Infections of the nervous system: an update on recent developments.
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The past decade has seen major changes in the field of infectious diseases. In particular, many new infections of the nervous system have been recognised, including the lethal infections of Enterovirus 71, and the Nipah and West Nile viruses. Increased interest in prion diseases has occurred, following the recognition of animal-to-human transmission in Europe. Familiar bacteria such as the pneumococcus continue to cause problems due to increasing resistance to multiple antibiotics. Furthermore, human immunodeficiency virus-infected and other immunocompromised patients are under the constant threat of opportunistic infections, many of which are targeted towards the brain and spinal cord. This paper reviews the changing world of nervous system infections, highlighting some of the most significant recent developments. (+info)
Infantile status epilepticus in Tunisia. Clinical, etiological and prognostic aspects.
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This retrospective study includes 139 infants (74 girls and 65 boys) treated for status epilepticus at two University hospitals in Tunisia between 1990 and 1997. Their mean age was 11 months. The majority of seizures were generalized (74%) and lasted between 30 minutes and 1 hour (70%). The cause of status epilepticus was classified as acute symptomatic in 56, febrile in 57, remote symptomatic in nine, progressive neurologic in 10 and idiopathic in seven. Overall mortality was 15.8% and neurological sequelae were identified in 36% of the cases during the mean follow-up time of 3.5 years. The incidence of significant sequelae was a function of aetiology (especially acute symptomatic causes) and age (under 1 year of age). We conclude that the most frequent causes of infantile status epilepticus in Tunisia were fever and acute symptomatic causes. Status epilepticus among infants is an important public health problem, with significant associated mortality and morbidity. Management of status epilepticus can be improved by more rapid access to appropriate medical care. (+info)
Human herpesvirus 6.
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The development of techniques for the culture of lymphoid cells and the isolation of viruses that infect these cells led to the discovery of human herpesvirus (HHV) 6 in 1986. At the time, HHV-6 was the first new human herpesvirus to be discovered in roughly a quarter of a century, and its isolation marked the beginning of an era of discovery in herpesvirology, with the identification of HHV-7 and HHV-8 (Kaposi's sarcoma-associated herpesvirus) during the following decade. Like most human herpesviruses, HHV-6 is ubiquitous and capable of establishing a lifelong, latent infection of its host. HHV-6 is particularly efficient at infecting infants and young children, and primary infection with the virus is associated with roseola infantum (exanthem subitum) and, most commonly, an undifferentiated febrile illness. Viral reactivation in the immunocompromised host has been linked to a variety of diseases, including encephalitis, and HHV-6 has been tentatively associated with multiple sclerosis. This article discusses the major properties of HHV-6, its association with human disease, and the pathobiological significance of viral reactivation. (+info)
Infections at high altitude.
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Every year, thousands of outdoor trekkers worldwide visit high-altitude (>2500 m) destinations. Although high-altitude areas per se do not harbor any specific agents, it is important to know the pathogens encountered in the mountains to be better able to help the ill sojourner at high altitude. These are the same pathogens prevalent in the surrounding lowlands, but various factors such as immunomodulation, hypoxia, physiological adaptation, and harsh environmental stressors at high altitude may enhance susceptibility to these pathogens. Against this background, various gastrointestinal, respiratory, dermatological, neurological, and other infections encountered at high altitude are discussed. Because there are few published data on infections at high altitude, this review is largely anecdotal and based on personal experience. (+info)
Central nervous system infection during immunosuppression.
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Suppression of the immune system by human immunodeficiency virus (HIV) infection or immunosuppressive therapy following transplantation increases susceptibility to CNS infection. Examination of the level and type of immunosuppression, in addition to the clinical and radiologic findings at the time of diagnosis can aid the clinician in determining the most likely etiology of infection. This article discusses how suppression of the host immune status modifies the presentation and diagnosis of selected CNS infections and the recommended treatment for these infections. (+info)
Immune-mediated protection from measles virus-induced central nervous system disease is noncytolytic and gamma interferon dependent.
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Neurons of the mammalian central nervous system (CNS) are an essential and largely nonrenewable cell population. Thus, virus infections that result in neuronal depletion, either by virus-mediated cell death or by induction of the cytolytic immune response, could cause permanent neurological impairment of the host. In a transgenic mouse model of measles virus (MV) infection of neurons, we have previously shown that the host T-cell response was required for resolution of infection in susceptible adult mice. In this report, we show that this protective response did not result in neuronal death, even during the peak of T-cell infiltration into the brain parenchyma. When susceptible mice were intercrossed with specific immune knockout mice, a critical role for gamma interferon (IFN-gamma) was identified in protection against MV infection and CNS disease. Moreover, the addition of previously activated splenocytes or recombinant murine IFN-gamma to MV-infected primary neurons resulted in the inhibition of viral replication in the absence of neuronal death. Together, these data support the hypothesis that the host immune response can promote viral clearance without concomitant neuronal loss, a process that appears to be mediated by cytokines. (+info)
Critical role for protein tyrosine phosphatase SHP-1 in controlling infection of central nervous system glia and demyelination by Theiler's murine encephalomyelitis virus.
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We previously characterized the expression and function of the protein tyrosine phosphatase SHP-1 in the glia of the central nervous system (CNS). In the present study, we describe the role of SHP-1 in virus infection of glia and virus-induced demyelination in the CNS. For in vivo studies, SHP-1-deficient mice and their normal littermates received an intracerebral inoculation of an attenuated strain of Theiler's murine encephalomyelitis virus (TMEV). At various times after infection, virus replication, TMEV antigen expression, and demyelination were monitored. It was found that the CNS of SHP-1-deficient mice uniquely displayed demyelination and contained substantially higher levels of virus than did that of normal littermate mice. Many infected astrocytes and oligodendrocytes were detected in both brains and spinal cords of SHP-1-deficient but not normal littermate mice, showing that the virus replicated and spread at a much higher rate in the glia of SHP-1-deficient animals. To ascertain whether the lack of SHP-1 in the glia was primarily responsible for these differences, glial samples from these mice were cultured in vitro and infected with TMEV. As in vivo, infected astrocytes and oligodendrocytes of SHP-1-deficient mice were much more numerous and produced more virus than did those of normal littermate mice. These findings indicate that SHP-1 is a critical factor in controlling virus replication in the CNS glia and virus-induced demyelination. (+info)
Cerebral aspergillosis caused by Neosartorya hiratsukae, Brazil.
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We report the first case of infection by Neosartorya hiratsukae, an ascomycete in which the conidial state resembles Aspergillus fumigatus. The fungus caused a brain infection in a Brazilian woman, who died despite itraconazole treatment. Diagnosis was established by direct microscopic examination, computed tomographic scan, and magnetic resonance imaging of the brain, and repeated cultures from the lesions. The in vitro antifungal susceptibility of the isolate is provided. (+info)