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At least 883 records · Page 49Linked to original sources
PubMed1988

Comparison of in situ DNA hybridization (ISH) and immunocytochemistry for diagnosis of herpes simplex virus (HSV) encephalitis in tissue.

Formol-fixed and paraffin-embedded brain tissue of 33 cases of human necrotizing encephalitis was investigated for Herpes simplex virus (HSV) by immunocytochemistry with a polyclonal antiserum, and by in situ hybridization (ISH) with a biotinylated cDNA probe. HSV antigens (VA) were found in various types of cells in the cytoplasm, cellular processes and nuclei. Labelling by ISH was mostly restricted to nuclei and intranuclear inclusions but otherwise matched the distribution of VA. Eighteen of 25 acute cases had HSV antigen detectable by immunocytochemistry, and 18 of the acute cases contained HSV DNA detectable by our ISH technique. However, results differed somewhat between the techniques: three brains negative for VA showed hybridization, and other 3 VA-positive cases remained negative by ISH. Thus 21 brains with acute necrotizing encephalitis were labelled with one or both techniques. In 8 cases with a subacute course (duration of disease was longer than 1 month), HSV antigens were never detectable although 4 brains showed hybridization. All brains labelled by one or both techniques contained nuclear inclusions bodies. Only one case, of subacute course, with inclusion bodies remained unlabelled. Brain tissue of 11 controls, including cytomegalic inclusion body disease, was never labelled. These results demonstrate that immunocytochemistry and ISH are techniques of comparable sensitivity (72%) for detection of HSV in paraffin sections of acute necrotizing encephalitis brains; their combined use enhanced sensitivity, in our hands, to 84%. In cases with a disease course longer than one month, ISH seems to be the method of choice to demonstrate HSV in situ.

Acute Disease↗
PubMed1992

Early diagnosis and successful treatment of acute cytomegalovirus encephalitis in a renal transplant recipient.

We report the case of a 40-year-old male HIV-negative renal transplant patient with allograft rejection and immunosuppressive therapy who presented with acute cytomegalovirus (CMV) encephalitis. CT and MRI of the brain were normal but EEG showed diffuse slowing and dysrhythmia. In cerebrospinal fluid (CSF) initially 81 cells/microliters were found and immunocytochemistry showed a decreased CD4/CD8 ratio and increased values of activated lymphocytes, natural killer cells and immunoglobulin-containing cells. CMV-specific IgM antibodies in CSF and serum, immunostaining of CMV antigen in CSF cells and virus culture from CSF and urine were negative. During the first 3 weeks of illness no intrathecal production of immunoglobulins could be detected. Early diagnosis of CMV encephalitis was made by in situ hybridization (ISH) on CSF cell preparations and the polymerase chain reaction (PCR) which was positive in CSF and blood. On day 26 diagnosis was confirmed by detection of CMV-specific intrathecal IgG production. The patient was treated with ganciclovir, anti-CMV immunoglobulins and intrathecal beta interferon. He recovered completely after 2 months. Our data demonstrate the usefulness of ISH and PCR in the early diagnosis of CMV encephalitis and perhaps may encourage the use of intrathecal beta interferon in other patients with this disease.

Acute Disease↗
PubMed1993

The inflammatory reaction of paraneoplastic ganglionitis and encephalitis: an immunohistochemical study.

To elucidate the cellular mechanisms of tissue injury in paraneoplastic states, tissues from two patients with small cell carcinoma of the lung and paraneoplastic neurological syndromes were studied. One patient had encephalitis with ganglionitis, and the other ganglionitis. Immunocytochemistry on brain and ganglia was performed using monoclonal and polyclonal antibodies. The majority of the inflammatory cells in brain and ganglia were T-cells, of both helper and cytotoxic subtypes. There were more macrophages in the inflammatory infiltrate of ganglia than in the brain of encephalitis. Major histocompatibility complex class I and II antigen expression was greater in the mononuclear cells in brain than in ganglia. There was no evidence of complement deposition and little evidence for antibody synthesizing cells. Our findings suggest a T-cell-mediated immune attack in paraneoplastic ganglionitis and encephalitis, with a greater role for macrophages in ganglionitis.

Aged↗
PubMed1983

Neurotransmitter synthesizing enzymes in experimental viral encephalitis.

Stereotactic intracerebral inoculation of a non-neuroadapted strain of herpes simplex virus type 1 into the left neostriatum of Sprague-Dawley rats induced clinical acute encephalitis within 3 to 5 days postinoculation, with microscopic evidence of inflammation in brain parenchyma, but with no gross areas of tissue destruction. Viral presence in brain was unequivocally confirmed by tissue culture, immunofluorescence and electron microscopy. Levels of activity of neurotransmitter synthesizing enzymes tyrosine hydroxylase (TH), glutamate decarboxylase (GAD), and choline acetyltransferase (ChAT) in the substantia nigra, caudate-putamen and frontal cortex of acutely encephalitic animals were not significantly different from those of PBS-inoculated controls; neither were there significant differences between the inoculated and non-inoculated sides of the individual animals. Our results show that locally injected herpes simplex virus may spread in brain causing neurological symptoms and death without major local structural changes or loss of neurotransmitter synthesizing enzymes. The degree and distribution of cell dysfunction and cell loss in viral encephalitis basically determine any alterations of enzyme activities specific to the involved cell population. The literature on neurotransmitter enzymes and experimental viral encephalitis is reviewed.

Acetylcholine↗
PubMed1984

Genetic and phenotypic characteristics of enterovirus 71 isolates from patients with encephalitis and with hand, foot and mouth disease.

Biological and biochemical characters of seven enterovirus 71 (E71) isolates were compared. Four isolates (two from patients with hand, foot and mouth disease [HFMD] and two from patients with encephalitis) grew in cynomolgus monkey kidney cells both at 39.5 and 35 degrees C. However, the remaining three strains (from patients with HFMD) grew at 35 degrees C, but not at 39.5 degrees C. Three temperature-resistant and two temperature-sensitive strains were tested for neurovirulence in monkeys. Temperature-resistant strains were shown to be neurovirulent, whereas temperature-sensitive strains were less neurovirulent. The results suggest correlation between temperature-sensitive growth and neurovirulence in monkeys of E71. Variation in the electrophoretic mobility of the viral polypeptides was detected in three out of seven strains. The fingerprinting of oligonucleotides generated from the viral genome showed similar patterns in two isolates from patients with HFMD and one from patient with encephalitis and variable patterns in each genomic map of remaining four strains. These variations of polypeptide patterns and of oligonucleotide maps could not be correlated with pathogenicity (encephalitis or HFMD), temperature-sensitive growth and neurovirulence in monkeys.

Animals↗
PubMed1996

Use of rifabutin in combination with atovaquone, clindamycin, pyrimethamine, or sulfadiazine for treatment of toxoplasmic encephalitis in mice.

The effectiveness of combinations of rifabutin with atovaquone, clindamycin, pyrimethamine, or sulfadiazine in the treatment of toxoplasmic encephalitis in a murine model was investigated. Doses of each drug that were not effective in reducing inflammation in the brain of mice with toxoplasmic encephalitis when used alone were used in combination with a dose of rifabutin which was minimally effective. At the end of each period of therapy (15 or 30 days), brains of mice were examined histopathologically and the severity of the inflammatory lesions scored. Treatment with rifabutin in combination with pyrimethamine or sulfadiazine did not reduce brain inflammation significantly when compared to treatment with each drug alone. In contrast, treatment with rifabutin plus atovaquone for 15 or 30 days or with rifabutin plus clindamycin for 15 days resulted in statistically significant reduction in the inflammation. These results suggest that combining rifabutin with certain drugs that are active against Toxoplasma gondii may be useful for the treatment of toxoplasmic encephalitis in humans and may allow for a reduction in dosage of either or both drugs with a resulting reduction in untoward side effects.

Animals↗
PubMedDate not supplied

Thrombocytopenia--a common finding in the initial phase of tick-borne encephalitis.

The aim of this prospective study was to assess the frequency of thrombocytopenia and abnormal liver function tests in the initial phase of tick-borne encephalitis. In 1994, 248 adult patients presented at the Department of Infectious Diseases, University Medical Centre Ljubljana, with acute lymphocytic meningitis or meningoencephalitis and serologically confirmed tick-borne encephalitis virus infection. In 180/248 (72.6%) patients, typical biphasic course of the illness was found and 28/180 (15.6%) patients with biphasic course were examined in both phases of the illness. In 20 out of these 28 (71.4%) patients, thrombocytopenia and leukopenia were found initially, in one (3.6%) patient only leukopenia was recorded and three (10.7%) patients had thrombocytopenia without leukopenia. In four (14.3%) patients leukocyte and thrombocyte values were within the normal range. The lowest leukocyte number was 1.4 x 10(9)/l and the lowest recorded thrombocyte number was 60 x 10(9)/l. Abnormal liver function tests were discovered in four out of 18 patients tested (22.2%). In conclusion, in the initial phase of tick-borne encephalitis thrombocytopenia and abnormal liver function tests may be found. Thrombocytopenia is a common finding with a frequency similar to that of well-known leukopenia, while abnormal liver function tests are relatively rare.

Adolescent↗
PubMed1992

Tick-borne encephalitis in a 3-month-old child.

Tick-borne encephalitis has not been reported in infants younger than 12 months of age. We report a 3.5-month-old child with a serologically proven tick-borne encephalitis. The infant had a history of a tick bite 3.5 weeks before the first symptoms of encephalitis appeared. The family lives in an endemic area of the disease. There were no prodromal signs and the course of the disease was monophasic. In an endemic area, prophylactic treatment with hyperimmunoglobulin after a tick bite should be considered even in very young infants, but in most children active immunization is probably not necessary because of infrequent exposure. Active immunization is still recommended after the 1st year of life.

Age Factors↗
PubMed1995

MR and CT imaging patterns in post-varicella encephalitis.

The aim of the investigation was to determine the patterns of cerebral involvement on computed tomography (CT) and magnetic resonance (MR) imaging in post-varicella encephalitis. Four children between the ages of 2 and 11 years presented over a 5-year period with a diagnosis of post-varicella encephalitis. Their imaging studies and clinical data were reviewed retrospectively. The medical histories of all four children were noncontributory except for recent bouts of chickenpox 1 week to 3 months prior to hospitalization. Three children presented with parkinsonian manifestations. Bilateral, symmetric hypodense, nonenhancing basal ganglia lesions were found on CT. These areas showed nonenhancing low signal intensity on T1-weighted images and high signal intensity on T2-weighted images on MR. One child presented with diffuse, multiple gray and white matter lesions of similar imaging characteristics; some lesions, however, did enhance. This child had no gait disturbances. Post-varicella encephalitis can produce two patterns of dramatic CT and MR findings. With an appropriate history and clinical findings, varicella as a cause of bilateral basal ganglia or diffuse cerebral lesions can be differentiated from other possible etiologies which include trauma, anoxia, metabolic disorders and demyelinating diseases.

Chickenpox↗
PubMed1991

Magnetic resonance imaging in a case of mumps postinfectious encephalitis with asymptomatic optic neuritis.

A 5-year-old male patient with asymptomatic optic neuritis and mumps postinfectious encephalitis or acute disseminated encephalomyelitis is reported. Magnetic resonance imaging (MRI) with a short inversion time inversion recovery sequence was valuable in detecting clinically silent lesions of the unilateral right optic nerve in addition to visual evoked potentials. Evidence of concurrent optic neuritis was useful for detecting more extensive neurological involvement, leading to the diagnosis of mumps postinfectious encephalitis. A systematic MRI study should be performed in children with mumps encephalitis, regardless of appreciable clinical deficits.

Child, Preschool↗
PubMed1994

Herpes simplex brainstem encephalitis with a relapsing course.

We report a patient with a relapsing form of acute brainstem encephalitis. Pathological examination demonstrated necrotizing encephalitis in the cerebral cortex and, more pronounced, throughout the diencephalon, as well as in the pes pontis. Neurons and glial cells in the cerebral cortex and brainstem contained herpesvirus antigens. The clinical interrelationship of brainstem encephalitis, Miller Fisher syndrome and Landry-Guillain-Barré syndrome is discussed.

Adolescent↗
PubMed1989

A case study of the cognitive and behavioral deficits of temporal lobe damage in herpes simplex encephalitis.

Herpes simplex viral encephalitis is a fairly common nonepidemic encephalitis which produces severe neurological sequelae in survivors. Most viral infections of the central nervous system produce diffuse damage, but the herpes simplex virus demonstrates a predilection for localization in the temporal and orbitofrontal regions of the brain. This case study illustrates the highly significant language difficulties, marked memory deficits, and propensity for physical aggression following temporal lobe damage brought about by herpes encephalitis, and presents the usefulness of a new diagnostic measure in delineating such a variable cognitive pattern.

Adolescent↗
PubMed2003

Suramin inhibits the in vitro expression of encephalitis B virus proteins NS3 and E.

In this study, the mechanism by which Suramin inhibits the replication of epidemic encephalitis B virus was explored to provide a theoretical basis for its further application in clinical practice. After viral infection of HepG2 and IMR-32 cells, different concentrations of Suramin were added to the culture media, and then the cultural supernatants and infected cells were collected 48 h later. For the evaluation of the curative effect, cytopathic effect (CPE), virus titers, the expression of viral protein and viral RNA were determined by Western blot, RT-PCR and in vitro RNA synthesis, respectively. At the concentration of 50 microg/ml of Suramin, HepG2 and IMR-32 infected with epidemic encephalitis B virus decreased by 51.8% and 0.03% respectively, as compared with controls. It was suggested that expression of encephalitis B virus proteins NS3 and E was notably reduced by Suramin. This is especially true of E protein. At RNA level, however, no difference in RNA virus was found between Suramin-treated virus and non-treated cells. Our results suggest that Suramin can inhibit viral replication by blocking the production of viral proteins.

Antiviral Agents↗
PubMed2004

[Herpes simplex virus type 1 encephalitis].

BACKGROUND: Herpes simplex virus type 1 encephalitis (HSE) is the most frequent cause of severe sporadic viral encephalitis. In spite of the advanced modern methods for the treatment of HSE it is still associated with high mortality. Early diagnosis and prompt antiviral therapy with acyclovir are essential to improve prognosis and to prevent severe neurologic sequels. PURPOSE: This review summarizes the current knowledge on the pathogenesis, diagnosis, clinical presentation, and treatment of herpes simplex virus type 1 encephalitis. Characteristic features including magnetic resonance imaging (MRI) are illustrated by a typical case.

Acyclovir↗
PubMed1998

[Bickerstaff encephalitis. Clinical and magnetic resonance follow-up studies].

We present a patient with Bickerstaff's brainstem encephalitis in whom MR imaging correlated with the clinical findings during the course of the disease. T2-weighted MR imaging showed increased signal intensity in the medulla oblongata, upper pons, pendunculi cerebelli and the cerebellum. In the course of the disease the lesions on MRI tended to descend more caudally. No anti-GQ1b antibody titers could be detected in the acute phase of the illness. Our findings suggest that MRI is the most valuable diagnostic tool in supporting the clinical diagnosis of Bickerstaff's brainstem encephalitis and may be helpful in the distinction between Miller Fisher syndrome and Bickerstaff's brainstem encephalitis.

Brain Stem↗
PubMed2001

Craniectomy in severe, life-threatening encephalitis: a report on outcome and long-term prognosis of four cases.

OBJECTIVE: To report the feasibility of craniectomy with duraplasty in four patients with life-threatening encephalitis and, in particular, their long-term outcome. DESIGN: Report of four cases, analysis of the acute clinical course and neurological long-term sequelae. RESULTS: Generous craniectomy with duraplasty was performed in four patients with life-threatening encephalitis leading to decortication and decerebration. This treatment approach reduced intracranial pressure. The long-term sequelae (1.5-8 years after craniectomy) confirmed its appropriateness, having led to full neurological (cerebral) function, resocialization, and reintegration into their professional life in all four patients. CONCLUSION: Craniectomy with dural augmentation is a treatment approach in cases of severe space-occupying encephalitis, not only saving the patient's life but also leading to favorable long-term outcome.

Adolescent↗
PubMed2002

MRI findings in a remitting-relapsing case of Bickerstaff encephalitis.

A case of remitting-relapsing Bickerstaff encephalitis is reported. The article focuses on its imaging findings and their significance when a clinical differentiation between Bickerstaff encephalitis and Miller-Fisher syndrome is attempted. Signs and symptoms may occasionally overlap. However, because Miller-Fisher syndrome is related to the peripheral nervous system and Bickerstaff encephalitis is a central disease, the recognition of brain stem hypointense lesions on T1-weighted images, which are hyperintense on T2-weighted sequences, could be a reliable tool when the clinical diagnosis is unclear.

Adult↗
PubMed1997

Neurological disease and encephalitis in cats experimentally infected with Borna disease virus.

Barrier-bred cats were inoculated intracerebrally with either the rabbit-adapted Borna disease virus (BDV) strain V or a newly isolated feline BDV, obtained from a cat with natural staggering disease (SD). Three out of eight inoculated cats developed neurological signs and non-suppurative encephalitis; all three recovered from the acute stage of disease. Sero-conversion and the development of neutralizing antibodies occurred in all of the virus-inoculated cats. In addition, cats inoculated with feline BDV showed an early peripheral T cell response not present in cats inoculated with BDV strain V, suggesting that the feline virus exerted a more vigorous effect on the immune system. Using immunohistochemistry and a reverse transcriptase-polymerase chain reaction assay, BDV-specific antigen and nucleic acid could be demonstrated in brain samples from each cat with encephalitis, showing that incomplete viral clearance was probably responsible for the maintenance of inflammation. The successful induction of neurological signs and encephalitis in one cat infected with feline BDV, together with the detection of BDV-specific antigen and nucleic acid in the brain, provides strong evidence for the notion that BDV is the etiological agent behind feline SD.

Animals↗