Enteroviruses

Enteroviruses are unenveloped single-stranded RNA viruses forming a genus in the family picornavirus. They account for 70 to 80 percent of cases of viral meningitis in which an agent is identified. Enteroviruses survive well in water and sewage, are transmitted by fecal-oral or hand-mouth routes, and replicate initially in the gastrointestinal tract. Enteroviruses were previously subdivided into three groups: polioviruses, echoviruses, and coxsackieviruses. Newer isolated enteroviruses have been assigned numbers (e.g., enterovirus 71 or EV 71). Coxsackievirus A9 and echoviruses E7, E9, E11, E19, and E30 have accounted for 70 percent of all cultured isolates from cerebrospinal fluid (CSF) in cases of enteroviral meningitis. Polioviruses have been largely eradicated, persisting only in Nigeria, Pakistan, and Afghanistan. Other enteroviruses have a worldwide distribution, and although cases of enteroviral meningitis occur throughout the year, infection is most likely to occur during summer and early fall months when conditions of sanitation are most lax. Acute enterovirus infection is usually asymptomatic or may result in mild gastroenteritis or pharyngitis; less than 5 percent of patients will develop meningitis or encephalitis.

Enteroviral CNS infection typically causes meningitis rather than encephalitis, with fever, headache, and stiff neck. These symptoms commonly last for 1 to 3 weeks in older children and adults. In occasional patients, enteroviruses may cause encephalitis or rarely a paralytic disease similar to polioviruses (see below) and may cause protracted, atypical infection in immunocompromised patients.

Herpes Simplex Virus Type 2

HSV-2 is a double-stranded DNA virus that is universal in human populations. HSV-2 is usually transmitted sexually, with antiviral antibodies first appearing in adolescence or early adult life. Following acute infection, the virus persists predominantly in spinal sensory ganglia and is subject to periodic reactivation, often without cutaneous or mucosal signs of infection. HSV-2 accounts for up to 10 to 20 percent of isolates in adults with viral meningitis and is roughly twice as common among women. HSV-2 as a cause of viral meningitis should be considered particularly in young, sexually active adults. Older data suggested that up to 36 percent of women and 11 percent of men had headache, fever, or nuchal rigidity at the time of their first attack of genital herpes. Some patients with HSV-2 meningitis following genital herpes may have focal lumbosacral symptoms including urinary retention suggesting nerve root infection, and the virus may also be associated with myelitis. HSV-2 DNA can frequently be detected in CSF by amplification using the polymerase chain reaction (PCR). Approximately 20 percent of individuals with acute HSV-2 meningitis may subsequently develop recurrent episodes of meningitis (Mollaret meningitis). Many individuals with recurrent meningitis have no history of genital herpes and lack genital lesions during attacks of meningitis.

Patients with HSV-2 meningitis usually recover without treatment. Although successful treatment with acyclovir has been described in individual cases, the efficacy of antiviral therapy in acute or recurrent HSV-2 meningitis is uncertain. In a recent trial, suppressive treatment with valacyclovir did not prohibit recurrence of HSV-2 meningitis.

Varicella Zoster Virus

VZV is a herpesvirus typically associated with chicken pox during acute infection and with cutaneous zoster (shingles) during reactivated infection. Like HSV-2, VZV is thought to account for 10 to 20 percent of identified cases of viral meningitis. Meningitis may occur during either primary or reactivated infection and may do so in the absence of rash. In contrast to many other viruses, VZV meningitis may result in significant CSF hypoglychorrachia and may be accompanied by a CSF pleocytosis characterized by atypical lymphocytes. As with HSV-2 meningitis, most immunocompetent patients with VZV meningitis recover without treatment. VZV infection may produce a wide variety of other neurologic conditions, which are discussed in greater detail later.

Less Common Causes of Viral Meningitis

The arthropod-borne agents—WNV, St. Louis encephalitis virus, California encephalitis virus, Powassan virus, and Colorado tick fever virus—are most commonly associated with encephalitis, but may also cause meningitis. WNV, St. Louis encephalitis virus, and California encephalitis virus are transmitted by mosquitoes and tend to be more common in summer and early autumn months. The tick-borne agents Powassan virus and Colorado tick fever virus can cause a rash and most frequently occur during spring and early summer months. An important consideration in patients with suspected Colorado tick fever is the tick-borne rickettsial illness Rocky Mountain spotted fever, which also has a peak incidence in spring and summer, usually has a rash, and requires antibiotic treatment.

LCMV is an arenavirus whose natural host is mice but which can cause meningitis and, less frequently, encephalitis in humans. The virus is present in mouse urine and is acquired by the respiratory route. At one time, it was thought to account for roughly 4 percent of diagnosed cases of viral meningitis, but in recent years it has become much less common, for unknown reasons. LCMV infections are classically most common in autumn and winter. Occasional outbreaks of infection have been associated with exposure to mice in animal facilities or to pet hamsters or guinea pigs. The meningitis associated with LCMV may be accompanied by low CSF glucose levels, which may persist in cases of prolonged recovery over weeks to months. In neonates, LCMV may cause a fatal systemic and CNS infection. Outbreaks of severe infection with high mortality have also been reported in which LCMV has been transmitted by organ transplantation. Reliable antiviral therapy for LCMV infection is not available; one patient with transplant-acquired LCMV infection recovered after reduction of the patient’s immunosuppressive regimen and treatment with ribavirin.

Mumps virus, once a major cause of meningitis worldwide, is now rare in developed countries but remains a significant cause of meningitis in areas where mumps immunization is not practiced. The virus has caused occasional epidemics in Western countries in unvaccinated populations exposed to individuals who have visited areas where mumps is still prevalent.

Human Immunodeficiency Virus

CNS invasion occurs early in the course of primary HIV infection, and meningitis due directly to HIV occurs in 9 to 24 percent of patients (see Chapter 44 ). The meningitis usually develops near the time of seroconversion and often occurs in the setting of an acute, mononucleosis-like retroviral syndrome characterized by fever, pharyngitis, and cervical lymphadenopathy; CNS findings of disorientation, confusion, or psychosis accompany this syndrome in some patients. Primary HIV meningitis should be considered in young adults with meningitis, particularly when they have HIV risk factors or a coexistent mononucleosis-like syndrome. The symptoms of meningitis are usually not severe and resolve in most but not all cases; in some patients, HIV meningitis becomes chronic. The CSF typically reveals a mild lymphocytic pleocytosis, mildly elevated protein content, and normal glucose level. Standard serologic tests for HIV (as well as tests for home use) are negative in many patients with this acute syndrome; serologic tests first become positive 22 to 27 days after onset of acute infection. The diagnosis of acute HIV meningitis is made by detecting viral RNA or viral p24 antigen in serum or plasma; the viral RNA usually becomes detectable 3 to 5 days prior to the detection of p24 antigen and is typically present in copy numbers greater than 50,000 copies/ml. Treatment of HIV is with antiretroviral therapy, and follow-up assay for antiviral antibodies is used to confirm the diagnosis. In approaching patients with suspected HIV meningitis, it must be kept in mind that lymphocytic meningitis in patients with HIV infection may be caused by a wide variety of other agents, many of which are treatable.

Approach to Patients with Viral Meningitis

Bacterial meningitis is the primary concern in any patient presenting with acute meningitis. If the patient is severely ill, bacterial meningitis should be suspected and presumptive antibiotic therapy should be initiated immediately, usually along with corticosteroids. Similarly, acyclovir should be initiated if HSV encephalitis is a significant diagnostic concern. Antibiotics and acyclovir can be discontinued once CSF studies are negative. In general, patients presenting with viral meningitis are less severely ill, and antibiotic and acyclovir treatment may often be deferred.

The diagnosis of viral meningitis is made by lumbar puncture and CSF analysis. In acute bacterial meningitis, there is often an elevated opening pressure and typically a marked neutrophilic pleocytosis, with significantly elevated protein and depressed glucose concentrations. In contrast, in viral meningitis the opening pressure is usually normal or mildly elevated, and the CSF white cell count is usually in the range of 50 to 2000/ml. Although viral meningitis typically produces a lymphocytic pleocytosis, polymorphonuclear leukocytes may constitute over 50 percent of the cells during the first 24 to 36 hours of the infection and may occasionally remain the predominant cell type for longer periods of time. Protein is usually elevated in the range of 50 to 100 mg/dl but is sometimes higher. The CSF glucose level in viral meningitis is usually greater than 50 percent of blood glucose; the absence of CSF hypoglychorrhachia is an important consideration in differentiating viral from bacterial meningitis. Depression of glucose to levels approaching those of bacterial meningitis may occasionally occur in meningitis caused by HSV-2, VZV, mumps, and LCMV. In the proper setting, lymphocytic pleocytosis with low CSF glucose may also raise concern about tuberculous or fungal meningitis.

Specific diagnosis of viral agents in CSF currently involves PCR amplification of viral RNA or DNA; at present, tissue culture isolation of virus is rarely performed for diagnostic purposes ( Table 43-1 ). PCR is rapid and has a high level of sensitivity in meningitis due to enteroviruses, HSV-2, and VZV during acute infection. PCR can identify all strains of enteroviruses but does not distinguish between individual strains. Enteroviral RNA can be identified in CSF in the first 1 or 2 days of meningitis, from throat for several days, and from stool for a few weeks. Because asymptomatic enterovirus infections are common in the summer months, enterovirus isolation from throat or stool does not make a definitive diagnosis of enterovirus meningitis. In one study, use of an enterovirus PCR assay in the emergency department in children with aseptic meningitis resulted in significantly less antibiotic use, shorter length of hospitalization, and lower hospital costs. Although it is the diagnostic study of choice in many viral meningitides, CSF PCR may be negative early in the disease course, and diagnostic yield may be highest when CSF is obtained within 3 to 14 days of onset of meningitis. In certain instances, the detection of CSF immunoglobulins may have greater diagnostic sensitivity than PCR. This is the case in WNV neuroinvasive disease and other arbovirus infections, in which detection of virus-specific immunoglobulin M (IgM) is more sensitive than PCR. Similarly, detection of virus-specific IgG in CSF may prove diagnostic in infections due to protracted or reactivated VZV where PCR is negative. Identification of the causative agent in viral meningitis may be made retrospectively by detecting a rise in IgG antibody titers between acute and convalescent (obtained after 3 to 6 weeks) serum or, at times, by detecting an abnormal serum:CSF ratio of antiviral antibodies.

Other laboratory studies in viral meningitis are usually unhelpful. Peripheral white blood cell count may be normal or elevated. Computed tomography (CT) scans and magnetic resonance imaging (MRI) of the brain are typically normal. The electroencephalogram (EEG) is usually normal but may occasionally show mild background slowing. Marked asymmetries or seizure foci should not be seen unless encephalitis predominates.

Viral meningitis is sometimes referred to by the older term “aseptic meningitis.” This term, however, subsumes a broad range of clinical entities characterized by a meningeal reaction but distinct from purulent bacterial meningitis. It may include not only viral meningitis but also infections by bacteria that are not readily detected in routine cultures ( Leptospira icterohaemorrhagiae , Borrelia burgdorferi , Treponema pallidum , Mycoplasma pneumoniae ), meningeal involvement by Rickettsia , Ehrlichia , or Anaplasma , and infection by parasites such as Toxoplasma gondii . The possibility of infection by one of these agents should be kept in mind in a patient with suspected viral meningitis, since all are amenable to antibiotic treatment. In particular, Borrelia burgdorferi can be a major cause of lymphocytic meningitis in endemic areas (see Chapter 40 ). Aseptic meningitis may also be associated with a variety of pharmacologic agents including nonsteroidal anti-inflammatory agents, trimethoprim-sulfamethoxazole, augmentin, carbamazepine, intravenous immunoglobulin G, and the murine monoclonal antibody OKT3.

Treatment of viral meningitis is supportive in most cases. Analgesics may be required for individuals with severe headaches, and antiemetics for those with considerable nausea and vomiting. Hospitalization is seldom required except when vomiting is severe enough to cause dehydration or when bacterial meningitis cannot be excluded. Acyclovir and valacyclovir have been used to shorten the duration of illness in acute meningitis due to HSV-2 and VZV ( Table 43-3 ). However, controlled studies do not exist, and no standardized regimen has been developed. Patients with recurrent HSV meningitis may wish to keep oral acyclovir or valacyclovir at home and take the drug at the onset of meningeal symptoms. Ongoing twice daily treatment with valacyclovir at a dose of 0.5 mg has not been shown to prevent recurrence, but higher dosages were not studied. The antiviral agent pleconaril, which prevents uncoating of viral RNA, has been used in enteroviral meningitis but is not routinely available in the United States.

As a group, patients with viral meningitis generally make a complete recovery within 1 to 2 weeks. Not all patients recover this quickly, however, and symptoms such as fatigue may last for weeks or even months. CSF abnormalities may also persist for well beyond the initial period of recovery. In addition, there have been occasional reports of permanent sequelae, usually but not always in small children, including cognitive impairment, deafness, and cranial nerve palsies. Aqueductal stenosis with hydrocephalus is a rare complication of HSV-2 and mumps meningitis.

Herpes Simplex Virus

Herpes simplex encephalitis represents only 10 to 15 percent of cases of viral encephalitis in the United States. However, it remains the most common cause of fatal nonepidemic viral encephalitis and is the only viral encephalitis for which effective antiviral therapy has been proven in clinical trials. HSV is ubiquitous in human populations. HSV-1 is most commonly acquired as a symptomatic or asymptomatic gingivostomatitis in early childhood. HSV-2 is more commonly sexually transmitted and is classically acquired during adolescence or adulthood. Both agents enter neuronal processes during primary infection and persist in neurons within sensory ganglia. HSV-1 may also persist within the CNS and is responsible for 90 percent of cases of herpes simplex encephalitis in adults; of these cases, roughly two-thirds represent reactivated infection. HSV-2 may be associated with myelitis.

The pathogenesis of herpes simplex encephalitis is not well understood. Encephalitis has been postulated to follow the spread of virus from the trigeminal ganglia through sensory fibers to the meninges overlying the temporal lobes and orbitofrontal cortex or, alternatively, to follow reactivation of virus in the olfactory bulbs prior to spread to the brain itself. HSV infects neurons, glia, and ependyma.

Herpes simplex encephalitis occurs throughout the year without seasonal incidence, affects men and women equally, and may occur at any age. Immunosuppression does not increase the risk of encephalitis, but the course may be atypical in these individuals. The virus has a predilection for orbitofrontal cortex and temporal lobes, which it may involve unilaterally or bilaterally. The cingulate cortex is also involved in many patients. Occasionally herpes simplex encephalitis involves the occipital cortex or brainstem, in rare cases without temporal lobe involvement. Vascular congestion and petechial or larger hemorrhages may be present; progression of the infection results in extensive and frequently hemorrhagic destruction of brain.

Herpes simplex encephalitis presents with an almost universal triad of headache (in over 90% of cases), fever, and alteration in mental state. Changes in mental state at presentation may range from confusion, frank psychosis, or somnolence to stupor or coma. Temporal lobe involvement may be manifested by olfactory or gustatory hallucinations, déjà vu phenomena, and upper quadrant visual field defects. Bilateral temporal involvement may result in the loss of ability to store and recall new information, and involvement of the dominant hemisphere can result in aphasia. Rare patients present with symptoms and signs referable to the occipital lobes. Focal or generalized seizures may occur at any point during the acute illness or after recovery.

The CSF typically contains a lymphocytic pleocytosis of 50 or more cells/mm ³ (median, 130 cells/mm ³ ). In occasional patients, however, the cell count is normal. Although herpes simplex encephalitis is frequently hemorrhagic, the presence or absence of red blood cells in CSF does not differentiate HSV infection from encephalitis due to other causes. CSF protein concentration has a median value of 80 mg/dl, but ranges from normal to over 700 mg/dl; CSF glucose is usually normal. MRI with gadolinium enhancement is the initial diagnostic procedure of choice and will usually demonstrate hyperintense T2-weighted signal along with gadolinium enhancement within the temporal lobe; it may also show involvement of the insula, orbitofrontal cortex, and cingulate gyrus ( Fig. 43-1 ). MRI abnormalities in other regions of cortex or brainstem, without temporal lobe involvement, do not exclude the diagnosis. The EEG may show temporal lobe slowing or spike-wave activity. CT with contrast and EEG are less sensitive, but used together may provide diagnostic information when MRI is not available.

A , Magnetic resonance imaging (MRI) of herpes simplex virus encephalitis. T2-weighted fluid-attenuated inversion recovery (FLAIR) sequence showing increased signal in right temporal lobe, insula, and orbitofrontal cortex. There is also involvement of the left insula. B , T1-weighted MRI 6 months after infection, showing massive destruction of the left temporal lobe.

A specific diagnosis of herpes simplex encephalitis is made by amplification of viral DNA from CSF using PCR. Overall diagnostic accuracy of PCR in patients with brain biopsy-proven HSV encephalitis is 98 percent. In some patients, however, PCR may be negative at presentation due to low copy numbers of DNA in the CSF; in these cases, repeat CSF PCR after 4 to 7 days is usually positive. Diagnostic yield of PCR falls to 21 percent in patients after 2 weeks of antiviral treatment. Determination of acute antibody titers is not of value in the acute diagnosis of HSV encephalitis; however, comparison of acute and convalescent serum titers may be useful retrospectively and, in rare cases, provides diagnostic information when PCR was negative or when CSF was not obtained initially. Retrospective serologic confirmation of herpes simplex encephalitis may also be made by determining serum:CSF ratios of HSV-specific antibodies to identify intrathecal antibody production.

Herpes simplex encephalitis is treated with intravenous acyclovir ( Table 43-3 ), which inhibits HSV synthesis by competing with deoxyguanosine triphosphate as a substrate for DNA polymerase and causing DNA chain termination. The drug is converted into its pharmacologically active monophosphate form by virally encoded thymidine kinase and thus only becomes active in infected cells. Acyclovir is administered intravenously at 10 mg/kg body weight every 8 hours for 21 days. Complications of acyclovir therapy are usually mild. The major concern is nephrotoxicity due to deposition of drug crystals, which can be avoided by careful hydration. Although acyclovir resistance has been reported in other conditions, acyclovir-resistant herpes simplex encephalitis is rare.

Prior to the introduction of acyclovir, overall mortality from herpes simplex encephalitis was over 70 percent, with mortality approaching 100 percent in patients over the age of 40 years. The advent of acyclovir has reduced the overall mortality to 28 percent, and instituting antiviral therapy at presentation when the diagnosis is suspected has reduced 1-year mortality to 14 percent. Patients who are alert or lethargic when treatment is initiated have an excellent likelihood of survival, but mortality in patients treated when semicomatose or comatose still approaches 25 percent. The likelihood of death or serious neurologic impairment is greater when the patient is elderly, initiation of acyclovir treatment is delayed, or evidence of extensive CNS involvement is present on initial neuroimaging. Even with prompt initiation of treatment, up to two-thirds of patients are left with permanent neurologic deficits including epilepsy, impaired cognition, aphasia, anterograde amnesia, or motor deficits. Neurologic improvement takes place over months, and some patients who are severely impaired immediately after treatment have a good functional recovery over time.

Varicella Zoster Virus

VZV, like HSV, is an enveloped double-stranded DNA virus that is worldwide in distribution. The virus is acquired by the respiratory route and replicates initially in tonsillar tissue to produce a viremia followed by seeding of multiple tissues including skin. Primary infection classically results in chicken pox, but individuals may also be infected acutely with little or no rash. Virus is then taken up by nerves supplying infected skin or other tissues and is transported to sensory ganglia, establishing lifelong persistence. VZV thus differs from HSV in that it produces an acute viremic illness and only then persists secondarily and spreads within neurons. Viral latency in sensory ganglia is heavily controlled by T-cell–mediated immunity, and reactivation of infection may occur with waning of immune response during old age or in states of compromised host immunity.

Cutaneous zoster (shingles), the most common manifestation of reactivated VZV infection, affects roughly 1 million adults in the United States annually. The likelihood of developing zoster is higher in individuals who acquired chicken pox during infancy. Most cases of zoster occur in patients older than 50 years. Neuropathologic correlates of cutaneous zoster include focal meningeal inflammation, necrosis of associated neurons, and degeneration of motor and sensory nerve roots in the involved area. Cutaneous zoster may develop without known precipitating cause or may be triggered by systemic cancer, spinal irradiation, HIV infection or other immunosuppressed states, or spinal trauma. Many patients experience a sharp, burning discomfort in a dermatomal distribution for 2 to 5 days before onset of the rash. A localized redness with red macules then develops and progresses to vesicles in the same dermatomal pattern as the pain. Additional vesicles may appear over the next 2 to 7 days. The distribution of herpes zoster is usually unilateral and involves a single dermatome. The rash involves the trunk in 50 percent, the head in 20 percent, the arms in 15 percent, and the legs in 15 percent of cases. Over the next month, the dermatomal pain slowly disappears, leaving residual hypoalgesia or hyperalgesia. Occasional patients may present with dermatomal pain without rash, termed zoster sine herpete . Treatment with oral valacyclovir (1 gram three times daily for 7 to 10 days) shortens the duration of rash and acute pain. Recommended treatment in immunocompromised individuals is 5 to 10 mg/kg of usually intravenous acyclovir given three times daily for 5 to 7 days.

Postherpetic neuralgia (PHN)—pain occurring in the distribution of the original rash and persisting for longer than 3 months—occurs in 9 to 14 percent of patients following shingles and increases with advancing age. The pain may be relentless, episodic, or paroxysmal and may be elicited by cutaneous contact or stimulation. Postherpetic itch is also common. The live attenuated Oka strain VZV vaccine has been shown to reduce the incidence of cutaneous zoster in healthy individuals by 50 percent and the incidence of postherpetic neuralgia by 67 percent. To what extent antiviral treatment of acute zoster lessens the likelihood of PHN has not been clearly demonstrated. Symptomatic treatment of PHN is often disappointing. Tricyclic antidepressants, gabapentin, pregabalin, controlled-release morphine sulfate, oxycodone, and lidocaine patches have moderate to high efficacy, but are sometimes completely unhelpful. Aspirin in cream or ointment form, topical capsaicin, and intrathecal methylprednisolone are less effective, limited by side effects, or both. For most of these medications, treatment involves escalating dosages of medication until pain relief is achieved or unacceptable side effects occur.

VZV may invade the CNS during primary or reactivated infection and, in reactivated infection, may do so in the absence of cutaneous zoster. Prior to the advent of PCR testing, CNS invasion by VZV was considered unusual. It is now realized, however, that CNS involvement by VZV is much more frequent; in one series VZV was found to be the most common agent identified in viral meningitis and encephalitis (29% of isolates). Studies from France and England have identified the agent in 5 to 15 percent of encephalitis isolates. The virus is now known to cause a wide range of syndromes of neurologic injury involving not only brain and spinal cord but also cranial nerves and brainstem or peripheral ganglia. CNS invasion in reactivated VZV infection occurs following spread of virus from trigeminal or spinal sensory ganglia; in this process, the virus may produce ophthalmic involvement or may produce Ramsay–Hunt syndrome, in which infection of the tympanic membrane and surrounding structures is accompanied by facial nerve palsy. Of greater concern and unlike HSV, VZV may infect both large and small vessels supplying the brain or spinal cord, at times followed by spread of the infection into neural parenchyma. Involvement of vessels may produce focal or multifocal ischemic injury or may cause vessel-wall necrosis with resulting arterial dissection, aneurysm formation, or hemorrhage within the subarachnoid space or brain parenchyma. The classic presentation of VZV vasculopathy is herpes zoster ophthalmicus, in which there is initial superficial zoster in the distribution of the ophthalmic branch of the trigeminal nerve followed days to weeks later by stroke in the territory of the carotid or middle cerebral artery. However, VZV vasculitis may occur with or without preceding cutaneous zoster or herpes zoster ophthalmicus or oticus and may involve virtually any vascular territory within the brain or spinal cord. VZV vasculitis may be significantly more severe in HIV infection or other immunosuppressed states, and immunosuppressed patients may develop a more slowly progressive CNS vasculopathy or myelitis.

CSF in acute VZV CNS infection may reveal a mononuclear pleocytosis, at times with red blood cells and sometimes hypoglychorrhachia. VZV encephalitis in the setting of acute VZV infection may be diagnosed by PCR; however, the reaction rapidly becomes negative, so a negative PCR does not exclude the diagnosis. Diagnosis of VZV vasculopathy in the setting of reactivated infection may also be made by the presence of elevated titers of anti-VZV IgG antibodies in CSF. Oligoclonal bands are commonly present and are reactive with VZV proteins.

Treatment of VZV encephalitis is with acyclovir, 10 mg/kg, usually intravenously, every 8 hours for a minimum of 14 days. Oral prednisone, 1 mg/kg, given daily for 5 days, may be used to treat the inflammatory component of the vasculitis; more prolonged treatment is avoided to prevent steroid-induced immunosuppression.

West Nile Virus

WNV, a single-stranded RNA flavivirus virus, is currently the most common cause of epidemic encephalitis in the United States. The virus infects multiple species of animals and birds, in particular crows, jays, magpies, and ravens. Culex species mosquitoes, predominantly C. tarsalis and C. pipiens , are the primary vectors for human infection. WNV produces infection predominantly in the summer and early autumn, when mosquitoes are most active. As of December 2012, 5,387 cases of WNV infection had been reported to the CDC for the year, with 243 deaths ( Fig. 43-2 ). Of these cases, 2,734 (51%) represented neuroinvasive disease ( Fig. 43-3 ). In most individuals, WNV infection is silent or produces only trivial symptoms. In 20 percent of infected patients, symptomatic West Nile fever develops, characterized by malaise, fatigue, anorexia, headache, nausea, vomiting, myalgia, fever, eye pain, and a nonspecific maculopapular rash. The illness usually lasts less than 7 days, although a minority of patients may remain symptomatic for as long as 6 weeks.

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