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At least 19 recordsLinked to original sources
PubMed2006

Mycobacterium tuberculosis invasion and traversal across an in vitro human blood-brain barrier as a pathogenic mechanism for central nervous system tuberculosis.

BACKGROUND: Central nervous system (CNS) tuberculosis is a serious, often fatal disease that disproportionately affects young children. It is thought to develop when Mycobacterium tuberculosis breaches the blood-brain barrier (BBB), which is composed of tightly apposed brain microvascular endothelial cells. However, the mechanism(s) involved in this process are poorly understood. METHODS: To better understand these processes, we developed an in vitro model of M. tuberculosis BBB infection using primary human brain microvascular endothelial cells. RESULTS: M. tuberculosis was found to both invade and traverse the model BBB significantly more than did M. smegmatis (a nonpathogenic mycobacterium). Invasion by M. tuberculosis across the BBB required host-cell actin cytoskeletal rearrangements. By microarray expression profiling, we found 33 M. tuberculosis genes to be highly up-regulated during the early stages of invasion of the BBB by M. tuberculosis; 18 of them belong to a previously described in vivo-expressed genomic island (Rv0960-Rv1001). Defined M. tuberculosis isogenic transposon mutants for the up-regulated genes Rv0980c, Rv0987, Rv0989c, and Rv1801 were found to be deficient in their ability to invade the BBB model. CONCLUSIONS: We developed an in vitro model of M. tuberculosis BBB infection and identified M. tuberculosis genes that may be involved in CNS invasion.

Actins↗
PubMed1999

Central nervous system tuberculosis.

Involvement of the central nervous system (CNS) by Mycobacterium tuberculosis, particularly meningitis, is the most severe form of tuberculous infection. Parenchymal CNS involvement can occur in the form of tuberculoma or, more rarely, abscess. Although surgery was initially advocated as the mainstay of therapy, more recent evidence suggests that parenchymal forms of CNS tuberculosis can be cured with medical treatment alone. Also, damage of the spinal cord, roots, and spine can occur in the form of spinal meningitis, radiculomyelitis, spondylitis, or spinal cord infarction.

Humans↗
PubMed2003

[Neuroradiologic manifestations of central nervous system tuberculosis in 122 adults].

PURPOSE: Central nervous system (CNS) tuberculosis remains a public health problem, particularly in developing countries. The aim of this study is to characterize neuroradiologic findings of various intracranial lesions. METHODS: We retrospectively reviewed data of 122 patients with CNS tuberculosis, without immunosuppression. CT scan was performed in all patients, whereas 17 patients had CT scan and MRI. RESULTS: We included 74 women (61%) and 48 men (39%) with a mean age of 37 years (17 -88y). 18 patients (14,7%) had a history of tuberculosis. Tuberculous meningitis was the most frequent clinical presentation (119 cases). Mycobacterium tuberculosis was isolated in cerebrospinal fluid of 18 patients (15%). Several types of lesions were identified : hydrocephalus (35 cases), tuberculomas (29 cases), leptomeningitis (26 cases), infarction (15 cases), abcesses (2 cases). Hydrocephalus was associated to other lesions in 26 cases. Communication hydrocephalus was present in 28 cases. Multiple tuberculomas were seen in 23 cases (80%), with miliary aspects in some cases. In 3 cases, tuberculoma was present without meningitis. Patients with leptomeningitis showed thick meningeal contrast enhancement involving all basal cisterns. Infarction resulted from arterial englobement or embols, and involved the area of middle cerebral artery (12 cases). CONCLUSION: Central nervous system tuberculosis has different appearences, mostly hydrocephalus and tuberculomas. MR with contrast is necessary for diagnosis and for follow-up during treatment.

Adolescent↗
PubMed1986

Central nervous system tuberculosis with the acquired immunodeficiency syndrome and its related complex.

Central nervous system tuberculosis occurred in three patients with the acquired immunodeficiency syndrome (AIDS) and seven patients with AIDS-related complex who were evaluated for 48 months. Nine patients were intravenous drug abusers and one was Haitian. Five patients had cerebral-ring-enhancing lesions and three had hypodense areas. The clinical spectrum included meningitis in two patients, multiple cerebral abscesses in one, and tuberculomas in four. All Mycobacterium tuberculosis isolates were sensitive to standard antituberculous drugs. All patients received treatment with isoniazid, rifampin, and pyrazinamide; six patients also received streptomycin. Three patients with AIDS died of opportunistic infection preceded by central nervous system tuberculosis. Among the patients with the AIDS-related complex, three improved with treatment, three were lost to follow-up, and one died. Tuberculosis should be considered in the differential diagnosis of central nervous system mass lesions in intravenous drug abusers with AIDS or AIDS-related complex. Because patients with tuberculosis can be cured, biopsy of accessible brain mass lesions should be mandatory. Preventive therapy may be indicated in drug abusers without disease.

Acquired Immunodeficiency Syndrome↗
PubMedDate not supplied

Central nervous system tuberculosis in HIV-infected patients: clinical and radiographic findings.

PURPOSE: To characterize the radiographic findings on neuroimaging of 25 human immunodeficiency virus (HIV)-seropositive patients with proved central nervous system tuberculosis and to correlate those findings with clinical data. METHODS: Twenty-five HIV-seropositive patients with central nervous system tuberculosis were identified, and their imaging studies (CT and, in some cases, MR) and medical records were reviewed. The diagnosis of central nervous system tuberculosis was based on cerebrospinal fluid culture (n = 20), biopsy (n = 4), and/or autopsy (n = 5), with a clinical diagnosis of central nervous system tuberculosis in one additional patient. Results also were correlated with CD4 counts and chest x-ray findings. RESULTS: Nine (36%) of 25 patients demonstrated meningeal enhancement. Eleven (44%) of 25 demonstrated enhancing parenchymal lesions; 6 patients had tuberculomata, and 5 had tuberculous abscesses. Communicating hydrocephalus was present in 8 (32%) of 25, and infarction was seen in 9 (36%) of 25. Fifteen of 23 chest x-rays were suggestive of pulmonary tuberculosis. Mean CD4 count was 162. Nine (38%) of 24 patients had a history of pulmonary tuberculosis, and 5 (21%) of 24 had no history of tuberculosis or any other opportunistic infection. Overall mortality was 79%. CONCLUSION: Central nervous system tuberculosis has a very high mortality among HIV-infected patients. Because cerebrospinal fluid cultures can take 6 to 8 weeks, the neuroradiologist can play a critical role in patient treatment by suggesting the correct diagnosis based on characteristic imaging findings. Radiographic clues include multiloculated abscess, cisternal enhancement, basal ganglia infarction, and communicating hydrocephalus, which are not findings associated with the more commonly encountered central nervous system lymphoma or toxoplasma encephalitis. Central nervous system tuberculosis may be the initial presentation of acquired immunodeficiency syndrome. In patients with suspected central nervous system tuberculosis, chest x-ray may provide additional support for the diagnosis of tuberculosis.

AIDS-Related Opportunistic Infections↗
PubMed2006

IFNgamma synergizes with IL-1beta to up-regulate MMP-9 secretion in a cellular model of central nervous system tuberculosis.

Matrix metalloproteinase-9 (MMP-9) activity is implicated in pathogenesis of central nervous system tuberculosis (CNS-TB). IFNgamma, a key cytokine in TB, usually inhibits MMP-9 secretion. Addition of IFNgamma to conditioned media from M. tb-infected monocytes (CoMTB) resulted in a 7-fold increase in MMP-9 activity detected by gelatin zymography (P<0.01). In contrast, tissue inhibitor of metalloproteinase (TIMP)-1 and -2 secretion, measured by ELISA, was suppressed. Dexamethasone abolished the synergistic increase in MMP-9 activity. Interleukin (IL)-1beta in CoMTB is a critical mediator of synergy with IFNgamma, and IL-1beta alone synergizes with IFNgamma to increase MMP-9 secretion from 51 +/- 31 to 762 +/- 136 U. IL-1beta activity is dependent on p38 mitogen-activated protein (MAPK) kinase, which was found to be phosphorylated in tissue specimens from patients with CNS-TB. Extracellular signal regulated kinase (Erk) and p38 MAPK activation did not affect IFNgamma signaling pathways. Inhibition of janus-activated kinase (JAK)-2 by 50 microM AG540 decreased MMP-9 secretion to 124 +/- 11.1 from 651 +/- 229 U of activity (P<0.01). However, signal transducer and activator of transcription (STAT)-3 but not STAT-1 phosphorylation was synergistically up-regulated by IFNgamma and CoMTB. In summary, synergy between IL-1beta and STAT-3 dependent IFNgamma signaling is key in control of up-regulation of MMP-9 activity in CNS-TB and may be a significant mechanism of brain tissue destruction.

Blotting, Western↗
PubMed1990

Central nervous system tuberculosis in children: a review of 30 cases.

The medical records of 30 children with central nervous system tuberculosis (CNS tuberculosis) who were treated between March, 1976, and February, 1989, were reviewed. All had cranial computerized tomography scans at presentation. The mean cerebrospinal fluid leukocyte count was 200/mm3, protein 239 mg/dl, glucose 25 mg/dl and CSF/serum glucose ratio 21%. Mantoux skin tests with 5 tuberculin units were greater than or equal to 10 mm induration in 50%, and chest radiographs were positive in 40% of patients. Hydrocephalus was demonstrated by cranial computerized tomography in all 30 patients (100%). Cranial computerized tomography scan demonstrating hydrocephalus is a sensitive radiographic nervous system tuberculosis and should be part of the early evaluation of children with suspected central nervous system tuberculosis.

Brain Diseases↗
PubMed1997

Neuroimaging of central nervous system tuberculosis in HIV-infected patients.

The recent resurgence of tuberculosis in the United States is in part attributable to the AIDS epidemic. Central nervous system tuberculosis has fairly specific radiographic features, and thus the alert radiologist may be the first to suggest this diagnosis. This article reviews the neuroimaging characteristics of central nervous system tuberculosis in HIV-seropositive patients, including intracranial manifestations, tuberculous spondylitis, and tuberculous arachnoiditis.

AIDS-Related Opportunistic Infections↗
PubMed2002

Early detection of central nervous system tuberculosis with the gen-probe nucleic Acid amplification assay: utility in an inner city hospital.

Central nervous system tuberculosis is a serious clinical problem, the treatment of which is sometimes hampered by delayed diagnosis. We investigated the utility of the Gen-Probe nucleic acid amplification assay for the rapid diagnosis of tuberculous meningitis and as a noninvasive method of identifying intracranial tuberculoma.

Diagnostic Techniques and Procedures↗
PubMed2001

[Central nervous system tuberculosis in children: 2. Treatment and outcome].

Neurologic damage is usual after central nervous system (CSN) tuberculosis recovery. Treatment is long, difficult and prone to complications. Many factors are enrolled as prognostic determinants. This study aimed to describe the treatment and outcome of 52 children with CNS tuberculosis of a tertiary pediatric hospital. All of them received standard triple drug regimen, and 41 (78.8%) received corticosteroids as adjunctive therapy. Hydrocephalus was common (28 of 41 tested), but only 8 (15.4%) patients underwent ventricular shunt surgery. Hepatotoxicity to anti tuberculosis drugs occurred in 32 (61.5%) cases, but in only 3 (9.4%) drug substitution was necessary. There were 8 (15.4%) deaths and 24 (46.1%) cases developed neurologic damage after therapy. Patients who did not receive steroids during treatment and those with advanced neurological involvement at diagnosis showed a tendency to worse prognosis.

Adolescent↗
PubMed1994

Central nervous system tuberculosis: MRI.

The MRI findings of 18 proven cases of central nervous system (CNS) tuberculosis were reviewed; 10 patients were seropositive for HIV. All had medical, laboratory, or surgical proof of CNS tuberculosis. Eleven patients had meningitis, of whom two also had arachnoiditis. Five patients had focal intra-axial tuberculomas: four brain masses and one an intramedullary spinal lesion. Two patients had focal extra-axial tuberculomas: one in the pontine cistern, and one in the spine. In all 11 patients with meningitis MRI showed diffuse, thick, meningeal enhancement. All intraparenchymal tuberculomas showed low signal intensity on T2-weighted images and ring or nodular enhancement. The extra-axial tuberculomas had areas isointense or hypointense relative to normal brain and spinal cord on T2-weighted images. Although tuberculous meningitis cannot be differentiated from other meningitides on the basis of MR findings, intraparenchymal tuberculomas show characteristic T2 shortening, not found in most other space-occupying lesions. In the appropriate clinical setting, tuberculoma should be considered.

Adult↗
PubMedDate not supplied

Magnetic resonance imaging in diagnosis of childhood central nervous system tuberculosis.

BACKGROUND: We investigated the role of magnetic resonance imaging (MRI) in diagnosis of central nervous system (CNS) tuberculosis. PATIENTS AND METHODS: The MRI findings (T1, T2 and T1 sequence after contrast) of 11 children with CNS tuberculosis were evaluated and the diagnostic value of contrast enhanced MRI and its correlation with the clinical findings were investigated. RESULTS: The median age of the patients was 6 years; seven were male and four female. MRI findings of the cases were meningeal enhancement (90.9%), hydrocephalus (63.6%), infarction (45.5%), tuberculomas (27.2%), cranial nerve involvement (27.2%) and severe cortical atrophy (9.1%). MRI provided early diagnosis in two cases by demonstrating tuberculomas, and supported the diagnosis in seven cases. However, in two cases MRI findings were inadequate to diagnose CNS tuberculosis, especially at the beginning. CONCLUSION: Contrast enhanced MRI is a very useful technique for diagnosing CNS tuberculosis, particularly by demonstrating the localized lesions, meningeal enhancement and the brain stem. However, a family history of tuberculosis, chest X-ray findings and the clinical picture are still very important for diagnosis.

Adolescent↗
PubMed1995

Paradoxical progression of tuberculous lesions during chemotherapy of central nervous system tuberculosis. Report of four cases.

The peculiar phenomenon of paradoxical progression during the treatment of central nervous system tuberculosis is discussed. A few cases with this phenomenon were reported in the past, and the authors have treated four such cases. During the treatment for tuberculous meningitis, the four patients developed new lesions, mainly in the form of tuberculomas, which progressed for some time and later regressed. In all these cases the initial drug regimen was not changed, except for the addition of steroids for a short period at the time of deterioration. All four patients underwent ventriculoperitoneal shunt insertion during the course of treatment. The authors discuss the significance of the changes in the lesions and management of such cases, and review the literature.

Adolescent↗
PubMed2000

[Central nervous system tuberculosis with and without HIV infection--clinical, neuroimaging, and neuropathological study].

Clinical data, neuroimaging, and neuropathology of 17 patients with central nervous system tuberculosis were reported. Of this population, 12 were men, 5, women; ages ranged from 23 to 75 years (mean, 46.9). There were three HIV positive patients among them. More than a half of patients had disturbance of consciousness as initial symptom. Neurological signs were variable such as visual acuity loss, hemiparesis, paraparesis, cerebellar ataxia, and tremor, though disturbance of consciousness was the most frequent (36%). Neuroimaging (X-ray CT and MRI) revealed meningeal enhancement (53%), tuberculoma (50%), hydrocephalus, infarction or bleeding and spinal cord tuberculoma. There were three patients who showed paradoxical progression. Eleven patients were performed CSF examination, all of them revealed increased cell count (mean, 206 counts/mm3) and protein (mean, 225 mg/dl), but only 4 patients were positive on bacteriological examination including PCR. Seven patients died and 5 patients were performed autopsy. Neuropathologically, all patients showed a stage of meningitis prominent on basal brain (basal cistern and/or Sylvian fissure). Cell infiltrations including lymphocyte, monocyte, and eosinocyte were most severe around blood vessels, and observed in all cases except one which showed only fibroblast and collagen fibers indicating healed stage. In some cases, there existed epithelioid cells and Langhans giant cells, and in some cases, fibrin exudate. There were three cases having tuberculoma, one HIV case and two non-HIV cases. Center of tuberculoma in non-HIV case was formed by caseous necrosis, and tuberculoma was surrounded by granuloma constituted by epithelioid cells and Langhans giant cells with lymphocyte cell infiltration and proliferation of blood vessels. In contrast, tuberculoma of HIV case did not include granuloma, and was formed with small cells with large nucleus which surrounded arteries. Our studies, as other studies, failed to show any differences between HIV and non-HIV patients clinically, as well as on neuroimaging study. But neuropathological study suggests that mechanism of tuberculoma formation may be different between in HIV positive patients and in non-HIV patients.

Adult↗