West Nile Virus
B. Denise Hemby and Theresa M. Campo
Definition
West Nile virus (WNV) is a viral illness caused by arthropodborne viruses that is transmitted to humans from infected mosquitoes, particularly Aedes, Culex, or Anophleles. The mosquitoes become infected by feeding on infected animals, especially birds. WNV has been found in a variety of birds, but more commonly in crows, hawks, owls, and jays. These birds become infected by eating on dead infected birds and animals. Usually people who get infected with WNV have no or mild symptoms (fever, headache, body aches, rash, or swollen glands). If WNV enters the brain, it can be life-threatening. WNV is a nationally notifiable condition. All cases should be reported to local public health departments to help authorities recognize outbreaks and implement control measures. Once a patient recovers from WNV disease, he or she is thought to have a lifelong immunity to the disease. There is no immunization for WNV. The two categories of WNV disease are nonneuroinvasive and neuroinvasive.
A.Nonneuroinvasive disease is less severe and often presents as a febrile illness.
B.Neuroinvasive disease leads to encephalitis, meningitis, and flaccid paralysis and requires much more intensive treatment.
Incidence
A.WNV is a reportable disease that allows the Centers for Disease Control and Prevention (CDC) to maintain significant surveillance data and statistics. A total of 47 states and the District of Columbia reported WNV infections in people, birds, or mosquitoes in 2017. Overall, 2,097 cases of WNV disease in people have been reported to CDC. Of these, 1,425 (68%) were classified as neuroinvasive disease (such as meningitis or encephalitis) and 672 (32%) were classified as nonneuroinvasive disease.
B.Approximately 1 in 150 patients develop severe neurological disease. About 1 out of 10 people who develop severe illness affecting the central nervous system (CNS) will die.
C.WNV was first noted in North America in 1999. WNV is endemic in the Middle East, Africa, and Asia.
D.Human WNV infections usually begin in midsummer and decline in September, correlating with peak mosquito activity. Mosquito bites are most likely to occur during peak feeding times during dawn and dusk. Prolonged contact or multiple mosquito bites increase the risk of developing WNV.
Pathogenesis
A.Mosquitoes are infected with WNV when feeding on an infected animal host. Wild birds are the most common source of infection, although other animals such as horses and chickens can be animal hosts. The virus is delivered to the human via mosquito bite when the mosquito’s saliva is deposited in the human skin cells. The virus replicates in the skin cells and migrates to the lymph nodes and various organs. Infected immune cells are able to transverse the blood–brain barrier and infect the brain parenchyma, leading to encephalitis and meningitis. The typical incubation period for WNV is 3 to 14 days.
Predisposing Factors
A.Time of year: Late summer and early fall.
B.Region: Living in or traveling to a region with a higher number of reported cases.
C.Work or recreational outdoor exposure.
D.Homelessness.
E.Age: Most serious disease occurring in the elderly and infants.
F.Blood transfusion.
G.Organ transplant.
Common Complaints
A.Nonneuroinvasive WNV:
1.Up to 80% of persons are asymptomatic.
2.Fever (>100.4°F or 38°C).
3.Headache.
4.Myalgia.
5.Arthralgias.
6.Fatigue.
7.Gastrointestinal (GI) symptoms: Nausea, vomiting, and diarrhea.
8.Maculopapular rash: Usually noted on chest, back, and arms; occurs in 20% to 50% of patients. The presence of the rash represents a decreased risk of neuroinvasive disease.
Other Signs and Symptoms
A.Abdominal pain.
B.Eye pain.
C.Irregular heart rhythm.
Potential Complications: Neuroinvasive Disease
A.Meningitis: Stiff neck, photophobia, focal neurological deficits, and higher fever (to 104°F).
B.Encephalitis: Mental status changes, stupor, confusion, coma, movement disorders, focal neurological deficits, personality changes, higher fever (to 104°F), and seizures.
C.Flaccid paralysis: Cranial nerve palsy, vertigo, dysarthria, dysphagia, respiratory failure.
D.Other rare complications:
1.Cardiac dysrhythmia.
2.Myocarditis.
3.Rhabdomyolysis.
4.Optic neuritis.
5.Uveitis.
6.Chorioretinitis.
7.Orchitis.
8.Pancreatitis.
9.Hepatitis.
Subjective Data
A.Review the onset, course, and duration of symptoms, especially fever, rash, headache, and myalgia.
B.Ask patient to describe any neurological symptoms, changes in mental status, stiff neck, photophobia, and seizures.
C.Review symptoms of other family members or coworkers who are also ill.
D.Ask the patient to recall what activity brought about or preceded his or her symptoms.
E.Ask patient what steps he or she has taken to treat symptoms at home.
F.Review the patient’s medical history for any chronic illnesses.
G.Review all medications, including over-the-counter (OTC) and herbal products.
H.Review history of mosquito bites and any preventive steps taken such as use of insect repellent:
1.Outdoor work activities.
2.Outdoor recreational activities.
3.Review recent travel.
I.Evaluate living conditions for exposure risks
Physical Examination
Patients presenting with neurological symptoms should be quickly assessed and referred to a neurologist for immediate evaluation of symptoms.
A.Check temperature, pulse, blood pressure, and respirations.
B.Inspect:
1.Observe general overall appearance, noting weakness, difficulty breathing, or changes in affect, speech, or level of consciousness (LOC).
2.Assess hydration status.
3.Ophthalmic examination: Assess the presence of papilledema.
4.Inspect face for muscle weakness or drooping.
5.Dermal inspection for the presence of a maculopapular rash, especially on the abdomen, back, and arms.
C.Auscultate:
1.Auscultate heart for dysrhythmias.
2.Auscultate all lung fields for adventitious breath sounds.
D.Palpate:
1.Palpate skin for signs of dehydration—poor skin turgor.
2.Palpate the neck and lymph nodes: Preauricular, posterior auricular, submental and sublingual, anterior cervical chain, and supraclavicular nodes.
3.Palpate abdomen for tenderness and/or organomegaly.
E.Mental status and neurologic examination:
1.Administer mental status exam to look for confusion, stupor, and changes in LOC.
2.Complete cranial nerve testing: Focus on visual fields, extraocular movement (EOM) of a transient downbeat nystagmus, facial muscle movement and strength, and gag reflex.
3.Muscle strength testing and testing for sensation in all extremities.
4.Test reflexes:
a.Deep tendon reflexes.
b.Babinski reflex is performed by running the reflex hammer up the midline of the sole of the foot from heel to the base of the toes (both feet are tested):
i.A normal reaction is for the toes to either remain still or else to curl downward.
ii.A positive Babinski is noted when the big toe points upward and the other toes fan out.
5.Assess for meningeal signs:
a.Signs of meningeal irritation include nuchal rigidity
b.Assess for positive Brudzinski’s and Kernig’s signs (refer to Figures 19.1 and 19.2):
i.Brudzinski’s sign: Place the patient supine and flex the head upward. Resulting flexion of both hips, knees, and ankles with neck flexion indicates meningeal irritation.
ii.Kernig’s sign: Place the patient supine, keeping one leg straight; flex the other hip and knee to a bent knee to form a 90-degree angle. Slowly extend the lower leg. This places a stretch on the meninges, resulting in pain and spasm for the hamstring muscle. Resistance to further extension can be felt.
Diagnostic Tests
A.WNV Immunoglobulin M (IgM) antibody capture ELISA (MACELISA) is the gold standard diagnostic test:
1.The presence of WNV-specific IgM in blood or cerebrospinal fluid (CSF) provides good evidence of recent infection but may also result from cross-reactive antibodies after infection with other flaviviruses or from nonspecific reactivity. According to product inserts for commercially available WNV IgM assays, all positive results obtained with these assays should be confirmed by neutralizing antibody testing of acute- and convalescent-phase serum specimens at a state public health laboratory or CDC.
2.If serum is collected within 8 days of illness onset, the absence of detectable virus-specific IgM does not rule out the diagnosis of WNV infection, and the test may need to be repeated on a later sample.
3.WNV immunoglobulin G (IgG) antibodies generally are detected shortly after IgM antibodies and persist for many years following a symptomatic or asymptomatic infection. Therefore, the presence of IgG antibodies alone is only evidence of previous infection and clinically compatible cases with the presence of IgG, but not IgM, should be evaluated for other etiologic agents.
B.If there is concern that the illness could have been caused by another type of flavivirus, an additional test, the plaque reduction neutralization test (PRNT), is used to identify false positive MAC-ELISA test results. PRNTs can also confirm acute infection by demonstrating a four-fold or greater change in WNV-specific neutralizing antibody titer between acute- and convalescent-phase serum samples collected 2 to 3 weeks apart.
C.Complete blood count (CBC) with differential.
D.For patients with neuroinvasive disease:
1.Lumbar puncture—for viral culture and tests to detect viral RNA on CSF or tissue specimens. Positive tests for WNV will show pleocytosis, increased lymphocytes, increased protein, and normal glucose. The MAC-ELISA test should be performed on CSF when lumbar puncture (LP) is completed.
2.Imaging: MRI of the brain and spinal cord is the preferred imaging test. MRI may show meningeal inflammation and bilateral lesions.
3.EEG: May show generalized slowness.
Differential Diagnoses
A.Nonneuroinvasive WNV:
1.WNV.
2.Other viral causes of febrile illness.
B.Neuroinvasive WNV:
1.Other viral causes of encephalitis: St. Louis equine encephalitis, California encephalitis (CE), Western and Eastern encephalitis.
2.Acute poliomyelitis.
3.Post-polio syndrome.
4.Guillain–Barré syndrome.
5.Multiple sclerosis.
6.Vertebrobasilar stroke.
Plan
A.Nonneuroinvasive disease:
1.Patient teaching:
a.Educate about expected signs and symptoms of WNV acute febrile illness.
b.Explain signs and symptoms that would require immediate medical evaluation such as mental status changes, stiff neck, and neurological symptoms.
c.Instruct the patient to rest as needed. The patient may expect fatigue to continue for up to 3 weeks.
d.Instruct that WNV disease will be reported to the health department for surveillance purposes. Special populations may be subject to follow-up.
e.Prevention strategies for WNV include ways to avoid mosquito bites:
i.Use mosquito repellent containing DEEP, picaridin, FR3535, or oil of lemon eucalyptus.
ii.Mosquitoes are most active from dusk to dawn; stay indoors during these peak times.
iii.Wear long sleeves and pants.
iv.Remove mosquito breeding sites; dump standing water in flower pots and buckets.
v.Change the water in bird baths weekly.
f.Finding dead birds may be a sign that WNV is circulated between birds and mosquitoes:
i.Do not handle a dead bird with bare hands.
ii.Report finding dead birds to the local health department for testing.
2.Dietary management:
a.There are no specific dietary recommendations for WNV.
b.Encourage the patient to drink plenty of fluids to prevent dehydration.
c.If the patient is experiencing nausea and vomiting, meals should be light and nonspicy, and should be taken in smaller amounts more frequently.
3.Pharmaceutical therapy: