A very young patient with Tubercular Meningitis and its complications

2020 ◽  
Vol 10 (2) ◽  
pp. 400-401
Author(s):  
Rowshan Jahan Akhter ◽  
BH Nazma Yasmeen
Keyword(s):  
Mycobacterium Tuberculosis ◽  
Cranial Nerve ◽  
Obstructive Hydrocephalus ◽  
Cns Infection ◽  
Communicating Hydrocephalus ◽  
Mycobacterium Tuberculosis Infection ◽  
Nerve Roots ◽  
Tubercular Meningitis ◽  
Medical College ◽  
The Brain

A case report on a successful management of an eight months old boy with Tubercular Meningitis with Multiple Tuberculoma in Brain with Obstructive Hydrocephalus with Left sided Lower motor neuron type Facial Palsy with Right Sided Hemiparesis. Tuberculous meningitis (TBM) is Mycobacterium tuberculosis infection of the Brain Meninges.1,2 In TBM inflammation occur mainly in the base of the brain and when the inflammation affect the brain stem subarachnoid area, cranial nerve roots then symptoms may occur like space-occupying lesions.3,4 TBM is more common in children than in adults, especially children aged 0-5 years.5 In children central nervous system tuberculosis usually presents as tubercular meningitis, post-tubercular meningitis hydrocephalus, and rarely a space-occupying lesions known as tuberculomas.6 TBM accounts for 2–5% of all active cases of Mycobacterium tuberculosis.7 Pulmonary infection coexists in 25–83% of TBM.8-10 Predominately primary CNS infection is found in children and leptomeningeal infection presents as meningitis, cranial nerve (CN) palsies (most commonly CN 2, 3, 4, and 7), and communicating hydrocephalus.11 Northern International Medical College Journal Vol.10 (2) Jan 2019: 400-401

scholarly journals LRRK2 regulates innate immune responses and neuroinflammation during Mycobacterium tuberculosis infection

2019 ◽  
Author(s):  
C.G. Weindel ◽  
S.L. Bell ◽  
T.E. Huntington ◽  
K.J. Vail ◽  
R. Srinivasan ◽  
...  
Keyword(s):  
Mycobacterium Tuberculosis ◽  
Glial Cells ◽  
Mycobacterial Infection ◽  
Type I Interferons ◽  
Type I ◽  
Innate Immune Responses ◽  
Mycobacterium Tuberculosis Infection ◽  
Inflammatory Molecules ◽  
Multiple Hit ◽  
The Brain

SUMMARYDespite many connections between mutations in leucine-rich repeat kinase 2 (LRRK2) and susceptibility to mycobacterial infection, we know little about its function outside of the brain, where it is studied in the context of Parkinson’s Disease (PD). Here, we report that LRRK2 controls peripheral macrophages and brain-resident glial cells’ ability to respond to and express inflammatory molecules. LRRK2 KO macrophages express elevated basal levels of type I interferons, resulting from defective purine metabolism, mitochondrial damage, and engagement of mitochondrial DNA with the cGAS DNA sensing pathway. While LRRK2 KO mice can control Mycobacterium tuberculosis (Mtb) infection, they exhibit exacerbated lung inflammation and altered activation of glial cells in PD-relevant regions of the brain. These results directly implicate LRRK2 in peripheral immunity and support the “multiple-hit hypothesis” of neurodegenerative disease, whereby infection coupled with genetic defects in LRRK2 create an immune milieu that alters activation of glial cells and may trigger PD.

scholarly journals Evaluation of the Mtb72F Polyprotein Vaccine in a Rabbit Model of Tuberculous Meningitis

2006 ◽  
Vol 74 (4) ◽  
pp. 2392-2401 ◽  
Author(s):  
Liana Tsenova ◽  
Ryhor Harbacheuski ◽  
Andre L. Moreira ◽  
Evette Ellison ◽  
Wilfried Dalemans ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Weight Loss ◽  
Cerebrospinal Fluid ◽  
Nervous System ◽  
Mycobacterium Tuberculosis ◽  
Tuberculous Meningitis ◽  
Protective Efficacy ◽  
Rabbit Model ◽  
Cns Infection ◽  
The Brain

ABSTRACT Using a rabbit model of tuberculous meningitis, we evaluated the protective efficacy of vaccination with the recombinant polyprotein Mtb72F, which is formulated in two alternative adjuvants, AS02A and AS01B, and compared this to vaccination with Mycobacterium bovis bacillus Calmette-Guérin (BCG) alone or as a BCG prime/Mtb72F-boost regimen. Vaccination with Mtb72F formulated in AS02A (Mtb72F+AS02A) or Mtb72F formulated in AS01B (Mtb72F+AS01B) was protective against central nervous system (CNS) challenge with Mycobacterium tuberculosis H37Rv to an extent comparable to that of vaccination with BCG. Similar accelerated clearances of bacilli from the cerebrospinal fluid, reduced leukocytosis, and less pathology of the brain and lungs were noted. Weight loss of infected rabbits was less extensive for Mtb72F+AS02A-vaccinated rabbits. In addition, protection against M. tuberculosis H37Rv CNS infection afforded by BCG/Mtb72F in a prime-boost strategy was similar to that by BCG alone. Interestingly, Mtb72F+AS01B induced better protection against leukocytosis and weight loss, suggesting that the polyprotein in this adjuvant may boost immunity without exacerbating inflammation in previously BCG-vaccinated individuals.

scholarly journals A Randomized Controlled Trial of Isoniazid to Prevent Mycobacterium tuberculosis Infection in Kenyan Human Immunodeficiency Virus–Exposed Uninfected Infants

2020 ◽  
Author(s):  
Sylvia M LaCourse ◽  
Barbra A Richardson ◽  
John Kinuthia ◽  
A J Warr ◽  
Elizabeth Maleche-Obimbo ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Mycobacterium Tuberculosis ◽  
High Risk ◽  
Adverse Events ◽  
Controlled Trial ◽  
Preventive Therapy ◽  
Infection Prevalence ◽  
Mycobacterium Tuberculosis Infection ◽  
Immunodeficiency Virus ◽  
Exposed Uninfected

Abstract Background Human immunodeficiency virus (HIV)–exposed uninfected (HEU) infants in endemic settings are at high risk of tuberculosis (TB). For infants, progression from primary Mycobacterium tuberculosis (Mtb) infection to TB disease can be rapid. We assessed whether isoniazid (INH) prevents primary Mtb infection. Methods We conducted a randomized nonblinded controlled trial enrolling HEU infants 6 weeks of age without known TB exposure in Kenya. Participants were randomized (1:1) to 12 months of daily INH (10 mg/kg) vs no INH. Primary endpoint was Mtb infection at end of 12 months, assessed by interferon-γ release assay (QuantiFERON-TB Gold Plus) and/or tuberculin skin test (TST, added 6 months after first participant exit). Results Between 15 August 2016 and 6 June 2018, 416 infants were screened, with 300 (72%) randomized to INH or no INH (150 per arm); 2 were excluded due to HIV infection. Among 298 randomized HEU infants, 12-month retention was 96.3% (287/298), and 88.9% (265/298) had primary outcome data. Mtb infection prevalence at 12-month follow-up was 10.6% (28/265); 7.6% (10/132) in the INH arm and 13.5% (18/133) in the no INH arm (7.0 vs 13.4 per 100 person-years; hazard ratio, 0.53 [95% confidence interval {CI}, .24–1.14]; P = .11]), and driven primarily by TST positivity (8.6% [8/93] in INH and 18.1% [17/94] in no INH; relative risk, 0.48 [95% CI, .22–1.05]; P = .07). Frequency of severe adverse events was similar between arms (INH, 14.0% [21/150] vs no INH, 10.7% [16/150]; P = .38), with no INH-related adverse events. Conclusions Further studies evaluating TB preventive therapy to prevent or delay primary Mtb infection in HEU and other high-risk infants are warranted. Clinical Trials Registration NCT02613169.

scholarly journals Diffuse leptomeningeal glioneuronal tumor with high-grade features masquerading as tubercular meningitis—a case report

2021 ◽  
Vol 52 (1) ◽  
Author(s):  
Sameer Peer ◽  
Vivek Murumkar ◽  
Karthik Kulanthaivelu ◽  
Chandrajit Prasad ◽  
Shilpa Rao ◽  
...  
Keyword(s):  
Case Report ◽  
Early Diagnosis ◽  
Histopathological Examination ◽  
Glioneuronal Tumor ◽  
Communicating Hydrocephalus ◽  
High Grade ◽  
Endemic Region ◽  
Tubercular Meningitis ◽  
Leptomeningeal Enhancement ◽  
Diffuse Leptomeningeal Glioneuronal Tumor

Abstract Background Diffuse leptomeningeal glioneuronal tumor (DLGNT) has been recently described in the literature. The complete neuroimaging spectrum and histopathological characteristics of this entity are yet to be elucidated. In an endemic region, diffuse leptomeningeal enhancement on neuroimaging with associated communicating hydrocephalus is usually suggestive of infective meningitis and the patients are started on empirical anti-microbial therapy. However, it is important to consider other differential diagnosis of leptomeningeal enhancement in such cases, particularly if the clinical condition does not improve on anti-microbial therapy. An early diagnosis of a neoplastic etiology may be of particular importance as the treatment regimens vary considerably depending on the underlying disease condition. Case presentation In this case report, we describe a case of DLGNT with high-grade histopathological features which was initially managed as tubercular meningitis based on the initial neuroimaging findings. Due to worsening of the clinical course and subsequent imaging findings at follow-up, a diagnosis of DLGNT was considered and subsequently proven to be DLGNT with features of anaplasia on histopathological examination of leptomeningeal biopsy specimen. Conclusion This case highlights the importance of recognizing certain subtle finding on MRI which may help in an early diagnosis of DLGNT which is crucial for appropriate treatment.

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