Indian Journal of Pediatrics, Volume 72—September, 2005 755
Original Article
Correspondence and Reprint requests : Dr. Sunil Karande, Flat 24,
Joothica, 5th Floor; Opposite Grant Road Post Office; 22A, Naushir
Bharucha Road; Mumbai 400 007, India. Fax No. : 91-22-2407 6100
Since the early 1990’s, human immunodeficiency virus
(HIV) infection is assuming alarming proportions in
Mumbai.1 This HIV epidemic has been accompanied by a
corresponding increase in the incidence of tuberculosis
(TB) and HIV-related TB cases. 2,3 Between 1-2% of
children with untreated tuberculous infection develop
tuberculous meningitis (TBM), a serious illness which has
a high rate of neuromorbidity and mortality. 4,5 Co-
infection of TBM and HIV is likely to further complicate
this problem.6
The objective of the present study was to: (i) find out
the incidence of HIV co-infection in children admitted
with TBM to our hospital, (ii) identify factors which are
associated with HIV-infected status and (iii) find out
whether HIV co-infection affects the in-hospital outcome.
MATERIALS AND METHODS
Patient Enrolment
All consecutive children, aged 1 month to 12 years of age,
who were admitted to our hospital with a diagnosis of
TBM, were enrolled prospectively. The study was
conducted from May 2000 to August 2003. The diagnosis
of TBM was based on a standard clinical case definition
(Table 1) devised by Doerr et al.7
At the time of admission, a complete physical
examination was performed. Cerebrospinal fluid (CSF)
Tuberculous Meningitis and HIV
Sunil Karande, Vishal Gupta, Madhuri Kulkarni, Anagha Joshi1 and Mhisti Rele2
Division of Pediatric Neurology, Department of Pediatrics, and Departments of 1Radiology and 2Microbiology,
Lokmanya Tilak Municipal Medical College and General Hospital, Sion, Mumbai, India
Abstract. Objective : To identify factors associated with HIV-infected status in children admitted with tuberculous meningitis
(TBM), and to find out whether HIV co-infection affects in-hospital outcome. Methods : This prospective hospital-based study
was conducted from May 2000 to August 2003. All consecutive children, aged 1 month to 12 years of age, admitted with a
diagnosis of TBM were enrolled. Relationship between 35 features viz., two demographic factors, nine clinical features, 13
neurological features, five laboratory (including cerebrospinal fluid) parameters, six radiological (including computed tomography
scan brain) features, and the two outcomes (disabled survivor or death); with HIV-infected status was assessed. Results : Of
a total 123 TBM cases enrolled, eight (6.5%) were HIV-infected. There was no significant difference between the two groups,
except that more children in the HIV-infected group had Hb< 8 gm/dl: both on bivariate analysis, (OR, 12.0; 95% CI, 2.6-55.9;
P = 0.001) and on multivariate analysis (OR, 12.30; 95% CI, 1.9-79.6; P = 0.008). Outcome was similar in both the groups.
Conclusion: Only presence of Hb< 8 gm/dl was associated with HIV-infected status. HIV co-infection did not affect the
outcome. [Indian J Pediatr 2005; 72 (9) : 755-760] E-mail:karandesunil@yahoo.com
Key words : HIV Infections; Multivariate Analysis; Tomography, X-Ray Computed; Treatment outcome; Tuberculosis;
Meningeal
examination and cranial computed tomography (CT) scan
were done soon after admission in every child. A
standardized data-entry form was used to document
demographic data, clinical symptoms and signs,
laboratory findings, Mantoux test result, chest radiograph
and ultrasound abdomen findings, CSF and Cranial CT
scan findings of each patient were conducted at
presentation. Histopathological examinations of lymph
nodes were carried out wherever appropriate.
Each patient was screened for HIV infection using the
enzyme-linked immunosorbent assay (ELISA) test. Pre
and post- test counseling was offered to the parents. The
ELISA kits were used in strict compliance with the
manufacturer's instructions. The kits detected antibodies
to both HIV-1 and HIV-2 viruses. They met the minimum
standards (sensitivity > 99 %, specificity > 95 %) as
recommended by World Health Organization (WHO).8
TABLE 1. Clinical Case Definition of Tuberculous Meningitis by
Doerr et al7
Abnormal neurological signs and/or symptoms, and  greaterequal 2 of the
following:
1. Discovery of adult source case with contagious tuberculosis
who had significant contact with child
2. Presence of Mantoux (5 TU) skin test reaction  greaterequal 10 mm of
induration, or greaterequal 5 mm of induration if child had close contact
with infected adult
3. CSF abnormalities without evidence of other infectious cause
4. Abnormalities on cranial CT consistent with CNS tuberculosis
CNS = central nervous system; CSF = cerebrospinal fluid; CT =
computed tomography; TU = tuberculin units.
Sunil Karande et al
756 Indian Journal of Pediatrics, Volume 72—September, 2005
The diagnosis of HIV infection was confirmed as per the
WHO strategy II: when two ELISA tests based on a
different antigen preparation and/or different principle
were positive.9 In children below 18 months of age, HIV
infection was confirmed only if they also fulfilled the
WHO criteria for symptomatic HIV infection.10
Nutritional status was assessed by the Wellcome
classification.11 The severity of the disease at admission
was classified into three stages, based on the Medical
Research Council (MRC) guidelines12: stage I (early) =
conscious, non-specific symptoms and no neurological
signs; stage II (intermediate) = signs of meningeal
irritation with slight or no clouding of sensorium, with or
without minor neurological deficit (cranial nerve palsy or
limb paresis); and, stage III (advanced) = severe clouding
of sensorium, convulsions, focal neurological deficit, and/
or involuntary movements. The children’s levels of
consciousness were assessed by the 15 point Glasgow
coma scale (GCS).13 Cranial CT scan has proved to be a
reliable method for the diagnosis of TBM.4,14 The degree
and significance of hydrocephalus were calculated by
ventricular size index (VSI), which is the relation between
bi-frontal diameter over the frontal horn diameter.15 A VSI
of 30-38% indicates mild hydrocephalus, 39-45%
moderate hydrocephalus, and >45% severe
hydrocephalus.15
Management of Cases
Standard anti-tuberculous therapy (ATT) 16: isoniazid (5
mg/kg/day), rifampicin (10 mg/kg/day), pyrazinamide
(25 mg/kg/day), and ethambutol (20 mg/kg/day); and
other supportive measures (corticosteroids,
anticonvulsants and mannitol) were started within 24- 48
hours of admission. Corticosteroids were administered
during the first month of therapy and were given as
intravenous dexamethasone (0.6 to 1.2 mg/kg/day in
three divided doses) for the first seven days, followed by
oral prednisolone (2 mg/kg/day in three divided doses)
and then gradually tapered over a week. Acetazolamide
(20 mg/kg/day orally in three divided doses) was started
in children with hydrocephalus to prevent its progression.
During hospitalization, if the patient had deteriorating
neurological symptoms and signs, Cranial CT scan was
repeated to detect development of hydrocephalus or
progression in its severity. A Neurosurgeon would do a
ventriculoperitoneal (VP) shunt surgery when Cranial CT
scan showed presence of moderate or severe
hydrocephalus and it was associated with deteriorating
neurological symptoms and signs.5,17 If the CSF protein
concentration was more than 1 g/l, the hydrocephalus
was initially treated by external ventricular drainage
using a chamber as high CSF protein content can cause
blockage of a VP shunt.17 After the protein concentration
fell below 1 g/l, shunt surgery was done. Family
screening was done to detect source of infection. Liver
function tests (LFTs) were done weekly, and whenever
appropriate, to detect ATT-induced hepatotoxicity.
In children who were HIV seropositive (HIV-P), CSF
examination was repeated to detect associated
cryptococcal meningitis by direct microscopy on
centrifuged deposits with wet and India ink preparation
and culture on Sabouraud dextrose agar.
Variables and Outcome Assessment
Almost all the features that were analyzed (except shunt
surgery being done, and development of ATT-induced
hepatotoxicity) were documented at presentation. The
outcome in each patient was assessed in terms of survival
or death. Survival meant that the patient was discharged
from the hospital: (i) having made a “complete recovery”,
or (ii) as a “disabled survivor” with neurological sequelae
such as altered sensorium, cranial nerve palsy,
extrapyramidal movements, focal neurological deficit,
mental retardation, optic atrophy, and/or tone
abnormalities. Survivors were discharged from hospital
after their clinical condition had stabilized and they were
able to take feeds either orally or via nasogastric tube.
Data Analysis
The data obtained was analyzed using the Statistical
Package for the Social Sciences, version 11 for Windows
(SPSS Ltd., Chicago, Illinois, USA). A bivariate analysis
was initially performed by the Chi square (chi2) test (with
Yates’ correction) to assess the relationship between the 35
variables, and the two outcomes (disabled survivor or
death); with the HIV-P status. Wherever appropriate, the
odds ratio (OR) was calculated and 95% confidence
intervals (CI) was estimated around the OR. A P value
<0.05 was considered significant. Two-tailed significance
was obtained in all cases. Further, multivariate analysis
was performed. Starting with a tentative logistic
regression model with all the variables obtained in
bivariate analysis, a step down variable selection
procedure was used to derive a suitable model predicting
the HIV-P status.
RESULTS
Clinical, Laboratory and Radiological Features
Of a total 123 children with TBM who were enrolled, eight
(6.5%) were detected to be HIV-P. There was no
significant difference (P = 0.060) in mean age of children
in the HIV-seronegative (HIV-N) and HIV-P groups: 34.5
months (S.D. 30.4 months, range 2.5 months to 11 years)
vs 67.0 months (S.D. 47.3 months, range 5 months to 12
years). The M : F ratio was 1.1 : 1 in the HIV-N group and
1.7 : 1 in the HIV-P group. There was no significant
difference (P = 0.100) in the mean symptom duration in
the HIV-N and HIV-P groups: 22.1 days (S.D. 30.1 days,
range 1 to 180 days) vs 42.0 days (S.D. 59.4 days, range 1
to 180 days).
On bivariate analysis, clinical and neurological features
in both the groups were similar at presentation (Tables 2
Tuberculous Meningitis and HIV
Indian Journal of Pediatrics, Volume 72—September, 2005 757
and 3). Most children (87.8% vs 62.5%) were already in
MRC TBM stage III at presentation. Laboratory and
radiological features did not differ significantly between
the two groups (Table 4), except that more children in the
HIV-P group had moderate-severe anemia i.e. Hb < 8
gm/dl (P = 0.001). Three children in the HIV-N group
developed ATT-induced hepatotoxicity, which
necessitated omitting isoniazid, rifampicin and
pyrazinamide, and adding streptomycin till LFTs
normalized. Cryptococcal meningitis was not detected in
any of the HIV-P cases.
When multivariate analysis was applied (Table 5),
again the same variable, viz. Hb < 8 gm/dl, proved to be
independently associated (P = 0.008) to the HIV-P status.
Outcome
Twenty-two (19.1%) HIV-N cases and three (37.5%) HIV-
P cases made a complete recovery. Table 6 shows that
there was no significant difference in the two groups as
regards disabled survivor (P = 0.557) or death (P = 0.779)
outcomes. Also, duration of hospital stay in HIV-N and
HIV-P children who survived was similar (P=0.120): 20.3
days (S.D. 11.9 days, range 5 to 68 days) vs.  13.7 days
(S.D. 5.1 days, range 7 to 22 days). The mean duration of
hospital stay in HIV-N children who died was 21.2 days
(range 3 to 90 days, S.D. 17.5 days). Only one patient, a 12-
year-old boy, in the HIV-P group died after 10 day
hospital stay.
DISCUSSION
To our knowledge, the present study is the first one in
India, and probably the second in the world, which has
compared the characteristics and outcome of children
having TBM with and without HIV co-infection. The
present study has revealed that eight (6.5%) of 123
TABLE 2. Clinical Features in HIV-Negative and HIV-Infected TB Meningitis Cases
Variable HIV-negative HIV-infected
(n = 115) (%) (n = 8) (%) OR# 95% CI P value*
Demographic Factors
Young age (< 3 years) 70/115 (60.9) 2/8 (25.0) 0.2 0.04-1.1 0.105
Male sex 60/115 (52.2) 5/8 (62.5) 1.5 0.3-6.7 0.842
Symptoms
Duration of illness > 2 weeks 52/115 (45.2) 3/8 (37.5) 0.7 0.2-3.2 0.955
Fever§ 111/115 (96.5) 8/8 (100.0)   -      - 0.636
Changes in personality 72/115 (62.6) 2/8 (25.0) 0.2 0.04-1.0 0.084
Weakness 85/115 (73.9) 4/8 (50.0) 0.4 0.08-1.5 0.292
Seizures 74/115 (64.3) 4/8 (50.0) 0.6 0.1-2.3 0.663
Contact with adult TB 42/115 (36.5) 6/8 (75.0) 5.2 1.0-27.0 0.075
Measles in previous 6 months 12/115 (10.4) 1/8 (12.5) 1.2 0.1-10.8 1.000
General Signs
BCG received 68/115 (59.1) 5/8 (62.5) 1.2 0.3-5.1 1.000
Malnutrition 33/115 (28.7) 5/8 (62.5) 4.1 0.9-18.3 0.108
#Odds ratio calculated by bivariate analysis; * P < 0.05 significant.
§Odds ratio cannot be computed. They are only computed for a 2 × 2 tables without empty cells.
TABLE 3. Neurological Features in HIV-Negative and HIV-Infected TB Meningitis Cases
Variable HIV-negative HIV-infected OR#   95% CI P value*
(n = 115) (%) (n = 8) (%)
Neurological factors (clinical)
Stage III of disease§ 101/115 (87.8) 5/8 (62.5)   -       - 0.129
Coma (GCS score < 6) 25/115 (21.7) 3/8 (37.5) 0.5 0.1-2.1 0.554
Meningeal signs 50/115 (43.5) 5/8 (62.5) 2.2 0.5-9.5 0.497
Tonic posturing§ 26/115 (22.6) 0/8 (0.0)   -      - 0.286
Papilloedema§ 4/115 (3.5) 0/8 (0.0)   -      - 1.000
Optic atrophy§ 6/115 (5.2) 0/8 (0.0)   -      - 1.000
Cranial nerve palsy 40/115 (34.8) 1/8 (12.5) 0.3 0.03-2.3 0.366
Focal neurological deficit 61/115 (53.0) 2/8 (25.0) 0.3 0.1-1.5 0.243
Hypertonia 47/115 (40.9) 2/8 (25.0) 0.5 0.1-2.5 0.608
Hypotonia 41/115 (35.7) 3/8 (37.5) 1.1 0.2-4.8 1.000
Ankle clonus 27/115 (23.5) 4/8 (50.0) 3.3 0.8-13.9 0.211
Extra-Pyramidal movements§ 14/115 (12.2) 0/8 (0.0)   -      - 0.636
Shunt surgery 67/115 (58.3) 2/8 (25.0) 0.2 0.05-1.2 0.143
#Odds ratio calculated by bivariate analysis; *P < 0.05 significant.
§Odds ratio cannot be computed. They are only computed for a 2 × 2 tables without empty cells.
Sunil Karande et al
758 Indian Journal of Pediatrics, Volume 72—September, 2005
TABLE 4. Laboratory and Radiological Features in HIV-Negative and HIV-Infected TB Meningitis Cases
Variable HIV-negative HIV-infected OR# 95% CI P value*
(n = 115) (%) (n = 8) (%)
Moderate-severe anemia 14/115 (12.2) 5/8 (62.5) 12.0 2.6-55.9 0.001
(Hb < 8 gm/dL)
Mantoux test positive 21/115 (18.3) 1/8 (12.5) 1.6 0.2-13.4 0.950
Cerebrospinal fluid parameters
Cells > 100 mm3 50/115 (43.5) 4/8 (50.0) 1.3 0.3-5.5 1.000
Proteins > 1 g/l 70/115 (60.9) 4/8 (50.0) 0.6 0.2-2.7 0.815
CT scan brain parameters
Moderate-severe hydrocephalus§ 53/115 (46.1) 4/8 (50.0)   -      - 0.168
Parenchymal enhancement 77/115 (67.0) 3/8 (37.5) 0.3 0.1-1.3 0.192
Basilar inflammation 89/115 (77.4) 5/8 (62.5) 0.5 0.1-2.2 0.597
Cerebral infarct ± edema 51/115 (44.3) 3/8 (37.5) 0.8 0.2-3.3 0.993
Tuberculoma 26/115 (22.6) 2/8 (25.0) 1.1 0.2-6.0 1.000
Presence of extra-cranial TB§ 86/115 (74.8) 8/8 (100.0)   -      - 0.232
ATT hepatotoxicity§ 3/115 (2.6) 0/8 (0.0)   -      - 1.000
#Odds ratio calculated by bivariate analysis; *P < 0.05 significant.
§Odds ratio cannot be computed. They are only computed for a 2 × 2 tables without empty cells.
TABLE 5. Multivariate Logistic Regression Model Showing the Variables Associated with HIV-Infected Status in TB Meningitis Cases
Variables Regression SE P value* df OR 95% CI
coefficient
Young age (< 3 years) - 1.06 0.95 0.267 1 0.4 0.05-2.2
Changes in personality - 1.92 1.01 0.057 1 0.2 0.02-1.1
Contact with adult TB   1.55 0.97 0.108 1 4.7 0.7-31.3
Malnutrition   0.14 0.95 0.884 1 1.2 0.2-7.4
Moderate-severe anemia (Hb < 8 gm/dl)   2.51 0.95 0.008 1 12.3 1.9-79.6
Constant   0.73 2.97 0.805 1 2.1        -
*P<0.05 significant.
SE = standard error; df = degree of freedom; OR = odds ratio; CI = confidence interval.
TABLE 6. Outcome in HIV-Negative and HIV-Infected TB Meningitis Cases
Outcome HIV-negative HIV-infected P value* OR 95% CI
(n) (%) (n) (%)
Disabled survivor 66/88 (75.0) 4/7 (57.1) 0.557 2.3 0.5-10.9
Died 27/115 (23.5) 1/8 (12.5) 0.779 2.2 0.3-18.2
*P < 0.05 significant.
OR = odds ratio; CI = confidence interval.
children admitted with TBM were HIV-infected. Except
for the significantly increased (P = 0.008) occurrence of
moderate-severe anemia (Hb < 8 gm/dl) in the HIV-
infected cases, all other features and in-hospital outcome
were similar.
There is scant data on TBM in HIV-infected children. A
prospective study by Topley et al18 from Durban, South
Africa has reported that 10 (25%) of 40 children admitted
with TBM were HIV-infected. In their study on bivariate
analysis, clinical features (including Hb levels) were
similar in HIV-negative and HIV-infected children with
TBM, but Cranial CT scans showed significantly (P = 0.01)
more parenchymal enhancement.18 Topley et al
hospitalized the children for at least six months to assess
their treatment outcome. In their experience, the short
term response to treatment was reasonable in 6 out of the
10 HIV-infected children. Four of their survivors who had
completed treatment left hospital being able to stand or
walk. But long-term outcome at six to twelve months was
poorer in the HIV-infected children, with 30% dying and
the remaining children surviving with moderate or severe
handicap.18  In the present study, patients did not
complete treatment in hospital. Since follow-up after
discharge from hospital is generally poor in the present
setting, the authors could not document the outcome after
completion of ATT. The present finding that HIV co-
infection does not appear to change the clinical
manifestations or the in-hospital outcome of TBM has
been reported in adult studies.19-21
Topley et al18 have not employed multivariate analysis
on their data. Multivariate analysis scores over bivariate
analysis, as it has the advantage of determining the
Tuberculous Meningitis and HIV
Indian Journal of Pediatrics, Volume 72—September, 2005 759
“independent” effect of each variable while controlling
the influence of other variables. The present study
confirmed on multivariate analysis, that Hb< 8 gm/dl
was independently associated (P = 0.008) to the HIV-
infected status. The authors believe that the probable
reason for this increased incidence of moderate-severe
anemia is the advanced immunosuppression, and this
finding will be useful to clinicians working in resource-
constrained settings to suspect HIV co-infection in
children admitted with TBM. Anemia is a common
feature in HIV-infected children and its pathogenesis is
often multi-factorial, including iron deficiency, the anemia
of chronic disease, malaria and opportunistic
infections.22,23 Anemia has also been shown to be a
statistically significant predictor of progression to the
acquired immunodeficiency syndrome and is
independently associated with an increased risk of death
in individuals with HIV.22,23
There are no guidelines available about the use of
corticosteroids in children with TBM and HIV co-
infection. However, the administration of corticosteroids
has been shown to significantly improve the survival and
intellectual outcome of children with TBM.24 Hence these
were used even if HIV co-infection was present. Topley et
al have also similarly used corticosteroids in their study.19
A recent study from Vietnam has documented that
adjunctive treatment with corticosteroids improves
survival in patients over 14 years of age with TBM and
HIV co-infection.25
The strengths of the present study are that: (i) it was
prospective, (ii) all patients received uniform treatment,
and (iii) 35 variables were analyzed by both bivariate and
multivariate analysis to identify those associated with
HIV co-infection. However, the present study has its
limitations. First, there was a low incidence of HIV co-
infection (8/123, 6.5%) in the TBM cases analyzed by the
authors. Hence, it must be kept in mind that the
sensitivity of the results of the present study may be less
than optimal. However, the authors still believe that these
results are important, as the present study was carried out
when the HIV sero-prevalence in the general population
was still < 2%. It is believed that the present study is
timely and that its results offer pediatricians in our
country an easy and inexpensive guideline to suspect HIV
co-infection in children with TBM, viz the presence of
moderate-severe anemia (Hb < 8 gm/dl). The only other
similar pediatric study is by Topley et al18, wherein there
was a much higher incidence of HIV co-infection (10/40,
25%) in the TBM cases analyzed. This study was carried
out in South Africa in 1995-1997, after the HIV sero-
prevalence in the general population had already reached
panic levels (>10%).18 Second, the diagnosis of TBM in the
present study patients was based on clinical criteria and
not on microbiological criteria. Although definitive
diagnosis of TBM depends on the detection of the tubercle
bacilli in the CSF, either by smear examination or by
bacterial culture; smears are usually positive in fewer than
10% of cases of TBM, while culture for M. tuberculosis
takes up to eight weeks and is also often negative.17 We
would like to point out three other pediatric studies in
which diagnosis of TBM was based on the clinical criteria
devised by Doerr et al.7,26,27 Third, due to financial
constraints we could not perform viral antigen detection
tests. Hence we followed the Joint UNAIDS-WHO
revised recommendations to diagnose HIV disease. 8
Strategy II was followed as it is applicable where the
prevalence of infection is 30% or less, as in Mumbai. 1
Combinations of ELISA can provide results as reliable as
the ELISA / Western blot combination and at a much
lower cost.8 Fourth, neurological outcome in children who
survived was assessed purely on clinical examination at
the time of discharge from the hospital. No  formal
intelligence quotient or audiological evaluations, were
performed
CONCLUSION
The present study documents that there are no significant
differences between HIV-infected and HIV-negative
children admitted with TBM, except for a lower Hb level
(< 8 gm/dl) among HIV-infected children. Also, HIV co-
infection does not change the in-hospital response to
therapy in childhood TBM.
Acknowledgements
We thank our Dean, Dr. M.E. Yeolekar for granting us permission to
publish this study; and our Biostatistician, Mr. Kailas Gandewar, and
Dr. D.P. Singh, Reader, Department of Research Methodology, Tata
Institute of Social Sciences, Deonar, Mumbai for their help in the
statistical analysis of the data.
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760 Indian Journal of Pediatrics, Volume 72—September, 2005
Contributors: SK designed the study, directed the data analysis,
performed the literature review and wrote the manuscript; he will
act as the guarantor of the paper. VG monitored the patients,
collected the data, performed the literature review and helped in
drafting the manuscript. MK helped in designing the study,
discussed the core ideas and analysis, and edited the manuscript. AJ
helped in designing the study, reported the Cranial CT scans, and
edited the manuscript. MR helped in designing the study and did the
HIV ELISA tests.
Funding: None.
Competing interests: None.
This paper is based on the dissertation submitted to the National
Board of Examinations, New Delhi for DNB (Pediatrics) degree
examination held in January 2004. Sunil Karande was the
Postgraduate Guide and Vishal Gupta was his Postgraduate Student.
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