scholarly journals Japanese encephalitis

2016 ◽  
Vol 8 (2) ◽  
Author(s):  
Novie H. Rampengan
Keyword(s):  
Japanese Encephalitis ◽  
Virus Isolation ◽  
Clinical Manifestations ◽  
Elisa Test ◽  
Culex Mosquito ◽  
Capture Elisa ◽  
Infective Disease ◽  
Pig Farm ◽  
The Central Nervous System ◽  
Intra Cranial Pressure

Abstract: Japanese encephalitis (JE) is an acute infective disease in the central nervous system. Pigs and birds are the main reservoirs of JE viruses, albeit, there is no transmission from human to human with mosquito bites. Clinical manifestations of JE in human vary from mild symptoms like rhinitis until severe symptoms, and even death. Incubation period of JE varies from 4 until 14 days. Development of JE symptoms are divided into 4 stadiums, as follows: prodormal, acute, sub-acute, and convalescent. Diagnosis is based on anamnesis about fever and the presence of pig farm around the house, and physical examination consisted of increased intra-cranial pressure and decreased consciousness, meanwhile, the definite diagnosis is confirmed with virus isolation either IgM capture ELISA test from serum or cerebrospinal fluid; both have sensitivity almost 100%. Treatment of JE is only symptomatic and supportive. Prevention and erradication of JE virus are aimed to human, mosquito Culex as vector and its larvae, and pig as the reservoir. Japanese encephalitis can be prevented with immunization. In severe cases, sequelae are found around 40%-75%.Keywords: Japanese encephalitis, culex mosquito, pig farm, vaccinationAbstrak: Japanese encephalitis (JE) merupakan penyakit infeksi akut pada SSP. Babi dan unggas merupakan reservoir virus ini, namun tidak terjadi penularan dari manusia ke manusia lain melalui gigitan nyamuk. Manifestasi klinis penyakit JE pada manusia bervariasi, mulai dari gejala ringan seperti demam flu biasa sampai berat bahkan kematian. Masa inkubasi JE bervariasi antara 4 sampai 14 hari. Perkembangan gejala JE terbagi atas 4 stadium yaitu stadium prodormal, akut, sub-akut, dan konvalesen. Diagnosis pasti dengan anamnesis adanya perternakan babi disekitar rumah dan demam, pemeriksaan fisik terdapat peningkatan tekanan intra kranial serta penurunan kesadaran, dan diagnosis pasti dengan isolasi virus maupun pemeriksaan IgM capture ELISA dari serum atau CSS dengan sensitivitas hampir 100%. Terapi JE hanya bersifat simtomatis dan suportif. Pencegahan dan pemberantasan JE virus ditujukan pada manusia, vektor nyamuk Culex beserta larvanya, dan reservoir babi. Penyakit JE dapat dicegah dengan imunisasi. Pada kasus berat, ditemukan gejala sisa sekitar 40%-75%.Kata kunci: Japanese encephalitis, nyamuk Culex, peternakan babi, imunisasi

scholarly journals Clinical profiles and some associated factors of Japanese encephalitis in Bali

2016 ◽  
Vol 46 (1) ◽  
pp. 13
Author(s):  
I Komang Kari ◽  
Wei Liu ◽  
I Made Kompiang Gautama ◽  
I Ketut Subrata ◽  
Zhi Yi Xu
Keyword(s):  
Aseptic Meningitis ◽  
Japanese Encephalitis ◽  
Associated Factors ◽  
Viral Encephalitis ◽  
Clinical Manifestations ◽  
Cross Sectional Study ◽  
Cross Sectional ◽  
Army Hospital ◽  
The Central Nervous System ◽  
Clinical Profiles

Background Japanese Encephalitis (JE) is a mosquito-borne vi-ral disease that can affect the central nervous system and causeseveral complications and death. In Indonesia, particularly in Bali,studies of JE in humans are still very limited.Objective To assess the clinical manifestations and outcome ofJE in Bali and to identify some possible associated factors andmonthly distribution of admission to the hospitals.Methods A cross-sectional study was conducted in 8 district hospi-tals, army hospital, and Sanglah central hospital, as surveillance cen-ters in Bali, from July 2001 through January 2003. Subjects less than12 years of age and residences of Bali province who were suspectedof having acute viral encephalitis, aseptic meningitis, and acute flac-cid paralysis referred from all health facilities were included in thisstudy. The diagnosis of JE was established by detection of virus-spe-cific IgM in CSF and serum, with IgM capture enzyme-linkedimmunosorbent assay (MAC ELISA)Results During the study, 158 subjects with encephalitis were in-cluded; 55 (34.8%) were caused by JE and 103 (65.2%) were causedby non-JE. It showed that pig owning and rice farming were signifi-cantly associated with JE (PR= 3.02, 95% CI 1.29; 7.10; P= 0.009and PR= 2.86, 95% CI 1.30; 6,31, P= 0.008, respectively). Mostsubjects (46.2%) were under 2 years old with mean age of 37.24(SD 32.24) months. Forty-two (26.6%) subjects had nuchal rigidity,and all of them had aseptic meningitis. Denpasar had the highestprevalence of non-JE cases. Bangli and Klungkung had the lowestprevalence of JE and non-JE. The highest prevalence of JE was inGianyar. Peak prevalences of JE were in April and May 2002. Peakprevalences of non-JE were during August-October 2001 and inMarch-April 2002. Four (7.3%) subjects of JE group and 25 (24.3%)subjects of non-JE died. There were 25 (45.5%) out of 55 subjectswho survived with disability. Twenty-four (43.6%) JE subjects and34 (33.0%) non-JE subjects had good outcome.Conclusions Around one third of the subjects were positively di-agnosed as JE. The highest prevalence of JE was found in Gianyar.Peak prevalences of JE are in April and May 2002. Pig owning andrice farming are associated factors. Almost half of JE subjects sur-vived with disability

Postoperative cognitive dysfunction: progress mechanisms and clinical characteristics

2019 ◽  
Vol 2 (19) ◽  
pp. 29-33
Author(s):  
K. B. Manysheva ◽  
M. A. Akhmedov ◽  
A. A. Rakhmanova ◽  
S. M. Khutalieva
Keyword(s):  
Cognitive Dysfunction ◽  
Clinical Characteristics ◽  
Cognitive Deficit ◽  
Neuropsychological Testing ◽  
Postoperative Cognitive Dysfunction ◽  
Clinical Manifestations ◽  
Postoperative Recovery ◽  
Neuropsychological Rehabilitation ◽  
Brain Barrier Permeability ◽  
The Central Nervous System

The article is devoted to the study of postoperative cognitive dysfunction — a syndrome that is often found in the postoperative period and does not depend on the volume of surgeon. Based on the analysis of the results of modern studies, the authors cite the most likely etiological causes of the syndrome, grouped according to different categories of risk factors. The pathogenetic algorithm for cognitive dysfunction includes the appearance of systemic inflammation, improving blood-brain barrier permeability with the endothelial dysfunction, the migration of inflammatory agents into the central nervous system, and the formation of oxidative stress. The clinical manifestations of cognitive deficit in the outcome of surgeon performed under general anesthesia, the authors illustrate with their own observations of patients with a neurosurgical profile with spinal pathology operated on with the use of propofol anesthesia, comparing the results of neuropsychological testing with an assessment of the level of anxiety. In conclusion, the authors outline a strategy for the prevention of postoperative cognitive dysfunction and recommend conducting neuropsychological rehabilitation as an important component of postoperative recovery for all patients with a diagnosed cognitive deficit that occurred after surgery.

scholarly journals Mild Clinical Presentation of Joubert Syndrome in a Male Adult Carrying Biallelic MKS1 Truncating Variants

Diagnostics ◽  
2021 ◽  
Vol 11 (7) ◽  
pp. 1218
Author(s):  
Raffaella Brunetti-Pierri ◽  
Marianthi Karali ◽  
Francesco Testa ◽  
Gerarda Cappuccio ◽  
Maria Elena Onore ◽  
...  
Keyword(s):  
Wide Spectrum ◽  
Clinical Manifestations ◽  
Brain Magnetic Resonance Imaging ◽  
Joubert Syndrome ◽  
Male Adult ◽  
Full Field ◽  
Pathogenic Variants ◽  
Disease Spectrum ◽  
Male Individual ◽  
The Central Nervous System

Pathogenic variants in the MKS1 gene are responsible for a ciliopathy with a wide spectrum of clinical manifestations ranging from Meckel and Joubert syndrome (JBTS) to Bardet-Biedl syndrome, and involving the central nervous system, liver, kidney, skeleton, and retina. We report a 39-year-old male individual presenting with isolated Retinitis Pigmentosa (RP), as assessed by full ophthalmological evaluation including Best-Corrected Visual Acuity measurements, fundus examination, Goldmann Visual Field test, and full-field Electroretinography. A clinical exome identified biallelic nonsense variants in MKS1 that prompted post-genotyping investigations for systemic abnormalities of ciliopathy. Brain magnetic resonance imaging revealed malformations of the posterior cranial fossa with the ‘molar tooth sign’ and cerebellar folia dysplasia, which are both distinctive features of JBTS. No other organ or skeletal abnormalities were detected. This case illustrates the power of clinical exome for the identification of the mildest forms of a disease spectrum, such as a mild JBTS with RP in the presented case of an individual carrying biallelic truncating variants in MKS1.

Tropheryma whipplei, Immunosuppression and Whipple's Disease: From a Low-Pathogenic, Environmental Infectious Organism to a Rare, Multifaceted Inflammatory Complex

2015 ◽  
Vol 33 (2) ◽  
pp. 190-199 ◽  
Author(s):  
Thomas Marth
Keyword(s):  
Heart Valves ◽  
Clinical Manifestations ◽  
Systemic Infection ◽  
Tropheryma Whipplei ◽  
Molecular Techniques ◽  
Whipple’S Disease ◽  
Whipple's Disease ◽  
New Findings ◽  
The Central Nervous System ◽  
Body Compartments

Background: The actinobacterium Tropheryma whipplei was detected 20 years ago by molecular techniques, and following its culture has been characterized as the cause of a systemic infection known as Whipple's disease (WD). T. whipplei occurs in the environment, is prevalent only in humans, is believed to be transmitted via oral routes and to be host dependent. Key Messages: The classical form of T. whipplei infection, i.e. classical WD (CWD), is rare. It is well defined as slowly progressing chronic infection with arthralgia, diarrhea and weight loss, mostly in middle-aged men. However, current research revealed a much broader spectrum of clinical features associated with T. whipplei infection. Thus, T. whipplei may cause acute and transient infections (observed primarily in children) and the bacterium, which is found in soil and water, occurs in asymptomatic carriers as well as in CWD patients in clinical remission. In addition, T. whipplei affects isolated and localized body compartments such as heart valves or the central nervous system. Subtle immune defects and HLA associations have been described. New findings indicate that the progression of asymptomatic T. whipplei infection to clinical WD may be associated with medical immunosuppression and with immunomodulatory conditions. This explains that there is a discrepancy between the widespread occurrence of T. whipplei and the rareness of WD, and that T. whipplei infection triggered by immunosuppression presents with protean clinical manifestations. Conclusions: This review highlights recent findings and the clinical spectrum of infection with T. whipplei and WD, focusing specifically on the role of host immunity and immunosuppression. Current concepts of the pathogenesis, diagnosis and therapy are discussed.

Carbon monoxide: mechanism of toxic action, pathogenesis and clinical manifestations of acute intoxication

2021 ◽  
pp. 4-9
Author(s):  
A. N. Grebenyuk ◽  
V. N. Bykov
Keyword(s):  
Carbon Monoxide ◽  
Clinical Manifestations ◽  
Acute Poisoning ◽  
Toxic Action ◽  
Acute Intoxication ◽  
Emergency Situations ◽  
Common Causes ◽  
The Central Nervous System ◽  
Regulatory Effects ◽  
Mitochondrial Cytochrome Oxidase

Introduction. Carbon monoxide (CO) remains one of the most common causes of acute poisoning and death, both in everyday life and in emergency situations, especially in fires.Material and methods. The paper summarizes information about the regulatory effects, mechanisms of toxic action, pathogenesis and clinical picture of intoxication, as well as predictors of the severity of CO poisoning.Results. The main mechanism of the toxic effect of CO is due to its ability to bind to the protohemal iron of hemoglobin (Hb) to form carboxyhemoglobin (HbCO). The toxicity of CO may also be enhanced by impaired functions of the myoglobin of the myocardium and skeletal muscles, mitochondrial cytochrome oxidase, and iron-containing enzymes of the antioxidant system. The leading link in the pathogenesis of acute CO intoxication is a violation of the oxygen transport function of hemoglobin and the associated development of hemic and tissue hypoxia. CO-induced cell and tissue damage due to the induction of mitochondrial dysfunction, oxidative stress, free radical hyperproduction, lipid peroxidation, inflammation, and apoptosis also play a role in the pathogenesis of intoxication.Conclusion. The mechanism of toxic action of CO, associated primarily with the formation of carboxyhemoglobin and the development of hypoxia, determines the clinical manifestations of acute intoxication, which depend on the concentration of CO and the duration of exposure, but are almost always associated with the central nervous system and cardiovascular system.

scholarly journals Precise Localization and Dynamic Distribution of Japanese Encephalitis Virus in the Brain Nuclei of Infected Mice

2020 ◽  
Author(s):  
Wei Han ◽  
Mingxing Gao ◽  
Changqing Xie ◽  
Jinhua Zhang ◽  
zikai Zhao ◽  
...  
Keyword(s):  
Nervous System ◽  
Japanese Encephalitis Virus ◽  
Japanese Encephalitis ◽  
Post Infection ◽  
Viral Antigen ◽  
Thalamic Nucleus ◽  
Encephalitis Virus ◽  
3D Images ◽  
The Central Nervous System ◽  
The Brain

AbstractJapanese encephalitis virus (JEV) is a pathogen that causes severe vector-borne zoonotic diseases, thereby posing a serious threat to human health. Although JEV is potentially neurotropic, its pathogenesis and distribution in the host have not been fully elucidated. In this study, an infected mouse model was established using a highly virulent P3 strain of JEV. Immunohistochemistry and in situ hybridization, combined with anatomical imaging of the mouse brain, were used to dynamically localize the virus and construct three-dimensional (3D) images. Consequently, onset of mild clinical symptoms occurred in some mice at 84h post JEV infection, while most mice displayed typical neurological symptoms at 144h post infection. Moreover, brain pathology revealed typical changes associated with non-suppurative encephalitis, which lasted up to 192h. The earliest detection of viral antigen was achieved at 72h post infection, in the thalamus and medulla oblongata. At 144h post infection, the positive viral antigen signals were mainly distributed in the cerebral cortex, olfactory area, basal ganglia, thalamus, and brainstem regions in mice. At 192h post infection, the antigen signals gradually decreased, and the localization of JEV tended to concentrate in the cerebrum and thalamus, while no viral antigen was detected in the brain at 504h post infection. In this model, the viral antigen was first expressed in the reticular thalamic nucleus (Rt), at a consistent concentration. The expression of the viral antigen in the hippocampal CA2 region, the anterior olfactory nucleus, and the deep mesencephalic nucleus was high and persistent. The 3D images showed that viral signals were mostly concentrated in the parietal cortex, occipital lobe, and hippocampus, near the mid-sagittal plane. In the early stages of infection in mice, a large number of viral antigens were detected in denatured and necrotic neurons, suggesting that JEV directly causes neuronal damage. From the time of its entry, JEV is widely distributed in the central nervous system thereby causing extensive damage.Author summaryThere are many theories regarding the mechanism of entry of the Japanese encephalitis virus (JEV) into the nervous system. The inflammation cascade effect, resulting from the virus entering the central nervous system (CNS), is a major cause of brain injury in JEV patients. In this study, we found that the earliest point at which viral antigen was detected in the brain tissues following peripheral infection of JEV was at 72h. The virus was located in the nerve nuclei of the thalamus and medulla oblongata and, subsequently, viral antigens were found in the anterior olfactory nucleus. At 96h post infection, the virus was extensively distributed in the brain tissue, and at 144h-192h the viral antigen was widely distributed and highly concentrated. The viral concentration detected in the ventromedial thalamic nucleus (VM), deep mesencephalic nucleus (DpMe), and motor trigeminal nucleus (Mo5) remained high throughout the experiment. The hypertrophic nerve nuclei of JEV include the early anterior olfactory (AO) nucleus and the late hippocampal CA2 region. In the early stages of viral infection (72-144h post infection), the changes in viral antigen concentration and mortality rate were consistent. It was hypothesized that this stage represents the activation of viral proliferation and brain inflammation.

scholarly journals Postoperative agitation syndrome in young children with perinatal damage to the central nervous system

2021 ◽  
Vol 16 (5) ◽  
pp. 355-360
Author(s):  
V.I. Snisar ◽  
O.S. Pavlysh
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Young Children ◽  
Postoperative Period ◽  
Anesthetic Management ◽  
Clinical Manifestations ◽  
Postoperative Recovery ◽  
Inhalation Anesthesia ◽  
Ventriculoperitoneal Shunting ◽  
The Central Nervous System

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.

scholarly journals Autoantibodies Against Ubiquitous and Confined Antigens in Patients With Ocular, Neuro-Ophthalmic and Congenital Cerebral Toxoplasmosis

2021 ◽  
Vol 12 ◽  
Author(s):  
Monica Goldberg-Murow ◽  
Carlos Cedillo-Peláez ◽  
Luz Elena Concha-del-Río ◽  
Rashel Cheja-Kalb ◽  
María José Salgar-Henao ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Molecular Mimicry ◽  
Clinical Manifestations ◽  
Protective Role ◽  
Cross Reactivity ◽  
Ocular Toxoplasmosis ◽  
Cerebral Toxoplasmosis ◽  
Blood Retinal Barrier ◽  
The Central Nervous System

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).

scholarly journals Neurobrucellosis mimicking primary vasculitis of the central nervous system: we should perform a metagenomic analysis of the cerebrospinal fluid prior to brain biopsy

2021 ◽  
Author(s):  
Marina Barrionuevo Mathias ◽  
Fernando Gatti ◽  
Gustavo Bruniera ◽  
Vitor Paes ◽  
Gisele Sampaio Silva ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Psychiatric Symptoms ◽  
Brain Mri ◽  
Genetic Material ◽  
Clinical Manifestations ◽  
Brain Biopsy ◽  
Metagenomic Analysis ◽  
Normal Brain ◽  
The Central Nervous System

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.

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