Fatal Parasitic Meningoencephalomyelitis Caused By Halicephalobus deletrix: A Case Report and Review of the Literature

2010 ◽  
Vol 134 (4) ◽  
pp. 625-629
Author(s):  
Sarah L. Ondrejka ◽  
Gary W. Procop ◽  
Keith K. Lai ◽  
Richard A. Prayson
Keyword(s):  
Fatal Case ◽  
Brain Biopsy ◽  
Altered Mental Status ◽  
Brain Parenchyma ◽  
Review Of The Literature ◽  
Inflammatory Infiltration ◽  
Granulomatous Vasculitis ◽  
Helminthic Infection ◽  
The Central Nervous System ◽  
The Brain

Abstract Infection with the saprophagous nematode Halicephalobus species is uncommon but has been reported in horses worldwide. Only 3 human cases have been previously described, all of which have been fatal. We report a fourth fatal case, which occurred in a 39-year-old woman who presented with meningeal signs, altered mental status, and a prodromal pruritic rash. Diagnostic evaluation included an open brain biopsy, which was diagnosed as granulomatous vasculitis. The patient subsequently died after a course of steroids and cyclophosphamide. At autopsy, a robust perivascular mixed inflammatory infiltration of the brain parenchyma, meninges, and ventricular system was present with larval forms and mature nematodes morphologically consistent with Halicephalobus deletrix. Although extremely rare, this organism needs to be considered in the differential diagnosis of human helminthic infection of the central nervous system.

scholarly journals Vascular Dysfunction Induced by Mercury Exposure

2019 ◽  
Vol 20 (10) ◽  
pp. 2435 ◽  
Author(s):  
Tetsuya Takahashi ◽  
Takayoshi Shimohata
Keyword(s):  
Oxidative Stress ◽  
Vascular Dysfunction ◽  
Brain Parenchyma ◽  
Transport Systems ◽  
Mehg Exposure ◽  
In Vivo Models ◽  
The Central Nervous System ◽  
The Brain

Methylmercury (MeHg) causes severe damage to the central nervous system, and there is increasing evidence of the association between MeHg exposure and vascular dysfunction, hemorrhage, and edema in the brain, but not in other organs of patients with acute MeHg intoxication. These observations suggest that MeHg possibly causes blood–brain barrier (BBB) damage. MeHg penetrates the BBB into the brain parenchyma via active transport systems, mainly the l-type amino acid transporter 1, on endothelial cell membranes. Recently, exposure to mercury has significantly increased. Numerous reports suggest that long-term low-level MeHg exposure can impair endothelial function and increase the risks of cardiovascular disease. The most widely reported mechanism of MeHg toxicity is oxidative stress and related pathways, such as neuroinflammation. BBB dysfunction has been suggested by both in vitro and in vivo models of MeHg intoxication. Therapy targeted at both maintaining the BBB and suppressing oxidative stress may represent a promising therapeutic strategy for MeHg intoxication. This paper reviews studies on the relationship between MeHg exposure and vascular dysfunction, with a special emphasis on the BBB.

scholarly journals Central nervous system paracoccidioidomycosis. Report of a case successfully treated with Itraconazol

2000 ◽  
Vol 42 (4) ◽  
pp. 231-234 ◽  
Author(s):  
Luis A. VILLA ◽  
Angela TOBÓN ◽  
Antonio RESTREPO ◽  
Daniel CALLE ◽  
David S. ROSERO ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Clinical Improvement ◽  
Brain Biopsy ◽  
Yeast Cells ◽  
Control Drug ◽  
Antibody Titers ◽  
The Central Nervous System ◽  
Clonic Seizures ◽  
The Brain

Paracoccidioidomycosis (PCM) is a primary pulmonary infection that often disseminates to other organs and systems. Involvement of the central nervous system (CNS) is rare and due to the fact that both clinical alertness and establishment of the diagnosis are delayed, the disease progresses causing serious problems. We report here a case of neuroparacoccidioidomycosis (NPCM), observed in a 55 year-old male, who consulted due to neurological symptoms (left hemiparesis, paresthesias, right palpebral ptosis, headache, vomiting and tonic clonic seizures) of a month duration. Upon physical examination, an ulcerated granulomatous lesion was observed in the abdomen. To confirm the diagnosis a stereotactic biopsy was taken; additionally, mycological tests from the ulcerated lesion and a bronchoalveolar lavage were performed. In the latter specimens, P. brasiliensis yeast cells were visualized and later on, the brain biopsy revealed the presence of the fungus. Treatment with itraconazole (ITZ) was initiated but clinical improvement was unremarkable; due to the fact that the patient was taking sodium valproate for seizure control, drug interactions were suspected and confirmed by absence of ITZ plasma levels. The latter medication was changed to clonazepam and after several weeks, clinical improvement began to be noticed and was accompanied by diminishing P. brasiliensis antigen and antibody titers. In the PCM endemic areas, CNS involvement should be considered more often and the efficacy of itraconazole therapy should also be taken into consideration.

scholarly journals Immune cells and CNS physiology: Microglia and beyond

2018 ◽  
Vol 216 (1) ◽  
pp. 60-70 ◽  
Author(s):  
Geoffrey T. Norris ◽  
Jonathan Kipnis
Keyword(s):  
Central Nervous System ◽  
Immune Cells ◽  
Brain Function ◽  
Brain Parenchyma ◽  
The Body ◽  
Immune Repertoire ◽  
Perivascular Macrophages ◽  
The Central Nervous System ◽  
Cns Immunity ◽  
The Brain

Recent advances have directed our knowledge of the immune system from a narrative of “self” versus “nonself” to one in which immune function is critical for homeostasis of organs throughout the body. This is also the case with respect to the central nervous system (CNS). CNS immunity exists in a segregated state, with a marked partition occurring between the brain parenchyma and meningeal spaces. While the brain parenchyma is patrolled by perivascular macrophages and microglia, the meningeal spaces are supplied with a diverse immune repertoire. In this review, we posit that such partition allows for neuro–immune crosstalk to be properly tuned. Convention may imply that meningeal immunity is an ominous threat to brain function; however, recent studies have shown that its presence may instead be a steady hand directing the CNS to optimal performance.

scholarly journals Immune System in the Brain: A Modulatory Role on Dendritic Spine Morphophysiology?

2012 ◽  
Vol 2012 ◽  
pp. 1-7 ◽  
Author(s):  
Oscar Kurt Bitzer-Quintero ◽  
Ignacio González-Burgos
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Immune System ◽  
Dendritic Spines ◽  
Cell Lineage ◽  
Myeloid Cell ◽  
Brain Parenchyma ◽  
Immune Mediators ◽  
The Central Nervous System ◽  
The Brain

The central nervous system is closely linked to the immune system at several levels. The brain parenchyma is separated from the periphery by the blood brain barrier, which under normal conditions prevents the entry of mediators such as activated leukocytes, antibodies, complement factors, and cytokines. The myeloid cell lineage plays a crucial role in the development of immune responses at the central level, and it comprises two main subtypes: (1) resident microglia, distributed throughout the brain parenchyma; (2) perivascular macrophages located in the brain capillaries of the basal lamina and the choroid plexus. In addition, astrocytes, oligodendrocytes, endothelial cells, and, to a lesser extent, neurons are implicated in the immune response in the central nervous system. By modulating synaptogenesis, microglia are most specifically involved in restoring neuronal connectivity following injury. These cells release immune mediators, such as cytokines, that modulate synaptic transmission and that alter the morphology of dendritic spines during the inflammatory process following injury. Thus, the expression and release of immune mediators in the brain parenchyma are closely linked to plastic morphophysiological changes in neuronal dendritic spines. Based on these observations, it has been proposed that these immune mediators are also implicated in learning and memory processes.

scholarly journals A Rhombencephalitis Revealing HIV Virorachia

2021 ◽  
Author(s):  
Annick Melanie MAGNEROU ◽  
Martine NIDA ◽  
Daniel MASSI GAMS ◽  
Hugues Martial ZANGA ◽  
Fidelie Scolastique NGOUNGOURE HALIMA ◽  
...  
Keyword(s):  
Viral Suppression ◽  
Treated Patient ◽  
Brain Mri ◽  
Undetectable Viral Load ◽  
Brain Parenchyma ◽  
Hiv Replication ◽  
Csf Analysis ◽  
Persistent Inflammation ◽  
The Central Nervous System ◽  
The Brain

Abstract One of the possible causes of persistent inflammation of the brain parenchyma in the age of antiretrovirals is residual HIV replication, despite effective viral suppression in the bloodstream with Antiretroviral treatment (ART). The central nervous system (CNS) is infected early during primary HIV infection and is one of the reservoirs of this virus during chronic infection. Inadequate penetration of certain ART into the CNS could promote some degree of intrathecal HIV replication.We describe the case of an HIV-infected patient compliant to ART with an undetectable viral load in the blood but present in the cerebrospinal fluid (CSF). The patient presented with subacute rhombencephalitis due to HIV which was fatal to him.An HIV-infected and treated patient, well controlled on ART, with new neurological disorders, should be promptly investigated by brain MRI and CSF analysis for exhaustive detection of viruses including that of HIV itself.

scholarly journals Unexpected intracranial location of a Cephenemyia stimulator larva in a roe deer, Capreolus capreolus, revealed by computed tomography

2021 ◽  
Vol 33 ◽  
pp. 1-7
Author(s):  
Luis E. Fidalgo ◽  
Ana M. López-Beceiro ◽  
Carlos Martínez-Carrasco ◽  
Noelia Caparrós-Fontarosa ◽  
Antonio Sánchez ◽  
...  
Keyword(s):  
Computed Tomography ◽  
Central Nervous System ◽  
Roe Deer ◽  
Capreolus Capreolus ◽  
Brain Parenchyma ◽  
Anatomical Location ◽  
Migration Route ◽  
The Central Nervous System ◽  
Hemorrhagic Lesion ◽  
The Brain

In this study we describe the finding of a Cephenemyia stimulator larva in the brain of a roe deer (Capreolus capreolus) after performing a computed tomography (CT) scan of its head. Despite this anatomical location of oestrid larvae could be relatively frequent in other genera, such as Oestrus, to our knowledge, this is the first reported case involving the genus Cephenemyia. Concretely, a second-instar C. stimulator larvae was found in the basis of the cranium. The location of a macroscopic hemorrhagic lesion involving the brain parenchyma peripheral to the location of the larva suggests that tissue colonization occurred before the animal was hunted. Since no detectable alterations or damage to the cranial bones were observed, we suggest a possible larval migration route drilling the skull bones. Finally, we propose the use of the term “neuromyiasis” to be referred to the invasion of the central nervous system by dipteran larvae, particularly oestrids.

scholarly journals Immovable Object Meets Unstoppable Force? Dialogue Between Resident and Peripheral Myeloid Cells in the Inflamed Brain

2020 ◽  
Vol 11 ◽  
Author(s):  
Alanna G. Spiteri ◽  
Claire L. Wishart ◽  
Nicholas J. C. King
Keyword(s):  
Myeloid Cells ◽  
Cell Types ◽  
Brain Parenchyma ◽  
Specific Cell ◽  
Novel Treatments ◽  
Experimental Systems ◽  
Immune Mediated ◽  
Recent Developments ◽  
The Central Nervous System ◽  
The Brain

Inflammation of the brain parenchyma is characteristic of neurodegenerative, autoimmune, and neuroinflammatory diseases. During this process, microglia, which populate the embryonic brain and become a permanent sentinel myeloid population, are inexorably joined by peripherally derived monocytes, recruited by the central nervous system. These cells can quickly adopt a morphology and immunophenotype similar to microglia. Both microglia and monocytes have been implicated in inducing, enhancing, and/or maintaining immune-mediated pathology and thus disease progression in a number of neuropathologies. For many years, experimental and analytical systems have failed to differentiate resident microglia from peripherally derived myeloid cells accurately. This has impeded our understanding of their precise functions in, and contributions to, these diseases, and hampered the development of novel treatments that could target specific cell subsets. Over the past decade, microglia have been investigated more intensively in the context of neuroimmunological research, fostering the development of more precise experimental systems. In light of our rapidly growing understanding of these cells, we discuss the differential origins of microglia and peripherally derived myeloid cells in the inflamed brain, with an analysis of the problems resolving these cell types phenotypically and morphologically, and highlight recent developments enabling more precise identification.

Herpetic Meningoencephalitis by Vertical Transmission: A Case Report and Systematic Review

2021 ◽  
Vol 2 (1) ◽  
pp. 35-41
Author(s):  
Julia Teles Triglia Pinto ◽  
◽  
Ana Carolina Tomasella Auad ◽  
Gabrielle Menegucci ◽  
Marília Gabriela Palácio Galbiatti ◽  
...  
Keyword(s):  
Specific Treatment ◽  
Brain Parenchyma ◽  
High Rate ◽  
Neurological Damage ◽  
Neurological Sequelae ◽  
Spontaneous Vaginal Delivery ◽  
The Central Nervous System ◽  
Herpetic Encephalitis ◽  
Simplex Virus ◽  
The Brain

Objective: To report a case of vertical herpetic meningoencephalitis. Results: The involvement of the central nervous system (CNS) in infection by HSV (herpes simplex virus), HSV-1 or HSV-2, causes an acute inflammatory process in the brain parenchyma, leading to herpetic encephalitis. It is a feared form of the disease due to its severity and its high rate of morbidity and mortality. Its rapid fatal progression can be prevented from early suspicion and treatment, which is essential when taking into account their neurological sequelae since survivors have motor sequelae, behavioral disorders, or epilepsy. The present work reports the case of a newborn male with spontaneous vaginal delivery who, at 19 days of age, started to experience fever, irritability, difficulty in eating, spasms, tremors of the upper limbs, deviation of the eyes, and seizures of difficult to control, together with CFE and serological changes, in addition to imaging tests compatible with herpetic meningoencephalitis, progressing with a very serious evolution despite the institution of specific treatment for CNS herpetic infection, evolving with important neurological sequelae. Conclusion: The sequels resulting from herpetic encephalitis not properly diagnosed, or even late, leads from severe neurological damage to death. Therefore, it is extremely important to start empirical treatment with antiviral drugs to reduce the sequelae mentioned above.

scholarly journals Physiology of Microglia

2011 ◽  
Vol 91 (2) ◽  
pp. 461-553 ◽  
Author(s):  
Helmut Kettenmann ◽  
Uwe-Karsten Hanisch ◽  
Mami Noda ◽  
Alexei Verkhratsky
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Immune Cell ◽  
Brain Parenchyma ◽  
Microglial Cells ◽  
Activation Process ◽  
Normal Brain ◽  
The Central Nervous System ◽  
Cellular Compartments ◽  
The Brain

Microglial cells are the resident macrophages in the central nervous system. These cells of mesodermal/mesenchymal origin migrate into all regions of the central nervous system, disseminate through the brain parenchyma, and acquire a specific ramified morphological phenotype termed “resting microglia.” Recent studies indicate that even in the normal brain, microglia have highly motile processes by which they scan their territorial domains. By a large number of signaling pathways they can communicate with macroglial cells and neurons and with cells of the immune system. Likewise, microglial cells express receptors classically described for brain-specific communication such as neurotransmitter receptors and those first discovered as immune cell-specific such as for cytokines. Microglial cells are considered the most susceptible sensors of brain pathology. Upon any detection of signs for brain lesions or nervous system dysfunction, microglial cells undergo a complex, multistage activation process that converts them into the “activated microglial cell.” This cell form has the capacity to release a large number of substances that can act detrimental or beneficial for the surrounding cells. Activated microglial cells can migrate to the site of injury, proliferate, and phagocytose cells and cellular compartments.

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