Varicella-zoster was 36 °C, and the rest of

Varicella-zoster virus
(VZV) is a human neurotropic virus, member of the Herpesviridae family. It
has the ability to remain dormant in cranial and dorsal root ganglia 1. Two
clinical syndromes are caused by this virus. The primary infection (chickenpox)
usually occurs during childhood and is extremely contagious, characterized by
fever, malaise, and a vesicular rash 2. Reactivation of VZV results in herpes
zoster (shingles), with dermatomal distribution of pain and rash. and it is
usually a disease of older or immunocompromised people 1,2. Central nervous
system (CNS) involvement may occur during primary infection or reactivation,
and may include meningitis, encephalitis, meningoencephalitis, vasculopathy,
myelitis, Guillain-Barré syndrome, and retinal inflammatory disorders 1,2.

Here, we present the
case of a previous healthy immunocompetent 37-year-old man with aseptic
meningitis without rash as a result of reactivated VZV infection, in whom
cerebrospinal fluid (CSF) analysis revealed hypoglycorrhachia.A 36-year-old Caucasian
male presented to our hospital with a 4-day history of persistent frontal
headache and low-grade fever, with no other symptoms. He had an episode of
varicella infection in his childhood, but no history of zoster. The rest of his
medical history was unremark­able. Apart from paracetamol, no other medications
had been taken in the previous days. He was an active smoker with a
10-pack-year history, with no use of alcohol or illicit drugs. His family
history was insignificant. He was married, lived in an urban area, worked as a
refrigerant, and with no contacts with animals.

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Initially, the patient
was evaluated by an otolaryngologist, without findings from the ear, nose and
throat examination, but neck stiffness was noted, and the patient was referred
to the emergency room. On examination, he was alert and oriented. His body
temperature was 36 °C, and the rest of the vital signs were
also normal. Neck stiffness was present, but no other neurological
abnormalities were detected. The remainder of the clinical examination,
including skin, respiratory and cardiovascular system, was normal.

A chest x-ray and a
computed tomography of the head and sinuses were carried out and showed no
abnormalities. Laboratory tests revealed a white blood cell (WBC) count of 6.1 x 109 /L (neutrophils: 61.3%,
lymphocytes: 24.5%, monocytes: 11.7%, eosinophils: 2.2%, basophils: 0.3%) and a
platelet count of 149 x 109 /L. The serum biochemical parameters of kidney
and liver function were normal. C-reactive protein and erythrocyte
sedimentation rate levels were within normal range also. Blood and urine
culture were drawn and serology for human immunodeficiency virus (HIV) was
obtained. A lumbar puncture (LP) was performed in the emergency room and yielded
clear cerebral spinal fluid (CSF), with 400 x 106/L WBC (94%
lymphocytes), 25 x 106/L red blood cells (RBC), an elevated total
CSF protein of 177 mg/dL, and a low CSF glucose of 45 mg/dL (serum glucose of 90
mg/dL), with a CSF to serum glucose ratio of 0.5. Gram stain, Ziehl–Neelsen
stain and Indian ink stain were negative, while CSF cultures were sent. CSF
volume was insufficient for performing polymerase chain reaction (PCR) studies.
The patient was started on intravenous ceftriaxone and acyclovir and he was
admitted to the internal medicine department with the diagnosis of probable
aseptic meningitis.

On day 3 of
hospitalization, the patient continued to be afebrile, while the headache and
the neck stiffness had resolved. Blood, urine and CSF cultures obtained on
admission did not demonstrate any bacterial growth, and ceftriaxone was stopped.
The HIV serology was negative too. A second LP was performed in order to
collect a CSF sample for neurotropic viruses’ PCR and assess the need for
continuing acyclovir treatment. Repeated LP revealed WBC count of 667 x 106/L
(93% lymphocytes), RBC count of 30 x 106/L, total protein level of
94 mg/dL, and a glucose level of 38 mg/dL (serum glucose of 94 mg/dL), with a
CSF to serum glucose ratio of 0.4. CSF cytology did not yield any malignant
cells. The PCR analysis of the CSF herpes simplex virus (HSV) I and II was
negative, but VZV DNA was detected. The patient received a total of 8 days of
intravenous acyclovir and he was discharged with instructions for an additional
6-day course of oral valacyclovir and for performing a magnetic resonance
imaging (MRI) of the brain as an outpatient. On his follow-up visit two weeks
later, the patient was in a good health condition, while the MRI showed no
abnormalities.VZV meningitis is an
uncommon complication of herpes zoster 3. Nevertheless, VZV represents one of
the commonest etiological agent for aseptic meningitis 4-6. The progress of
the technology has allowed a more detailed attribution of central nervous
system (CNS) disorders to VZV. PCR and other molecular amplification methods
are characterized by high sensitivity and specificity in detecting viral DNA in
CSF, and have become essential tools in the diagnostic armory 1. In contrast
with VZV encephalitis or meningoencephalitis, VZV meningitis is associated with
a favorable clinical outcome in immunocompetent hosts, and the need for
treatment with antiviral agents in these patients is controversial 6.

It is well established
that aging causes a multitude of changes in the immune system leading to
numerous defects, and to a subsequent vulnerability to pathogens 7. Additionally,
disease-related or iatrogenic immunosuppression have deleterious effects on
host defense 8. Defects in specific functional compartments of the immune
system are associated with susceptibility to specific infectious agents 8.
Herpes zoster is most frequent in the elderly and in immunocompromised patients
1,2. The reason relies on the fact that VZV-specific, cell-mediated immunity
declines with age or immunosuppression, and it is the adaptive T cell response
that is crucial for preventing the reactivation of the latent virus 7-9. A
recent study demonstrated that the incidence of herpes zoster was twice as high
in immunocompromised than in immunocompetent hosts, and that higher incidences
were observed among individuals with severe immunosuppression 10. Higher
incidences were also observed among women and older patients 10.

Herpes zoster is manifested
by a unilateral dermatomal rash, which is painful and/or pruritic. It starts as
papules and quickly evolves into vesicles or bullae. Occasionally, a dermatomal
distribution of pain and/or pruritus occurs in the absence of an antecedent skin
eruption. This condition is known as zoster sine herpete 1. The dormant virus has also the ability, during its
reactivation, to travel from the ganglia to the central nervous system, without
concurrent skin manifestations 11. Indeed, in cases of VZV meningitis, the
rash can be absent in a significant proportion of patients 5, 12-14.

The CSF analysis in viral
meningitis typically includes lymphocytic pleocytosis, a slightly elevated
protein level, and a normal glucose level. A CSF hypoglycorrhachia is defined
as CSF glucose less than 45 mg/dL, and is usually detected in bacterial,
tuberculous, and fungal meningitis 15. Less common causes of
hypoglycorrhachia include acute syphilitic meningitis, Mycoplasma pneumoniae meningitis, primary amebic meningitis,
meningeal cysticercosis, carcinomatous meningitis, subarachnoid hemorrhage, sarcoidosis,
rheumatoid meningitis, and lupus myelopathy 16. Viruses that may cause low
CSF glucose levels when they invade meninges are mumps and, occasionally only, HSV,
enteroviruses, lymphocytic choriomeningitis virus and VZV 13,14,16. It must
be emphasized that CSF glucose level may be falsely low in case of concurrent
hypoglycemia. A serum glucose must be drawn before the LP, and a CSF to serum
glucose ratio must be calculated. A normal ratio is around 0.6, and ratios less
than 0.5 are considered abnormal 15.

We report an
unusual presentation of VZV meningitis in previously healthy young adult,
without a rash and with hypoglycorrhachia. Only few similar cases have been
previously reported 17-19. Mayo and Booss 17 reported four young adult patients
without exanthem and with clinical and serological diagnosis of VZV meningitis.
Three of them had low CSF glucose, and the other patient an abnormal CSF to
serum glucose ratio, while all had a favorable outcome. Habib et al. 18
presented an immunocompetent 26-year-old woman who was diagnosed with VZV
meningitis using PCR in CSF, without a rash and with low CSF glucose and CSF to
serum glucose ratio. The patient was successfully treated with intravenous
acyclovir. Pasedag et al. 19 reported an 18-year-old previously healthy man
with molecular and serological diagnosis of VZV meningitis, presented with hypoglycorrhachia
and treated successfully with acyclovir and valacyclovir. Finally, three other
similar cases exist in the literature concerning three patients under the age
of 16 years, all with a benign course 20-22.


In conclusion, our
case emphasizes the importance of considering reactivated VZV as a cause of
aseptic meningitis in young and immunocompetent individuals, even in the
absence of an exanthem. It is also highlight the fact that VZV meningitis can
be accompanied by hypoglycorrhachia. The widespread use of molecular methods in
CSF analysis allows the prompt recognition of CNS involvement during the course
of this viral disease and the early initiation of treatment.


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