Monday, April 26, 2021

Meningitis/Encephalitis Case File

Posted By: Medical Group - 4/26/2021 Post Author : Medical Group Post Date : Monday, April 26, 2021 Post Time : 4/26/2021
Meningitis/Encephalitis Case File
Eugene C. Toy, MD, Manuel Suarez, MD, FACCP, Terrence H. Liu, MD, MPH

Case 17:
A 45-year-old male resident of Minnesota was brought to the emergency department (ED) in january  because of fever, confusion, and "inability  to  talk." His wife reported that he had generalized malaise, headache, and low-grade fever for 3 days with no other specific symptoms. Several  hours  before coming to the ED, he was noted to have progressive lethargy and confusion and lost his ability to  speak.  He had not had nausea, vomiting, diarrhea nor focal weakness or seizures.  He was previously in good health, took  no medications, and denied recent travel outside of the United  States. There  were  no recent insect  bites or pet exposures. On physical examination, his temperature was  38.3°C (101°F)  and other  vital signs were normal. Expressive aphasia was  noted, but there were  no focal findings or nuchal rigidity and the pupils were equal and reactive to light. There were no petechiae, splinter hemorrhages, subconjunctival  hemorrhages, or heart murmurs. The fundi were normal without papilloedema. A lumbar puncture was  performed and the findings from the cerebrospinal fluid (CSF) were as follows: leukocyte count 150/μL with 90% lymphocytes, erythrocytes  500/μL,  protein 125 mg/dl, glucose 50 mg/dl, and no organisms were seen on a Gram stain. After the lumbar puncture  he developed progressive weakness of the right upper extremity.

 What is the most likely diagnosis? 
 What is the best treatment for this patient? 
 What other diagnostic tests may be performed to support the diagnosis?



Summary: A previously healthy 45-year-old man from Minnesota developed a sudden onset of fever, headache, expressive aphasia, and focal weakness in January. A lumbar puncture reveals no organisms, but elevated protein and leukocytes with lymphocyte predominance. He has progressive weakness of his right upper extremity.
  • Most likely diagnosis: Herpes simplex virus type 1 (HSV- 1) encephalitis.
  • Best treatment: Admit to the ICU and immediately start intravenous acyclovir.
  • Confirmatory tests: A brain biopsy is definitive (usually not done if the HSV PCR test is positive and/or empiric acyclovir results in clinical improvement) . A PCR o n the CSF for HSV-1 should be performed and i s often positive. MRI of the brain and EEG added support to the diagnosis.


  1. To describe the most common causes of meningitis and encephalitis.
  2. To find the differences in the CSF examination in meningitis and encephalitis etiologic agents.
  3. To discuss the options for treating meningitis and encephalitis.
This patient has a typical presentation of sporadic HSV-1 encephalitis. His acute onset of low-grade fever, generalized malaise, and headache which progressed to lethargy, aphasia, and then focal weakness of the right upper extremity is strongly suggestive of HSV-1 encephalitis. Seizure is often present. Encephalitis viruses include, Eastern equine encephalitis, St. Louis encephalitis, La Crosse encephalitis, California encephalitis, Powassan fever, and all others, which are less common than West Nile virus (WNV) and HSV-1 encephalitis. In the absence of a known outbreak of WNV, the presentation suggests that the most likely diagnosis is viral encephalitis due to HSV-1. Herpes encephalitis is the most common cause of fatal sporadic encephalitis in the United States and should always be considered in the differential diagnosis "treatable" with antiviral medication. The CSF findings of a lymphocytic pleocytosis with a significant number of RBCs and an elevated protein on LP are suggestive of HSV encephalitis. Decreased CSF glucose levels may also be present in HSV encephalitis, but rarely in other viral encephalitis. A positive PCR for HSV-1 in the CSF would confirm the diagnosis. Supporting information for HSV-1 encephalitis may include CT or MRI of the brain, EEG, brain biopsy, and culture of the CFS for HSV. Other considerations would rickettsia (RMSF); nonspirochetal treponemes (lyme); fungal (cryptococcosis ); protozoal (acanthoamoeba, Nagleria); and bacterial etiologies. Therapies should consider geographic exposures, vector exposure (ticks, mosquitoes), occupation, hobbies and immune defects.

Approach To:

CNS infections are medical emergencies. These include meningitis due to a bacterial or viral infection of tissues surrounding the cerebral cortex (meninges) and encephalitis which is a viral infection of the cerebral cortex. There may be a combination of meningitis and encephalitis (meningoencephalitis) which is most often viral in etiology.

Early diagnosis and appropriate therapy (within 2 hours of presentation) of bacterial meningitis is crucial. More than 75% of all cases of bacterial meningitis in the United States are due to Streptococcus pneurrwniae or Neisseria meningitidisMeningitis due to Haemophilus influenzae has markedly decreased due to widespread immunization with the Haemophilus B influenza conjugate vaccine. Listeria monocytogenes remains an infection of at-risk patients and infections by this bacterium are sporadic. Less commonly, meningitis due S. agalactiae (Group B Streptococcus) and Escherichia coli may be seen in at-risk patients (neonates, infants, and immunocompromised patients) .

Streptococcus pneurrwniae is the most common etiologic agent of community acquired bacterial meningitis and is often seen in patients with other foci of infection: pneumonia, otitis media, mastoiditis, sinusitis, or endocarditis. It may also be one of the causes of meningitis following CSF leaks due to trauma, iatrogenesis, or congenital defects of the meninges. The pneumococcal 13-valent for children and 23-valent vaccine for adults are effective in preventing invasive disease.

Neisseria meningitidis is the second most common sporadic agent of bacterial meningitis and the most common cause of outbreaks and epidemics of bacterial meningitis in the United States. It occurs primarily in children and young adults. Patients with persistent deficiencies in the terminal complement components (C5-C9) are predisposed to infection with N. meningitidis. A quadravalent (A, C, Y, or W-135 ) conjugate vaccine is available, but does not protects against serogroup B, the agent of one-third of cases in the United States. The ACIP has recommended vaccination be used for the prevention of meningococcal disease in the following individuals:
  1. Routine vaccination of adolescents at age 11 to 12 years with a booster at age 16
  2. A 2-dose primary series administered 2 months apart for persons aged 2 to 54 years with persistent complement deficiency (C5-C9), or functional or anatomic asplenia, or HIV infection
Other less common causes of bacterial meningitis include Listeria monocytogenes, Group B streptococci (S. agalactiae), aerobic gram-negative bacilli and staphylococcus species. Listeria monocytogenes meningitis is associated with extremes of age, neonates and persons >50 years of age. Alcoholism, malignancy, immunosuppression, diabetes mellitus, hepatic failure, renal failure, iron overload, collagen vascular disorders, and HIV infection are also predisposing factors. Group B streptococcal meningitis, an important cause of infection in neonates, can be seen in adults with
the same underlying conditions that predispose to listerial meningitis. Aerobic gramnegative bacilli (Klebsiella species, E. coli, Serratia marcescens, and Pseudomonas aeruginosa). S taphylococcus aureus and S. epidermidis may cause meningitis in patients with head trauma, subsequent to neurosurgical procedures and placement of CSF shunts, or following bacteremia due to catheters, indwelling devices, and urinary tract infection. Community-acquired Methicillin-resistant Staphylococcus aureus (CA-MRSA) is an emerging cause of community-acquired meningitis. The differential diagnosis of bacterial meningitis is broad and includes organisms such as mycobacterial, fungal, protozoal, and viral.

Diagnosis of Meningitis
Meningitis should be considered if a patient has fever, headache, neck stiffness, and altered mental status. On examination "jolt accentuation" of the headache elicited with rapid horizontal movement of the head is considered to be more sensitive for the diagnosis of meningitis than the traditional Kernig or Brudzinski signs of meningeal irritation. Nuchal rigidity is the inability to flex the head forward due to rigidity of the neck muscles. Kemig sign is positive when the leg is bent at the hip and knee at an angle of 90 degrees, and subsequent extension of the knee is painful. Brudzinski sign is the appearance of involuntary lifting of the legs when the patient's head is lifted from the examining couch when the patient is lying supine. These findings are not specific and may indicate subarachnoid hemorrhage as well as meningitis. Nuchal rigidity, altered mental status, and Kernig and Brudzinski signs may be absent but this should not deter an evaluation for meningitis.

The diagnosis of meningitis is established by the analysis of a CSF specimen (Table 17-1) . At times CT imaging may be necessary prior to performing a lumbar puncture to reduce the risk of brain herniation; however, this imaging should not delay empiric antibiotic therapy. Specific indications for a CT imaging prior to an LP include: focal neurological findings (including seizure), increased intracranial pressure or papilledema, age >65 years, underlying immune deficiency, and coma. A CSF white cell count >500/μL, a CSF lactate acid >3.5 mmol/L, or a CSF- to-serum

Cerebrospinal fluid findings in patients with mengingitis
Cerebrospinal fluid findings in patients with mengingitis

bPolymorphonuclear neutrophils.

glucose ratio <0.4 are highly predictive of bacterial meningitis. Latex agglutination testing is available for the evaluation of bacterial meningitis (H. infiuenzae type b; S. pneumoniae; N. meningitidis groups A, B, C, Y, or W135; S. agalactiae and E. coli K1; BD Directigen Meningitis Combo Test). A polymerase chain reaction (PCR) should be considered as a diagnostic aid especially for meningitis due to enteroviruses which cause about 85% of the viral meningitis seen in the United States (echovirus, coxsackievirus A and B, and the nonpolio enteroviruses).

Tuberculous meningitis can mimic enteroviral and herpes simplex virus infections. IgM antibody capture enzyme-linked immunosorbent assay (ELISA) testing is useful in identifying arbovirus infections especially those due to WNV, St. Louis encephalitis, California encephalitis, Eastern equine encephalitis, La Crosse encephalitis, and Powassan viruses. This is especially important in patients whose CSF evaluation is consistent with aseptic meningitis. Aseptic meningitis is meningeal inflammation without identification of a causative bacterial agent and accompanied by a monocytic pleocytosis of the CSF. Seasonality, geography, exposure to ticks or mosquitoes, and concomitant symptoms and signs are usually helpful in determining the etiology.

The natural history of aseptic meningitis is usually benign and often subclinical or underappreciated due to its low-grade presentation (eg, mumps, enteroviral infections) . However, at times, especially WNV can cause devastating effects with severe morbidity and mortality. Testing for fungal, mycobacterial, HIV, and nontreponemal spirochetal agents (Lyme disease ) should be performed when clinically indicated ( eg, immunosuppression, exposure history) in nonbacterial meningitis. A Venereal Disease Research Laboratory (VDRL) test should be considered on all abnormal CSF samples to exclude syphilis. Noninfectious causes of meningitis should be considered, including drug-induced causes (nonsteroidal anti-inflammatory drug [NSAID] use and collagen vascular diseases, especially systemic lupus erythematosus).

Empiric antimicrobial therapy for purulent meningitis

aGentamicin may be added for synergy in Listeria, 5. aureus, and gram-negative meningitis.

Treatment of Meningitis
If the examination of CSF reveals the presence of purulent meningitis and a positive Gram stain suggests a specific etiology, targeted antimicrobial therapy must be initiated as quickly as possible (optimally within 30 minutes of arrival in the ED) . If the Gram stain is negative, empiric antibiotic therapy is determined by the patient's age and underlying conditions (Table 1 7-2) . The administration of dexamethasone concomitant with or just prior to the first dose of antimicrobial therapy will attenuate the inflammatory response created by the lysis of certain meningeal pathogens (H. influenzae, Mycobacterium tuberculosis, S. pneumoniae, and Cryptococcus neoformans) by antimicrobial agents. If Listeria monocytogenes is proven or suspected, ampicillin should be included in the antibacterial regimen to which gentamicin may be added for synergy.

In the treatment of bacterial meningitis, time is of the essence. Antimicrobial treatment should not be delayed while awaiting the results of a CT scan or an MRI. If a CT scan is indicated prior to an LP, antibiotics should be started empirically after an appropriate examination and septic workup.

Viruses are by far the most common cause of encephalitis. Approximately 20,000 cases of encephalitis occur in the United States each year, with the predominant endemic sporadic cause being the HSV-1. The most common epidemic cause of viral meningitis is WNV followed by other sporadic and epidemic viral etiologies. Rabies encephalitis is now rare in North America. Viral encephalitis presents as an acute-onset, febrile illness associated with headache, altered level of consciousness, and occasionally focal neurologic signs. The clinical presentation of encephalitis can be similar to meningitis but the 2 differ in that meningitis is not always characterized by focal neurologic signs and change in mental status. While fever and headache are the principal manifestations of both syndromes, nuchal rigidity is characteristic only of meningitis.

Arboviral diseases such as Eastern equine encephalitis and St. Louis encephalitis have affected humans in the United States for years. These viral infections may be fatal or have significant morbidity, the prevalence in humans has been low and effective treatments and human vaccines have not been developed. This situation changed in 1999 when the first cases of WNV occurred in the United States. The virus spread throughout the United States and has now been diagnosed in thousands of patients annually with significant morbidity and mortality. WNV encephalitis is most severe in the older age groups with the highest mortality and morbidity rates occurring in those >65 years of age. While most cases of WNV infection are subclinical or mild, the disease can be severe and most often occurs during seasonal outbreaks or epidemic conditions. These severe clinical presentations of WNV include encephalitis, meningitis, flaccid paralysis, and fever. Vaccines have been developed for veterinary use in preventing WNV as early as 2001 ; however, there are currently no approved vaccines for human use for WNV.

In the United States nonepidemic, sporadic, or focal encephalitis is most frequently due to HSV-1 with one-third of the cases occurring in patients < 20 years of age and one-half occurring in those over 50 years old. HSV-1 encephalitis results from a reactivation of the latent virus in the trigeminal ganglion, resulting in inflammatory necrotic lesions in the temporal cortex and limbic system. Most HSV-1 cases occur in the absence of an antecedent illness.

Diagnosis of Encephalitis
After a history and physical examination is completed, CSF analysis should be performed including cell count, glucose, protein, cultures (both viral and bacterial); PCR for specific viral diagnoses including HSV-1, and IgM antibody capture ELISA tests based upon suspected viral etiologies. CSF cultures for HSV-1 and arboviruses are usually negative, but the sensitivity of the PCR for HSV and the arboviral IgM antibody capture ELISA exceeds 90%. In HSV encephalitis, MRI typically demonstrates unilateral or bilateral abnormalities in the medial and inferior temporal lobes, which may extend into the frontal lobe. The EEG findings include focal delta activity over the temporal lobes and periodic lateralizing epileptiform discharges (PLEDs) . Brain biopsy with fluorescent antibody and histopathology is reserved for patients who do not respond to empiric acyclovir or have negative PCRs of the CSF. CT imaging is not as sensitive as MRI with gadolinium.

The CSF typically shows a lymphocytic pleocytosis, an increased number of erythrocytes and an increased concentration of protein; glucose levels are usually normal, but may be low early in the infection. With early HSV-1 encephalitis, the CSF may initially show a PMN predominance which then shifts to a lymphocytosis. Acyclovir should be started immediately when HSV-1 infection is suspected. PCR for HSV-1 DNA in CSF should be obtained but treatment should not be delayed waiting for results. A temporal lobe abnormality on MRI (eg, a hemorrhagic lesion) is considered to be a poor prognostic sign for neurologic recovery, although CMV, EBV, and echoviruses can cause the same syndrome of encephalitis infection.

WNV infection is more frequently associated with a poliomyelitis, Parkinsonlike syndrome, or a Guillain-Barre type of presentation. Vector-borne diseases such as WNV infection are unlikely events during a Minnesota winter especially when there is no evidence of an outbreak or epidemic. The diagnosis of HSV-1 encephalitis is critical because it is the only viral infection of the CNS for which antiviral therapy with acyclovir has been proven effective. In HSV encephalitis, prompt acyclovir treatment reduces mortality to approximately 25% in adults and older children. Unfortunately over 50% of the patients who survive will have neurologic sequelae.

HIV-infected individuals are susceptible to CNS toxoplasmosis infection when their CD4 lymphocyte counts are below 200/μL, and are at high risk with CD4 counts below 50/μL. Localized or focal encephalitis is the most common presentation of toxoplasmosis. Toxoplasmosis is the most common cause of a CNS mass lesion in AIDS followed by CNS lymphoma (B cell or non-Hodgkin) which occurs in approximately 2% to 12% of HIV- infected individuals. Unlike the situation in immunocompetent hosts, HIV-associated lymphoma is strongly associated with Epstein-Barr virus infection. In patients with AIDS, lymphoma was second only to toxoplasmosis as the most common source of central nervous system mass lesions. A negative PCR for Epstein-Barr virus and the diffuse nature of an MRI abnormality exclude central nervous system lymphoma.

Cryptococcal meningitis (CM) is a subacute infection of the central nervous system associated with a CSF pleocytosis of 40 to 400 cells/μL with lymphocyte predominance and slightly low glucose levels. Diagnosis of cryptococcal CNS infection can be made in >98% of patients by combining the use of rapid antigen detection tests for cryptococcal antigen, India ink preparation, and CSF cultures for fungi.

Progressive multifocal leukoencephalopathy (PML) is an opportunistic infection caused by polyomavirus JC, associated with gradual demyelination of the central nervous system and thereby expressed as a progressive neurologic deficit. The lesions of PML are generally bilateral, asymmetric, nonenhancing or with delayed peripheral enhancement, and are peri ventricular or subcortical in distribution. Radiographic studies reveal no unusual tissue mass effects. This is in contrast to primary central nervous system lymphoma and toxoplasmosis in which mass effect may occur.

Risk factors for AIDS-related opportunistic infections include late-stage HIV infection (CD4 cell count <100/μL ) , no prior treatment, and the presence of thrush. Patients with PML usually display focal neurologic signs and an MRI will reveal multiple white matter lesions without mass effect, involving the right lateral frontal, right frontoparietal, and left frontal lobes, right pons, bilateral brachium pontis, and right cerebellum. In addition, the PCR is positive for polyomavirus JC in PML. While the gold standard for the diagnosis of PML is brain biopsy, the CNS lesions are usually quite deep and relatively inaccessible. When the preponderance of clinical evidence supports a diagnosis of PML, biopsy can usually be deferred. Approximately 50% of patients with AIDS and PML will survive the PML if highly active antiretroviral therapy is administered, presumably because of the effects of immune reconstitution in arresting the disease process. Neurologic deficits typically persist in survivors proportionate to the disease severity at the time of presentation.

Primary amoebic meningoencephalitis may be due to any of the 4 free-living amoebae, for example, Naegleria fowleri, Balamuthia mandrillaris, Sappinia diploidea, and Acanthoemba castelanii. Other parasitic infections such as those caused by Trypanosoma brucei, T. cruzi, and Toxoplasma gondii are among those with a protozoan etiology. These pathogens are uncommon causes of CNS infections in North America. Naegleria fowleri produces primary amebic meningoencephalitis (PAM) and symptoms of PAM are indistinguishable from acute bacterial meningitis. Other amebae cause granulomatous amebic encephalitis (GAE), which is more apt to be subacute and can present as an indolent or asymptomatic chronic infection. Amebic meningoencephalitis can mimic a brain abscess, aseptic or chronic meningitis, or even a CNS malignancy. Infection with Strongyloides stercoralis can lead to a devastating systemic infection often involving the CNS with polymicrobial bacterial meningitis. Termed "hyperinfection syndrome," it is seen in severely immune compromised: HIV, HTLV 1 and 2, and those receiving anti-TNF therapies.

  • See also Case 18 (Antimicrobial Use in ICU), Case 19 (Sepsis), and Case 20 (Immune-Compromised Patient With Sepsis). 


17.1  A 44-year-old man who is HIV infected is hospitalized because of a 1 -week history of progressive weakness of the left lower extremity and an inability to walk. He has also had a rapid loss of weight, night sweats, and frequent lowgrade fever. His CD4 cell count at the time of diagnosis was 88/μL. On physical examination he appears cachectic and chronically ill. His temperature is 38.1°C (100.6°F). Other significant findings included the presence of oral thrush, splenomegaly, bilateral lower extremity weakness, and hyperreflexia. An LP is performed and examination of his CSF shows the following: opening pressure normal; leukocyte count 21/μL with 98% lymphocytes and 2% neutrophils; erythrocyte count 1/μL; protein 85 mg/dL, and glucose 55 mg/dL. The India ink stain, cryptococcal antigen test, and culture for fungi were negative. The PCR was positive for polyomavirus JC and negative for EBV virus. Which of the following is the most likely diagnosis?
A. Cerebral lymphoma
B. Cerebral toxoplasmosis
C. Cryptococcal meningitis
D. Progressive multifocal leukoencephalopathy
E. Tuberculosis

17.2  A 25 -year-old man is evaluated in the ED for fever, headache, and mental status changes of 4 hours' duration. He underwent a cadaveric kidney transplantation 10 months ago, and his immunosuppressive regimen includes prednisone and azathioprine. He has no allergies. On physical examination, his temperature is 38.7°C (101.6°F) , heart rate is 115 beats/minute, respiratory rate is 25 breaths/minute, and blood pressure is 100/60 mm Hg. He is oriented as to the year and his name but cannot recall the month. His neck is supple, and Kernig and Brudzinski signs are absent. The neurologic examination is normal. His peripheral leukocyte count is 20,000/μL. A CT scan of the head shows no sign of hemorrhage, hydrocephalus, mass effect, or midline shift. An LP is performed and examination of the CSF shows leukocyte count 2000/μL (60% neutrophils, 40% lymphocytes), erythrocyte count 20/μL, glucose 25 mg/dL, protein 150 mg/dL, and a negative Gram stain. The opening spinal pressure is normal. Results of blood, urine, and CSF cultures are pending. Which of the following is the most appropriate empiric antibiotic therapy?
A. Ampicillin and ceftriaxone
B. Ampicillin, ceftriaxone, and vancomycin
C. Ceftriaxone and moxifloxacin
D. Ceftriaxone and vancomycin
E. Moxifloxacin


17.1  D. The most likely diagnosis is PML. PML is an opportuntsttc infection caused by polyomavirus JC, leading to demyelination of the CNS that causes gradually progressive neurologic deficits. Radiographically, there is no mass effect. The lesions are generally bilateral, asymmetric, nonenhancing, and peri-ventricular or subcortical in distribution. This late-stage HIV infection is based on a CD4 cell count <100/μL The presence of thrush in this patient has a high-risk status for AIDS-related opportunistic infections. He also has focal neurologic signs and an MRI that shows multiple white matter lesions without mass effect involving the right lateral frontal, right frontoparietal, and left frontal lobes and cerebellum. A PCR analysis is positive for polyomavirus JC. The gold standard for diagnosis of PML is a brain biopsy but with the preponderance of evidence supporting a diagnosis of PML, a biopsy can be deferred. If HAART is administered, 50% of AIDS patients will survive PML. Neurologic deficits typically persist in survivors. In patients with HIV infection and CD4 cell counts <200/μL, localized or focal encephalitis is the most common presentation of toxoplasmosis and is the most common CNS system mass lesion. A negative serologic test for toxoplasma-specific IgM would add additional support to the exclusion of toxoplasmic encephalitis. CNS lymphoma occurs in approximately 2% to 12% of HIV- infected individuals. It is strongly associated with Epstein-Barr virus infection. In patients with AIDS, lymphoma was second only to toxoplasmosis as the most common CNS mass lesion.

17.2  B. Risk factors for listerial meningitis include immunosuppression, neonatal status or age >50 years, alcoholism, malignancy, diabetes mellitus, hepatic failure, renal failure, iron overload, CVDs, and HIV infection. The most appropriate empiric therapy is ampicillin (the drug of choice for Listeria) , with ceftriaxone and/or vancomycin. The CSF fluid supports a diagnosis of meningitis. Empiric vancomycin and ceftriaxone are recommended for the treatment of meningitis in patients 2 to 50 years of age. This covers S. pneumoniae and N. meningitidis, the most common organisms responsible for meningitis in this age group. The analysis of CSF in patients with listerial meningitis often fails to reveal typical gram-positive rods with characteristic "tumbling motility" in wet mount preparations, but often shows pleocytosis and may demonstrate a significant number of lymphocytes in addition to neutrophils. Patients usually have ↑ CSF protein levels; ↓ CSF glucose levels are found less commonly and less profoundly with listerial meningitis. The fluoroquinolones may be effective but do not penetrate the CNS well. Gentamicin is synergistic with ampicillin despite poor CNS penetration.


 Meningitis has a high morbidity and mortality rate, especially in high-risk patients. 
 LP and CNS imaging are  central to the diagnosis of meningitis and encephalitis. 
 Each year 20,000 cases of encephalitis occur in the United States, with the predominant sporadic cause being HSV and the most common epidemic cause being WNV. 
 PML is caused  by polyomavirus JC, with demyelination of the CNS and neurologic deficits. 
 If HART is administered, 50% of patients with AIDS and PML will survive the latter disease. 
 HSV  is the most common cause of fatal  sporadic encephalitis in the United States. 
 HSV encephalitis has fever,  headache, seizures, focal  neurologic signs, and impaired multiple sclerosis (MS). 


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Fitch MT, van de Beek D. Emergency diagnosis and treatment of adult meningitis. Lancet Infect Dis . 2007 ; 7 : 1 9 1 -200. 

Kennedy PG . Viral encephalitis. ] Neural. 2005 ; 2 5 2 : 268-272. Epub 2005 Mar 1 1 . [PMID: 1 5 7 6 1 6 7 5 .]


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