The 1959 Outbreak of Eastern Encephalitis in New Jersey: I. Introduction and Description of Outbreak12

Goldfield, Martin; Sussman, Oscar

doi:10.1093/oxfordjournals.aje.a120789

Cited by 27 publications

(15 citation statements)

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“…Cases occur at migration time, summer and autumn, and children are most affected, with an acute encephalitis which may be abrupt and virulent, with a mortality rate of 70%. 26 Western equine encephalitis This is less severe, occurring in eastern, central and western United States, Canada, and eastern South America.…”

Section: Epidemic Encephalitismentioning

confidence: 99%

Management of cerebral infection.

Anderson¹

1993

Journal of Neurology, Neurosurgery & Psychiatry

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Section: Epidemic Encephalitismentioning

confidence: 99%

Management of cerebral infection.

Anderson¹

1993

Journal of Neurology, Neurosurgery & Psychiatry

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“…Goldfield et al reported that one in eight young children developed fulminant encephalitis and only 1 in 23 had an inapparent infection. 4 Similarly, EEE tends to be more severe in elderly patients. 5 Histologically, infection in the human central nervous system (CNS) is characterized by a diffuse meningoencephalitis with widespread neuronal necrosis, perivascular cuffing with polymorphonuclear neutrophils and mononuclear cells, and vasculitis with vessel occlusion.…”

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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“…[8][9][10] Eastern equine encephalitis virus neuroinvasive disease is estimated to have a 30% case fatality rate and results in neurologic sequelae in more than 50% of survivors. 8,[11][12][13] Although veterinary EEEV vaccines are available for use in horses, there are no licensed vaccines or effective treatment of humans.…”

Section: Introductionmentioning

confidence: 99%

“…8 Human EEEV disease cases have occurred sporadically and in small clusters, primarily along the Atlantic and Gulf coasts of the United States. 9,11,14 The largest recorded EEEV outbreak occurred in New Jersey in 1959, with 32 laboratory-confirmed human cases during an 8-week period. 11 From 1997 through 2007, a median of eight neuroinvasive disease cases were reported to the Centers for Disease Control and Prevention annually.…”

Section: Introductionmentioning

confidence: 99%

“…9,11,14 The largest recorded EEEV outbreak occurred in New Jersey in 1959, with 32 laboratory-confirmed human cases during an 8-week period. 11 From 1997 through 2007, a median of eight neuroinvasive disease cases were reported to the Centers for Disease Control and Prevention annually. 15 This report summarizes the national EEEV surveillance data for 2003 through 2016, including human disease cases and nonhuman infections.…”

Section: Introductionmentioning

confidence: 99%

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Eastern Equine Encephalitis Virus in the United States, 2003–2016

Lindsey

Staples

Fischer

2018

The American Journal of Tropical Medicine and Hygiene

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Eastern equine encephalitis virus (EEEV) is a mosquito-borne alphavirus found in the eastern United States. Eastern equine encephalitis virus disease in humans is rare but can result in severe, often fatal, illness. This report summarizes the national EEEV surveillance data for 2003 through 2016, including human disease cases and nonhuman infections. Over the 14-year period, 633 counties from 33 states reported EEEV activity; 88% of those counties reported EEEV activity only in nonhuman species. A total of 121 human cases of EEEV disease were reported, with a median of eight cases reported annually. The national average annual incidence of EEEV neuroinvasive disease was 0.03 cases per million population. States with the highest average annual incidence included New Hampshire, Massachusetts, Vermont, Maine, and Alabama. Eastern equine encephalitis virus neuroinvasive disease incidence was highest among males and among persons aged < 5 and > 60 years. Overall, 118 (98%) case patients were hospitalized and 50 (41%) died. The case fatality ratio was highest among case patients aged ≥ 70 years. Nonhuman surveillance data indicate that the geographic range of EEEV is much greater than human cases alone might suggest. In areas where the virus circulates, health-care providers should consider EEEV infection in the differential diagnosis for meningitis and encephalitis. Providers are encouraged to report suspected cases to their public health department to facilitate diagnosis and consider interventions to mitigate the risk of further transmission. Because human vaccines against EEEV are not available, prevention depends on community efforts to reduce mosquito populations and personal protective measures to decrease exposure to mosquitoes.

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The 1959 Outbreak of Eastern Encephalitis in New Jersey: I. Introduction and Description of Outbreak12

Cited by 27 publications

References 0 publications

Management of cerebral infection.

Management of cerebral infection.

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

Eastern Equine Encephalitis Virus in the United States, 2003–2016

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