Acute Flaccid Paralysis and West Nile Virus Infection

Sejvar, James J.; Leis, A. Arturo; Stokić, Dobrivoje S.; Gerpen, Jay A. van; Marfin, Anthony A.; Webb, Richard A.; Haddad, Maryam B.; Tierney, Bruce C.; Slavinski, Sally; Polk, Jo Lynn; Dostrow, Victor; Winkelmann, Michael; Petersen, Lyle R.

doi:10.3201/eid0907.030129

Cited by 176 publications

(114 citation statements)

References 30 publications

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“…Recently, viremia in asymptomatic donors has been shown to persist for longer periods of time (up to 104 days). There is a greater incidence of encephalitis than meningitis, which develops in around 1 in 150 infected patients (294,333,334). Elderly patients have been shown to be at greater risk of developing severe neurological disease.…”

Section: Infections Caused By West Nile Virusmentioning

confidence: 99%

Transmission of Tropical and Geographically Restricted Infections during Solid-Organ Transplantation

et al. 2008

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SUMMARY In recent years, the increasing number of donors from different regions of the world is providing a new challenge for the management and selection of suitable donors. This is a worldwide problem in most countries with transplantation programs, especially due to the increase in immigration and international travel. This paper elaborates recommendations regarding the selection criteria for donors from foreign countries who could potentially transmit tropical or geographically restricted infections to solid-organ transplant recipients. For this purpose, an extensive review of the medical literature focusing on viral, fungal, and parasitic infections that could be transmitted during transplantation from donors who have lived or traveled in countries where these infections are endemic has been performed, with special emphasis on tropical and imported infections. The review also includes cases described in the literature as well as risks of transmission during transplantation, microbiological tests available, and recommendations for each infection. A table listing different infectious agents with their geographic distributions and specific recommendations is included.

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Section: Infections Caused By West Nile Virusmentioning

confidence: 99%

Transmission of Tropical and Geographically Restricted Infections during Solid-Organ Transplantation

et al. 2008

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“…Human infection is associated with a febrile illness that can progress to a severe neuroinvasive disease characterized by seizures, muscle weakness, cognitive impairment, and a poliomyelitis-like flaccid paralysis (2,50,51). WNV induces neuronal damage and loss in several brain regions, including the hippocampus, brain stem, cerebellum, and anterior horn of the spinal cord (13,21).…”

mentioning

confidence: 99%

Caspase 3-Dependent Cell Death of Neurons Contributes to the Pathogenesis of West Nile Virus Encephalitis

Samuel¹,

Morrey

Diamond

2007

J Virol

162

176

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West Nile virus (WNV) is a neurotropic, arthropod-borne flavivirus that has become a significant global cause of viral encephalitis. To examine the mechanisms of WNV-induced neuronal death and the importance of apoptosis in pathogenesis, we evaluated the role of a key apoptotic regulator, caspase 3. WNV infection induced caspase 3 activation and apoptosis in the brains of wild-type mice. Notably, congenic caspase 3 ؊/؊ mice were more resistant to lethal WNV infection, although there were no significant differences in the tissue viral burdens or the kinetics of viral spread. Instead, decreased neuronal death was observed in the cerebral cortices, brain stems, and cerebella of caspase 3 ؊/؊ mice. Analogously, primary central nervous system (CNS)-derived neurons demonstrated caspase 3 activation and apoptosis after WNV infection, and treatment with caspase inhibitors or a genetic deficiency in caspase 3 significantly decreased virus-induced death. These studies establish that caspase 3-dependent apoptosis contributes to the pathogenesis of lethal WNV encephalitis and suggest possible novel therapeutic targets to restrict CNS injury.

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“…Table 1 provides an overview and summary of specific symptoms, neurologic findings and frequency of respiratory and intensive care unit support required for patients with Zika-associated GBS. Although there is no particular neurologic finding that would suggest Zika virus over an alternate etiology, clinical symptoms typically appear distally and symmetrically, as opposed to West Nile virus infection, which typically produces an asymmetric flaccid paralysis similar to polio (14) .…”

Section: Guillain-barré Syndrome Associated With Zika Virus Infectionmentioning

confidence: 99%

Manifestaciones neurológicas de la infección por el virus zika

Zunt¹

2017

An Fac med

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Zika virus is a flavivirus transmitted via mosquito bite, blood transfusion, sexual intercourse or from motherto-child during gestation. Although neurologic complications of Zika virus infection are rare, Guillain-Barré syndrome (GBS) is the most common manifestation and typically develops soon after the initial systemic manifestations of Zika virus infection. This syndrome typically starts in the distal limbs with symmetric sensory abnormalities and progresses to involve weakness and decreased or absent deep tendon reflexes. Severe cases may also involve respiratory and cardiovascular impairment requiring care in an intensive care unit, and ventilator or circulatory support. A review of 166 published cases of GBS associated with Zika virus is notable for lower mortality than seen with sporadic GBS, but limited data regarding long-term outcome. When available, treatment with intravenous IgG (IVIg) or plasmapheresis, can reduce the severity and duration of symptoms. Keywords: Zika Virus; Neurologic Manifestations; Central Nervous System Infection; Guillain-Barré Syndrome. Resumen El virus zika es un flavivirus transmitido a través de la mordedura de mosquito, transfusión de sangre, la relación sexual o de madre a hijo durante la gestación. Aunque las complicaciones neurológicas de la infección por el virus zika son raras, el síndrome de Guillain-Barré (GBS) es la manifestación más común y normalmente se desarrolla poco después de las manifestaciones sistémicas iniciales de la infección por el virus. Este síndrome comienza en las extremidades distales con alteraciones sensoriales simétricas y progresa hasta involucrar la debilidad y la disminución o ausencia de reflejos tendinosos profundos. Los casos graves pueden implicar deterioro respiratorio y cardiovascular, requiriendo atención en una unidad de cuidados intensivos, así como ventilador o soporte circulatorio. Una revisión de 166 casos publicados de GBS asociados con el virus zika se caracteriza por una menor mortalidad que los observados con GBS esporádica, pero los datos son limitados con respecto a resultados a largo plazo. Cuando esté disponible, el tratamiento con IgG intravenoso (IVIg) o plasmaféresis puede reducir la gravedad y duración de los síntomas. Palabras clave. Virus Zika; Manifestaciones Neurológicas; Infección del Sistema Nervioso Central; Síndrome de Guillain-Barré. SIMPOSIO VIRUS ZIKA

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Acute Flaccid Paralysis and West Nile Virus Infection

Cited by 176 publications

References 30 publications

Transmission of Tropical and Geographically Restricted Infections during Solid-Organ Transplantation

Transmission of Tropical and Geographically Restricted Infections during Solid-Organ Transplantation

Caspase 3-Dependent Cell Death of Neurons Contributes to the Pathogenesis of West Nile Virus Encephalitis

Manifestaciones neurológicas de la infección por el virus zika

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