Systemic and Ophthalmic Manifestations of West Nile Virus Infection

Yos Priestley; Marcia Thiel; Steven B. Koevary


Expert Rev Ophthalmol. 2008;3(3):279-292. 

In This Article

Systemic Clinical Features of Infection

The incubation period of WNV prior to the onset of symptoms ranges from 2 to 14 days. This said, most patients infected with WNV are asymptomatic and many cases go unreported. Symptoms are estimated to develop in only 20-40% of individuals who are infected by the virus.[19] Three clinical categories of infection have been defined: asymptomatic, WNF, and WN meningoencephalitis (WNM). WNF occurs much more frequently than WNM. The most common symptoms of WNF are flu-like and include fever, headache, myalgia, malaise, diarrhea, vomiting and fatigue.[4,6,21,38] Other reported, but less common, features include a maculopapular rash on the chest, back and lower extremities, pharyngitis, arthralgias, seizures and hearing loss.[11,39,40,41,42,43] Less-common organ involvement includes hepatitis, pancreatitis, myocarditis and orchitis. One patient with diagnosed WNV presented with diffuse monomorphic skin eruptions comprised of erythematous papules that spread to the patient's face, palms, and soles.[44] A maculopapular rash is seen most often in patients with WNF or WNM rather than WNE.[42] Symptoms of WNF usually subside in less than a week and patients generally recover within days to months.[11,45,46]

In less than 1% of cases, individuals develop severe, potentially fatal neurologic disease that has been variously classified as WNM, WNE, and WN poliomyelitis (WNP; acute flaccid paralysis). Table 1 highlights the percentages of cases in each category of WNV disease in humans and the most common symptoms of each. As evidenced, many symptoms overlap in given individuals, making diagnosis difficult; however, given the high mortality rate and more severe complications of the encephalitic form of the disease, settling on a correct diagnosis is critical.

WNM presents as would a typical meningitis, with symptoms including fever, headache, stiff neck, nuchal rigidity and photophobia.[4,11,20,21] Other symptoms may include respiratory failure, limb weakness and cardiac arrhythmia.[11] WNE can develop as the disease begins to involve the brain. When this occurs, additional, serious symptoms may develop, including altered mental status and state of consciousness, dysarthria, seizures, tremor, ataxia, involuntary movements, parkinsonism and cranial nerve palsies.[4,11,20,21] In one reported case by Bode et al. only 21% of patients with WNE who survived acute disease returned to their original level of neurological function following hospitalization.[11] It is not clear why or how the infection targets certain regions of the CNS; regions of the brain that were shown to be susceptible include the medulla,[6] basal ganglia[2,6,47,48] and thalamus.[2,21,48]

A rare but clearly important neuroinvasive condition that has been associated with WNV infection is acute flaccid paralysis, which develops as a result of a reduction in anterior horn motor response amplitudes.[20] Many of these patients initially present with the typical flu-like symptoms of WNF and go on to develop muscle weakness a week or two later.[19] Symptoms were reported to range from weakness in one limb to flaccid quadriplegia.[20,50,51,52] At autopsy, a 41 year old patient with WNP was reported to have severe neuronal loss and gliosis in his spinal cord anterior horns and substantia nigra; his anterior horn nerve roots and substantia nigra also showed severe atrophy and neurofibrillary tangle formation, respectively.[53] While many patients with severe flaccid paralysis due to WNP are misdiagnosed with Guillain-Barre syndrome (GBS), very few have had confirmed demyelinating neuropathy in nerve conduction studies.[6,19,20,54] Prognosis is variable, with some patients recovering fully in weeks while others have continued to suffer long-term complications.[55] Cranial nerve involvement, while uncommon, has also been reported in these patients, with CN7 being preferentially affected, resulting in facial paralysis and weakness.[20,56]


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