Clinical and Neuroradiographic Manifestations of Eastern Equine Encephalitis

Deresiewicz, Robert L.; Thaler, Scott J.; Hsu, Liangge; Zamani, Amir A.

doi:10.1056/nejm199706263362604

Cited by 289 publications

(223 citation statements)

References 27 publications

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“…Following an incubation period of 5 to 15 days, infection may progress to systemic then encephalitic disease [5]. Systemic disease presents with headache, fever, malaise, myalgia, nausea, and vomiting.…”

Section: Togaviridaementioning

confidence: 99%

“…VEEV, WEEV, and EEEV are all widely distributed in North, Central, and South America. Human infection can progress rapidly to encephalitis, with fatality rates of~1 % in cases of VEEV and WEEV, and 50 % to 75 % in cases of EEEV cases [5,6]. Of the 3, VEEV is considered the most important zoonotic pathogen, with several reported human outbreaks in South and Central Americas, primarily by enzootic VEEV strains [7].…”

Section: Epidemiology Of Encephalitic Arbovirusesmentioning

confidence: 99%

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Encephalitic Arboviruses: Emergence, Clinical Presentation, and Neuropathogenesis

2016

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Arboviruses are arthropod-borne viruses that exhibit worldwide distribution, contributing to systemic and neurologic infections in a variety of geographical locations. Arboviruses are transmitted to vertebral hosts during blood feedings by mosquitoes, ticks, biting flies, mites, and nits. While the majority of arboviral infections do not lead to neuroinvasive forms of disease, they are among the most severe infectious risks to the health of the human central nervous system. The neurologic diseases caused by arboviruses include meningitis, encephalitis, myelitis, encephalomyelitis, neuritis, and myositis in which virus-and immune-mediated injury may lead to severe, persisting neurologic deficits or death. Here we will review the major families of emerging arboviruses that cause neurologic infections, their neuropathogenesis and host neuroimmunologic responses, and current strategies for treatment and prevention of neurologic infections they cause.

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Section: Togaviridaementioning

confidence: 99%

Section: Epidemiology Of Encephalitic Arbovirusesmentioning

confidence: 99%

Encephalitic Arboviruses: Emergence, Clinical Presentation, and Neuropathogenesis

2016

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“…However, in some cases, EEE virus crosses the blood-brain barrier and causes a severe, and often fatal, acute encephalitis, which kills 50 to 75% of infected humans and leaves many survivors with serious neurological sequelae. 1,3 It has long been recognized that EEE infection in children tends to have a more rapid onset and to be more severe. Goldfield et al reported that one in eight young children developed fulminant encephalitis and only 1 in 23 had an inapparent infection.…”

mentioning

confidence: 99%

Early Events in the Pathogenesis of Eastern Equine Encephalitis Virus in Mice

Vogel

Kell

Fritz

et al. 2005

The American Journal of Pathology

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To elucidate the pathogenesis of eastern equine encephalitis (EEE) virus infections, we used histopathology, immunohistochemistry, and in situ hybridization to track the spread and early cellular targets of viral infection in mice. Young mice were inoculated with virulent EEE virus in their right rear footpad and were followed in a time-course study for 4 days. Virulent EEE virus produced a biphasic illness characterized by an early self-limiting replication phase in peripheral tissues followed by an invariably fatal central nervous system (CNS) phase. In the early extraneural phase, there was primary amplifying replication of virus within fibroblasts at the inoculation site and within osteoblasts in active growth areas of bone that resulted in a transient high-titer viremia. Pathological changes and viral infection were observed as early as 12 hours post-infection (PI) in osteoblasts, skeletal muscle myocytes, and in fibroblasts along fascial sheaths. The severity and extent of infection in peripheral tissues peaked at day 1 PI. In the neural phase of infection, virus was first detected in the brain on day 1 PI, with rapid interneuronal spread of infection leading to death by day 4 PI. EEE virus appeared to be directly cytopathic for neurons. The very rapid onset and apparently random and widely dispersed infection in the CNS, with concurrent sparing of olfactory neuroepithelium, strongly suggests that invasion of the CNS by EEE occurs by a vascular route, rather than via peripheral nerves or the olfactory neuroepithelium. Our finding that metaphyseal osteoblasts are an early site of amplifying viral replication may explain the higher-titer viremias and higher incidence of neuroinvasion and fulminant encephalitis seen in the young, and may also explain why mature animals become refractory to encephalitis after peripheral inoculation with EEE virus. Eastern equine encephalitis (EEE) virus is a singlestranded RNA virus in the genus Alphavirus (family Togaviridae) that can cause a severe mosquito-borne encephalitis in humans, horses, and game birds. 1 In North America, EEE virus is prevalent in freshwater swamps along the Atlantic and Gulf coasts of the United States where both its mosquito vector, Culiseta melanura, and its passerine bird reservoir hosts live. 2 The virus has a very wide host range, but as Culiseta mosquitoes rarely feed on mammalian hosts, other bridging mosquito species actually transmit the virus from infected birds to horses, and occasionally, to humans. Most EEE infections in humans are inapparent or produce a low-grade fever followed by malaise, arthralgia, and myalgia. However, in some cases, EEE virus crosses the blood-brain barrier and causes a severe, and often fatal, acute encephalitis, which kills 50 to 75% of infected humans and leaves many survivors with serious neurological sequelae. 1,3 It has long been recognized that EEE infection in children tends to have a more rapid onset and to be more severe. Goldfield et al reported that one in eight young children developed fulminant ence...

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“…This pattern is similar to that seen in ADEM. The presence of neutrophils rather than lymphocytes, as the predominant cell type, occurs frequently in patients with West Nile virus (WNV) neuroinvasive disease [50], and tick borne encephalitis virus [51], and can also occur with Eastern equine encephalitis [52].…”

Section: Viral Encephalitismentioning

confidence: 99%

Neuro-Intensive Care of Patients with Acute CNS Infections

Beckham

Tyler

2012

Neurotherapeutics

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Summary Infections in the central nervous system (CNS) are caused by a wide range of microorganisms resulting in distinct clinical syndromes including meningitis, encephalitis, and pyogenic infections, such as empyema and brain abscess. Bacterial and viral infections in the CNS can be rapidly fatal and can result in severe disability in survivors. Appropriate identification and acute management of these infections often occurs in a critical care setting and is vital to improving outcomes in this group of patients. This review of diagnosis and management of acute bacterial and viral infections in the CNS provides a general approach to patients with a suspected CNS infection and also provides a more detailed review of the diagnosis and management of patients with suspected bacterial meningitis, viral encephalitis, brain abscess, and subdural empyema.

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Clinical and Neuroradiographic Manifestations of Eastern Equine Encephalitis

Cited by 289 publications

References 27 publications

Encephalitic Arboviruses: Emergence, Clinical Presentation, and Neuropathogenesis

Encephalitic Arboviruses: Emergence, Clinical Presentation, and Neuropathogenesis

Early Events in the Pathogenesis of Eastern Equine Encephalitis Virus in Mice

Neuro-Intensive Care of Patients with Acute CNS Infections

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