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Encephalitis and Its Mimics in the Critical Care Unit
Published in Cheston B. Cunha, Burke A. Cunha, Infectious Diseases and Antimicrobial Stewardship in Critical Care Medicine, 2020
A critically ill patient presents to the emergency department with a low-grade fever and altered mental status. Is this a brain infection? Is it a stroke? Is it the “toxic metabolic” encephalopathy so commonly seen in patients who are septic, hypotensive, hypoxic, or otherwise severely compromised? How far must one go to exclude the possibility of a central nervous system (CNS) damaging process? How does one most rationally approach this all too frequent occurrence? This chapter will attempt to provide a framework to address these frequent and challenging questions.
Neuropathogenesis of viral infections
Published in Avindra Nath, Joseph R. Berger, Clinical Neurovirology, 2020
Avindra Nath, Joseph R. Berger
Infected leukocytes infect resident brain cells via cell to cell contact resulting in localized areas of brain infection. Viral replication may be restricted at the level of viral entry, such that the virus may infect only those cells that have specific receptors. For example, polio virus infection is dependent upon expression of its receptor, CD155, in the gut [14] and neurons [15]. Other viruses may easily enter cells, but replication may be determined availability of certain host proteins. For example, JCV enters a wide variety of cell types but it replicates in those brain derived cells such as astrocytes that have NF-1D protein [16] while, JCV does not replicate in neurons even if the viral genome is microinjected into the nucleus due to the lack of NF-1D [17]. However, JCV may rarely infect cerebellar granule cells [18] and cortical pyramidal neurons [19]. Similarly, herpes and adenoviruses are capable of entering a large number of cell types but infection gets established only in a few cell types. The ability of viruses to infect multiple cell types and use multiple receptor and non-receptor mediated mechanisms for invading an organism aids their survival in nature.
Introduction
Published in Arvind Kumar Bansal, Javed Iqbal Khan, S. Kaisar Alam, Introduction to Computational Health Informatics, 2019
Arvind Kumar Bansal, Javed Iqbal Khan, S. Kaisar Alam
A disease can be caused either through the pathogenicity that refers to the disease generating cause in the microorganisms, through genetic mutations, or through insertion/deletion of genes through a host pathogen (disease causing agent such as virus or bacteria). Pathogenicity includes production or deletion of chemicals (toxins) that would adversely affect the biochemical environment of the human cells. Many times, there is a delayed link between bacterial infection and diseases. For example, gastrointestinal infection is caused by pathogenic strains of Escherichia coli, brain infection can be caused by meningitis strains and HIV is caused by a virus.
Subgingival microbiome at different levels of cognition
Published in Journal of Oral Microbiology, 2023
Nele Fogelholm, Jaakko Leskelä, Muhammed Manzoor, Jacob Holmer, Susanna Paju, Kaija Hiltunen, Hanna-Maria Roitto, Riitta Kt Saarela, Kaisu Pitkälä, Maria Eriksdotter, Kåre Buhlin, Pirkko J Pussinen, Päivi Mäntylä
Although older adults with declining cognition have limited capability to maintain oral hygiene and often develop oral health problems, epidemiological studies have suggested a bi-directional association between oral health and declining cognition/dementia [19,20]. This bidirectional relationship between some neurodegenerative diseases and periodontitis is associated with an increase in inflammatory biomarkers, in IgG related to periodontopathogenic bacteria, and in periodontitis severity [21]. Mild cognitive impairment (MCI) may progress in some people to dementia, but others may remain stable or recover full function [22]. It has been argued based on experimental animal studies that brain infection is an early event much before cognitive decline and diagnosis of dementia [13]. It seems plausible that the oral dysbiosis promoting systemic inflammation may play a role in several of these neurodegenerative diseases [23].
SARS-CoV-2 invasion of the central nervous: a brief review
Published in Hospital Practice, 2021
Ruqaiyyah Siddiqui, Mohammad Ridwane Mungroo, Naveed Ahmed Khan
While SARS-CoV-2 is known to affect the respiratory system, mounting evidence suggests that it invades the CNS. Several case reports have demonstrated that patients showed symptoms related to brain infection. Based on the symptoms, the parietal lobe and the cerebellum might be the likely targets of SARS-CoV-2; however, further work is needed to elucidate this. The presence of ACE2, used by SARS-CoV-2 for cell entry, in the brain as well as detection of the virus in the CSF, further assert that SARS-COV-2 targets the brain. Therefore, medical practitioners should take that into account when dealing with patients suffering from COVID-19.
Staphylococcus aureus infected embolic stroke upregulates Orm1 and Cxcl2 in a rat model of septic stroke pathology
Published in Neurological Research, 2019
Lærke Boye Astrup, Kerstin Skovgaard, Rune Skovgaard Rasmussen, Tine Moesgaard Iburg, Jørgen Steen Agerholm, Bent Aalbæk, Henrik Elvang Jensen, Ole Lerberg Nielsen, Flemming Fryd Johansen, Peter Mikael Helweg Heegaard, Páll Skúli Leifsson
The brain plays a fundamental role in the development of sepsis as it controls the sepsis-related response at behavioural, neuroendocrine and autonomic levels. Sepsis-related brain pathology may therefore create a vicious cycle of unfavourable neuro-immune signalling and cardiovascular failure leading to increased mortality [1,2]. Post-mortem examinations have revealed that especially ischaemic brain lesions but also brain abscesses are frequent in both human and animal cases of sepsis [1,3–5]. However, the pathophysiological brain responses after septic stroke are difficult to investigate, as autonomic dysfunction can be difficult to study in severely ill patients, and as access to human post-mortem tissue from such patients is limited [6]. This creates a strong need for animal models of septic stroke and associated brain abscesses. Unfortunately, no such model exists. Existing models of bacterial brain infection mainly use transcranial inoculation of bacteria embedded in agarose or in vitro examination of the isolated brain cell responses towards bacterial components [7,8]. As such, the existing models do not reflect the haematogenous spread of bacteria to the brain, the blood-brain barrier reaction during septic embolic stroke, nor the concurrent presence of brain ischaemia and bacterial infection, which are all central to septic stroke pathology [1]. Therefore, we established a rat model of septic embolic stroke to investigate outcome of brain ischaemia and haematogenous brain infection with likely blood-brain barrier disruption. This combined scenario was achieved by creating focal brain ischemia using an infectious fibrin clot. The fibrin clot was designed to create an area of ischaemic damage at similar anatomical locations in all rats, and the clot contained a defined number of live bacteria. Staphylococcus aureus (S. aureus) was used as this bacterium is one of the main causes of sepsis and brain abscesses in man [9–11].