Acute cysticercal meningitis--missed diagnosis.
ABSTRACT Neurocysticercosis is the commonest CNS parasitic disease worldwide but cysticercal meningoencephalitis is relatively rare, especially in Indian patients. We herein report a girl with cysticercal meningitis that was initially not suspected and later diagnosed on the basis of cerebrospinal fluid (CSF) eosinophilia. The need for CSF examination with wright-giemsa staining to avoid missing CSF eosinophilia is discussed.
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ABSTRACT: In disease-endemic areas, severe cysticercal meningitis (SCM) is characterized by intense inflammatory cerebrospinal fluid (CSF) and negative bacterial and fungal cultures. There have been no systematic studies of SCM. We characterized patients with SCM and compare them with neurocysticercosis (NC) patients with mild CSF abnormalities by conducting a nine-year retrospective review at a neurological referral center. Two groups of patients were compared: group A, those with severe CSF pleocytosis > 1,000 cells/mm(3) (n = 12), and group B, those with CSF pleocytosis <or= 1,000 cells/mm(3) (n = 126). All patients had positive CSF results in an enzyme-linked immunosorbent assay for cysticercal antigens and negative CSF cultures for bacteria, fungi, and mycobacteria. Intracranial hypertension, meningeal signs, CSF hypoglycorrachia, and a longer clinical course of NC were more frequently seen in group A. It is likely that SCM often goes unrecognized. Its correct identification may reduce morbidity and risks of unnecessary surgery in patients with chronic NC and CSF shunts.The American journal of tropical medicine and hygiene 01/2010; 82(1):121-5. · 2.53 Impact Factor
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ABSTRACT: Central nervous system infections account for 1% of primary hospital admissions and 2% of nosocomial infections and when encountered require prompt diagnosis and initiation of specific treatment. Imaging findings are mostly nonspecific with respect to the causative pathogen. This article describes the anatomy of cranial meninges and extra-axial spaces of the brain. Characteristic findings and recent advances in neuroimaging of meningitis and its complications and ventriculitis are summarized, and certain noninfectious causes of meningitis and meningitis mimics are described.Neuroimaging Clinics of North America 11/2012; 22(4):557-83. · 1.29 Impact Factor
Acute Cysticercal Meningitis – Missed Diagnosis
Devendra Mishra, Suvasini Sharma, Sanjeev Gupta1, Manoja Das and Dinesh Chauhan1
Departments of Pediatric Medicine and 1Laboratory Medicine, Chacha Nehru Bal Chikitsalaya, (Maulana Azad
Medical College), Geeta Colony, Delhi-110031.
Neurocysticercosis is the commonest CNS parasitic disease worldwide but cysticercal meningoencephalitis is relatively rare,
especially in Indian patients. We herein report a girl with cysticercal meningitis that was initially not suspected and later
diagnosed on the basis of cerebrospinal fluid (CSF) eosinophilia. The need for CSF examination with wright-giemsa staining
to avoid missing CSF eosinophilia is discussed. [Indian J Pediatr 2006; 73 (9) : 835-837] E-mail: email@example.com
Key words : CSF analysis; CSF eosinophilia; Neurocysticercosis; Lumbar puncture
Neurocysticercosis (NC) is the most frequent parasitic
infestation of the central nervous system in the world. It
has varied manifestations like seizures, raised intracranial
tension, stroke, hydrocephalus, meningoencephalitis etc.,
depending on the number and localization of the cysts.
Cysticercal meningitis is uncommon in India.1 In the
world literature also; acute cysticercal meningitis has been
described infrequently, especially in children. We herein
describe a 9-year-old girl who presented with acute
The patient was a 9-year-old girl who presented with one
day history of high grade, continuous fever, frontal
headache, and projectile vomiting. There was no history
of alteration in sensorium or convulsions. She had a
history of fever with rhinorrhea 1-week back for which
she had received oral amoxycillin for 5 days. There was
no history of rash, cough, bleeding, ear-discharge, and
any urinary or bowel complaints. She was
developmentally normal. Family history and past history
were not significant, they had a vegetarian dietary
pattern, and there was no history of contact with
tubercular patient. On examination, she was conscious but
irritable and febrile. V itals were stable and fundus
examination was normal. General physical examination
and systemic examination were normal except for
Correspondence and Reprint requests : Dr. Devendra Mishra, 163,
Sahyog Apartments, Mayur Vihar Phase I, Delhi-110091. Tel: 011
Indian Journal of Pediatrics, Volume 73—September, 2006
positive meningeal signs without focal neurological
The child was admitted with a provisional diagnosis of
meningitis. Investigations revealed total leukocyte count
of 10,470/ cumm with; polymorphonuclear cells, 68%;
lymphocytes, 24%; monocyte 6%; and eosinophils; 2%.
Lumbar puncture revealed turbid cerebrospinal fluid
(CSF) with 950 cells (polymorphonuclear cells, 90%;
lymphocytes, 10%), protein-610 mg/ dL, and sugar
45mg/ dL (concurrent blood sugar, 72 mg/ dL). CSF gram
stain and culture revealed no abnormality. Chest X-ray,
blood and urine cultures, serum biochemistry, and
platelet count were non-contributory. On the basis of
compatible clinical and CSF profile, a diagnosis of acute
bacterial meningitis was made and treatment with
Ceftriaxone, steroids (for 48 hours), and mannitol (single
dose, due to raised intracranial pressure) was started.
Fever, headache and vomiting subsided within 24 hours.
The patient remained well for the next 6 days.
On the 7th day of hospital stay, she developed
headache, projectile vomiting and irritability. She had no
recrudescence of fever or any convulsions. Examination
revealed neck rigidity and positive Kernig sign. There
were no focal neurological findings or papilledema. A
contrast enhanced computed tomograph (CECT) of the
cranium revealed an 8X7 mm hypodense lesion with an
eccentric mural nodule, minimal enhancement, but no
perilesional edema, in the left periventricular region. On
the basis of the radiological picture the lesion was
considered to be due to neurocysticercosis. A lumbar
puncture was repeated with a specific request to the
pathologist to look for eosinophils. CSF was grossly clear
with leukocytes-500/ cumm;
polymorphonuclear cells-25%, eosinophils-10%; protein
35mg/ dL, and sugar-51mg/ dL (concurrent blood sugar
Devendra Mishra et al
82mg/ dL). CSF gram stain and culture did not reveal any
abnormality. Tuberculin test with 5TU was negative.
Serum IgG-ELISA enzyme-linked immunosorbent assay
tests for Cysticercosis and for Tuberculosis were
Negative. Serum and CSF immunoblot studies and MRI
brain to look for subarachnoid cysts could not be done.
The patient was started on dexamethasone, and
decongestive measures (mannitol, acetazolamide). Her
symptoms improved over the next 12 hours. Indirect
ophthalmoscopy ruled out intra-ocular cysts.
Subsequently she received albendazole at dose of 15mg/
kg/ day for 28 days and anticonvulsants. She made an
uneventful recovery. At last follow-up (ten month later),
she was asymptomatic with no recurrence of symptoms,
no evidence of meningeal irritation or raised intracranial
pressure (ICT), and no neurodeficiet. Repeat CECT
revealed resolution of the lesion.
The initial clinical presentation was consistent with the
diagnosis of pyogenic meningitis. The previous course of
oral antibiotics could have been responsible for the
negative CSF gram stain and culture; the rapid
improvement on antibiotics, however, supported the
diagnosis. When the patient deteriorated after 6 days;
subdural effusion, ventriculitis or a concurrent brain
abscess were the likely possibilities. The re-appearance of
signs of meningeal irritation prompted us to repeat the
lumbar puncture. In view of the presence of granuloma
on CT, the possibility of cysticercal meningitis was
considered, and a Wright Giemsa staining of the CSF was
asked for. In the absence of this staining, eosinophils can
be mistaken for polymorphonuclear cells.1
The finding of the viable NC granuloma on CECT in
the absence of any past history of teniasis, seizures,
headaches, or any neurological problem was surprising.
This finding could also have been coincidental, as viable
cysts are known to remain asymptomatic for long periods
and reported to be present in up to 1.3% of normal
persons (autopsy study).2 The presence of CSF
eosinophilia and the coexistent inflammatory granuloma
suggested the possibility of cysticercal meningitis.
Cysticercosis is by far the commonest cause of CSF
eosinophilia in endemic areas.3 The CSF findings in
cysticercal meningitis consist of pleocytosis (usually
lymphocytic but frequently polymorphonuclear), reduced
glucose and elevated protein, with up to 70% patients
with cysticercal meningitis having CSF eosinophilia
between 2-40%.4-6 The presence of eosinophils more than
4% of leukocytes in the CSF is of diagnostic significance4
and is seen in the initial phases of the illness only. For
visualizing eosinophils in the CSF, Wright-Giemsa
staining of the CSF is required which is not routinely done
in wardside-laboratories in most hospitals. In the absence
of this staining, eosinophils can be mistaken for
polymorphonuclear cells.1 Other causes of eosinophilic
meningitis include coccidioidal meningitis; parasitic
infestation with Angiostrongylus cantonensis, Paragonimus
westermani, Gnathostoma spinigerum; intrathecal injection
of foreign proteins, and the insertion of rubber tubing into
the central nervous system in the course of neurosurgery.7
Cysticercal meningoencephalitis is caused by
infiltration of the meninges and the parenchyma of the
brain by a large number of parasites and inflammation in
the surrounding tissue is responsible for meningitis and
encephalitis.8 Although described in 42-48% of patients in
Latin American series, cysticercal meningoencephalitis
has been reported in less than 10% adults patients with
NC in India.1,9 Of the two large series of Indian children
with NC, only one reported meningoencephalitis in 0.3%
of the subjects.10,11 Slightly higher proportions have been
reported in a small case-series.8 Around 60% cysticercal
meningoencephalitis cases have been reported to have
associated parenchymal lesions.11 Most cases described
are chronic in evolution12 and isolated acute meningitis
has rarely been described. A case report from Thailand
describes two children presenting as pyogenic meningitis,
with normal cranial CT but not responding to antibiotic
therapy.6 Cysticercal meningitis was diagnosed based on
the presence of CSF eosinophilia and positive serum
serology, and both responded to praziquantel. Both
cysticercus ELISA and Electro-Immuno Transfer Blot
Assay (EITB) assays in the CSF have high sensitivity for
cysticercal meningitis, but these studies in CSF and EITB
in serum were not feasible in our setup.
There are no guidelines for the treatment of acute
cysticercal meningitis. A nti-parasitic therapy is
recommended for chronic meningitis.13 The decision to
treat in this patient was also justified by the radiological
presence of a viable cyst. To conclude, we describe a 9
year-old Indian child with acute cysticercal meningitis
that initially presented as pyogenic meningitis. Given the
high prevalence of cysticercosis in Indian patients, this
entity should be suspected in all patients; and CSF
eosinophilia specifically looked for, more so when a
concurrent parenchymal lesion suggestive of cysticercosis
1.? Singh G. Neurocysticercosis in the south-central America and
the Indian subcontinent. Arq Neuropsiquiatr 1997; 55: 349-356.
2.? Mahajan RC. Geographical distribution of human
cysticercosis. In, Cysticercosis: Present state of Knowledge and
Perspectives, (Ed.) Ana Flisser, et al. Academic Press 1982, 39-46.
3.? Tasker WG, Plotkin SA. Cerebral Cysticercosis. Pediatrics 1979;
4.? Wang CH, Gao SF, Guo YP. Diagnostic significance of
eosinophilia of the cerebro-spinal fluid in cerebral
cysticercosis. Chinese Medical Journal 1993; 106: 282-284.
5.? Wilber RR, King EB, Howes EL. Cerebrospinal fluid cytology
in five patients with cerebral cysticercosis. Acta Cytologica 1980;
24 : 421-426.
6.? Visudhipan P, Chiemchanya S. Acute cysticercal meningitis in
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Acute Cysticercal Meningitis – Missed Diagnosis
children: response to praziquantel. Ann Trop Ped 1997; 17: 9-13.
7.? Char DFB, Rosen L. Eosinophilic meningitis among children in
Hawaii. J Pediatr 1967; 70 : 28-35.
8.? Puri V, Sharma DK. Neurocysticercosis in children. Indian
Pediatr1991; 28 : 1309-1317.
9.? V enkatraman S, Roy A K , Dhamija RM, Sanchetee PC.
Cysticercal meningoencephalitis - Clinical presentation and
autopsy findings. J Assoc Phys India 1990; 38: 763-765.
10.? Singhi P, Ray M, Singhi S, Khandelwal P. Clinical spectrum of
500 children with neurocysticercosis and response to
albendazole therapy. J Child Neurol 2000; 15: 207-213.
11. Kalra V, Mittal R, Rana KS, Gupta A . Neurocysticercosis:
Indian experience. Perat MV (Ed), New Developments in
Neurology, Monduzzi Editore S.P.A. Bologna, Italy; 1998 pp
12. Joubert J. Cysticercal meningitis- a pernicious form of
neurocysticercosis which responds poorly to praziquantel. S
Afr Med J 1990; 77: 528-530.
13. Garcia HH, Evans CAW, Nash TE et al. Current consensus
guidelines for the treatment of Neurocysticercosis. Clin
Microbiol Rev 2002; 15: 747-756.
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