avenue Claude Vellefaux, 75475 Paris cedex ples were obtained and records kept by the virology
10, France (jean-michel.molina@sls.ap-hop-paris.fr).
laboratory. A large percentage (30%) of patients ad-
Clinical Infectious Diseases 2003; 37:152733
 2003 by the Infectious Diseases Society of America. All rights reserved.
mitted to this hospital have hematological diseases or
1058-4838/2003/3711-0015$15.00 HIV infection. CSF samples, which were obtained for

HIV/AIDS CID 2003:37 (1 December) 1527

diagnostic purposes, were prospectively tested by PCR for de-
tection of HSV DNA.
Clinical and radiological data for patients with positive re-
sults of CSF PCR were reviewed by 2 investigators who classified
the patients as having meningitis or encephalitis. The diagnoses
of meningitis and encephalitis were made on the basis of criteria
reported elsewhere [6, 7, 11]. Patients were considered to have
herpetic encephalitis if HSV was detected in CSF by PCR, in
association with at least 1 of the following conditions: (1) an
alteration in mental status, (2) a focal neurological symptom,
(3) any abnormal result of electroencephalography, and (4) a
necrotic lesion on a CT scan or MRI. Patients were considered
to have HSV-induced meningitis if CSF PCR was positive for
HSV DNA, in association with at least 1 of the following con-
ditions: (1) any symptoms associated with meningitis (e.g.,
headache, vomiting, nausea, or neck stiffness), without alter-
ation of mental status and without focal CNS symptoms; (2)
normal brain CT scan or MRI findings, if performed; (3) ab-
normal results of cytological or biochemical testing of CSF, with
negative results of cultures for bacteria, mycobacteria, and
fungi; and 4) no evidence of any other virus in the CSF, in-
cluding varicella-zoster virus (VZV), cytomegalovirus (CMV),
human herpes virus type 6 (HHV-6), and Epstein-Barr virus
(EBV), as assayed by PCR. Data collected from the medical
charts included demographic characteristics, past medical his-
tory, and neurological and general signs and symptoms at hos-
pital admission. The following biological data were also ob-
tained: results of CSF hematological and biochemical tests,
serum biochemical tests, and whole blood hematological tests.
Detection of HSV DNA in CSF. Detection of HSV DNA
in CSF specimens was performed by PCR analysis. PCR was
assayed using the Herpes Consensus Generic and herpes iden-
tification Hybridowell tests (Arge`ne-Biosoft), in accordance
with the manufacturers instructions [12]. If brief, by means
of the Herpes Consensus Generic kit, amplification was per-
formed using primers located in the relatively conserved region
of the DNA polymerase genes of 6 Herpesviridae species (HSV-
1, HSV-2, CMV, VZV, EBV, and HHV-6). Amplified products
were detected by hybridization with biotinyled probes. After
the subsequent addition of a streptavidine-peroxydase conju-
gate and a tetramethylbenzidene component, optic density was
measured at 450 nm. Samples in which the generic probe de-
tected a positive signal were subsequently identified via hy-
bridization with 6 single-specific probes using the herpes iden-
tification Hybridowell kit.
CSF samples obtained from 1994 through 1999 were initially
tested with a global (i.e., not type-specific) HSV PCR assay [4].
Amplified products were detected using microplate hybridi-
zation with a biotinyled probe (Gen-Eti-K DEIA; DiaSorin), in
accordance with the manufacturers instructions. CSF samples
that were initially positive for HSV DNA and stored at 80C
1528 CID 2003:37 (1 December) HIV/AIDS
were retested in our study using the Herpes Consensus Generic
assay.
Detection of anti-HSV antibodies in serum. The synthesis
of specific antibodies to HSV-1 and HSV-2 in serum was as-
sessed by an immunoenzymatic assay (HSV-1 and HSV-2 re-
combinant IgG ELIT; Eurobio).
Isolation of HSV-1 and HSV-2. HSV isolation was per-
formed using tissue culture. Secretions obtained from periph-
eral blisters were inoculated in MRC5 diploid cells and incu-
bated at 37C. After a 48-h incubation period, HSV infection
was determined by staining with monoclonal antibodies against
HSV-1 and HSV-2 (CHA437; Arge`ne-Biosoft). When the test
results were positive, the HSV type was determined using im-
munofluorescence with type-specific monoclonal antibodies
(Microtrak; Dade Behring).
RESULTS
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Patients with HSV-induced meningitis. Of the 919 CSF sam-
ples obtained during the study period and tested for HSV DNA
using PCR, 30 (3.3%) tested positive for HSV DNA. Three
samples were obtained from patients admitted to other hos-
pitals, and their medical records were not available. Two pa-
tients most likely had false-positive PCR results. Among the
remaining 25 patients, 7 (28%) had encephalitis, with alteration
of their mental status and focal neurological symptoms.
Eighteen patients had HSV-induced meningitis, on the basis
of our criteria. The prevalence of HSV-induced meningitis was,
therefore, 2% in our study. Two patients had herpetic men-
ingitis concomitant with a primary genital infection, and 2 had
a typical case of recurrent benign lymphocytic meningitis. One
patient was lost to follow-up 3 days after diagnosis.
Of interest, 13 patients were severely immunocompromised
at the time of diagnosis; these patients are the focus of this
study. Ten patients were infected with HIV and had AIDS di-
agnosed a median of 5.5 years (range, 113 years) before the
episode of meningitis. The median CD4+ cell count for these
10 patients was 103 cells/mm3 (range, 4303 cells/mm3), and
the median plasma HIV-1 RNA load was 11,500 copies/mL.
All but 1 of these HIV-infected patients were treated with an-
tiretroviral therapy when they had meningitis, and 8 also re-
ceived chemotherapy for the treatment of non-Hodgkin lym-
phoma. The 3 other immunocompromised patients had an
acute transformation of a case of chronic myelogenous leu-
kemia (n p 1) or lymphoma (n p 2) and were also receiving
chemotherapy. Table 1 summarizes the demographic and clin-
ical characteristics of these 13 patients and their symptoms at
the onset of meningitis.
Clinical presentation involved acute meningeal syndrome,
with headache (100% of patients), asthenia (100%), fever
(92%), and neck stiffness (77%). None of the patients presented
Table 1. Demographic characteristics and initial clinical data
for 13 immunocompromised patients with herpetic meningitis,
Saint-Louis Hospital (Paris), 19942001.
Characteristic
Age, median years (range)
Male sex
History of herpes genitalis
Underlying condition
AIDS
Lymphoma
Leukemia
Symptom
Headache
Asthenia
Fever, temperature of 138C
Neck stiffness
Nausea/vomiting
Radiculalgia
Muscle pain
Back pain
Photophobia
Concomitant mucocutaneous herpes
NOTE. Data are no. (%) of patients, unless otherwise indicated.
with seizures, altered mental status, or focal central neurological
deficit at admission. Six had initial radiculalgia, with sphincter
involvement in 2 cases. The median duration of clinical symp-
toms before CSF samples were obtained was 8 days (range, 1
36 days). Eight patients (62%) presented with cutaneous or
mucosal lesions suggestive of HSV infection before (median, 4
days) or concomitant with meningitis. All patients underwent
brain CT and/or MRI, the findings of which were always nor-
mal. Funduscopic examination was performed for 11 patients,
and findings were normal.
Of note, before CSF was obtained, all 13 immunocompro-
mised patients had neutropenia (defined as a WBC count of
!1000 cells/mm3), and 12 had lymphopenia at the onset of
meningeal symptoms. The median WBC count at the onset of
clinical symptoms was 400 cells/mm3 (range, 1001000 cells/
mm3). Neutropenia was due to chemotherapy in 11 patients
and due to high-dose cotrimoxazole therapy for Pneumocystis
carinii pneumonia and maintenance ganciclovir therapy for
CMV retinitis in 2 of the HIV-infected patients. Findings from
other blood tests were unremarkable. The median interval be-
tween the initiation of chemotherapy and the onset of menin-
geal symptoms was 10 days. It is interesting that none of these
patients were receiving anti-HSV prophylaxis at the onset of
symptoms, and only 1 was receiving low doses of ganciclovir.
CSF findings. The CSF cytological findings and protein
and glucose concentrations are summarized in table 2. The
WBC count was !400 cells/mm3 in all patients, with a median
WBC count of 74 cells/mm3 and an elevated protein concen-
tration of 0.72 g/L. Mononuclear cells were predominant in all
samples tested. In 7 (54%) of 13 patients, there was a low CSF
Value
glucose concentration (i.e., !50% of the plasma concentration).
Mononuclear cells were described as activated or atypical in 7
37 (2977)
patients, with great polymorphism in size and large cytoplasmic
8 (62)
granulations, and were suspected to be associated with lym-
8 (62)
phoma with meningeal involvement. Cultures for bacteria, my-
cobacteria, and fungi remained sterile for all patients. No con-
10 (77)
comitant viral infection in the CSF was detected by PCR.
10 (77)
Virological results. By means of PCR, HSV DNA was de-
1 (8)
tected in all CSF samples and HSV-2 was identified in 7 of 7
samples. HSV-1 was never identified in CSF. HSV-2 was isolated
13 (100)
from specimens of concomitant cutaneous lesions obtained from
13 (100)
5 patients, 2 of whom had an untyped HSV meningeal infection.
12 (92)
One patient with untyped HSV meningitis had isolated serum
10 (77)
antibodies against HSV-2. In 3 cases, patients had both anti
6 (46)
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HSV-1 and antiHSV-2 antibodies detected in serum, and the
6 (46)
type of HSV-induced meningitis could not be determined. Over-
5 (38)
all, HSV-2 was likely to be responsible for at least 10 (77%) of
5 (38)
the 13 cases of meningitis. All but 1 patient (for whom no serum
1 (8)
sample was available for testing) had evidence of a positive HSV-
8 (62)
2 serology at or before the onset of meningitis.
Clinical course and outcome. Patients were observed for
a median duration of 90 days (range, 81800 days) after the
episode of meningitis. Two of the patients did not receive any
treatment, and 11 patients (85%) received antiviral therapy with
intravenous acyclovir (1015 mg/kg per day t.i.d.) or foscavir
(1 patient) for at least 3 days. The median duration of treatment
was 13.5 days (range, 335 days). A favorable outcome was
noted in 7 patients, 5 of whom received antiviral therapy. The
median time between symptom onset and initiation of therapy
was 2 days for these patients.
Patients 7 and 5 (table 3), for whom the initiation of antiviral
Table 2. CSF characteristics at the time of
diagnosis for 13 patients with herpetic men-
ingitis, Saint-Louis Hospital (Paris), 19942001.
Characteristic Value
WBC count, cells/mm 3
74 (4340)
Neutrophil level, % 4 (020)
Lymphocyte level, % 97 (80100)
Specimens with activated
lymphocytes, no. (%) 7 (54)
RBC count, cells/mm3 5 (0110)
Protein level, g/L 0.72 (0.324.41)
Specimens with low
glucose level, no. (%)a 7 (54)
NOTE. Data are median values (range), unless oth-
erwise indicated.
a
CSF glucose level was !50% of the blood glucose
level.
HIV/AIDS CID 2003:37 (1 December) 1529
 Table 3. Demographic and clinical characteristics for 13 immunocompromised patients with herpetic meningitis, Saint-Louis
Hospital (Paris), 19942001.

Time from
CD4+ cell count, Received WBC count at chemotherapy to Prior history
Sex/age, HIV cells/mm3 Hematological cytotoxic symptom onset, symptom onset, of herpes
Patient years infection (% lymphocytes) disease chemotherapy cells/mm3 days genitalis
1 F/36 Yes 221 (15) Burkitts lymphoma Yes 900 5 No
2 M/29 Yes 59 (22) Hodgkin disease Yes 400 9 Yes

3 M/42 Yes 246 (17) Anaplastic lymphoma Yes 400 8 No

4 M/39 Yes 120 (16) T cell lymphoma Yes 100 5 Yes

5 F/30 No ND Acute transformation Yes 400 23 No

of CML
6 M/33 Yes 303 (30) Burkitts lymphoma Yes 500 27 No

7 M/68 No ND T cell lymphoma Yes 900 18 Yes

8 M/34 Yes 131 (5) B cell lymphoma Yes 800 14 Yes

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9 M/37 Yes 103 (11) Hodgkin disease Yes 300 10 Yes

10 F/59 Yes 80 (20) Hodgkin disease Yes 100 7 No

11 M/77 No 22 (5) B cell lymphoma Yes 100 11 Yes

12 F/39 Yes 47 (6) Neutropenia due to No 1000 Yes

cotrimoxazole
13 F/35 Yes 4 (1) Neutropenia due to No 900 Yes
ganciclovir

NOTE. Acv, acyclovir; CML, chronic myelogeneous leukemia; Fcn, foscarnet; HCV-2, herpes simplex virus type 2; ND, not determined.

therapy was delayed by 17 and 44 days, respectively, developed
severe neuropathy with pain in both legs, associated with par-
aparesia, urinary retention, and anal incontinence. The first
patient developed meningitis during treatment for lymphoma.
Because of the presence of activated lymphocytes in the CSF,
a diagnosis of lymphomatous meningitis was suspected. He
received intravenous and intrathecal corticosteroid therapy. In-
travenous acyclovir was started 17 days after the onset of symp-
toms. Despite this treatment, the symptoms persisted as defin-
itive sequelae. For the second patient, the delay from the onset
of symptoms to the treatment of HSV-induced meningitis was
44 days. Sixty days after the initiation of antiviral therapy, how-
ever, the symptoms eventually improved.
Four immunocompromised patients died after the episode
of meningitis. Two deaths were associated with the underlying
hematological malignancy, but the other 2 were likely due to
HSV-induced encephalitis. These 2 patients developed enceph-
alitis 17 and 50 days after the onset of meningitis. The first
patient was infected with HIV and had a low CD4+ cell count.
She initially received no treatment for HSV-induced meningitis.
Forty-five days later, however, she developed an altered mental
status and received anti-HSV therapy. A second lumbar punc-
ture confirmed the presence of HSV-2 in CSF. She died 4 days
later from acute HSV-2associated encephalitis, with temporal
necrosis revealed on MRI. The second patient had lymphoma
without HIV infection. Because of the low glucose concentra-
tion and the presence of activated lymphocytes in the CSF, a
meningeal extension of the lymphoma was suspected. The pa-
tient subsequently received intravenous and intrathecal che-
motherapy and developed encephalitis. An MRI of the brain
showed bilateral temporal necrosis. He died 3 days later, despite
the initiation of intravenous acyclovir therapy.
It is interesting to note that 6 patients received prophylactic
anti-HSV therapy with valacyclovir (n p 3 ), oral acyclovir
(n p 2), and intravenous acyclovir (n p 1 ) during 13 following
courses of chemotherapy for their malignancies, and none ex-
perienced a relapse of HSV-induced meningitis.
DISCUSSION
During the 7-year period of this study, we identified 18 cases
of HSV-induced meningitis in our institution, on the basis of
detection of HSV DNA in CSF by PCR. The prevalence of
HSV-induced meningitis was 2% and was comparable to that
of previous reports, in which the prevalence ranged from 0.5%
to 3.9% [6, 1315].
We focused our attention on the 13 severely immunocom-
promised patients who presented with HSV-induced menin-

1530 CID 2003:37 (1 December) HIV/AIDS

 Time from
Cutaneous symptom onset
herpes during to treatment,
meningitis Initial presentation Treatment days Outcome
Vulva, cervix Fever, meningeal syndrome Favorable 8 days after diagnosis
None Fever, meningeal syndrome Acv 30 mg/kg/d iv 0 Favorable 9 days after diagnosis, without
sequelae
Lumbar (HSV-2) Fever, meningeal syndrome Acv 30 mg/kg/d iv 0 Favorable 7 days after diagnosis, without
sequelae
Buttock, anal (HSV-2) Fever, meningeal syndrome, lower Acv 30 mg/kg/d iv 2 Favorable 10 days after diagnosis, without
limb monoplegia, anal incontinence sequelae
Leg, genital (HSV-2) Fever, meningeal syndrome, axonal Acv 45 mg/kg/d iv 44 Sensory neuropathy during the 60-day pe-
neuropathy, sphincter involvement riod after diagnosis
Buttocks Meningeal syndrome, radiculalgia Acv 30 mg/kg/d iv 34 Favorable for meningitis but died because
of tumor progression
None Fever, meningeal syndrome (meningo- Acv 30 mg/kg/d iv 17 Persistent sequelea 5 years after diagnosis
myelitis)
Hand, foot, head (HSV-2) Fever, meningeal syndrome, Acv 30 mg/;kg/d iv 26 Favorable 45 days after diagnosis, without

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radiculalgia sequelae
Genital ulceration Fever, flu-like syndrome Acv 30 mg/kg/d iv 3 Favorable 6 days after diagnosis, without
sequellae
Vulva, buttocks (HSV-2) Sciatic pain,fever,flu-like syndrome Acv 30 mg/kg/d iv 8 Tumor progression and death
None Fever, headache Acv 30 mg/kg/d iv 19 Death associated with encephalitis, urinary
retention
None Fever, meningeal syndrome Favorable 7 days after diagnosis, without
sequelae
None Fever, meningeal syndrome Fcn 100 mg/kg/d iv 55 Death due to encephalitis (temporal necro-
sis) 50 days after diagnosis

gitis. The majority (11 of 13) of these patients were receiving
chemotherapy for the treatment of lymphoma or leukemia.
Also, 10 patients had AIDS, of whom 8 had HIV-associated
lymphoma. In these patients, the causative process responsible
for meningitis was likely a viral reactivation, because all but 1
patient had antibodies against HSV-2 detected in serum at the
onset of symptoms. Furthermore, 8 patients had a history of
previous herpes genitalis. The absence of previous HSV recur-
rences should not rule out reactivation however, because only
25% of patients with anti-HSV antibodies usually report having
a prior history of HSV infection [16, 17].
HSV-2 was the likely cause of meningitis in our patients,
and cases of HSV-induced meningitis have indeed been re-
ported as being mainly due to HSV-2 [18]. HSV-2 reactivation
in our patients may have been triggered by lymphopenia and/
or neutropenia. Indeed, HSV-1 recurrences during neutropenia
have been well described and cause mucitis in patients with
cancer [19]. Also, relationships between immunity and HSV
infections have been studied in various animals with corneal
(for HSV-1) and vaginal (for HSV-2) infections. In these an-
imals, the infection caused fatal encephalitis in animals that
were not previously immunized [2022]. When animals were
previously immunized with a less neuroinvasive strain, they
were capablefollowing rechallenge with a wild strainto
mount a rapid cellular immune response, allowing for a rapid
viral clearance and prevention of CNS involvement [2022].
In such immunized animals, however, drug-induced neutro-
penia led to a less efficient and delayed viral clearance and to
virus loads that were 1001000-fold more than those seen in
nonneutropenic animals [20, 22]. Similarly, low CD4+ T lym-
phocyte counts before reinfection led to the same consequences,
with high local virus load [23]. On the basis of these data [20
23], we think that HSV-induced meningitis in our immuno-
compromised patients was triggered both by neutropenia and
CD4+ T cell deficiency. Neutropenia and low CD4+ T cell counts
could also explain the high rate (62%) of HSV cutaneous re-
currences noted in our study. HSV viremia, however, was un-
likely, because none of the patients had evidence of lung, liver,
or gut involvement during the course of meningitis [24].
The clinical symptoms, biological parameters, and CSF char-
acteristics for our patients were similar to those reported in
the literature for immunocompetent patients. Of interest, we
noted hypoglycorachia in 7 of our patients, a feature that is
rarely reported as being associated with the course of this in-
fection [3, 6]. Also, the activated aspect of lymphocytes in the
CSF in 7 patients, who had hematological malignancies, delayed
the diagnosis of HSV-induced meningitis. Indeed, some of these
patients received a misdiagnosis of lymphomatous meningitis

HIV/AIDS CID 2003:37 (1 December) 1531

and received corticosteroid and/or chemotherapy that most
likely altered the course of HSV-induced meningitis. These data
underscore the need for a systematic screening for HSV DNA
in CSF in such clinical situations.
Compared with HSV-1induced encephalitis, the outcome
of HSV-induced meningitis has been reported to be sponta-
neously favorable without the use of antiviral therapy in oth-
erwise healthy hosts [6]. However, in immunocompromised
patients, neurological complications were occasionally de-
scribed. Myelitis was reported in 5 patients with cancer or
diabetes [25]. HSV-associated myelitis has also been described
in HIV-infected patients with CD4+ cell counts of !50 cells/
mm3, leading to encephalitis in some instances [2528]. The
outcome in these patients was usually unfavorable, despite the
use of antiviral therapy. However, it was difficult to sort out
the direct role of HSV infection in these patients, because they
also had CSF CMV coinfection [26]. Four of our patients also
developed severe complications, leading to encephalitis and
death in 2 cases. The severity of clinical symptoms in our study
could also be associated with a low CD4+ T cell count. Indeed,
the 2 patients who developed encephalitis had very low CD4+
T cell counts (22 and 4 cells/mm3).
The benefit of using antiviral therapy to treat HSV-induced
meningitis is unclear [29]. Our data may suggest that anti-HSV
therapy should be started as soon as possible for immunocom-
promised patients with HSV-induced meningitis. Indeed, a de-
lay in the administration of antiviral therapy seems to have
been associated with severe complications in our patients. The
dogma of early diagnostic and treatment developed for anti-
herpetic treatment in HSV-induced encephalitis might therefore
be applicable to herpetic meningitis in immunocompromised
patients. In addition, for such patients, the use of acyclovir
prophylaxis to prevent new episodes of HSV-induced menin-
gitis during further episodes of neutropenia should be consid-
ered. Indeed, no patient (except 1 who received low-dose gan-
ciclovir) was receiving anti-HSV prophylaxis at the time of
meningitis onset, and 6 of our patients who subsequently re-
ceived anti-HSV prophylaxis did not experience any recurrence
of HSV-induced meningitis, despite having undergone 13 sub-
sequent chemotherapy courses with neutropenia. However,
caution should be taken in this patients population, because
of the risk of selection of resistance [27].
In conclusion, we believe that HSV-induced meningitis
should be considered as a cause of lymphocytic meningitis in
immunocompromised patients, especially when neutropenia
and/or lymphopenia are present and when concomitant cu-
taneous recurrences are observed. Results of PCR for detection
of HSV DNA in CSF should be obtained as soon as possible.
We suggest that immunocompromised patients should receive
immediate antiviral therapy and that antiviral prophylaxis
1532 CID 2003:37 (1 December) HIV/AIDS
should be considered for such patients if they are at risk for
recurrence of neutropenia.
Acknowledgment
This study was supported, in part, by the CERI (Centre
dEtudes et de Recherche en Infectiologie).
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