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West Nile Virus - 10/12/2012

posted Oct 12, 2012, 1:33 PM by Monique Tanna   [ updated Dec 27, 2012, 6:43 AM by Purnema Madahar ]

Today we had a very interesting CRS case of a 67 year old man who presented with severe headache and fever for 3 days along with several nonspecific complaints including muscle aches, nausea, abdominal pain, diarrhea and anorexia.  The teams did a great job of teasing out the history including a recent URI 3 weeks prior to admission, and onset of symptoms upon returning from a 4-day stay in Florida.  The patient had a temperature of 102.7, and his neurologic exam was notable for lethargy, disorientation (A&O to person and time), intact cranial nerves and muscle strength, with an upgoing Babinski bilaterally.  He also had a supple neck and a macular rash on bilateral ankles.  The teams narrowed their differential to viral encepahlitis, with West Nile virus high on the list given his presentation in the early Fall.  He was found to have West Nile virus, a single stranded RNA virus, diagnosed by a positive IgM titer in the serum and CSF.  In this edition of the Daily, I'd like to review the epidemiology, clinical manifestations, and diagnosis of West Nile virus.

Let’s start with some history.  When was the West Nile virus first described, and what is the epidemiology?

The West Nile virus was first isolated in 1937 in a patient from the West Nile province of Uganda (1).  It has been reported throughout Africa, the Middle East, parts of Europe, western Russia, southwestern Asia, and Australia (1).  The virus first emerged in North America in 1999, causing 62 cases of encephalitis and 7 deaths in NY, capturing the attention of the public and media.

What time of year is it?  (One of Darlene’s favorite questions!)

Approximately 85% of infections occur in August and September, which is the peak transmission within the bird-mosquito-bird cycle.  In the US, human illness has been reported from May through December (1).

What are the clinical manifestations?

Most patients are asymptomatic.  Symptoms are seen in only 20-40% of patients, and can range from a nonspecific febrile illness to severe meningoencephalitis.  The incubation period ranges from 2 to 14 days, but may be longer in immunosuppressed patients.  The illness usually lasts 3 to 6 days, with an acute onset of symptoms including headache, nausea, vomiting, abdominal pain, diarrhea, anorexia, eye pain, malaise, myalgia, phayngitis and rash (maculopapular, morbilliform).  Less than 1% develop meningitis, encephalitis, or acute flaccid paralysis (AFP).  These patients can have severe weakness or movement disorders (tremor, myoclonus, parkinsonian features).  AFP can occur without overt meningoencephalitis, but with asymmetric weakness affecting both the upper and lower limbs, hyporeflexia or areflexia, acute bowel or bladder dysfunction, without sensory abnormalities.  These manifestations are thought to be due to the destruction of spinal anterior horn cells, causing a poliomyelitis-like syndrome (1). 

How is West Nile virus diagnosed?

Serum leukocyte count can be normal or elevated.  CSF usually has a predominance of lymphocytes and elevated protein levels.  The diagnosis is made by detection of IgM antibodies using ELISA in the serum and/or CSF.  Detection of antibodies in the CSF indicates CNS infection as IgM antibodies do not cross the blood-brain barrier.  90% of patients with CNS infection have detectable IgM antibodies in the CSF within 8 days of symptom onset, and these may persist for longer than 500 days.  In patients with a prior West Nile infection, a 4-fold or higher increase in titer is consistent with acute infection.  Head CT is usually normal, but MRI may show focal lesions in the pons, basal ganglia, thalamus, and/or enhancement of the leptomeninges and periventricular areas. 

What is the treatment and clinical outcome?

Treatment is largely supportive.  Case-fatality rates range from 4-18% (1).  Advanced age is the most important risk factor for death, and other possible risk factors include severe muscle weakness, altered mental status, and a history of diabetes or immunosuppression (1).  Many patients have persistent neurologic deficits; in 2000, fewer than half returned to their baseline functional level, and only one third were fully ambulatory (1). 

Attached are some review articles on West Nile virus, as well as a review of the pathogenic flaviviruses.

West Nile Virus Review: JAMA 2002
Petersen LR, Marfin AA, Gubler DJ. West Nile virus. JAMA. 2003 Jul 23;290(4):524-8.

West Nile Virus Review: BMJ 2003
Solomon T, Ooi MH, Beasley DW, Mallewa M. West Nile encephalitis. BMJ. 2003 Apr 19;326(7394):865-9.

West Nile Virus Review: Annals 2002
Petersen LR, Marfin AA. West Nile virus: a primer for the clinician. Ann Intern Med. 2002 Aug 6;137(3):173-9.

Pathogenic Flaviviruses
Gould EA, Solomon T. Pathogenic flaviviruses. Lancet. 2008 Feb 9;371(9611):500-9.
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