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PubMed1998

Herpes simplex encephalitis and bilateral acute retinal necrosis syndrome after craniotomy.

PURPOSE: Acute retinal necrosis (ARN) syndrome is associated with members of the herpes virus family, but the mechanisms of infection remain unclear. The purpose of this study is to report a unique case of acute retinal necrosis syndrome associated with herpetic encephalitis in order to elucidate possible factors involved in herpetic central nervous system disease. METHOD: Case report. RESULTS: A 64-year-old woman who developed acute herpes simplex virus encephalitis associated with bilateral acute retinal necrosis syndrome after craniotomy for resection of a suprasellar craniopharyngioma is presented. The results of lumbar puncture, magnetic resonance imaging, and ophthalmologic examination are consistent with herpetic infection. The origin of acute retinal necrosis syndrome and the association of acute retinal necrosis syndrome with encephalitis are reviewed. CONCLUSIONS: After craniotomy, we hypothesize reactivation of previously latent herpes simplex virus in the area of the inferior frontal lobe and optic chiasm. Reactivated virus may have migrated to the retina by axonal transport, through the optic nerves, to produce the acute retinal necrosis syndrome.

Acyclovir↗
PubMed2005

Early events in the pathogenesis of eastern equine encephalitis virus in mice.

To elucidate the pathogenesis of eastern equine encephalitis (EEE) virus infections, we used histopathology, immunohistochemistry, and in situ hybridization to track the spread and early cellular targets of viral infection in mice. Young mice were inoculated with virulent EEE virus in their right rear footpad and were followed in a time-course study for 4 days. Virulent EEE virus produced a biphasic illness characterized by an early self-limiting replication phase in peripheral tissues followed by an invariably fatal central nervous system (CNS) phase. In the early extraneural phase, there was primary amplifying replication of virus within fibroblasts at the inoculation site and within osteoblasts in active growth areas of bone that resulted in a transient high-titer viremia. Pathological changes and viral infection were observed as early as 12 hours post-infection (PI) in osteoblasts, skeletal muscle myocytes, and in fibroblasts along fascial sheaths. The severity and extent of infection in peripheral tissues peaked at day 1 PI. In the neural phase of infection, virus was first detected in the brain on day 1 PI, with rapid interneuronal spread of infection leading to death by day 4 PI. EEE virus appeared to be directly cytopathic for neurons. The very rapid onset and apparently random and widely dispersed infection in the CNS, with concurrent sparing of olfactory neuroepithelium, strongly suggests that invasion of the CNS by EEE occurs by a vascular route, rather than via peripheral nerves or the olfactory neuroepithelium. Our finding that metaphyseal osteoblasts are an early site of amplifying viral replication may explain the higher-titer viremias and higher incidence of neuroinvasion and fulminant encephalitis seen in the young, and may also explain why mature animals become refractory to encephalitis after peripheral inoculation with EEE virus.

Animals↗
PubMed2002

Macrophages relate presynaptic and postsynaptic damage in simian immunodeficiency virus encephalitis.

Neurodegeneration observed in lentiviral-associated encephalitis has been linked to viral-infected and -activated central nervous system macrophages. We hypothesized that lentivirus, macrophages, or both lentivirus and macrophages within distinct microenvironments mediate synaptic damage. Using the simian immunodeficiency virus (SIV)-infected macaque model, we assessed the relationship between virus, macrophages, and neurological damage in multiple brain regions using laser confocal microscopy. In SIV-infected macaques with SIV encephalitis (SIVE), brain tissue concentrations of SIV RNA were 5 orders of magnitude greater than that observed in nonencephalitic animals. In SIVE, staining for postsynaptic protein microtubule-associated protein-2 was significantly decreased in the caudate, hippocampus, and frontal cortical gray matter compared to nonencephalitic controls, whereas staining for presynaptic protein synaptophysin was decreased in SIV-infected macaques with and without encephalitis. These data suggest that presynaptic damage occurs independent of pathological changes associated with SIVE, whereas postsynaptic damage is more tightly linked to regional presence of both activated and infected macrophages.

Animals↗
PubMed1999

Blood-brain barrier tight junction disruption in human immunodeficiency virus-1 encephalitis.

The blood-brain barrier (BBB) plays a critical role in regulating cell trafficking through the central nervous system (CNS) due to several unique anatomical features, including the presence of interendothelial tight junctions that form impermeable seals between the cells. Previous studies have demonstrated BBB perturbations during human immunodeficiency virus encephalitis (HIVE); however, the basis of these permeability changes and its relationship to infiltration of human immunodeficiency virus type 1 (HIV-1)-infected monocytes, a critical event in the pathogenesis of the disease, remains unclear. In this study, we examined CNS tissue from HIV-1-seronegative patients and HIV-1-infected patients, both with and without encephalitis, for alterations in BBB integrity via immunohistochemical analysis of the tight junction membrane proteins, occludin and zonula occludens-1 (ZO-1). Significant tight junction disruption (P < 0.001), as demonstrated by fragmentation or absence of immunoreactivity for occludin and ZO-1, was observed within vessels from subcortical white matter, basal ganglia, and, to a lesser extent, cortical gray matter in patients who died with HIVE. These alterations were also associated with accumulation of activated, HIV-1-infected brain macrophages, fibrinogen leakage, and marked astrocytosis. In contrast, no significant changes (P > 0.05) were observed in cerebellar tissue from patients with HIVE compared to HIV-seronegative patients or HIV-1-infected patients without encephalitis. Our findings demonstrate that tight junction disruption is a key feature of HIVE that occurs in regions of histopathological alterations in association with perivascular accumulation of activated HIV-1-infected macrophages, serum protein extravasation, and marked astrocytosis. We propose that disruption of this key BBB structure serves as the main route of HIV-1-infected monocyte entry into the CNS.

AIDS Dementia Complex↗
PubMed1998

Is EEG useful in assessing patients with acute encephalitis treated with acyclovir?

EEG has been used widely in diagnosing encephalitis, as it demonstrates rather typical abnormalities, especially in herpes simplex virus encephalitis (HSVE). We analysed 204 EEG recordings from 98 consecutive acyclovir-treated patients with acute encephalitis between 1984 and 1994. Periodic complexes (PC) in the acute phase predicted poor outcome (Kendall tau 0.40, P < 0.001). However, unlike in many other diseases, e.g. stroke and intracerebral haemorrhage, the diffuse slowing of the background activity at acute phase did not predict outcome (Kendall tau -0.6, P = 0.35). At follow-up, the emergence of diffuse slow background activity was significantly associated with a less favourable outcome (Kendall tau 0.33, P = 0.0016). Among clinical variables, only epileptic seizures early during the course of the disease correlated significantly with outcome. EEG does have value as a prognostic indicator in acute encephalitides, but it seems that diffuse slowing of background activity or irritative features acutely are not as important as previously thought, based on the experiences of the pre-acyclovir era.

Acute Disease↗
PubMed1995

Expanded spectrum of herpes simplex encephalitis in childhood.

We designed a polymerase chain reaction method to detect herpes simplex virus (HSV) DNA in spinal fluid from patients with encephalitis. The polymerase chain reaction amplified a 211 base-pair segment of the HSV DNA polymerase gene. Applying this method, we diagnosed HSV type 1 infection in three young children, aged 7 to 13 months, who had atypical forms of the illness. On the basis of magnetic resonance imaging, their disease was diffuse or multifocal in two cases and, in all three, lacked the temporal lobe involvement considered characteristic of HSV encephalitis beyond the neonatal period. Most of the diffuse or multifocal abnormalities detected by magnetic resonance imaging were not apparent by computed tomography. Restriction enzyme analysis of the polymerase chain reaction products from all three patients indicated that their disease was caused by HSV type 1. We conclude that in preschool-age children beyond the neonatal period, the spectrum of HSV encephalitis includes multifocal or diffuse involvement of the brain, which may be detected most efficiently by magnetic resonance imaging. The polymerase chain reaction method has the potential for providing an early diagnosis, but further studies are required to define the sensitivity and specificity of the polymerase chain reaction before it can be used for routine clinical decision making.

Antibodies, Viral↗
PubMed2002

Encephalitis related to primary varicella-zoster virus infection in immunocompetent children.

INTRODUCTION: Encephalitis is a rare complication of primary varicella-zoster virus (VZV) infection in immunocompetent children. METHODS: The clinical and laboratory findings of two girls with VZV-related encephalitis are reported. RESULTS: Both children presented with focal epileptic seizures, corresponding to cortical/subcortical as well as white matter lesions. The first showed a typical vesicular skin rash. She was easily diagnosed and made a rapid recovery during acyclovir and steroid treatment. In the second girl, a preceding measles-mumps-rubella virus vaccination and the absence of skin vesicles were misleading with respect to the diagnosis, which was finally proven by IgG seroconversion and intrathecal synthesis of IgG antibodies to VZV. She developed left parieto-occipital tissue necrosis and recovered only transiently during initial acyclovir/steroid treatment. Eight weeks after onset, progressive white matter demyelination and the occurrence of erythema nodosum in the lower limbs necessitated a second 4-month course of oral steroids. The VZV PCR from cerebrospinal fluid was negative in both children. CONCLUSIONS: Primary VZV infection may cause severe encephalitis that may occur without skin vesicles and lead to a chronic course with systemic vasculitis. The coincidence of vaccination and neurologic diseases offers no proof per se of a causal relationship.

Acyclovir↗
PubMed1999

Herpes simplex virus encephalitis in pregnancy.

BACKGROUND: Although polymerase chain reaction (PCR) can detect herpes simplex virus (HSV) in the cerebrospinal fluid (CSF), HSV encephalitis remains a significant cause of neurologic impairment in pregnant women. Assessment of fetal contamination also remains a problem. CASES: We report two cases in which HSV encephalitis initially was not suspected and led to significant maternal neurologic impairment. In both cases, HSV PCR of CSF confirmed the diagnosis. In one case, fetal serum HSV PCR excluded fetal contamination. CONCLUSION: As soon as encephalitis in pregnancy is suspected, a combination of acyclovir and penicillin is recommended because the potential benefits far outweigh the risks. Using the HSV PCR, HSV infection in the fetus can be diagnosed.

Adult↗
PubMed1988

Herpes simplex virus encephalitis in children.

Herpes simplex encephalitis (HSE) is an uncommon disease, yet 25 to 30 per cent of cases involve children. The initial clinical findings are nonspecific (fever, altered mental status), but most cases evolve to demonstrate focal neurologic signs and symptoms. The CSF is abnormal in over 90 per cent of cases. The EEG, CT, and MRI will further help in detecting focal encephalitis. The clinician caring for a child with focal encephalitis should institute broad-spectrum antimicrobial therapy plus acyclovir, pending definitive diagnosis by ancillary tests or brain biopsy, which is positive for HSE 33 to 55 per cent of the time and is diagnostic for other treatable conditions 10 to 20 per cent of the time. Acyclovir is the drug of choice for HSE and substantially reduces mortality and morbidity. The management of HSE in a child requires an experienced team of specialists and laboratory support in a tertiary intensive care setting.

Acyclovir↗
PubMed1987

Cytomegalovirus encephalitis in patients with acquired immunodeficiency syndrome: an autopsy study of 30 cases and a review of the literature.

The pathology of cytomegalovirus (CMV) encephalitis was studied at autopsy in thirty patients with acquired immunodeficiency syndrome. Lesions could be segregated into five major categories: microglial nodules, isolated inclusion-bearing cells, focal parenchymal necrosis, necrotizing ventriculo-encephalitis, and necrotizing radiculo-myelitis. Microglial nodules and CMV inclusions were present in all brains. Microglial nodules were found with variable frequency and had greatest density in subcortical grey matter. Only a small percentage (average, 6.5 per cent) contained CMV inclusion-bearing cells. Isolated inclusion-bearing cells unaccompanied by microglial nodules or inflammatory infiltrates were seen in half the patients. CMV inclusions were identified in capillary endothelia, astrocytes, and neurons. Focal CMV necrosis, ventriculo-encephalitis, and radiculo-myelitis were less frequent. The presence of CMV inclusions in capillary endothelia suggests a vascular portal of entry for the virus into the central nervous system. The diffuse ependymal and/or subpial distribution of CMV in several patients suggests additional dissemination via the cerebrospinal fluid. Isolated inclusion-bearing cells may reflect the relative nonpermissiveness of surrounding central nervous system parenchyma for CMV infection.

Acquired Immunodeficiency Syndrome↗
PubMed1988

Diagnosis of acute herpes simplex encephalitis by brain perfusion single photon emission computed tomography.

Brain perfusion was studied in 14 patients with acute encephalitis by use of 123I-iodoamphetamine or 99mTc-hexamethylpropyleneamine oxime and single photon emission computed tomography (SPECT), the first examination being made 4-11 days after onset of encephalitis symptoms. All 6 patients with herpes simplex virus encephalitis (HSVE) had strongly increased accumulation of radiotracer in the affected temporal lobe; in the remaining 8 results were normal. At the time of the first SPECT conventional CT images were normal in all patients. The SPECT abnormality in HSVE gradually converted over 4-10 weeks from increased tracer accumulation to greatly subnormal accumulation. Brain perfusion SPECT may be helpful in the early diagnosis of HSVE.

Acute Disease↗
PubMedDate not supplied

Treatment regimens for patients with toxoplasmic encephalitis.

Toxoplasma gondii is an obligate intracellular parasitic protozoan that infects a variety of warm-blooded animals, including humans. Infection is usually asymptomatic in immunocompetent individuals but may be devastating in immunocompromised individuals such as those with acquired immunodeficiency syndrome (AIDS). Clinical manifestations of infection in immunocompromised patients include the development of encephalitis. It has been estimated that approximately 30% of patients with AIDS who are latently infected will eventually develop toxoplasmic encephalitis. The most common regimen used to treat toxoplasmic encephalitis is a combination of pyrimethamine 50 to 100 mg/d and sulfadiazine 4 to 8 g/d, with or without folinic acid 10 mg/d. This regimen, however, commonly leads to adverse effects or relapses. Other pharmacologic approaches include the use of clindamycin rather than sulfadiazine, the macrolide antibiotics, atovaquone, 5-fluorouracil, trimethoprim/sulfamethoxazole, minocycline or doxycycline, trimetrexate with folinic acid, dapsone, rifabutin, pentamidine, and diclazuril. None of these alternative regimens has been proven to be more effective than the standard pharmacologic therapy. An evolving approach is the use of immunotherapy, such as interleukin-2, -6, and -12; interferon-gamma; and alpha-tumor necrosis factor. Restoring a competent immune system may be the only cure for toxoplasmosis and other opportunistic infections.

AIDS-Related Opportunistic Infections↗
PubMed2003

Maternal Herpes simplex virus type 2 encephalitis following Cesarean section.

Herpes simplex virus type 2 (HSV-2) encephalitis is rare especially during pregnancy. In immunocompetent patients, HSV-2 meningitis (contrary to HSV-1 meningitis) is usually mild, without encephalitis. We report a rare case of maternal HSV-2 encephalitis following Cesarean section. The woman had no symptomatic genital lesion, and the infant was not infected. The route of meningeal infection (neuronal or hematogenous) is discussed.

Acyclovir↗
PubMed1996

Mimicry of a 21.5 kDa myelin basic protein peptide by a Maedi Visna virus polymerase peptide does not contribute to the pathogenesis of encephalitis in sheep.

Epitope mimicry is the theory that an infectious agent such as a virus causes pathological effects via mimicry of host proteins and thus elicits a cross-reactive immune response to host tissues. Weise and Carnegie (1988) found a region of sequence similarity between the pol gene of the Maedi Visna virus (MVV), which induces demyelinating encephalitis in sheep, and myelin basic protein (MBP), which is known to induce experimental allergic encephalitis (EAE) in laboratory animals. In this study, cross-reactions between sera raised in sheep against synthetic peptides of MVV (TGKIPWILLPGR) and 21.5 kDa MBP (SGKVPWLKPGR) were demonstrated using enzyme-linked immunosorbant assay (ELISA) and thin layer chromatography (TLC) immunoprobing. The antibody responses of MVV-infected sheep were investigated using ELISA against the peptides, and MBP protein, immunoprobing of the peptides on TLC plates and Western blotting against MBP. Slight significant reactions to the 21.5 kDa MBP peptide (P < 0.001) and to a lesser extent sheep MBP (P < 0.004) were detected in ELISA. The MBP peptide evoked stronger responses from more sera than the MVV peptide on immunoprobed TLC plates. On the Western blots, eight of the 23 sheep with Visna had serum reactivity to MBP. This slight reaction to MBP in MVV-infected sheep is of interest because of the immune responses to MBP evident in multiple sclerosis and EAE, but its relevance in Visna is limited since no correlation with disease severity was observed. The cell-mediated immune responses of MVV-infected sheep against similar peptides was assessed. The peptides did not stimulate proliferation of peripheral blood lymphocytes of MVV-infected sheep. Since the MVV peptide was not recognised by antibodies or T lymphocytes from MVV-infected and encephalic sheep, it was concluded that epitope mimicry of this 21.5 kDa MBP peptide by the similar MVV pol peptide was not contributing to the immunopathogensis of Visna. The slight antibody response to MBP and the MBP peptide can be attributed to by-stander effects of the immunopathology of MVV-induced encephalitis.

Animals↗
PubMed2003

[Hodgkin's disease manifesting as paraneoplastic limbic encephalitis].

INTRODUCTION: Malignancy is a possible cause of unexplained encephalitis. EXEGESIS: We describe a 59-years-old woman with limbic encephalitis, not explained by other causes, preceding diagnosis of Hodgkin's disease. Successful treatment of Hodgkin's disease was effective against neurological disturbance. CONCLUSION: This case provides evidence that Hodgkin's disease can be uncovered by paraneoplastic limbic encephalitis.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed2001

A novel permissive role for glucocorticoids in induction of febrile and behavioral signs of experimental herpes simplex virus encephalitis.

Herpes simplex virus type 1 (HSV-1) encephalitis may present with fever and behavioral changes, to the extent of a psychotic state and psychomotor agitation. We developed a clinically relevant experimental model of HSV-1 encephalitis and investigated host brain responses associated with its clinical signs and whether these responses depend on the presence of circulating glucocorticoids. Intracerebral inoculation of HSV-1 in rats induced fever, motor hyperactivity and aggressive behavior. In adrenalectomized rats HSV-1 failed to induce these signs, although mortality rate was identical to sham-operated rats. Hypophysectomy or blocking glucocorticoid receptors also prevented HSV-1-induced fever. Dexamethasone replacement therapy to adrenalectomized rats restored the HSV-1-induced fever and behavioral abnormalities. HSV-1 inoculation produced hyperproduction of prostaglandin E(2) by brain slices. This effect was abolished in adrenalectomized rats and was restored by dexamethasone treatment. In intact rats HSV-1 induced brain interleukin-1beta (IL-1beta) gene expression. Adrenalectomy alone caused brain IL-1beta expression, which did not increase after HSV-1 infection. Similarly, HSV-1 induced IL-1beta expression in astrocyte cultures. Removal of cortisol from the culture medium caused basal IL-1beta mRNA expression which was not increased by infection. In conclusion, fever, motor hyperactivity and aggressive behavior during experimental HSV-1 encephalitis are dependent on brain responses, including prostaglandin E(2) and IL-1beta synthesis. Circulating glucocorticoids play an essential permissive role in the induction of these host brain responses.

Adrenalectomy↗
PubMed2002

Low-voltage activity in EEG during acute phase of encephalitis predicts unfavorable neurological outcome.

The purpose of this study was to evaluate the risk factors responsible for the onset of postencephalitic epilepsy during the acute phase of encephalitis. We retrospectively studied 19 patients with acute encephalitis admitted to the Division of Pediatrics at our hospital from January 1989 to December 1998. Nine cases were complicated by postencephalitic epilepsy and 10 were non-complicated cases. Significant risk factors for postencephalitic epilepsy were seizures, more severe impairment of consciousness, abnormalities in cranial computed tomography/magnetic resonance imaging/single photon emission computed tomography examination and low-voltage EEG activity, which was defined as EEG findings showing less than 20 microV of background activity without the appearance of a hump or spindle, during the acute phase of encephalitis. In particular, cases with low-voltage EEG activity were all complicated by intractable epilepsy after less than 1 year. Low-voltage EEG activity during the acute phase predicts an unfavorable neurological outcome, reflecting severe widespread impairment in the whole of the cortex.

Acute Disease↗
PubMed1983

Computed tomography in postinfluenzal encephalitis.

A 2-year-old girl developed encephalitis following influenza A virus infection. Brain computed tomography (CT) showed symmetrical hypodense areas in the putamina. Contrast enhancement was noted surrounding the hypodense areas 2 days after the onset of encephalitis. These localized lesions demonstrated on CT have not been reported in the literature of postinfluenzal encephalitis.

Child, Preschool↗