Neuromuscular Manifestations of West Nile Virus Infection

Abstract

The most common neuromuscular manifestation of West Nile virus (WNV) infection is a poliomyelitis syndrome with asymmetric paralysis variably involving one (monoparesis) to four limbs (quadriparesis), with or without brainstem involvement and respiratory failure. This syndrome of acute flaccid paralysis may occur without overt fever or meningoencephalitis. Although involvement of anterior horn cells in the spinal cord and motor neurons in the brainstem are the major sites of pathology responsible for neuromuscular signs, inflammation also may involve skeletal or cardiac muscle (myositis, myocarditis), motor axons (polyradiculitis), and peripheral nerves [Guillain–Barré syndrome (GBS), brachial plexopathy]. In addition, involvement of spinal sympathetic neurons and ganglia provides an explanation for autonomic instability seen in some patients. Many patients also experience prolonged subjective generalized weakness and disabling fatigue. Despite recent evidence that WNV may persist long-term in the central nervous system or periphery in animals, the evidence in humans is controversial. WNV persistence would be of great concern in immunosuppressed patients or in those with prolonged or recurrent symptoms. Support for the contention that WNV can lead to autoimmune disease arises from reports of patients presenting with various neuromuscular diseases that presumably involve autoimmune mechanisms (GBS, other demyelinating neuropathies, myasthenia gravis, brachial plexopathies, stiff-person syndrome, and delayed or recurrent symptoms). Although there is no specific treatment or vaccine currently approved in humans, and the standard remains supportive care, drugs that can alter the cascade of immunobiochemical events leading to neuronal death may be potentially useful (high-dose corticosteroids, interferon preparations, and intravenous immune globulin containing WNV-specific antibodies). Human experience with these agents seems promising based on anecdotal reports.

Evaluation of Prolonged Fatigue Post–West Nile Virus Infection and Association of Fatigue with Elevated Antiviral and Proinflammatory Cytokines

“…This has particularly been demonstrated by neuropathogens (13). WNV causes a neuroinvasive disease in a small percentage of those infected (17) and can result in long-term mental and physical impairments (2,14,21). Extended IgM antibody titers have been documented several years postinfection in humans (22,26,28), and persistent neurologic and renal infection has been documented in animal models (25,30,31).…”

“…While most infected individuals do not develop any signs or symptoms of disease, roughly 20% will develop febrile illness, and less than 1% will develop neuroinvasive disease, characterized as encephalitis, meningitis, and/or acute flaccid paralysis (17). Symptomatic WNV patients are likely to suffer from extended morbidity and mortality several years postinfection, particularly neurologic impairment (2,14,15). Common outcomes include short-term memory loss, concentration impairment, muscular weakness, and fatigue (2).…”

Zika virus: what do we know about the viral structure, mechanisms of transmission, and neurological outcomes?

“…Most viruses from this family are transmitted by mosquito or tick bites causing mild to potentially lethal infections in humans, the latter resulting from myelitis, encephalitis, and hemorragia reported for yellow fever, dengue, West Nile fever, Japanese encephalitis, and others (26) (27) (28) .…”

“…Guillain-Barre syndrome is an acute auto-immune polyradiculoneuropathy that may be caused by infections, many of which involve Flavivirus (27) and other arboviruses such as Chikungunya (75) . It is characterized by superior/ inferior limb extremity paresthesia, ascending muscular weakness, and paralysis that can evolve into respiratory and deglutition disorders, and death (76) .…”

Guillain–Barré Syndrome Associated with Zika Virus Infection in a Traveler Returning from Guyana

“…[14][15][16][17] The current ZIKV outbreak in the Americas began in May 2015 with confirmed autochthonous transmission in Brazil. 18 ZIKV has since spread rapidly throughout the region and, as of September 2016, endemic transmission has been reported in nearly every country or territory in the Americas and Caribbean including the United States.…”