scholarly journals Lyssaviruses and the Fatal Encephalitic Disease Rabies

2021 ◽  
Vol 12 ◽  
Author(s):  
Terence Peter Scott ◽  
Louis Hendrik Nel

Lyssaviruses cause the disease rabies, which is a fatal encephalitic disease resulting in approximately 59,000 human deaths annually. The prototype species, rabies lyssavirus, is the most prevalent of all lyssaviruses and poses the greatest public health threat. In Africa, six confirmed and one putative species of lyssavirus have been identified. Rabies lyssavirus remains endemic throughout mainland Africa, where the domestic dog is the primary reservoir – resulting in the highest per capita death rate from rabies globally. Rabies is typically transmitted through the injection of virus-laden saliva through a bite or scratch from an infected animal. Due to the inhibition of specific immune responses by multifunctional viral proteins, the virus usually replicates at low levels in the muscle tissue and subsequently enters the peripheral nervous system at the neuromuscular junction. Pathogenic rabies lyssavirus strains inhibit innate immune signaling and induce cellular apoptosis as the virus progresses to the central nervous system and brain using viral protein facilitated retrograde axonal transport. Rabies manifests in two different forms - the encephalitic and the paralytic form - with differing clinical manifestations and survival times. Disease symptoms are thought to be due mitochondrial dysfunction, rather than neuronal apoptosis. While much is known about rabies, there remain many gaps in knowledge about the neuropathology of the disease. It should be emphasized however, that rabies is vaccine preventable and dog-mediated human rabies has been eliminated in various countries. The global elimination of dog-mediated human rabies in the foreseeable future is therefore an entirely feasible goal.

2021 ◽  
Vol 16 (5) ◽  
pp. 355-360
Author(s):  
V.I. Snisar ◽  
O.S. Pavlysh

One of the complications of the postoperative period in children is postanesthetic agitation, a significant emotional and uncontrollable worry, clouding of consciousness, feeling of anxiety and fear, inappropriate behavior, irritability, inconso­lable crying, aggressive and negative attitude towards parents and medical staff. Postoperative agitation is very important for clinicians and hospitals, it has a risk of harming a patient, staying longer in the ward after anesthesia, and increasing the period of postoperative recovery. The frequency of postoperative agitation depends on age group. Most often agitation occurs in young children. There is evidence that agitation can also be due to the immature nervous system and a consequence of pathological conditions of the central nervous system (asthenoneurotic syndrome, encephalopathy, hyperactivity syndrome, perinatal posthypoxic and organic brain lesions, history of prematurity, epilepsy, psychophysical and speech delay, etc.). That is why the goal of our research was to study the patterns of clinical manifestations of postoperative agitation syndrome in children with prenatal da­mage to the central nervous system. The work was performed based on the analysis of the postoperative period in 109 young children: 59 patients with acquired hydrocephalus, who underwent ventriculoperitoneal shunting, and 50 children without neurological disorders in whom reconstructive surge­ries were carried out. Depending on the type anesthetic management, each group was divided into two subgroups: children, who received inhalation anesthesia with sevoflurane, and those, who received total intravenous anesthesia using propofol. In the postoperative period, the behavior of children was assessed on a Pediatric Ane­sthesia Emergence Delirium scale 30 minutes after anesthesia was completed. Criterion for the development of agitation was the presence of excitement in a child with a score of ≥ 10 points. Study showed that young children with perinatal damage to the central nervous system and children whose anesthetic provision is carried out using sevoflurane are the most vulnerable to the development of agitation syndrome. Agitation in such children is more pronounced and longer. These cases require prediction, detection and active surveillance.


2021 ◽  
Vol 12 ◽  
Author(s):  
Monica Goldberg-Murow ◽  
Carlos Cedillo-Peláez ◽  
Luz Elena Concha-del-Río ◽  
Rashel Cheja-Kalb ◽  
María José Salgar-Henao ◽  
...  

Toxoplasma gondii infection can trigger autoreactivity by different mechanisms. In the case of ocular toxoplasmosis, disruption of the blood-retinal barrier may cause exposure of confined retinal antigens such as recoverin. Besides, cross-reactivity can be induced by molecular mimicry of parasite antigens like HSP70, which shares 76% identity with the human ortholog. Autoreactivity can be a determining factor of clinical manifestations in the eye and in the central nervous system. We performed a prospective observational study to determine the presence of autoantibodies against recoverin and HSP70 by indirect ELISA in the serum of 65 patients with ocular, neuro-ophthalmic and congenital cerebral toxoplasmosis. We found systemic autoantibodies against recoverin and HSP70 in 33.8% and 15.6% of individuals, respectively. The presence of autoantibodies in cases of OT may be related to the severity of clinical manifestations, while in cases with CNS involvement they may have a protective role. Unexpectedly, anti-recoverin antibodies were found in patients with cerebral involvement, without ocular toxoplasmosis; therefore, we analyzed and proved cross-reactivity between recoverin and a brain antigen, hippocalcin, so the immunological phenomenon occurring in one immune-privileged organ (e.g. the central nervous system) could affect the environment of another (egg. the eye).


2021 ◽  
Author(s):  
Marina Barrionuevo Mathias ◽  
Fernando Gatti ◽  
Gustavo Bruniera ◽  
Vitor Paes ◽  
Gisele Sampaio Silva ◽  
...  

Context Primary angiitis of the central nervous system (PACNS) is characterized by the inflammation of small and medium CNS arteries; the clinical manifestations include headache, cognitive impairment and focal neurological deficits. The gold standard test for diagnosis is brain biopsy. Neurobrucellosis is an infection associated with cattle farming, which leads to neurological and psychiatric symptoms. We report a case of neurobrucellosis mimicking PACNS. Case report Male, 32 years old, with fever, headache, dizziness and cognitive impairments for 30 days. History of stroke 2 years before, with mild sequelae right hemiparesis; investigation showed suspected intracranial dissection. On physical examination, he had apathy, preserved strength, reduced reflexes with plantar flexor responses. General laboratory tests, autoantibodies and serology were normal. Brain MRI showed deep left nucleocapsular gliosis and cerebral angiography revealed stenosis of the ICA and MCA. CSF showed 42 cells/ mm³, glucose 46 mg/dL, protein 82 mg/dL. Blood PCR was negative for Brucella. Immunophenotyping of the CSF and PET-CT excluded neoplasia. Brain biopsy was inconclusive for vasculitis. Metagenomic analysis of the CSF detected 78% of Brucella genetic material. Serum agglutination test was 1:40 for brucella. Conclusions PACNS is diagnosed by exclusion. The patient filled criteria for possible PACNS, image compatible with vascular stenosis, but inconclusive brain biopsy. Brucellosis is an endemic disease in underdeveloped countries that can present as CNS vasculitis. Metagenomic analysis allows the detection of different pathogens using a single method. The case illustrates the use of metagenomics in rare diseases characterized by vasculitis, with change in clinical outcomes and conduct.


2019 ◽  
Author(s):  
Liza Malong ◽  
Ilaria Napoli ◽  
Ian J White ◽  
Salome Stierli ◽  
Alessandro Bossio ◽  
...  

The specialised blood barriers of the nervous system are important for protecting the neural environment but can hinder therapeutic accessibility1,2. Studies in the central nervous system (CNS) have shown the importance of the cellular components of the neuro-vascular unit for blood-brain barrier (BBB) function. Whilst the endothelial cells (ECs) confer barrier function with specialised tight junctions (TJs) and low levels of transcytosis, pericytes and astrocytes provide complete coverage of the ECs and both deliver essential signals for the development and maintenance of the BBB3–9. In contrast, the blood-nerve barrier (BNB) of the peripheral nervous system (PNS) remains poorly defined10. Here, we show that the vascular unit in the PNS has a distinct cellular composition with only partial coverage of the BNB-forming ECs. Using a mouse model, in which barrier function can be controlled11, we show the BNB, while less tight than the BBB, is maintained by low levels of transcytosis and the TJs of the ECs, with opening of the barrier associated with increased transcytosis. Importantly, we find that while ECs of the PNS have higher transcytosis rates than those of the CNS, the barrier is reinforced by resident macrophages that specifically engulf leaked material. This identifies a distinct role for macrophages as an important component of the BNB acting to protect the PNS environment with implications for improving therapeutic delivery to this tissue.


1995 ◽  
Vol 37 (2) ◽  
pp. 137-143
Author(s):  
C.L.P. Lancellotti ◽  
C.E.P. Corbett ◽  
M.I.S. Duarte

Histopathological and ultrastructural studies of 23 patients who died with clinical diagnosis of measles were carried out. In 12 cases viral nucleocapsids were searched by electron microscopy and detected in 100% of the cases in the lungs and in 50% of the cases in the central nervous system. They were mostly intranuclear. Histopathological changes associated to neurological alterations and the detection of virion are discussed in relation to acute and delayed clinical manifestations.


2013 ◽  
Vol 2013 ◽  
pp. 1-4 ◽  
Author(s):  
Nicolás Coronel-Restrepo ◽  
Fabio Bonilla-Abadía ◽  
Omar A. Cortes ◽  
Jorge H. Izquierdo ◽  
Alberto M. Shinchi ◽  
...  

The primary angiitis of the central nervous system (PACNS) is an entity with a very low incidence and prevalence. It is not clear why the inflammatory process of this entity is limited to the cerebral vasculature without systemic manifestations. Its clinical manifestations are very heterogeneous and make clinical diagnosis difficult. In most cases, a brain biopsy is required. Only the clinical suspicion and the ability to recognize the possible clinical and imagenological patterns of presentation make an accurate diagnosis possible. The vast majority of the treatment recommendations are given by series of case reports. The following paper described the clinical, imagenological, and histopathological characteristics of three Colombian patients with PACNS. The strategic therapeutic used in shown.


2021 ◽  
Vol 17 (2) ◽  
pp. 6-15
Author(s):  
L.A. Dziak ◽  
O.S. Tsurkalenko ◽  
K.V. Chekha ◽  
V.M. Suk

Coronavirus infection is a systemic pathology resulting in impairment of the nervous system. The involvement of the central nervous system in COVID-19 is diverse by clinical manifestations and main mechanisms. The mechanisms of interrelations between SARS-CoV-2 and the nervous system include a direct virus-induced lesion of the central nervous system, inflammatory-mediated impairment, thrombus burden, and impairment caused by hypoxia and homeostasis. Due to the multi-factor mechanisms (viral, immune, hypoxic, hypercoagulation), the SARS-CoV-2 infection can cause a wide range of neurological disorders involving both the central and peripheral nervous system and end organs. Dizziness, headache, altered level of consciousness, acute cerebrovascular diseases, hypogeusia, hyposmia, peripheral neuropathies, sleep disorders, delirium, neuralgia, myalgia are the most common signs. The structural and functional changes in various organs and systems and many neurological symptoms are determined to persist after COVID-19. Regardless of the numerous clinical reports about the neurological and psychiatric symptoms of COVID-19 as before it is difficult to determine if they are associated with the direct or indirect impact of viral infection or they are secondary to hypoxia, sepsis, cytokine reaction, and multiple organ failure. Penetrated the brain, COVID-19 can impact the other organs and systems and the body in general. Given the mechanisms of impairment, the survivors after COVID-19 with the infection penetrated the brain are more susceptible to more serious diseases such as Parkinson’s disease, cognitive decline, multiple sclerosis, and other autoimmune diseases. Given the multi-factor pathogenesis of COVID-19 resulting in long-term persistence of the clinical symptoms due to impaired neuroplasticity and neurogenesis followed by cholinergic deficiency, the usage of Neuroxon® 1000 mg a day with twice-day dosing for 30 days. Also, a long-term follow-up and control over the COVID-19 patients are recommended for the prophylaxis, timely determination, and correction of long-term complications.


2001 ◽  
Vol XXXIII (3-4) ◽  
pp. 71-77
Author(s):  
I. G. Salikhov ◽  
E. I. Bogdanov ◽  
A. T. Zabbarova

Cerebral vasculitis (CV) is a severe, potentially disabling disease that usually develops in the presence of rheumatic, infectious, medicinal, or malignant diseases. In rare cases, isolated (primary) vasculitis of the central nervous system (CNS) is observed [17, 33]. The complex pathogenesis, polymorphism of clinical manifestations, and the absence in most cases of reliable non-invasive diagnostic criteria for CV complicate early diagnosis and treatment. In this regard, it seems relevant to analyze the features of clinical manifestations and diagnostic capabilities in cerebrovascular pathology caused by vasculitis.


Author(s):  
Veronica Murta ◽  
Alejandro Villarreal ◽  
Alberto Javier Ramos

With confirmed COVID-19 cases surpassing the 8.5 million mark around the globe, there is an imperative need to deepen the efforts from the international scientific community to gain comprehensive understanding of SARS-CoV-2. Although the main clinical manifestations are associated with respiratory or intestinal symptoms, reports of specific and non-specific neurological signs and symptoms, both at presentation or during the course of the acute phase, are increasing. Approximately 25-40% of the patients present neurological symptoms. The etiology of these neurological manifestations remains obscure, and probably involves several direct pathways, not excluding the direct entry of the virus to the Central Nervous System (CNS) through the olfactory epithelium, circumventricular organs, or disrupted blood-brain barrier (BBB). Furthermore, neuroinflammation might occur in response to the strong systemic cytokine storm described for COVID-19, or due to dysregulation of the CNS angiotensin system. Descriptions of neurological manifestations in patients in the previous coronavirus (CoV) outbreaks have been numerous for the SARS-CoV and lesser for MERS-CoV. Strong evidence from patients and experimental models suggests that some human variants of CoV have the ability to reach the CNS and that neurons, astrocytes and/or microglia can be target cells for CoV. A growing body of evidence shows that astrocytes and microglia have a major role in neuroinflammation, responding to local CNS inflammation and/or to dysbalanced peripheral inflammation. This is another potential mechanism for SARS-CoV-2 damage to the CNS. In this work we will summarize the known neurological manifestations of SARS-CoV-2, SARS-CoV and MERS-CoV, explore the potential role for astrocytes and microglia in the infection and neuroinflammation, and compare them with the previously described human and animal CoV that showed neurotropism. We also propose possible underlying mechanisms by focusing on our knowledge of glia, neurons, and their dynamic intricate communication with the immune system.


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