Cases reported "Encephalitis, Viral"

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1/47. bk virus as the cause of meningoencephalitis, retinitis and nephritis in a patient with AIDS.

    BACKGROUND: The two widely spread human polyomaviruses, bk virus (BKV) and jc virus (JCV) establish latency in the urinary tract, and can be reactivated in AIDS. JCV might cause progressive multifocal leucoencephalopathy, but although up to 60% of AIDS patients excrete BKV in the urine there have been few reports of BKV-related renal and/or neurological disease in AIDS. OBJECTIVE: To report on an AIDS patient with progressive renal and neurological symptoms involving the retina. DESIGN: Case report. SETTING: Venhalsan, Soder Hospital, Stockholm, sweden. methods: The brain, eye tissue, cerebrospinal fluid, urine and peripheral blood mononuclear cells were analysed by nested PCR for polyoma-virus dna. Macroscopical and microscopical examination were performed of the kidney and brain post mortem. Immunohistochemical stainings for the two BKV proteins, the VP1 and the agnoprotein, were performed on autopsy material and virus infected tissue culture cells. RESULTS: BKV could be demonstrated in the brain, cerebrospinal fluid, eye tissues, kidneys and peripheral blood mononuclear cells. CONCLUSION: During 6 years, approximately 400 cerebrospinal fluid samples from immunosuppressed individuals with neurological symptoms have been investigated by PCR for the presence of polyomaviruses. BKV dna has, so far, only been found in the case reported here. Although reports of BKV infections in the nervous system are rare, there is now evidence for its occurrence in immunocompromised patients and the diagnosis should be considered in such patients with neurological symptoms and signs of renal disease. The diagnosis is simple to verify and is important to establish.
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2/47. Interferon gamma (IFN-gamma) deficiency in generalized Epstein-Barr virus infection with interstitial lymphoid and granulomatous pneumonia, focal cerebral lesions, and genital ulcers: remission following IFN-gamma substitution therapy.

    A 26-year-old previously healthy woman developed granulomatous pneumonitis, encephalitis, and genital ulceration during primary Epstein-Barr virus (EBV) infection. EBV dna was demonstrated by polymerase chain reaction analysis of serum, lung tissue, and genital ulcer specimens. serology verified primary EBV infection. The patient lacked lymphocytes cytotoxic to autologous EBV-transformed B lymphocytes. No spontaneous or in vitro EBV-induced interferon gamma (IFN-gamma) production was evident in peripheral blood. The cells had normal IFN-gamma production when stimulated with staphylococcus aureus exotoxin A. In the bone marrow and peripheral blood, the number of large granular CD56 lymphocytes (natural killer cells) increased 39%-55%, but no CD4 or CD8 cell lymphocytosis was initially found. A partial clinical response was achieved with treatment with acyclovir, corticosteroids, and intravenous gamma-globulin. Because of persistent granulomatous central nervous system and lung involvement, subcutaneous IFN-gamma therapy was started but was discontinued after 3 months because of development of fever, pancytopenia, and hepatitis. This therapy initiated a complete clinical recovery, which occurred parallel to development of EBV-specific cytotoxic CD8 T lymphocytes and normalization of natural killer cell lymphocytosis. These findings provide evidence for an EBV-induced lymphoproliferative disorder due to a T lymphocyte dysfunction associated with a selective lack of IFN-gamma synthesis.
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3/47. Fatal encephalitis due to nipah virus among pig-farmers in malaysia.

    BACKGROUND: Between February and April, 1999, an outbreak of viral encephalitis occurred among pig-farmers in malaysia. We report findings for the first three patients who died. methods: Samples of tissue were taken at necropsy. Blood and cerebrospinal-fluid (CSF) samples taken before death were cultured for viruses, and tested for antibodies to viruses. FINDINGS: The three pig-farmers presented with fever, headache, and altered level of consciousness. myoclonus was present in two patients. There were signs of brainstem dysfunction with hypertension and tachycardia. Rapid deterioration led to irreversible hypotension and death. A virus causing syncytial formation of vero cells was cultured from the CSF of two patients after 5 days; the virus stained positively with antibodies against hendra virus by indirect immunofluorescence. IgM capture ELISA showed that all three patients had IgM antibodies in CSF against Hendra viral antigens. Necropsy showed widespread microinfarction in the central nervous system and other organs resulting from vasculitis-induced thrombosis. There was no clinical evidence of pulmonary involvement. inclusion bodies likely to be of viral origin were noted in neurons near vasculitic blood vessels. INTERPRETATION: The causative agent was a previously undescribed paramyxovirus related to the hendra virus. Close contact with infected pigs may be the source of the viral transmission. Clinically and epidemiologically the infection is distinct from infection by the hendra virus. We propose that this Hendra-like virus was the cause of the outbreak of encephalitis in malaysia.
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4/47. Acute encephalopathy and intractable seizures in a 10-year-old boy.

    We report a 10-year-old child with Robinow's syndrome who had a 2-week history of headaches and dizziness. On the day of admission, he developed a focal onset seizure with rapid secondary generalization. The seizures were intractable despite adequate doses of benzodiazepine, phenytoin, and phenobarbital, requiring a pentobarbital drip. Continuous electroencephalogram (EEG) monitoring showed persistence of the epileptiform discharges for 13 days. cerebrospinal fluid and brain biopsy studies were unrevealing. Mycoplasma pneumonia titers showed elevation of both immunoglobulins G and M that doubled during the tenth hospital day. High-dose methylprednisolone was begun, and within 12 hours of initiation the patient sat up and began to follow commands appropriately. The overall EEG background markedly improved. central nervous system mycoplasma pneumoniae infection should be suspected in patients with an encephalopathy of unclear etiology.
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5/47. Brainstem encephalitis resulting from Epstein-Barr virus mimicking an infiltrating tumor in a child.

    A case of a child with subacute neurologic features and imaging findings consistent with a brainstem encephalitis that was discovered to be related to a primary central nervous system infection caused by Epstein-Barr virus is presented. A brainstem tumor was initially suspected, but a correct diagnosis was formulated on the basis of the favorable clinical course and the detection of positive Epstein-Barr virus serology. In contrast to a prompt recovery of neurologic signs the neuroimaging alterations persisted for a longer time. The present report emphasizes the possible role of Epstein-Barr virus in the pathogenesis of infectious neurologic disorders in childhood, underlining the unusual presentation of a brainstem encephalitis, and considers the discrepancy between the course of neurologic features and the evolution of imaging alterations.
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6/47. Hypothetical pathophysiology of acute encephalopathy and encephalitis related to influenza virus infection and hypothermia therapy.

    BACKGROUND: To establish a treatment strategy for acute encephalopathy and encephalitis associated with influenza virus infection, the pathophysiology of the disease was investigated through manifestations and laboratory findings of patients. patients AND methods: A child with central nervous system (CNS) complications during the course of influenza virus infection was analyzed in view of immunologic abnormalities. In addition, four children with acute encephalopathy and encephalitis were enrolled in the hypothermia treatment for the purpose of stabilizing the cytokine storm in the CNS. RESULTS: The CNS symptoms preceded the systemic progression to the failure of multiple organs (MOF) and disseminated intravascular coagulopathy (DIC). The mild hypothermia suppressed the brain edema on computed tomography (CT) scanning and protected the brain from the subsequent irreversible neural cell damage. CONCLUSION: The replicated viruses at the nasopharyngeal epithelium may disrupt the olfactory mucosa and gain access to the brain via the olfactory nerve system. The direct virus-glial cell interaction or viral stimulation of the glial cells induces the production and accumulation of the pro-inflammatory cytokines, especially tumor necrosis factor (TNF)-alpha, in the CNS. The cytokine storm results in neural cell damage as well as the apoptosis of astrocytes, due to the TNF-alpha-induced mitochondrial respiratory failure. The disruption of the blood-brain barrier progresses to the systemic cytokine storm, resulting in DIC and MOF. Mild hypothermia appears promising in stabilizing the immune activation and the brain edema to protect the brain from ongoing functional, apoptotic neural and glial damage and the systemic expansion of the cytokine storm.
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7/47. An outbreak of enterovirus 71 infection in taiwan 1998: a comprehensive pathological, virological, and molecular study on a case of fulminant encephalitis.

    BACKGROUND: In a recent enterovirus outbreak in taiwan, serotype 71 was the culprit of encephalitis causing rapid clinical deterioration and death among young children. OBJECTIVES: Since knowledge of enterovirus 71 (EV71) infection in the central nervous system is still limited, the purpose of the present case study was attempted to uncover the pathogenesis of the virus. STUDY DESIGN: We performed a detailed pathological examination, virological and molecular studies on a case of EV71 infection with a rapidly fatal outcome. In addition, the whole genome of the virus was sequenced to determine the genetic relationships to other enteroviruses and two other EV71 strains (a prototype BrCr and a neurovirulent MS strain), and to provide the genetic basis of its neurovirulence of the new isolate, NCKU9822 strain. RESULTS: Characteristic features of acute encephalomyelitis were observed, with most prominent lesions in the spinal cord and brain stem. Mild myocarditis and pancreatitis were also noticed. EV71 antigen was localized to neurons on immunohistochemical staining. EV71 was recovered from all organs with inflammatory reaction. sequence analysis showed that overall NCKU9822 and the two EV71 strains shared 80% nucleotide identity and 95% amino acid identity. It had only 45% amino acid and 52% nucleotide identities with polioviral P1 capsid region. CONCLUSION: The spinal cord and brain stem were the main targets of EV71 in the fatal cases in this outbreak, however, heart and pancreas might also be involved. Since the amino acid sequences in the P1 region are conserved (97% identity) among the three EV71 strains as compared to other enteroviruses and polioviruses, these EV71 neurovirulent strains might share the same mechanisms of neurovirulence, and the mechanisms might be different from those in polioviruses.
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8/47. Acute encephalomyelitis during an outbreak of enterovirus type 71 infection in taiwan: report of an autopsy case with pathologic, immunofluorescence, and molecular studies.

    We report a fatal case of enterovirus type 71 (EV 71) infection in an 8-year-old girl during a summer outbreak of hand, foot, and mouth disease in 1998 in taiwan. The clinical course was rapidly progressive, with manifestations of hand, foot, and mouth disease, aseptic meningitis, encephalomyelitis, and pulmonary edema. The patient died 24 hours after admission. Postmortem study revealed extensive inflammation in the meninges and central nervous system and marked pulmonary edema with focal hemorrhage. brain stem and spinal cord were most severely involved. The inflammatory infiltrates consisted largely of neutrophils involving primarily the gray matter with perivascular lymphocytic cuffing, and neuronophagia. The lungs and heart showed no evidence of inflammation. EV 71 was isolated from the fresh brain tissues and identified by immunofluorescence method with type-specific EV 71 monoclonal antibody. It was also confirmed by neutralization test and reverse-transcriptase polymerase chain reaction with sequence analysis. The present case was the first example in which EV 71 was demonstrated to be the causative agent of fatal encephalomyelitis during its epidemic in taiwan.
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9/47. Correlation of clinical and neuroimaging findings in a case of rabies encephalitis.

    BACKGROUND: rabies encephalitis is a feared, virtually uniformly fatal form of central nervous system infection. The incidence of rabies encephalitis in the united states is almost certainly underestimated because of the predominance of bat-borne rabies, which can be spread without traumatic exposure. Because of its rarity in developed countries, rabies encephalitis has been seldom studied with modern imaging techniques. SETTING: University-based teaching hospital. PATIENT: A case of pathologically confirmed rabies encephalitis is presented. diagnosis of rabies was made by seroconversion testing while the patient was alive and was confirmed postmortem by the presence of rabies antigens and Negri bodies in the brain. The patient had 2 magnetic resonance studies done that showed dramatic abnormalities in the medulla and pons that correlated with features of the neurologic examination and hypothalamic-pituitary abnormalities. RESULT: The patient had a fulminant encephalitic course that ended in death. CONCLUSION: rabies is an uncommon cause of fatal encephalitis. Anatomic imaging studies such as computed tomographic and magnetic resonance scans have generally been negative in confirmed cases of rabies. We report a case of confirmed rabies with extensive brainstem and hypothalamic-pituitary abnormalities on magnetic resonance imaging. Although these findings are nonspecific, they should raise the clinical suspicion of rabies in the setting of aggressive encephalitis of unclear cause, and appropriate diagnostic tests should be performed.
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10/47. Case of fatal encephalitis by HHV-6 variant A.

    A fatal case is reported of encephalitis in an 85-year-old man caused by the human herpesvirus 6 variant A. The virological diagnosis was based on the findings of the virus variant genomic sequences both in the cerebrospinal fluid and serum of the patient. Moreover, virus replication in nervous tissue was suggested by a viral load higher in the cerebrospinal fluid than in the peripheral blood. The association of a central nervous system infection with the A variant of human herpesvirus 6 is interesting because of the difficulty in establishing a pathological role for this virus strain. Epstein-Barr virus dna was detected in the patient's cerebrospinal fluid in association with human herpesvirus 6 dna. The presence of the Epstein-Barr virus genomic sequences in the cerebro-spinal fluid was considered to be unimportant clinically.
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