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19 - Clinical management of viral encephalitis
- from Section III - Introduction: immunity, diagnosis, vector, and beneficial uses of neurotropic viruses
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- By Kenneth L. Tyler, Department of Neurology, Microbiology, and Medicine, University of Colorado at Denver, and Neurology Service, Denver Veterans Affairs Medical Center, Denver, CO, USA, Donald H. Gilden, Departments of Neurology and Microbiology, University of Colorado School of Medicine, Denver, CO, USA
- Edited by Carol Shoshkes Reiss, New York University
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- Book:
- Neurotropic Viral Infections
- Published online:
- 22 August 2009
- Print publication:
- 16 October 2008, pp 347-361
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Summary
Introduction
Most cases of viral encephalitis are acute, although a few viruses can cause chronic progressive encephalitis. Rarely, systemic virus infection may trigger post-infectious encephalomyelitis. Viral encephalitis typically reflects viral invasion of the brain parenchyma. Encephalitis patients usually have alterations in their state of consciousness. Some viruses produce “diffuse” encephalitis in which the predominant features are impaired consciousness, signs of generalized central nervous system (CNS) dysfunction such as generalized seizures, and a cerebral spinal fluid (CSF) pleocytosis. Conversely, other viruses produce “focal encephalitis,” in which altered consciousness and CSF abnormalities are accompanied by prominent focal abnormalities on neuroimaging tests or clinical examination including hemiparesis, aphasia, hemisensory loss, ataxia, focal as well as generalized seizures, and, less often, involuntary movements, visual field defects, and cranial nerve deficits. Personality changes, language, and memory disturbances and psychotic features are frequent. Viral encephalitis must be distinguished from nonviral conditions that can present a similar clinical picture, including Lyme disease, tuberculosis, syphilis, Listeria, Mycoplasma, fungal and parasitic infections, brain abscess, subdural hematoma or abscess, brain tumors, CNS vasculitis, and toxic/metabolic encephalopathies.
Viral encephalitis may be epidemic or sporadic (see also Chapter 17). Causes of epidemic viral encephalitis include the togaviruses, enteroviruses (see Chapter 17), mumps and lymphocytic choriomeningitis (LCM) virus (see Chapter 1). The toga-viruses are RNA viruses transmitted by mosquitoes or ticks (arthropod-born) (see Chapters 6, 7, and 20), with a peak incidence in the Northern Hemisphere in the warm summer months.
58 - Simian varicella virus
- from Part IV - Non-human primate herpesviruses
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- By Ravi Mahalingam, Departments of Neurology, University of Colorado Health Sciences Center, Denver, CO, USA, Donald H. Gilden, Microbiology, University of Colorado Health Sciences Center, Denver, CO, USA
- Edited by Ann Arvin, Stanford University, California, Gabriella Campadelli-Fiume, Università degli Studi, Bologna, Italy, Edward Mocarski, Emory University, Atlanta, Patrick S. Moore, University of Pittsburgh, Bernard Roizman, University of Chicago, Richard Whitley, University of Alabama, Birmingham, Koichi Yamanishi, University of Osaka, Japan
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- Book:
- Human Herpesviruses
- Published online:
- 24 December 2009
- Print publication:
- 16 August 2007, pp 1043-1050
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Summary
Introduction
After primary infection (chickenpox) in children, varicella zoster virus (VZV) becomes latent in cranial, dorsal root and autonomic ganglia along the entire neuraxis and may reactivate decades later to produce zoster. The incidence of zoster and its attendant neurological complications is related to a natural decline in cell-mediated immunity (CMI) to VZV that occurs with aging, and which also develops in immunocompromised organ transplant recipients, and patients with cancer or AIDS. Yet the mechanism of reactivation and the cascade of events that are precipitated by impaired CMI to VZV are still unknown. To study such events require an animal model of varicella. While experimental animal models of latency and pathogenesis exist for closely related viruses such as herpes simplex types 1 and 2, VZV causes disease exclusively in humans. Thus, lack of a good animal model has hampered the studies of varicella latency and pathogenesis. Several attempts to produce disease by experimental inoculation of animals have led to seroconversion without clinical symptoms (Takahashi et al., 1975; Myers et al., 1980, 1985; Matsunaga et al., 1982; Wroblewska et al., 1982; Walz-Cicconi et al., 1986). Subcutaneous inoculation of the Oka VZV (vaccine strain) into the breast of a chimpanzee has been shown to produce viremia and mild rash restricted to the site of inoculation (Cohen et al., 1996). VZV DNA was detected in blood mononuclear cells (MNCs) of the chimpanzee during the 10-day incubation period.
15 - Postherpetic neuralgia and other neurologic complications
- from Part III - Epidemiology and Clinical Manifestations
- Edited by Ann M. Arvin, Stanford University School of Medicine, California, Anne A. Gershon, Columbia University, New York
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- Book:
- Varicella-Zoster Virus
- Published online:
- 02 March 2010
- Print publication:
- 23 November 2000, pp 299-316
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Summary
Zoster (shingles) epidemiology
Herpes zoster is a common disorder. More than 300000 cases are estimated to occur annually in the United States. With the exception of immunocompromised individuals (particularly AIDS patients), zoster is a disease of the elderly. The incidence among people over age 50 is double that of people under 50 (Harnisch, 1984), which translates into an 8–10 fold increased frequency in people over age 60 compared with those under 60. As the aging population increases (currently 13% of Americans are older than 65), the incidence of zoster-associated morbidity and mortality is also expected to increase. Varicella in infancy may predispose to zoster earlier in life (Guess et al., 1985). The incidence of recurrent zoster is less than 5% (Hope-Simpson, 1965). Although varicella outbreaks occur most often in the spring, zoster may develop at any time of the year. The risk of zoster in vaccinated individuals compared with those who developed naturally occurring chickenpox will not be known for decades. Meanwhile, some investigators have predicted an increased incidence of zoster with widespread use of the live attenuated varicella vaccine (Garnett & Grenfell, 1992; Wharton, 1996).
Pathology and pathogenesis
Despite the ubiquitous nature and frequency of VZV infection, the pathogenesis of zoster remains largely unknown. Our present understanding of virus spread, localization and replication is based on in vitro studies of infected human or primate cells in tissue culture, correlation of the presence of VZV in human tissues with pathologic changes in different clinical situations, and attempts to produce disease experimentally.
The histologic features caused by zoster focus on the dorsal root ganglia and adjacent nerves.