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Journal of Medical Case Reports Apr 2018Staphylococcus epidermidis can cause nosocomial meningitis in the presence of prosthetic devices. We describe a case of Staphylococcus epidermidis meningitis in a... (Review)
Review
Staphylococcus epidermidis meningitis in the absence of a neurosurgical device secondary to catheter-related bloodstream infection: a case report and review of the literature.
BACKGROUND
Staphylococcus epidermidis can cause nosocomial meningitis in the presence of prosthetic devices. We describe a case of Staphylococcus epidermidis meningitis in a patient with neutropenia who had no intracranial foreign body, and we review the literature on meningitis that is caused by coagulase-negative Staphylococcus spp. without a neurosurgical device.
CASE PRESENTATION
A 47-year-old Japanese man with acute myeloid leukemia receiving chemotherapy through a totally implantable central venous catheter developed fever and headache. The patient had a history of craniotomy for anaplastic oligodendroglioma without an indwelling neurosurgical device. The results of two blood cultures and a cerebrospinal fluid culture were positive for Staphylococcus epidermidis. Clinical improvement was observed with treatment with vancomycin and removal of the central venous catheter despite prolonged neutropenia.
CONCLUSIONS
To the best of our knowledge, this is the first reported case of Staphylococcus epidermidis meningitis in a patient with neutropenia without a neurosurgical device who was successfully treated.
Topics: Administration, Intravenous; Anti-Bacterial Agents; Brain; Catheter-Related Infections; Catheters, Indwelling; Central Venous Catheters; Fatal Outcome; Humans; Leukemia, Myeloid, Acute; Magnetic Resonance Imaging; Male; Meningitis, Bacterial; Middle Aged; Staphylococcus epidermidis; Tomography, X-Ray Computed; Vancomycin
PubMed: 29690925
DOI: 10.1186/s13256-018-1646-7 -
Cureus Dec 2022() is a common nosocomial pathogen. However, associated meningitis and brain abscess formation are extremely rare in the United States. We present a case of a...
() is a common nosocomial pathogen. However, associated meningitis and brain abscess formation are extremely rare in the United States. We present a case of a 73-year-old male who initially presented for a tonsillar abscess of unknown etiology. While awaiting an abscess biopsy, the patient underwent molar extraction for chronic periodontitis and decay. The patient subsequently developed bacteremia and meningitis. As he clinically declined, repeat imaging revealed a brain abscess with eventual hemorrhagic transformation. Notably, the patient had underlying hypogammaglobulinemia from chronic lymphocytic leukemia (CLL), which we believe contributed to the invasive disease. Given the global spread of virulent strains of (such as hypervirulent or hypermucoviscous ), clinicians must bear this pathogen in mind while treating critically ill and immunocompromised patients.
PubMed: 36644065
DOI: 10.7759/cureus.32479 -
Cancer Management and Research 2017Acute myeloid leukemia (AML) rarely involves the central nervous system (CNS). Little is known about the clinical course in adult AML patients since most studies...
INTRODUCTION
Acute myeloid leukemia (AML) rarely involves the central nervous system (CNS). Little is known about the clinical course in adult AML patients since most studies examined pediatric patients. Therefore, this study analyzed the data of patients treated in three prospective trials of the "Study Alliance Leukemia" (SAL) study group for CNS involvement.
METHODS
In all, 3,261 AML patients included in the prospective AML96, AML2003, and AML60+ trials of the SAL study group were analyzed. Symptomatic patients underwent cerebrospinal fluid (CSF) puncture and CNS involvement was diagnosed depending on morphology and/or flow cytometry of the CSF. Cytogenetic, molecular, clinical, and laboratory parameters were analyzed in order to identify risk factors.
RESULTS
A total of 55 patients had proven symptomatic CNS involvement. Significantly more patients revealed CNS involvement at relapse (34 patients, 2.9%) compared with first diagnosis (21 patients, 0.6%), <0.001. CNS involvement at initial diagnosis had a significantly higher frequency in patients with complex aberrant karyotypes, high serum lactate dehydrogenase activity, French-American-British M5 subtype, -internal tandem duplication (ITD) mutations alone, and co-occurrence of a -ITD and mutation. Furthermore, AML patients with CNS involvement at diagnosis had an inferior outcome compared with patients without CNS involvement even if treated with intrathecal chemotherapy with an overall survival of 11% versus 30% at 5 years, =0.004.
CONCLUSION
This study analyzed the largest data set of adult AML patients with proven CNS involvement reported so far. The data demonstrated very low prevalence of CNS involvement at initial diagnosis in adult patients with AML, and described new risk factors. In patients with risk factors, intense diagnostic and treatment strategies should be employed in the future.
PubMed: 28435324
DOI: 10.2147/CMAR.S125259 -
Revista Chilena de Infectologia :... Aug 2018Cryptococcosis is a severe opportunistic mycotic infection, caused mainly by Cryptococcus neoformans. It can present as meningitis, pneumonia or cryptococcemia.
BACKGROUND
Cryptococcosis is a severe opportunistic mycotic infection, caused mainly by Cryptococcus neoformans. It can present as meningitis, pneumonia or cryptococcemia.
AIM
To characterize patients with Cryptococcus infection between January 1°, 2013 and June 30, 2016, in Hospital Carlos van Buren, Valparaíso, Chile.
METHODS
We identified retrospectively those cultures with Cryptococcus sp. growth, and then obtained their clinical files which were analyzed by two independent reviewers.
RESULTS
We were able to obtain data from 13 of 15 patients who presented with Cryptococcus neoformans infection. Out of all, 11 (84.6%) were males, with a median age of 35 years old. 11 (84,6%) were HIV positive, 1 (7,7%) had chronic lymphocytic leukemia, and 1 (7,7%) refered alcohol abuse. Out of the 15 episodes, 9 (60%) had meningeal infection; 5 (33.3%) were cryptococcemia without meningeal involvement and 1 (6.6%) presented as a pulmonary infection. Eight patients were deceased at one year follow up.
CONCLUSIONS
Cryptococcus sp. infection must be suspected in patients with cellular immunodeficiencies. Meningeal involvement is the most frequent form of clinical presentation. It still has a high mortality rate.
Topics: Adult; CD4-Positive T-Lymphocytes; Chile; Cryptococcosis; Cryptococcus neoformans; Deoxycholic Acid; Female; Fluconazole; Humans; Male; Retrospective Studies
PubMed: 30534929
DOI: 10.4067/s0716-10182018000400420 -
Turkish Journal of Haematology :... Dec 2022
Topics: Child; Humans; Methotrexate; Arachnoiditis; Precursor Cell Lymphoblastic Leukemia-Lymphoma
PubMed: 36172826
DOI: 10.4274/tjh.galenos.2022.2022.0379 -
Cold Spring Harbor Molecular Case... Sep 2016Here, we report the case of an acute promyelocytic leukemia (APL) patient who-although negative for FLT3 mutations at diagnosis-developed isolated FLT3 tyrosine kinase...
Here, we report the case of an acute promyelocytic leukemia (APL) patient who-although negative for FLT3 mutations at diagnosis-developed isolated FLT3 tyrosine kinase II domain (FLT3-TKD)-positive meningeal relapse, which, in retrospect, could be traced back to a minute bone marrow subclone present at first diagnosis. Initially, the 48-yr-old female diagnosed with high-risk APL had achieved complete molecular remission after standard treatment with all-trans retinoic acid (ATRA) and chemotherapy according to the AIDA (ATRA plus idarubicin) protocol. Thirteen months after the start of ATRA maintenance, the patient suffered clinically overt meningeal relapse along with minute molecular traces of PML/RARA (promyelocytic leukemia/retinoic acid receptor alpha) in the bone marrow. Following treatment with arsenic trioxide and ATRA in combination with intrathecal cytarabine and methotrexate, the patient achieved a complete molecular remission in both cerebrospinal fluid (CSF) and bone marrow, which currently lasts for 2 yr after completion of therapy. Whole-exome sequencing and subsequent ultradeep targeted resequencing revealed a heterozygous FLT3-TKD mutation in CSF leukemic cells (p.D835Y, c.2503G>T, 1000/1961 reads [51%]), which was undetectable in the concurrent bone marrow sample. Interestingly, the FLT3-TKD mutated meningeal clone originated from a small bone marrow subclone present in a variant allele frequency of 0.4% (6/1553 reads) at initial diagnosis. This case highlights the concept of clonal evolution with a subclone harboring an additional mutation being selected as the "fittest" and leading to meningeal relapse. It also further supports earlier suggestions that FLT3 mutations may play a role for migration and clonal expansion in the CSF sanctuary site.
PubMed: 27626069
DOI: 10.1101/mcs.a001123 -
Journal of Cytology 2017Carcinomatous meningitis is a rare manifestation of malignancy. It is increasingly being recognized in lung carcinoma, breast carcinoma, melanomas, gastrointestinal...
Carcinomatous meningitis is a rare manifestation of malignancy. It is increasingly being recognized in lung carcinoma, breast carcinoma, melanomas, gastrointestinal malignancies, lymphomas, and leukemia and it is almost never seen in gallbladder malignancies. We present a case whose primary presentation was as a carcinomatous meningitis that was subsequently found to be secondary to a gallbladder primary.
PubMed: 28469324
DOI: 10.4103/0970-9371.203571 -
BMC Infectious Diseases Jan 2020Bacillus cereus sometimes causes central nervous system infection, especially in compromised hosts. In cases of meningitis arising during neutropenia, CSF abnormalities... (Review)
Review
Survival of a case of Bacillus cereus meningitis with brain abscess presenting as immune reconstitution syndrome after febrile neutropenia - a case report and literature review.
BACKGROUND
Bacillus cereus sometimes causes central nervous system infection, especially in compromised hosts. In cases of meningitis arising during neutropenia, CSF abnormalities tend to be subtle and can be easily overlooked, and mortality rate is high. We report a survived case of B. cereus meningitis/brain abscess in severe neutropenia, presenting as immune reconstitution syndrome.
CASE PRESENTATION
A 54-year-old Japanese female with acute myelogenous leukemia developed B. cereus bacteremia and meningitis during consolidation chemotherapy. At the onset, she presented with mild meningism. She had marked leukocytopenia (WBC <100/μL, neutrophils 0/μL) and lumbar puncture yielded only mild pleocytosis. She was transferred to intensive care unit, and meropenem, linezolid and vancomycin was started. With intensive therapy, she recovered and once became afebrile. On day 19, however, her fever, meningism and consciousness level dramatically worsened despite recovery of bone marrow function. The antimicrobial chemotherapy was continued and finally she was cured with no complications.
CONCLUSIONS
With early diagnosis and prompt initiation and of antibiotics, the case was successfully treated without any sequelae. It is important to remember that, even under optimal antimicrobial therapy, bone marrow recovery can cause transient reaggravation of the disease. In such cases, timely and appropriate evaluation should be done to make the clinical decision to change, continue, or intensify treatment.
Topics: Anti-Bacterial Agents; Antineoplastic Combined Chemotherapy Protocols; Bacillus cereus; Bacteremia; Brain Abscess; Chemotherapy-Induced Febrile Neutropenia; Female; Humans; Immune Reconstitution Inflammatory Syndrome; Leukemia, Myeloid, Acute; Meningitis, Bacterial; Middle Aged; Treatment Outcome
PubMed: 31906936
DOI: 10.1186/s12879-019-4753-1 -
Journal of Hematology & Oncology Oct 2016DNMT3A mutations are frequently discovered in acute myeloid leukemia (AML), associated with poor outcome. Recently, a relapse case report of AML extramedullary disease...
BACKGROUND
DNMT3A mutations are frequently discovered in acute myeloid leukemia (AML), associated with poor outcome. Recently, a relapse case report of AML extramedullary disease has showed that AML cells harboring DNMT3A variation were detected in the cerebral spinal fluid. However, whether a causal relationship exists between DNMT3A mutation (D3Amut) and extramedullary infiltration (EMI) is unclear.
METHODS
We took advantage of DNMT3A (R882C) mutation-carrying AML cell strain, that is, OCI-AML3, assessing its migration ability in vitro and in vivo. By RNA interfering technology and a xenograft mouse model, we evaluated the effect of DNMT3A mutation on cell mobility and explored the possible mechanism.
RESULTS
OCI-AML3 displayed extraordinary migration ability in vitro and infiltrated into meninges of NOD/SCID mice after intravenous transfusion. We found that this leukemic migration or infiltration capacity was significantly compromised by the knockdown of DNMT3A mutant. Notably, TWIST1, a critical inducer of epithelial-mesenchymal transition, which underlies the metastasis of carcinomas, was highly expressed in association with R882 mutations. Abrogation of TWIST1 in DNMT3A mutated cells considerably weakened their mobility or infiltration.
CONCLUSIONS
Our results demonstrate that D3Amut in OCI-AML3 strain enhances leukemic aggressiveness by promoting EMI process, which is partially through upregulating TWIST1.
Topics: Animals; Cell Line, Tumor; Cell Movement; DNA (Cytosine-5-)-Methyltransferases; DNA Methyltransferase 3A; Epithelial-Mesenchymal Transition; Heterografts; Humans; Leukemia, Myeloid, Acute; Mice; Mutation; Neoplasm Invasiveness; Nuclear Proteins; Twist-Related Protein 1
PubMed: 27724883
DOI: 10.1186/s13045-016-0337-3 -
The Journal of Biological Chemistry 2021Meningiomas (MNs), arising from the arachnoid/meningeal layer, are nonresponsive to chemotherapies, with ∼50% showing loss of the Neurofibromatosis 2 (NF2) tumor...
Meningiomas (MNs), arising from the arachnoid/meningeal layer, are nonresponsive to chemotherapies, with ∼50% showing loss of the Neurofibromatosis 2 (NF2) tumor suppressor gene. Previously, we established NF2 loss activates mechanistic target of rapamycin complex 1 (mTORC1) and mechanistic target of rapamycin complex 2 (mTORC2) signaling, leading to clinical trials for NF2 and MN. Recently our omics studies identified activated ephrin (EPH) receptor and Src family kinases upon NF2 loss. Here, we report increased expression of several ligands in NF2-null human arachnoidal cells (ACs) and the MN cell line Ben-Men-1, particularly neuregulin-1/heregulin (NRG1), and confirm increased NRG1 secretion and activation of V-ERB-B avian erythroblastic leukemia viral oncogene homolog 3 (ERBB3) receptor kinase. Conditioned-medium from NF2-null ACs or exogenous NRG1 stimulated ERBB3, EPHA2, and mTORC1/2 signaling, suggesting pathway crosstalk. NF2-null cells treated with an ERBB3-neutralizing antibody partially downregulated mTOR pathway activation but showed no effect on viability. mTORC1/2 inhibitor treatment decreased NRG1 expression and downregulated ERBB3 while re-activating pAkt T308, suggesting a mechanism independent of NRG1-ERBB3 but likely involving activation of another upstream receptor kinase. Transcriptomics after mTORC1/2 inhibition confirmed decreased ERBB3/ERBB4 while revealing increased expression of insulin-like growth factor receptor 1 (IGF1R). Drug treatment co-targeting mTORC1/2 and IGF1R/insulin receptor attenuated pAkt T308 and showed synergistic effects on viability. Our findings indicate potential autocrine signaling where NF2 loss leads to secretion/activation of NRG1-ERBB3 signaling. mTORC1/2 inhibition downregulates NRG1-ERBB3, while upregulating pAkt T308 through an adaptive response involving IGF1R/insulin receptor and co-targeting these pathways may prove effective for treatment of NF2-deficient MN.
Topics: Antibodies, Monoclonal, Humanized; Autocrine Communication; Benzamides; Benzoxazoles; Cell Line, Tumor; Cell Movement; Cell Proliferation; Dose-Response Relationship, Drug; Gene Expression Regulation; Humans; Lapatinib; Meningeal Neoplasms; Meningioma; Morpholines; Neuregulin-1; Neurofibromin 2; Proto-Oncogene Proteins c-akt; Pyrazoles; Pyrimidines; Receptor, EphA2; Receptor, ErbB-3; Receptor, IGF Type 1; Signal Transduction; Sirolimus; TOR Serine-Threonine Kinases; Transcriptome; Triazines
PubMed: 33273014
DOI: 10.1074/jbc.RA120.014960