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PubMed1993

[Rubella encephalitis].

Morbidity in rubella is generally mild, and neurological complications are rare, varying from 1:6000-1:24,000. We describe an 11-year-old girl with severe manifestations of rubella encephalitis. The onset of encephalitis most often occurs within 1-6 days after development of the typical rash. Neurological features vary and include encephalitis, carotid artery thrombosis, myelitis, optic neuritis, Guillain-Barre syndrome, and peripheral neuritis. Rubella should be considered in the differential diagnosis of encephalitis despite the current vaccination program in Israel. Such cases should be prevented by encouraging widespread early childhood vaccination.

Acyclovir↗

PubMed1993

[A case of herpes simplex encephalitis presenting complete destruction of the medial portions in the bilateral temporal lobes].

A 57-year old man, who had suffered from herpes simplex encephalitis and had been cured without antiviral agents, was admitted to our hospital three years after the encephalitis. He had a complete loss of memory for events subsequent to the encephalitis and a retrograde amnesia for the several years leading up the encephalitis. MRI revealed the abnormalities located in the limbic system, especially the medial portions in the bilateral temporal lobes of the cerebrum were completely destroyed. We consider that this case suggests the specific affinity of herpes simplex virus especially for the medial portions in the temporal lobes of the cerebrum.

Amnesia, Retrograde↗

PubMed1994

[Brain stem encephalitis due to herpes simplex].

Brainstem encephalitis is an unusual infection caused by a variety of agents, among them the herpes simplex (HS) virus. The difficulty of establishing a diagnosis by neurophysiological and radiological examination is greater in this type of encephalitis than in the usual form produced by HS. We describe a fatal case of brainstem encephalitis. Inflammatory and necrotic lesions in the pous and medulla confirmed the clinical diagnosis, while the etiology was determined by immuno-histo-chemical techniques and viral culture of the cerebral parenchyma. Early diagnosis of this form of encephalitis, based on new virological techniques, allows more effective antiviral treatment.

Acyclovir↗

PubMed1993

Herpes simplex encephalitis. Early diagnosis and immune activation in the acute stage and during long-term follow-up.

From a series of in all 93 patients with herpes simplex encephalitis (HSE), verified by biopsy and/or the demonstration of intrathecal synthesis of antibodies to the virus, cerebrospinal fluid (CSF) and serum samples were analysed and compared with samples from 80 patients with non-HSE, i.e. acute encephalitis of non-HSV origin (approximately 50% with other known aetiology, 50% of unknown origin) treated on the suspicion of HSE but in whom no signs of intrathecal HSV antibody synthesis were found, and samples from an additional 42 patients with other verified or suspected diseases of the CNS. To improve the early non-invasive diagnosis of HSE, a HSV IgG capture enzyme linked immunosorbent assay (ELISA) was developed to demonstrate intrathecal synthesis of antibodies to the virus and the results were compared to those of the indirect ELISA. The capture ELISA was found to be advantageous in detecting the early antibody response and yielded more clear-cut results. No correction for damage to the blood-CSF barrier was needed and the method was therefore less labour-intensive than the indirect ELISA. Furthermore, a polymerase chain reaction (PCR) assay, with two "nested" primers pairs selected in the glycoprotein D gene of HSV-1, was developed for the amplification of HSV DNA in CSF. The method was found to be a rapid and non-invasive means of diagnosing HSE in a very early stage of the disease; it was highly sensitive and specific. With a combination of nested PCR assays for HSV-1 and HSV-2 (primers in the glycoprotein G gene) in 10 microliters of CSF, HSV DNA was detected in CSF from 88 out of 93 patients (95%) with HSE. Evidence of HSV-2 aetiology was found in 6 of 93 consecutive cases of HSE in immunocompetent patients by type-specific assays for the demonstration of HSV-2 DNA (primers in the gG gene) and HSV-2 antibodies (to gG2 antigen) in the CSF. Five of the 6 patients with HSV-2 encephalitis exhibited a clinical picture of severe HSE indistinguishable from that of "classical" HSV-1 encephalitis. The combined use of PCR for the detection of HSV DNA in the CSF and the demonstration of intrathecal synthesis of antibodies to the virus will yield a reliable diagnosis and is now the method of choice for the diagnosis of HSE.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗

PubMed1993

[Chronic herpes simplex encephalitis initially presenting with persistent myoclonus].

A 59-year-old female patient with atypical chronic herpes simplex encephalitis was reported. Initial symptom was persistent myoclonus involving the trunk and limb muscles, and later lateral gaze palsy to the left side, cerebellar ataxia, consciousness disturbance and other brainstem symptoms including absence of corneal and gag reflex and vocal cord palsy developed. The patient was successfully treated with high dose of acyclovir. Electroencephalogram was normal in the initial stage but later showed diffuse slow waves. Although CT scan and MRI showed no abnormal finding in the cerebral cortex, brainstem lesion was observed on PD weighted image of MRI. Lumbar puncture yielded a clear cerebrospinal fluid, with slightly elevated protein, increased lymphocytes, and elevated titer of herpes simplex virus type I. The serological data, albumin ratio (10.3), antibody index (12.3) and antibody ratio (7.1) were consistent with herpes simplex encephalitis. Ten days' administration of acyclovir, 1,200 mg a day and repeated three times, was prominently effective for the myoclonus and consciousness disturbance. A diagnosis of chronic herpes simplex encephalitis initially presenting with brainstem encephalitis was made. Judging from the clinical and EEG findings, the brainstem lesion was initially thought to be a cause of myoclonus in this case. However, somatosensory evoked potential (SPE) of both upper and lower extremities revealed enlarged amplitude (giant SEP), and long loop reflex was enhanced (C-reflex) on the left. Giant SEP and C-reflex imply cerebral cortex as the origin of the myoclonus. Brainstem inflammatory lesion might have involved the ascending inhibitory system, thus disinhibiting the cortical sensorimotor area and causing cortical myoclonus.

Chronic Disease↗

PubMed1993

Prevalence of Toxoplasma infection in a cohort of homosexual men at risk of AIDS and toxoplasmic encephalitis.

The purpose of this study was to characterize the epidemiologic, clinical, and laboratory parameters of a cohort of men at risk of AIDS-associated toxoplasmic encephalitis. One hundred seventeen (11%) of the 1,073 participants at the time of enrollment into the Chicago Multicenter AIDS Cohort Study (MACS) were seropositive for Toxoplasma antibodies. Significant differences in prevalence of antibodies between African-American, Hispanic, or white men were not observed (p = 0.49). One hundred one (86%) of the 117 antibody-positive participants had at least one follow-up serology performed and 6 (6%) of the 101 had a significant rise in IgG antibody titer on subsequent visits. Five of six participants with a significant rise in titer were also seropositive for HIV-1 at entry or seroconverted during the study. A trend toward higher IgG Toxoplasma titers and prevalence of IgM antibodies in participants seropositive for HIV-1 was observed, but the differences did not reach statistical significance. There was no evidence that the presence of Toxoplasma infection predisposed to development of CD4+ depletion or AIDS. None of the 183 individuals in the cohort who developed AIDS and who were seronegative for Toxoplasma antibodies developed toxoplasmic encephalitis. In contrast, of the 13 persons who developed AIDS and who were positive for Toxoplasma antibodies, 5 (38%) developed toxoplasmic encephalitis. Prevalence of Toxoplasma antibodies in the MACS population was independent of HIV-1 serostatus. Toxoplasma infection does not appear to predispose to progression of HIV-1 infection. The risk of development of toxoplasmic encephalitis in persons with AIDS and chronic Toxoplasma infection may have been underestimated by previous retrospective studies.

Acquired Immunodeficiency Syndrome↗

PubMed1996

[Virological diagnostics in acute encephalitis. Experience with nucleic acid detection and ratio examination during the period 1991-94].

In every single case of acute encephalitis it is important to confirm the clinical diagnosis by means of virological investigations. Previously, examination by brain biopsy was regarded as the gold standard for detecting the presence of virus or virus antigen in suspected cases of encephalitis caused by herpes simplex virus, but the extraction of the sample material requires experience, and is not without risk. In recent years, detection of herpes simplex DNA using the polymerase chain reaction is recommended as the method of choice during the acute state of the illness, followed by ratio determination, e.g. the relation between IgG antibodies in serum and cerebrospinal fluid during the reconvalescence period. Between 1991 and 1994, the clinical diagnosis of acute encephalitis was confirmed by laboratory investigations in 42 cases in our laboratory. Detection of viral DNA and subsequent ratio determination showed the encephalitis to have been caused by herpes simplex virus in 21 cases, and by varicella zoster virus in eight cases. Nucleic acid was detected in 21 cases, and 16 patients showed pathological ratio values. These results show that the polymerase chain reaction is a valuable diagnostic tool during the first two weeks of the illness, whereas ratio determination is a better way of investigating samples taken after this period.

Adult↗

PubMed1996

[Periodical EEG pattern modifications in herpetic encephalitis treated with acyclovir].

The presence of PLED or localized or lateralized periodic activity in encephalitis strongly suggests that the encephalitis is due to the herpes simplex virus. Nevertheless, there has been controversy over its clinical significance. In addition, since the introduction of antiviral drugs in the treatment of herpes encephalitis in its initial stages, the prognosis of the disease has improved. We studied nine patients all diagnosed as having herpes encephalitis and treated with acyclovir. The presence or absence of periodic activity and its characteristics were analyzed. It was seen that either there was no such activity, or if there was, it was not exactly as classically described.

Acyclovir↗

PubMed1995

Antigenic similarity of central European encephalitis and louping-ill viruses.

Twenty isolates of Central European encephalitis (CEE) virus were compared with 20 isolates of louping-ill (LI) virus in indirect immunofluorescence test (IIFT), using a panel of 17 monoclonal antibodies (MoAbs) prepared against the prototype LI virus. Three Asian members of the tick-borne encephalitis (TBE) complex were also included in the comparison: Turkish sheep encephalitis (TSE), Russian spring-summer encephalitis (RSSE) and Langat (LGT) viruses. Antigenic relationships of the viruses were evaluated by Dice similarity coefficient and cluster analysis. The results revealed antigenic heterogeneity of LI isolates, antigenic homogeneity of CEE isolates, and indicated that CEE and LI are related varieties of Eurasian TBE flavivirus that also includes TSE and RSSE strains.

Animals↗

PubMedDate not supplied

A mouse model of herpes simplex virus encephalitis: diagnostic brain imaging by magnetic resonance imaging.

Herpes simplex virus encephalitis is a severe sporadic encephalitis in man with high mortality and morbidity. A critical step in the establishment of therapy is early diagnosis. Magnetic resonance imaging is a noninvasive, accurate diagnostic test for the detection of central nervous system disease. In an effort to monitor morphological changes in vivo we present a new diagnostic neuroimaging model of experimental herpes simplex virus encephalitis. A mouse model of herpes simplex virus encephalitis was used. 40 SJL mice were intranasally inoculated with an infectious dose of wild-type strain HSV-I F. Morphological abnormalities were studied by cranial magnetic resonance imaging (MRI). These findings were correlated with sequential neuropathological studies. 95% of animals developed cerebral abnormalities on MRI. resembling human HSVE. Areas of increased signal intensity on T2-weighted sequences and focal pathological contrast enhancement were mostly found in the frontal and temporal lobes and thalamic and cerebellar regions. All animals with MRI abnormalities had neuropathological signs of neuronal degeneration and reactive astrocytosis in corresponding regions. The described monitoring system offers a new approach for studies on neurovirulence and therapeutic strategies.

Animals↗

PubMed1996

[Encephalitis due to measles].

OBJECTIVE: We present seven cases of acute encephalitis following measles, which were diagnosed during the epidemic that occurred in Spain in 1986. PATIENTS AND METHODS: We studied seven patients diagnosed of encephalitis due to measles. The diagnosis of measles was a made by the presence of a characteristic morbiliform rash and the detection of specific IgM antibodies. The diagnosis of encephalitis was based on the symptoms and the routine examinations of blood, CSF, EEG, CT, ophthalmic exploration and the study of the audiovisual evoked potentials. RESULTS: The patients were between 5 and 9 years of age. None of them had been previously vaccinated for measles. The symptoms of encephalitis occurred 1 to 12 days after the appearance of the rash and the most frequent symptoms were drowsiness and vomiting. All of the patients had EEG abnormalities that returned to normal 1 to 18 months after the diagnosis. One patient presented CT abnormalities. CSF examination revealed an increase of the cell count in one case. The ophthalmic exploration was normal except in one of the patients which had optic neuritis. There were no abnormalities in the audiovisual evoked potentials. All of the cases showed good evolution. Five years later, all of the patients have had a normal development. CONCLUSIONS: The correct vaccination of measles can eradicate this disease.

Child↗

PubMed1997

[Proinflammatory cytokine levels in cerebrospinal fluid from children with acute encephalitis].

We investigated interleukin-1 beta (IL-1 beta), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha), and soluble TNF receptor 1 (sTNF-R 1) during the acute stage in the cerebrospinal fluid (CSF) from children with acute encephalitis by means of a sandwich enzyme immunoassay. We divided the 24 children with acute encephalitis into two groups: those who survived without neurological sequelae (Group 1, n = 15), and those who died or were left with sequelae (Group 2, n = 9). The IL-1 beta, IL-6, TNF-alpha and sTNF-R 1 levels in CSF in the two groups were significantly higher than those in control subjects (n = 23). The CSF sTNF-R 1 levels in Group 2 were significantly higher than those in Group 1. Our findings suggest that the IL-1 beta, IL-6 and TNF-alpha in CSF are related to the pathogenesis of acute encephalitis, and that the CSF level of sTNF-R1 during the acute stage of encephalitis is an important index for predicting the neurological outcome.

Acute Disease↗

PubMed1997

[A case of chronic encephalitis due to double infection with herpes simplex and measles viruses].

In a healthy 49-year-old man, a decrease in job efficiency was noticed along with bizarre behavior. On admission, he was euphoric, childish, superficial and had increased libido. Neurological findings were normal. There were no abnormal findings on routine blood tests, hematochemistry or urine analysis. MRI showed no abnormal findings. However, single photon emission CT (SPECT) showed diffuse hypoaccummulation of tracer from the temporal to frontal regions. Lumbar puncture showed clear cerebrospinal fluid (CSF) with pleocytosis and an elevated protein level. Moreover, antibody IgG titers to herpes simplex virus (HSV) and measles virus were elevated, according to EIA [serum HSV -1,202.2x, measles virus 47.1x: CSF HSV-116.1x, measles virus 9.9x]. The ratio of serum to CSF antibody titers of HSV and measles virus were 12.5 and 4.75, respectively. The antibody index values of HSV and measles virus IgG titers were 8.42 and 22.22. The ratio of albumin was 105.7. Chronic, progressive HSV encephalitis is rare, and there have been very few reports of encephalitis due to double infection by HSV and another virus. Our patient was diagnosed as having encephalitis due to double infection with HSV and measles virus, because the ratio of serum to CSF antibody titers was less than 20 and the antibody index values were over 1.91. Moreover, since the IgG index was elevated and the ratio of albumin was not low, it was suggested that the blood-brain-barrier had not been disrupted, and antibodies were being produced chronically in the medullary cavity. Hyperaccummulation of tracer on SPECT studies has been reported in the early stages of HSV encephalitis. In our case, while CT and MRI showed no abnormal findings, SPECT showed diffuse hypoaccummulation. SPECT appears to be a useful tool in the diagnosis of this disorder. In case of chronic, progressive personality change in middle-aged adults, we must be aware of double virus infection of the brain as a possible causal factor.

Antibodies, Viral↗

PubMed1997

[Re-emergence of Venezuelan equine encephalitis virus in French Guiana. Apropos of 1 confirmed case].

Venezuelan equine encephalitis (VEE) is a mosquito-borne viral disease that occurs in equine species and in man. The strains can be grouped epidemiologically into two major categories: enzootic and epizootic. Enzootic strains cause sporadic human disease and are not associated with disease among equines. These strains are found throughout Florida. Central America, northern South America and Brazil. Epizootic strains are associated with enormous morbidity and mortality in equine species. In man, VEE virus infections are largely asymptomatic and in children and young adults there is an increased risk of encephalitis and dead. We report the first case in French Guiana of Venezuelan equine encephalitis. Clinical examination and biological studies showed encephalitis, interstitial pneumonia and acute liver failure. Despite an adequate symptomatic treatment, the young patient died five days after her admission in multiple organ dysfunction syndrome. Diagnosis is establishing by virologic test: VEE virus is isolated from the blood. These example of re-emerging infectious disease vividly illustrate that we remains vulnerable and emphasizes the need for an active surveillance system.

Blood↗

PubMed1997

[The difficulties of clinical diagnosis of mixed-infection of tick-born encephalitis and Lyme disease].

The authors report 49 cases of mixed infection (Lyme disease + tick-born encephalitis). All the patients were citizens of the Russian North-West. Clinically, there were symptoms of Lyme disease (erythema) and tick-born encephalitis (serous meningitis, neuritides of the cranial and peripheral nerves). In patients with mixed infection in the presence of erythema symptoms of tick-born encephalitis were less evident. The diagnosis of Lyme disease erythema-free form in combination with tick-born encephalitis may be made only by dynamic serological tests for both of these infections.

Aged↗

PubMed1998

Chemokines and receptors in HIV encephalitis.

BACKGROUND: Chemokines are involved in the migration of leukocytes and have been implicated in several inflammatory diseases of the central nervous system. Some of their receptors have been proposed to mediate HIV infection. OBJECTIVE: To determine changes in chemokine and receptor expression in HIV encephalitis, and to determine whether upregulation leads to recruitment of infected monocytes across the blood-brain barrier and participates in HIV neuropathology. METHODS: Immunocytochemistry and double-label immunofluorescent laser confocal microscopy was performed with antibodies to chemokines and their receptors on brain tissues from patients who died with or without HIV encephalitis. In vivo distribution was compared with in vitro cultures of human neuroglial cells. RESULTS: The beta-chemokines monocyte chemotactic protein-1, macrophage inflammatory protein-1alpha, and RANTES were detected on brain macrophages. Their presence was associated with the histopathological signs of HIV encephalitis. The alpha-chemokines IP-10 (10 kDa inflammatory protein) and interleukin-8 were expressed by astrocytes in all tissues, including controls. Presence of the CXC-chemokine receptor (CXCR)-4 was seen on brain macrophages/microglia, neurons, and astrocytes. CC-Chemokine receptor (CCR)-5 was detected only on macrophages/microglia. CCR-3 and CCR-1 were expressed by macrophages and endothelial cells. In vitro studies examining the presence of CCR-3, CCR-5, and CXCR-4 on human brain cell cultures demonstrated abundant neuronal and microglial expression. CONCLUSIONS: Expression of a variety of chemokines and receptors was shown to be increased in HIV encephalitis brain tissues particularly in areas of neuroglial reaction. The expression pattern supported their involvement in the recruitment of inflammatory infiltrates and formation of microglial nodules. Presence of chemokine receptors on neurons may be involved in the pathogenesis of neurologic damage in AIDS patients.

AIDS Dementia Complex↗

PubMed1998

[Clinical importance of the quantification of HIV-1 RNA in cerebrospinal fluid for the diagnosis of HIV encephalitis].

We evaluated prospectively the HIV-1 RNA level in CSF as a marker of HIV encephalitis diagnosis. 110 HIV-1 infected patients (mean age: 39 years; sex-ratio M/F: 94/16) were tested for HIV-1 RNA in plasma and CSF. Lumbar punctures were performed to explore cognitive deficit, seizure or fever. HIV encephalitis was diagnosed in 15 patients (14%), other CNS disease in 34 (31%), and fever without CNS disease in 61 (55%). HIV-1 RNA was detectable in 93% of the plasma and in 62% of the CSF. No significant difference was observed in CSF HIV-1 RNA between patients with or without HIV encephalitis. CSF HIV-1 RNA was correlated with plasma HIV-1 RNA (p < 0.01), CSF protein (p < 0.01) and CSF white cell counts (p < 0.01). The absence of any significant difference between patients with or without HIV encephalitis, suggests that the CSF HIV-1 RNA level is not a good marker for its diagnosis.

AIDS Dementia Complex↗

PubMed2025

Proteome Profiling in Cerebrospinal Fluid Reveals Increased Levels of Peroxiredoxin 2 Discriminating Japanese Encephalitis Virus and Scrub Typhus Infection.

Japanese encephalitis virus (JEV) and scrub typhus (ST) are major etiological agents of acute encephalitis syndrome (AES) in India and South Asia. The pathophysiological changes at the molecular level caused by JEV and ST have yet to be studied in detail. The cerebrospinal fluid (CSF) proteomic landscape is a critical indicator of CNS pathology. Here, we conducted label-free quantitative proteomics on CSF from AES patients (n = 15) to identify etiology-specific differentially expressed proteins (DEPs) linked to encephalitis. The key DEPs were validated via ELISA in CSF (n = 49) and serum (n = 33). Our findings revealed 50 proteins exhibited differential expression across JEV and ST groups, with a notable subset of three proteins, PRDX2, KLK6, and TTR. PRDX2 and KLK6 were markedly elevated in JEV CSF (AUC: 0.8933 and 0.9689) but not in ST or non-JEV AES, while TTR was reduced in JEV yet elevated in ST (AUC: 0.5619 vs. 0.8238). Further, PRDX2 upregulation was validated in JEV-infected mouse brains and cortical neurons. Overexpression of PRDX2 in human neuroblastoma cells correlated with enhanced antiviral gene expression, p-STAT1, p-AKT (ser473), and viral replication. Thus, our comprehensive proteomic analysis of CSF identifies PRDX2 as an important circulatory protein, differentially expressed between JEV and ST, with high specificity and enhancing viral propagation, underscoring its role in viral propagation and pathogenesis.

Humans↗