’ Case Report

Diagnostic challenges in tuberculous meningitis: a

case report with negative genexpert result
Bardan Ghimire, MDa,*, Ishwor Thapaliya, MBBSb, Jeshika Yadav, MBBSb, Sujata Bhandari, MBBSc,
Man B. Paudyal, MBBSb, Neha Mehta, MBBSb, Sagar Bhandari, MBBSd, Yagya R. Adhikari, MBBSb,
Sanjaya Sapkota, MBBSb, Madhur Bhattarai, MBBSb

Introduction: Tuberculous meningitis (TBM) is a severe form of tuberculosis affecting the meninges, primarily caused by
Mycobacterium tuberculosis. Diagnosis of TBM poses numerous challenges due to its nonspecific clinical presentation and the
limitations of diagnostic tests like GeneXpert.
Case presentation: The authors report a case of a 22-year-old female from Eastern Nepal presenting with acute-onset fever,
headache, vomiting, and neck pain. Cerebrospinal fluid (CSF) analysis showed lymphocytic pleocytosis, elevated protein, low
glucose levels, and cobweb coagulum indicative of TBM. However, the GeneXpert test revealed negative results.
Discussion: In resource-limited settings like Nepal, where access to GeneXpert MTB/Rif is limited, CSF analysis and clinical
algorithms play a crucial role in diagnosing TBM. Relying solely on GeneXpert results may lead to false negatives, so a high level of
suspicion based on patient risk factors is essential. Prompt initiation of empirical antitubercular therapy is vital for a favorable outcome
in TBM cases.
Conclusion: Negative MTB PCR results from CSF can be misleading in diagnosis of tubercular meningitis. Therefore,
comprehensive evaluations, including detailed patient history, physical examination, and CSF fluid analysis, are crucial in high
tuberculous prevalence countries to ensure accurate and timely diagnosis.
Keywords: adenosine deaminase, genexpert, lumbar puncture, lymphocytic pleocytosis, tubercular meningitis

Introduction
HIGHLIGHTS
Tuberculous meningitis (TBM) is an extrapulmonary form of
• Tuberculous meningitis (TBM) is challenging to diagnose
tuberculosis (TB) caused by Mycobacterium tuberculosis infect-
due to nonspecific symptoms and low sensitivity of
ing the meninges. The primary infection usually starts in the lungs
GeneXpert MTB/RIF test.
and then spreads to the lymph nodes. In TBM, the bacteria form • Acute symptoms in TBM can be misdiagnosed or cause
collections in the brain called Rich foci, leading to an intense delays in treatment, leading to neurological complications
inflammatory response and meningitis symptoms[1]. Children and poor outcomes.
aged 0–4 years are more susceptible, especially in regions with • Cerebrospinal fluid analysis and clinical presentation are
higher TB prevalence. In developed countries, TBM is more crucial for TBM diagnosis when GeneXpert results are
commonly seen in adults due to TB reactivation or underlying inconclusive in resource-limited settings.
immunocompromised conditions like chronic steroid use, dia- • TBM requires a high index of suspicion, especially in
betes, or alcoholism[2]. TBM generally accounts for about 1% of tuberculous-endemic areas, to ensure early detection and
treatment.
a
College of Medical Sciences Teaching Hospital, Kathmandu University, Bharatpur,
b
Tribhuvan University, Institute of Medicine, Maharajgunj, cNobel Medical College,
Biratnagar and dNational Medical College, Birgunj, Nepal all extrapulmonary TB cases and varies in prevalence based on
Sponsorships or competing interests that may be relevant to content are disclosed at regional TB rates. HIV-positive individuals, especially those with
the end of this article. low CD4 counts, are more susceptible to CNS involvement and
*Corresponding author. Address: College of Medical Sciences Teaching Hospital, disseminated TB[3,4]. The diagnostic procedure involves the
Kathmandu University, Bharatpur 44200, [Link].:+977 984 184 0264 examination of cerebrospinal fluid (CSF), which typically shows
E-mail bardang08@[Link] (B. Ghimire).
low glucose levels, elevated protein levels, and a higher count of
Copyright © 2023 The Author(s). Published by Wolters Kluwer Health, Inc. This is an
white blood cells, predominantly lymphocytes[4]. GeneXpert test
open access article distributed under the Creative Commons Attribution-
NoDerivatives License 4.0, which allows for redistribution, commercial and non- does not exclude TBM. GeneXpert should be used in combina-
commercial, as long as it is passed along unchanged and in whole, with credit to the tion with other diagnostic tests, clinical findings, and when pos-
author. sible, radiologic data to inform their overall suspicion for TBM[5].
Annals of Medicine & Surgery (2023) 85:5731–5735 First-line antitubercular treatments have good penetration into
Received 1 August 2023; Accepted 8 September 2023 the CSF so used as the primary regimen for the treatment of TBM.
Published online 22 September 2023 Treatment may be adjusted based on drug sensitivity results
[Link] received later[6].

5731
Ghimire et al. Annals of Medicine & Surgery (2023) Annals of Medicine & Surgery

In our case report, we presented the challenging diagnosis of Table 1. The patient had hypomagnesemia, hyponatremia, and
TBM in a 22-year-old female from Eastern Nepal. The case report hypocalcemia but normal blood urea, serum creatinine, random
emphasizes the difficulties encountered when the result of blood sugar, and potassium levels (Table 1). HIV, Hepatitis B
GeneXpert testing came back negative, leading to uncertainties in surface antigen, Hepatitis C Virus, and Venereal Disease
the diagnostic process in TB endemic countries with low-resource Research Laboratory/ Rapid plasma reagin testing were non-
settings. This case report is in line with the CARE reporting reactive. The serological tests for dengue fever were negative. The
checklist[7]. sputum sample was examined for presence of any acid-fast bacilli
(AFB) and found to be AFB negative. The patient has normal
noncontrast computed tomography scan of the brain and normal
Case presentation chest radiography findings as shown in Figures 1 and 2, respec-
A 22-year-old female from Eastern Nepal presented to the tively. She had albuminuria of 2 + on the dipstick test but no
emergency department with an acute-onset fever of 103°F and bacterial growth on the urine culture.
agitation that had persisted for 2 days. She also complained of Initially, the patient had presented to primary health center,
earache, severe headache, nausea, vomiting, dizziness, and neck where she was suspected as a case of bacterial or viral meningitis
pain. She had no chest pain, palpitations, shortness of breath, based on acute clinical presentation and negative sputum for
hemoptysis, weight loss, or night sweating. The patient had no AFB. The patient was treated there with intravenous ampicillin
known comorbidities and had not experienced similar symptoms along with other empiric treatment prior to transfer to our
in the past. teaching hospital. Then on presentation to our teaching hospital,
Physical examination revealed a blood pressure of 130/ she was admitted to the ICU and was given empiric intravenous
80 mm Hg, temperature of 103°F, pulse rate of 96 beats per antibiotics, namely ceftriaxone and vancomycin and empiric
minute, respiratory rate of 22 breaths per minute, and oxygen intravenous acyclovir therapy, respectively, while awaiting the
saturation of 99% on ambient air. Clinically, she appeared irri- CSF analysis reports. A lumbar puncture was performed under an
table and ill-looking, but there were no signs of pallor, icterus, aseptic condition and CSF analysis showed clear, light yellow
cyanosis, clubbing, lymphadenopathy, edema, or dehydration. fluid with cobweb coagulum (Fig. 3). The total cell count in CSF
Upon further examination, the patient exhibited neck stiffness, was 195/μl with lymphocyte predominance (90% lymphocytes
and both Kernig’s and Brudzinski’s signs were positive. and 10% neutrophils) (Table 1). CSF glucose level was low while
Given the presenting symptoms and clinical findings, a differ- albumin level was significantly elevated (Table 1). The adenosine
ential diagnosis of meningitis and encephalitis were considered. deaminase (ADA) enzyme level in CSF fluid was high (12 IU/l).
Laboratory tests revealed raised erythrocyte sedimentation rate, CSF GeneXpert test was negative but qualitative serum
low hemoglobin level (10.4 g/dl), increased white blood cell count C-reactive protein was positive in the patient. The serological test
of 23 500/mm3, neutrophilia (90%, normal range: 40–70%), for Japanese Encephalitis (anti-JE IgM in serum and CSF) was
lymphocytopenia (7%), low packed cell volume, mean cell also negative.
volume, and mean cell hemoglobin, respectively, as shown in

Table 1
Laboratory findings of the patient at the time of presentation
Laboratory parameters Results Units Reference range
Complete blood cell count
Hemoglobin 10.2 g/dl 12–15
WBC count 23 500 /mm3 4000–11 000
Platelet count 286 000 /mm3 150 000–450 000
Differential count
Neutrophils 90 % 40–70
Lymphocytes 7 % 20–40
Eosinophils 1 % 1–6
Monocytes 2 % 2–10
Packed cell volume 32 % 36–42
Mean cell volume 77 fl 80–100
Mean cell hemoglobin 26 pg 27–32
Mean cell hemoglobin concentration 32 g/dl 30–35
Erythrocyte sedimentation rate 58 mm/h 0–20
Serum electrolyte levels
Serum Na + 133 mmol/l 135–145
Serum K + 3.8 mmol/l 3.5–5.5
Serum calcium 8.0 mg/dl 8.6–10.3
Serum magnesium 1.2 mg/dl 1.6–2.5
Cerebrospinal fluid analysis
Total leukocyte count 195 /μL 0–5
Glucose 23 mg/dl 40–70
Albumin 200 mg/dl 15 –45 Figure 1. Normal noncontrast computed tomography of the brain.
WBC, white blood cell.

5732
Ghimire et al. Annals of Medicine & Surgery (2023)

condition, antitubercular therapy was started on second day of

admission as per the National Tuberculosis Management
Guidelines 2019. She was initiated on intensive phase treatment
of 2 months, consisting of isoniazid, rifampicin, pyrazinamide,
and ethambutol along with dexamethasone in the dose of 0.4 mg/
kg/day for 2 weeks. Within 2 days of initiation of therapy, her
health condition markedly improved with resolution of symp-
toms and laboratory abnormalities and all the empirical therapy
were stopped. The patient was shifted to ward and eventually
discharged in good health on 10th day of admission. Following
the initial 2 weeks, the oral dexamethasone was tapered at a rate
of 0.1 mg/kg/week until reaching a maintenance dose of 0.1 mg/
kg/day. Thereafter, the dose was reduced to 4 mg/day and gra-
dually tapered by 1 mg/week until it was eventually discontinued,
with the total duration of dexamethasone treatment spanning 10
weeks. Intensive phase treatment was followed by continuation
phase with isoniazid, rifampicin, and ethambutol for an addi-
tional 7 months. Throughout the treatment period, the patient
showed a steady recovery. Follow-up examinations indicated no
neurological deficits, and the patient remained asymptomatic at
subsequent visits.

Discussion
TB can affect any organ system of the body including the central
Figure 2. Normal chest radiography findings. nervous system[8]. About one-third of the world’s population is
assumed to have MTB infection[1]. CNS is involved in 1–2% of all
TB cases and 7–8% of all Extra-pulmonary tuberculosis cases
among immunocompetent patients[9]. In Nepal, TB has an annual
Considering the clinical history, examination, and relevant
incidence of 245 cases per 100 000 people in the
investigations, bacterial and viral meningitis/encephalitis were
population[10,11]. The National Tuberculosis Programme (NTP)
ruled out and thus based on the CSF analysis reports, a diagnosis
registered 37 861 all forms of TB cases in Fiscal year 2021/2022
of tubercular meningitis was established. Despite the empirical
out of which 28% were extrapulmonary TB cases[12]. Although,
treatment, as there was no improvement in the patient’s
the exact prevalence of TBM cases is not yet determined, a study
conducted by Bhatta et al.[13] revealed that 16% of 585 TB cases
within their study population were diagnosed with TBM. The
frequency of TBM has been influenced by several factors
including the global burden of TB, the prevalence of HIV, and
age-related aspects[14]. In developed countries, tubercular
meningitis accounts for 6% of all meningitis cases, while in
developing countries, it makes up one-third to one-half of all
bacterial meningitis cases[1]. Tubercular meningitis is the most
severe clinical manifestation of extrapulmonary TB[9] character-
ized by subacute or chronic inflammation of the meninges
enveloping the brain and spinal cord resulting from the invasion
of Mycobacterium tuberculosis in the subarachnoid space[1,15].
Recognition of TBM is frequently difficult in routine clinical
practice due to its nonspecific presentation[16]. The clinical fea-
tures of TBM resemble those of other bacterial meningitis,
characterized by symptoms such as fever, headache, vomiting,
altered mental status, and neck stiffness[16,17]. A history of latent
TB or prior TB exposure is found in 10% of TBM cases[16]. So, it
is important to know TB status, particularly in developing
countries with low socioeconomic status to facilitate the diag-
nosis and management of CNS complications, such as tubercular
meningitis[18]. TBM has further imposed challenges in diagnosis
compared to the other forms of bacterial meningitis due to its
slower onset of symptoms and the paucibacillary nature of the
Figure 3. Gross cerebrospinal fluid finding showing clear light yellow fluid with
cobweb coagulum. infection, making it harder to detect in CSF[9,19]. The acute onset
of symptoms in our patient closely resembles bacterial or viral

5733
Ghimire et al. Annals of Medicine & Surgery (2023) Annals of Medicine & Surgery

meningitis, leading to difficulties in making a definitive TBM from nontubercular meningitis in immunocompetent
diagnosis[20]. Based on acute clinical presentation and negative patients due to its higher sensitivity (75–94%) and specificity
AFB sputum, the patient was given antibiotics and antiviral (86–97%)[18]. CSF ADA levels are elevated in TBM as compared
therapy but the lack of the patient’s response to medications for to non-TBM like viral meningitis[23]. A study by Solari et al.[24]
bacterial or viral meningitis has further complicated the diag- highlighted the significance of CSF parameters like protein, glu-
nostic challenges. The presentation of TBM may resemble that cose, chloride, and ADA levels, along with lymphocytic pleocy-
of meningoencephalitis, and its diagnosis requires a high level of tosis, in early TBM diagnosis. In a study by Ghosh et al.[18], it was
clinical suspicion, especially in a country with a high burden found that the CSF ADA level cutoff point of 8.5 IU/l is indicative
of TB[21]. The negative result of the serological testing excludes of a diagnosis of TBM which further adds a diagnostic value to
the possibility of Japanese Encephalitis in the patient. our case. It is more sensitive than AFB smear and culture and can
Timely detection and proper treatment are essential in mini- be suggestive of the diagnosis of TBM[22]. In addition, this diag-
mizing morbidity and mortality associated with TBM[22]. A nostic tool is simple, rapid, inexpensive, easily accessible and can
conclusive diagnosis depends on the integration of clinical, be performed even with minimal training, making it particularly
radiological, and laboratory findings[14]. Laboratory diagnostic beneficial in areas with limited resources[25]. It can facilitate
procedures for TBM primarily rely on the identification of acid- clinicians in decision making process soon after admission and
fast bacilli in CSF smear or isolation of MTB in either solid or enables timely antitubercular therapy to prevent complications
liquid culture media[9,14]. Ziehl–Neelsen staining provides rapid associated with disability and morbidity[24]. For this reason,
results but has lower sensitivity of 10–20% while culture is more lumbar puncture and CSF ADA estimation need to find a place as
sensitive (60–70%) but takes greater than or equal to 2 weeks to a routine investigation in a resource-limited country like ours
produce observable bacterial replication which is too slow to aid where there is high prevalence of TB and TBM.
in clinical diagnosis[5]. Thus, clinicians must not wait for culture If there arise any difficulties in differentiating TBM from other
results and should initiate empirical therapy promptly as death forms of meningitis based on the initial CSF test or GeneXpert,
can occur[9]. Rapid diagnostic tests with higher sensitivity and empirical antitubercular therapy should be considered[4]. Delays in
specificity are necessary to support the presumptive diagnosis[22]. diagnosis and treatment have resulted in poor prognosis[4]. The
Genotypic methods have now emerged to address the need for mortality rate in TBM is influenced by the patient’s age, clinical
rapid diagnosis of TBM[9]. PCR-based assays have been reported condition at admission, length of delay in initiating therapy, and
to have 56% sensitivity and 90% specificity with GeneXpert the specific treatment approach employed[4]. Although tubercular
sensitivity ranging from 50 to 80%[14]. In 2013, WHO approved meningitis has an insidious onset of symptom ranging from 1 day
the GeneXpert MTB/RIF assay as the preferred initial test over to 9 months before diagnosis, but when a patient presenting with
conventional microscopy and culture for diagnosing TBM in low- acute symptoms is either misdiagnosed or have delayed diagnosis,
resource settings like Nepal[3,9,14]. However, PCR testing of CSF it may lead to tuberculoma formation and long-term neurological
for TBM diagnosis has significant limitations[5]. The patient of sequelae, including mental retardation, hydrocephalus, cranial
our case shows negative results to PCR despite having positive nerve palsy, sensorineural hearing loss, stroke-related lateralizing
gross CSF findings. The lower sensitivity of GeneXpert in TBM neurological deficits, seizures, coma, and even death[6]. Hence, a
diagnosis may be attributed to the very low bacillary load in the favorable outcome in TBM is only possible if early diagnosis and
CSF sample to reach the detection threshold limit as detection is treatment are done before the condition advances to later stages[4].
possible only when the required threshold limit is reached[5]. It In the resource-limited settings of Nepal, access to the
could be due to the presence of PCR inhibitors such as ery- GeneXpert MTB/Rif test may be limited[26,27]. In such cases,
throcytes in the CSF sample that causes errors in the result[9] or
alternative diagnostic tests like CSF analysis become
due to the low volume of the sample tested[5]. The absence of the
important[16]. The use of diagnostic algorithms based on CSF
target gene in TB isolates can also result in a false negative
values and patient clinical presentation can be helpful to differ-
result[6]. Additionally, failure of the procedure to capture and lyse
entiate it from other forms of meningitis[1]. So, relying solely on
the bacilli may lead to an inaccurate outcome as the accuracy of
GeneXpert MTB/Rif results is not enough. Instead, doctors
the GeneXpert assay primarily depends on the effective capture of
should maintain a high level of suspicion for TB meningitis based
intact bacilli from the specimen within the cartridge[9]. Brain
on patient risk factors to make an accurate diagnosis, especially in
imaging can be a valuable tool in aiding the diagnosis of TBM but
endemic countries with low-resource settings[1].
is not sufficient on its own to confirm the diagnosis[16]. Thus,
Considering the CSF analysis and raised ADA level, the deci-
normal brain imaging does not exclude the diagnosis. As per the
sion was made to shift the treatment from antibiotics to anti-
WHO guidelines, when patients are suspected of having TBM but
tubercular therapy adhering to National Tuberculosis
show negative results on GeneXpert assay, additional diagnostic
Management Guidelines 2019 promptly. She was put under
studies are recommended for further evaluation[19].
intensive phase therapy for 2 months, consisting of rifampicin,
Lumbar puncture is important in differentiating between var-
isoniazid, pyrazinamide, and ethambutol followed by continua-
ious types of meningitis. In the case of TBM, CSF analysis reveals
tion phase with isoniazid, rifampicin, and ethambutol for an
lymphocytic pleocytosis, elevated protein levels, and low glucose
additional 7 months[26]. After the initiation of therapy, there was
levels[16]. The findings in our patient are consistent with TBM as
observed in CSF analysis. Viral meningitis may show similar CSF a significant improvement in the health of the patient.
findings[1,4]. However, it is of utmost importance to consider
TBM as part of differential diagnosis for patients who came from Conclusion
TB endemic areas and present with unclear meningitis, particu-
larly when lymphocytic pleocytosis is observed[16]. Determination It is important to note that negative MTB PCR results from CSF can
of ADA levels in CSF adds a diagnostic value in distinguishing be misleading. Thus, in cases like ours, where no improvement is

5734
Ghimire et al. Annals of Medicine & Surgery (2023)

seen within 2 days; TBM should remain a significant consideration References

until it is ruled out through lumbar puncture and CSF analysis even [1] Slane VH, Unakal CG. Tuberculous Meningitis. Treasure Island, FL:
if the GeneXpert result is negative. Lumbar puncture is mandatory StatPearls Publishing; 2023. [Link]
and can be the main modality for doctors to get a more accurate [2] Chin JH. Tuberculous meningitis: diagnostic and therapeutic challenges.
Neurol Clin Pract 2014;4:199–205.
diagnosis of TB meningitis in limited health facilities. [3] Bourgi K, Fiske C, Sterling TR. Tuberculosis meningitis. Curr Infect Dis
Comprehensive and clear guidance is essential for establishing the Rep 2017;19:39.
investigative pathway for TBM. The detailed history of the patient, [4] Lee SA, Kim SW, Chang HH, et al. A new scoring system for the differ-
thorough physical examination, and CSF fluid analysis can greatly ential diagnosis between tuberculous meningitis and viral meningitis.
J Korean Med Sci 2018;33:e201.
aid in the diagnosis of TBM, particularly in patients living in [5] Bahr NC, Marais S, Caws M, et al. GeneXpert MTB/Rif to diagnose
countries with a higher prevalence of TB like Nepal. Prompt action, tuberculous meningitis: perhaps the first test but not the last. Clin Infect
timely diagnosis and appropriate therapy help in substantial Dis 2016;62:1133–5.
improvement in patients with TBM. [6] Marx GE, Chan ED. Tuberculous meningitis: diagnosis and treatment
overview. Tuberc Res Treat 2011;2011:1–9.
[7] Riley DS, Barber MS, Kienle GS, et al. CARE guidelines for case reports:
explanation and elaboration document. J Clin Epidemiol 2017;89:218–35.
Ethical approval [8] Galimi R. Extrapulmonary tuberculosis: tuberculous meningitis new
developments. Eur Rev Med Pharmacol Sci 2011;15:365–86.
None. [9] Patel S, Dadheech M, Maurya AK, et al. Assessment of the diagnostic
utility of GeneXpert Mycobacterium tuberculosis/Rifampicin (MTB/RIF)
assay in the suspected cases of tuberculous meningitis. Cureus 2023;15:
Consent e37761.
[10] KC P, Bhattarai M, Adhikari S, et al. Intestinal tuberculosis can mas-
Written informed consent was obtained from the parents for the querade as Crohn’s disease: a teachable moment. SAGE Open Med Case
Rep 2023;11:2050313X231184342.
publication of this case report and accompanying images. A copy
[11] Ministry of Health and Population. National TB prevalence survey
of the written consent is available for review by the Editor-in-Chief (2018-19), 2020. Accessed 2 September 2023. [Link]
of this journal on request. wp-content/uploads/2020/03/[Link]
[12] Department of Health Services -Annual-Report-FY-2021-22. Accessed 1
September 2023. [Link]
Sources of funding [13] Bhatta S, Pant N. Epidemiological profile and determinants of tubercu-
losis in Urban Nepalese population. Nepal Med J 2019;2:250–4.
None. [14] Wakode P, Siddaiah N, Manjunath N, et al. GeneXpert: a rapid and
supplementary diagnostic tool for tuberculous meningitis, experience
from tertiary neurocenter. J Neurosci Rural Pract 2022;13:204.
Author contribution [15] Seddon JA, Tugume L, Solomons R, et al. The current global situation for
tuberculous meningitis: epidemiology, diagnostics, treatment and out-
B.G., I.T., and J.Y. wrote the original manuscript, reviewed, and comes. Wellcome Open Res 2019;4:167.
[16] Chesdachai S, Katz B, Sapkota S. Diagnostic challenges and dilemmas in
edited the original manuscript. S.B., M.B.P., N.M., S.B., Y.R.A., tuberculous meningitis. Am J Med Sci 2020;359:372–7.
S.S., and M.B. reviewed and edited the original manuscript. [17] Foppiano Palacios C, Saleeb PG. Challenges in the diagnosis of
tuberculous meningitis. J Clin Tuberc Other Mycobact Dis 2020;20:
100164.
Conflicts of interest [18] Ghosh GC, Sharma B, Gupta BB. CSF ADA determination in early
diagnosis of tuberculous meningitis in HIV-infected patients. Scientifica
Authors have no conflict of interest to declare. (Cairo) 2016;2016:1–4.
[19] Metcalf T, Soria J, Montano SM, et al. Evaluation of the GeneXpert
MTB/RIF in patients with presumptive tuberculous meningitis. PLoS One
2018;13:e0198695.
Research registration [20] Agarwal AK. A hospital based study on estimation of adenosine deami-
nase activity in cerebrospinal fluid in various types of meningitis. J Clin
1. Name of the registry: none. Diagn Res 2014;8:73–6.
2. Unique identifying number or registration ID: none. [21] Tan JL, Nordin S, Besari AM. Rare clinical presentation of tuberculous
3. Hyperlink to your specific registration (must be publicly meningitis: a case report. Malays J Med Sci 2017;24:119–23.
[22] Chacko F, Modi M, Lal V, et al. Diagnostic efficacy of adenosine dea-
accessible and will be checked): none. minase levels in cerebrospinal fluid in patients of tubercular meningitis: a
comparison with PCR for Mycobacterium tuberculosis. Ann Neurosci
2010;17:126–30.
Guarantor [23] Chander A, Shrestha CD. Cerebrospinal fluid adenosine deaminase levels
as a diagnostic marker in tuberculous meningitis in adult Nepalese
Bardan Ghimire. patients. Asian Pac J Trop Dis 2013;3:16–9.
[24] Solari L, Soto A, Agapito JC, et al. The validity of cerebrospinal fluid
parameters for the diagnosis of tuberculous meningitis. Int J Infect Dis
2013;17:e1111–5.
Data availability statement [25] Gupta B. Adenosine deaminase levels in CSF of tuberculous meningitis
patients. J Clin Med Res 2010;2:220–4.
All available data are within the manuscript itself. [26] National Tuberculosis Management Guidelines 2019. Accessed 1
September 2023. [Link]
National-Tuberculosis-Management-Guidelines-2019_Nepal.pdf
Provenance and peer review [27] Pant P, Joshi A, Adhikari YR, et al. Pattern of tuberculosis, trend and
outcome of patients registered at DOTS Centre of a Tertiary Care
Not commissioned, externally peer-reviewed. Hospital. J Nepal Health Res Counc 2022;20:54–8.

5735