1/24. Organ recovery from a donor with presumed viral encephalitis: a case report and review.This article reviews the pathophysiology of viral encephalitis, which is specifically infectious to transplant recipients, and discusses the potential infectivity of donors who had this virus. In addition, the case report demonstrates one center's experience in placing organs from a donor who was presumed--but not confirmed--to have viral encephalitis. When a patient with viral encephalitis is considered for organ donation, it is recommended that a brain biopsy be obtained prior to organ placement to identify the suspected virus or confirm the absence of any viral entity.- - - - - - - - - - ranking = 1keywords = organ (Clic here for more details about this article) |
2/24. 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.- - - - - - - - - - ranking = 0.33333333333333keywords = organ (Clic here for more details about this article) |
3/24. 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.- - - - - - - - - - ranking = 0.42988220719797keywords = organ, nerve (Clic here for more details about this article) |
4/24. 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.- - - - - - - - - - ranking = 0.33333333333333keywords = organ (Clic here for more details about this article) |
5/24. Human herpesvirus 6 encephalitis associated with hypersensitivity syndrome.Hypersensitivity syndrome, a serious systematic reaction to a limited number of drugs, is associated with the reactivation of human herpesvirus 6. A 56-year-old man developed acute limbic encephalitis followed by multiple organ failure during the course of toxic dermatitis induced by aromatic anticonvulsants. The clinical features of skin eruptions, high fever, eosinophilia, and atypical lymphocytosis were compatible with drug hypersensitivity syndrome. The patient showed seroconversion for human herpesvirus 6, and polymerase chain reaction detected human herpesvirus 6 dna in the cerebrospinal fluid. To our knowledge, this is the first report of human herpesvirus 6 encephalitis associated with hypersensitivity syndrome.- - - - - - - - - - ranking = 0.33333333333333keywords = organ (Clic here for more details about this article) |
6/24. Neurological complications of acute and persistent Epstein-Barr virus infection in paediatric patients.Neurological complications of Epstein-Barr virus (EBV) have been reported almost exclusively in the course of acute primary infections. The role of EBV in paediatric neurological disease was investigated prospectively over a 2-year period, searching for acute primary, chronic, and reactivated EBV infections. Active EBV infections were diagnosed in 10/48 patients, including two with acute primary EBV infections (cranial neuritis and cerebellitis), one with chronic active infection (T/NK cell lymphoma with cranial neuritis), and seven with reactivated infections. Among these seven patients, three showed "Alice in Wonderland" syndrome, one facial nerve palsy, one progressive macrocephaly, and two prolonged encephalitic illness. The prognosis was good except for the patient with lethal T/NK cell lymphoma and the two girls with encephalitic illness. Despite steroid treatment, these girls suffered prolonged cognitive impairment and epileptic seizures. Both developed left-sided hippocampal atrophy, and one of them hippocampal sclerosis. Like primary infections, reactivated EBV infections cause neurological complications in a considerable number of paediatric patients, lead to serious long-term complications, and may contribute to the pathogenesis of hippocampal lesions.- - - - - - - - - - ranking = 0.096548873864637keywords = nerve (Clic here for more details about this article) |
7/24. Case of stroke in a 7-year-old male after parvovirus B19 infection.A 7-year-old male presented sudden-onset left hemiparesis, left-sided paresthesia, central paralysis of the left VII cranial nerve, and subsequent headache. Magnetic resonance scans were obtained 24 hours after admission. T(2)-weighted images disclosed hyperintensities located mainly in the posterior portion of the lenticular nucleus and in the head and body of the right caudate nucleus. A diagnosis of ischaemic stroke was made on the basis of neuroradiologic findings. Laboratory tests undertaken to establish the cause of stroke revealed parvovirus B19 infection preceding the neurologic abnormalities. In the absence of other known risk factors for stroke the possibility of parvovirus B19's being correlated with stroke onset is discussed.- - - - - - - - - - ranking = 0.096548873864637keywords = nerve (Clic here for more details about this article) |
8/24. adult post-infectious thalamic encephalitis: acute onset and benign course.We report on two young patients with an encephalitic syndrome and bilateral thalamic lesions following a presumably viral or mycoplasma respiratory tract infection with the main clinical symptoms of organic psychosis in the first and a prolonged amnestic syndrome and ataxia in the second case. Four months later the patients had recovered clinically and the thalamic lesions had resolved on magnetic resonance imaging in one case and almost completely in the other. We interpret the patients' illness as rare cases of a post-infectious acute thalamic encephalitis in adults. The cases and their relationship to possible post-infectious autoimmune inflammatory or toxic pathophysiological mechanisms are discussed and a review of the literature is provided.- - - - - - - - - - ranking = 0.33333333333333keywords = organ (Clic here for more details about this article) |
9/24. Community-acquired west nile virus infection in solid-organ transplant recipients.BACKGROUND: west nile virus (WNV) is rapidly spreading through north america. In the general population, the majority of WNV infections are asymptomatic. During 2002, an outbreak of WNV occurred in Toronto, canada. We observed four cases of severe symptomatic community-acquired WNV infection in our organ-transplant population. methods: Patient data were obtained from chart review. WNV was diagnosed by acute and convalescent serology. incidence was compared with data obtained from a population-based surveillance program. RESULTS: Four transplant patients had WNV encephalitis (n=3) or meningitis (n=1). Mean age was 44.5 (range 26-58) years and transplant type included kidney (n=2), liver (n=1), and heart (n=1). The mean time posttransplant was 3.8 years (range 2 months-8 years). The presenting symptoms were fever (4/4), confusion (3/4), headache (4/4), and weakness (2/4). cerebrospinal fluid showed a pleocytosis in all patients and elevated protein in three of four. All patients had identifiable occupational or recreational risk factors. There was no evidence that the infection was acquired by transfusion or the transplanted organ. Outcomes were full recovery (2/4), lower limb paralysis (1/4), and death (1/4). On the basis of active population surveillance data, the rate of WNV meningoencephalitis in the general population in the Toronto area was approximately 5 per 100,000. This compares to four cases in a transplant population of 2,000 patients (rate 200 per 100,000) (P<0.001). CONCLUSIONS: Transplant patients are likely at greater risk of severe neurologic disease caused by community-acquired WNV compared with the general population. Prevention of transmission and patient education may be more important in this population.- - - - - - - - - - ranking = 2keywords = organ (Clic here for more details about this article) |
10/24. Neuropathology of the brain and spinal cord in human west nile virus infection.OBJECTIVE: To describe the histopathology of the brain and spinal cord in human west nile virus (WNV) infection. MATERIALS AND methods: Single case report, including premortem clinical and laboratory findings, and autopsy. RESULTS: An 83-year-old female presented with acute confusion, high fevers, dysarthria and generalized subjective weakness, with decreased deep tendon reflexes and weakness on physical examination. electromyography showed evidence of a sensorimotor axonal polyneuropathy of the right-sided extremities. She became ventilator-dependent and died after a 2-week ICU stay, following withdrawal of life support. WNV infection was confirmed premortem by detection of IgM antibodies from serum and CSF and postmortem by RT-PCR from brain tissue. Examination of the brain parenchyma showed scattered microglial aggregates accompanied by perivascular chronic inflammation. The leptomeninges showed focal lymphocytic infiltrates. Examination of the spinal cord showed lymphocytic infiltrates in nerve roots and within the cord proper, with focal microglial nodules and neuronophagia in the ventral horns. Special stains were negative for a demyelinating process. General autopsy revealed only emphysema and atelectasis. CONCLUSIONS: The findings in this case suggest direct viral infection of the spinal cord and nerve roots as the mechanism of the flaccid paralysis often observed in patients infected with WNV. Findings are reviewed in comparison with other reports of neuropathologic findings in human WNV infection.- - - - - - - - - - ranking = 0.19309774772927keywords = nerve (Clic here for more details about this article) |
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