Virus signaling and apoptosis in the central nervous system infection

10.2741/1737 ◽  
2005 ◽  
Vol 10 (1-3) ◽  
pp. 2804 ◽  
Author(s):  
Dana, Perkins
2019 ◽  
Vol 5 (3) ◽  
pp. 70 ◽  
Author(s):  
James Riddell ◽  
L. Joseph Wheat

Histoplasmosis is an endemic fungal infection that may affect both immune compromised and non-immune compromised individuals. It is now recognized that the geographic range of this organism is larger than previously understood, placing more people at risk. Infection with Histoplasma capsulatum may occur after inhalation of conidia that are aerosolized from the filamentous form of the organism in the environment. Clinical syndromes typically associated with histoplasmosis include acute or chronic pneumonia, chronic cavitary pulmonary infection, or mediastinal fibrosis or lymphadenitis. Disseminated infection can also occur, in which multiple organ systems are affected. In up to 10% of cases, infection of the central nervous system (CNS) with histoplasmosis may occur with or without disseminated infection. In this review, we discuss challenges related to the diagnosis of CNS histoplasmosis and appropriate treatment strategies that can lead to successful outcomes.


1996 ◽  
Vol 40 (1) ◽  
pp. 218-220 ◽  
Author(s):  
P F Viladrich ◽  
C Cabellos ◽  
R Pallares ◽  
F Tubau ◽  
J Martínez-Lacasa ◽  
...  

We treated nine patients (10 episodes) with meningitis caused by Streptococcus pneumoniae isolates with decreased susceptibilities to broad-spectrum cephalosporins with high doses of cefotaxime (300 mg/kg of body weight per day; maximum dose, 24 g/day). Early adjunctive therapy with dexamethasone was also administered. Cefotaxime MICs were 0.5 (three episodes), 1 (five episodes), and 2 (two episodes) micrograms/ml, and MBCs ranged from 1 to 4 micrograms/ml. Therapy was well tolerated, and all patients experienced prompt clinical improvement. One patient died 8 days after the end of therapy, the central nervous system infection had already been cured, and the remaining patients recovered without relapses.


2020 ◽  
Author(s):  
Lis Høy Marbjerg ◽  
Christina Jacobsen ◽  
Jannik Fonager ◽  
Claus Bøgelund ◽  
Morten Rasmussen ◽  
...  

Abstract Background: The case presented here illustrates that interdisciplinary teamwork can be essential for the understanding of the COVID-19 disease presentation and enlightening of the pathophysiology. Case presentation: A 60-years-old overweight woman without any comorbidities was found dead in her apartment after 14 days of home isolation due to suspicion on the Coronavirus disease 2019 (COVID-19). She had reported symptoms of tachycardia, fever, and increasing respiratory difficulty one day before her death. Due to the Danish legal act on sudden deaths a forensic autopsy was performed including a thorough examination and biosampling. The results of the forensic autopsy displayed sever densified, almost airless, firm lungs, and an unspecific reactive minimal focal perivascular inflammation consisting of macrophages of the brain tissue. The final diagnosis, COVID-19 with involvement of the central nervous system was established by use of the RT-RNA analysis on cerebrospinal fluid, as well as by serologic detection of the specific antibodies for SARS-CoV-2 in cerebrospinal fluid and serum. The genetic analysis displayed a 2 % variation between SARS-CoV-2 isolates recovered from the tracheal sample, cerebrospinal fluid, and tissues from both lungs.Conclusion: The combination of all available results revealed that the cause of death was COVID-19 with severe pulmonary disease and neuroinvasion, as well as renal affection resulting in hyponatremia. To our knowledge, it was not shown previously that neuroinvasion could be confirmed by the detection of specific antibodies for SARS-CoV-2 and SARS-CoV-2 specific RNA in cerebrospinal fluid. This case supports hypotheses that SARS-CoV-2 may cause central nervous system infection. The genetic distinction between SARS-CoV-2 isolates was done by whole-genome sequencing, where the isolate recovered from the cerebrospinal fluid was the most different.


2014 ◽  
Vol 27 (4) ◽  
pp. 691-726 ◽  
Author(s):  
Samantha J. Dando ◽  
Alan Mackay-Sim ◽  
Robert Norton ◽  
Bart J. Currie ◽  
James A. St. John ◽  
...  

2020 ◽  
Author(s):  
Pan Xiang ◽  
Xinmin Xu ◽  
Xin Lu ◽  
Lili Gao ◽  
Huizhu Wang ◽  
...  

Abstract Background: SARS-Coronavirus-2 (SARS-CoV-2), the pathogen of coronavirus disease 2019 (COVID-19), not only infects the respiratory tract, but also other organs. About a third of the inpatients of COVID-19 have neurological symptoms and in vitro experiments revealed that SARS-CoV-2 could infect human neural progenitor cells and brain organoids. However, the traditional test often reports negative owing to the low number of virus in the cerebrospinal fluid. To date, timely diagnosis of central nervous system infection of SARS-CoV-2 remains a challenge.Case presentation: On day 14 of COVID-19, seizures, maxillofacial convulsions, intractable hiccups and significant increase in intracranial pressure developed in a 56-year-old man. The RT-PCR of SARS-CoV-2 was negative. SARS-CoV-2 nucleic acid were detected in cerebrospinal fluid (CSF) by ultrahigh depth sequencing. The patient was successfully treated after 14 days of mechanical ventilation and treatment of pneumonia and neurological dysfunction.Conclusions: This case suggests SARS-CoV-2 can invade the central nervous system and relevant examinations with CSF including ultrahigh depth sequencing of SARS-CoV-2 are needed among COVID-19 patients with neurological dysfunction.


2021 ◽  
Vol 54 (3) ◽  
pp. 198-203
Author(s):  
Lillian Gonçalves Campos ◽  
Thaylla Maybe Bedinot da Conceição ◽  
Marília Sfredo Krüger ◽  
Juliano Adams Perez ◽  
Juliana Ávila Duarte

Abstract Fungal infections of the central nervous system (CNS) are rare. However, because of the increase in the number of immunocompromised individuals, they have been gaining prominence in the differential diagnosis of CNS infections. Imaging techniques are sensitive for detecting and localizing an abnormality, in many cases allowing the origin of a lesion to be categorized as infectious, inflammatory, neoplastic, or vascular. This essay illustrates the magnetic resonance imaging and computed tomography findings of the most common fungal infections of the CNS, based on the experience of the Radiology Department of the Hospital de Clínicas de Porto Alegre, in the city of Porto Alegre, RS, Brazil.


2003 ◽  
Vol 77 (4) ◽  
pp. 2775-2778 ◽  
Author(s):  
Norman W. Marten ◽  
Stephen A. Stohlman ◽  
Jiehao Zhou ◽  
Cornelia C. Bergmann

ABSTRACT CD8+ T cells control acute infection of the central nervous system (CNS) by neurotropic mouse hepatitis virus but do not suffice to achieve sterile immunity. To determine the lag between T-cell priming and optimal activity within the CNS, the accumulation of virus-specific CD8+ T cells in the CNS relative to that in peripheral lymphoid organs was assessed by using gamma interferon-specific ELISPOT assays and class I tetramer staining. Virus-specific CD8+ T cells were first detected in the cervical lymph nodes. Expansion in the spleen was delayed and less pronounced but also preceded accumulation in the CNS. The data further suggest peripheral acquisition of cytolytic function, thus enhancing CD8+-T-cell effector function upon cognate antigen recognition in the CNS.


2020 ◽  
Vol 7 ◽  
pp. 2329048X2094244
Author(s):  
Ryosuke Sato ◽  
Kazuo Okanari ◽  
Tomoki Maeda ◽  
Kimihiko Kaneko ◽  
Toshiyuki Takahashi ◽  
...  

Myelin oligodendrocyte glycoprotein is a major target of the humoral immune response in children affected by inflammatory demyelinating diseases of the central nervous system. Although myelin oligodendrocyte glycoprotein causes autoimmune encephalitis in different animal models, the relevance of this mechanism in human autoimmune diseases of the central nervous system is unclear. We herein report a child with acute disseminated encephalomyelitis possibly triggered by central nervous system infection of primary herpes simplex virus in the presence of antimyelin oligodendrocyte glycoprotein antibody. A healthy 5-year-old Japanese boy suffered from acute disseminated encephalomyelitis. He was positive for antimyelin oligodendrocyte glycoprotein antibody in both the serum and the cerebrospinal fluid, and herpes simplex virus-1 DNA on polymerase chain reaction of the cerebrospinal fluid. We speculated that the central nervous system infection of primary herpes simplex virus disrupted the blood–brain barrier, and antimyelin oligodendrocyte glycoprotein antibody already present in serum was transferred to the cerebrospinal fluid, resulting in the onset of acute disseminated encephalomyelitis. This might be the mechanism underlying postinfectious acute disseminated encephalomyelitis associated with myelin oligodendrocyte glycoprotein antibody.


2017 ◽  
Vol 91 (23) ◽  
Author(s):  
Sheng-Wen Huang ◽  
Yi-Hui Huang ◽  
Huey-Pin Tsai ◽  
Pin-Hwa Kuo ◽  
Shih-Min Wang ◽  
...  

ABSTRACT RNA viruses accumulate mutations to rapidly adapt to environmental changes. Enterovirus A71 (EV-A71) causes various clinical manifestations with occasional severe neurological complications. However, the mechanism by which EV-A71 evolves within the human body is unclear. Utilizing deep sequencing and haplotype analyses of viruses from various tissues of an autopsy patient, we sought to define the evolutionary pathway by which enterovirus A71 evolves fitness for invading the central nervous system in humans. Broad mutant spectra with divergent mutations were observed at the initial infection sites in the respiratory and digestive systems. After viral invasion, we identified a haplotype switch and dominant haplotype, with glycine at VP1 residue 31 (VP1-31G) in viral particles disseminated into the integumentary and central nervous systems. In vitro viral growth and fitness analyses indicated that VP1-31G conferred growth and a fitness advantage in human neuronal cells, whereas VP1-31D conferred enhanced replication in human colorectal cells. A higher proportion of VP1-31G was also found among fatal cases, suggesting that it may facilitate central nervous system infection in humans. Our data provide the first glimpse of EV-A71 quasispecies from oral tissues to the central nervous system within humans, showing broad implications for the surveillance and pathogenesis of this reemerging viral pathogen. IMPORTANCE EV-A71 continues to be a worldwide burden to public health. Although EV-A71 is the major etiological agent of hand, foot, and mouth disease, it can also cause neurological pulmonary edema, encephalitis, and even death, especially in children. Understanding selection processes enabling dissemination and accurately estimating EV-A71 diversity during invasion in humans are critical for applications in viral pathogenesis and vaccine studies. Here, we define a selection bottleneck appearing in respiratory and digestive tissues. Glycine substitution at VP1 residue 31 helps viruses break through the bottleneck and invade the central nervous system. This substitution is also advantageous for replication in neuronal cells in vitro. Considering that fatal cases contain enhanced glycine substitution at VP1-31, we suggest that the increased prevalence of VP1-31G may alter viral tropism and aid central nervous system invasion. Our findings provide new insights into a dynamic mutant spectral switch active during acute viral infection with emerging viral pathogens.


2021 ◽  
Author(s):  
Jaida Hopkins ◽  
Samantha Sweck ◽  
Sean Richards

Rabies, despite available vaccines, causes approximately 55,000 deaths every year. Diagnosing relies on noting physical behaviors such as hydrophobia, vomiting, fever, behavior changes, paralysis, and consciousness, as well as, using several methodologies to molecularly detect the presence of the virus. RABV often enters through a bite wound given that it is transmissible through saliva. Infection spreads from muscle fibers into the peripheral nervous system traveling to the central nervous system. Infection of the central nervous system can lead to encephalitis (furious rabies) or acute flaccid paralysis (paralytic rabies). Treatment relies heavily on the time of exposure. If the patient is diagnosed prior to being symptomatic, post-exposure prophylaxis (PEP) can be administered. However, once the patient has begun displaying symptoms, therapy success rates sharply decline. Prevention includes vaccinating during both pre- and post-exposures, as well as utilizing Stepwise Approach towards Rabies Elimination (SARE) to aid impoverished countries in declining their rabies mortality rates.


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