A Toxic Infant with Aseptic Meningitis
Radiology Cases in Pediatric Emergency Medicine
Volume 7, Case 9
Kevin H. Higashigawa, Medical Student
Loren G. Yamamoto, MD, MPH
Kapiolani Medical Center For Women And Children
University of Hawaii John A. Burns School of Medicine
    An 8-month-old female is brought into the emergency 
department by her mother.  The infant was in her usual 
state of good health until three days ago, when her 
mother noted that she felt warm.  She was less active, 
but eating well and had no vomiting, diarrhea, or other 
complaints.  The following day (2 days ago), she 
refused to eat.  She continued to have fevers and 
remained less active than normal.  That evening she 
was taken to the ED and was found to have a 
temperature of 39.5 degrees C.  She was described by 
her mother as being less active, not eating well, and 
having a decreased urine output.  CBC showed a white 
count of 12.1 (32 segs, 2 bands, 53 lymphs, 9 monos), 
hemoglobin 11.1, and hematocrit 32.8.  A blood culture 
was obtained.  A chest radiograph was felt to be 
normal.  The infant was given antipyretics and 
discharged home.
     The next day (yesterday), she continued to have 
fevers.  Her temperature was 38.5 degrees C.  She was 
less active and was not eating or drinking.  She had not 
voided according to her mother.  There was no 
vomiting, diarrhea, or respiratory symptoms.  Her 
mother also noted on this morning that she had some 
skin lesions which resembled insect bites.  They were 
red and raised.  She was taken to see her primary care 
physician, who evaluated her and discharged her.
     She is brought to the ED today because of 
increasing lethargy, very poor oral intake, no urine 
output for 24 hours and continued fever.
      Past Medical History:  She was born via normal 
spontaneous vaginal delivery.  Prenatal and postnatal 
courses were uncomplicated.  She is usually on formula 
but has taken some solid foods.  Her immunizations are 
up to date.  She had one prior hospitalization at 4 
weeks of age for fever during which time a sepsis 
workup was negative.  Her family history is 
     Exam:   VS  T 39 degrees C, P 160, R 35, BP 95/46.  
She is very lethargic.  She is not cooing, smiling, or 
vocalizing.  She has a weak cry and is tachypneic.  She 
does not respond to painful stimuli. She assumes a 
position of comfort, in which her lower and upper 
extremities are flexed and her head is turned to the 
right.  Attempts to place her head midline result in a 
weak cry.  There is slight nuchal rigidity.  She is pale 
with mottling of her lower extremities.  There are 
multiple skin lesions across her face and a few on her 
arm.  They are irregularly crusted (questionably 
pustular) centrally, surrounded by some erythema.  She 
appears to have a facial droop on the right.  Her 
anterior fontanelle is small but sunken.  Her mucus 
membranes are sticky and she does not produce any 
tears when she cries.  She does open her eyes, but will 
not follow objects and has a dysconjugate gaze.  Breath 
sounds are bilaterally coarse.  She has some upper 
airway rhonchi.  She has no wheezes, crackles, or 
rales.  Heart regular without murmurs.  Abdomen flat 
and soft.  Radial pulses are 2-3+ bilaterally and equal.  
Her hands and feet are cool.

     An IV is started and IV fluid is infused.  She is also 
given an IV dose of ceftriaxone.  She begins to have 
extensor posturing with arching of her back.  She keeps 
her head to the right.  She also develops tonic-clonic 
movements of her left upper extremity, and is therefore 
given a IV lorazepam followed by phenytoin.

What work-up would you recommend?  

     Because of the infant's fever, nuchal rigidity, 
lethargy, and focal neurologic abnormalities, a 
diagnosis of meningitis and/or encephalitis is 
suspected.  A lumbar puncture is performed which 
shows fluid that is questionably hazy (minimally).  She 
is given IV acyclovir and vancomycin (ceftriaxone was 
given earlier).  The laboratory analysis of the CSF 
shows 105 RBCs and 40 WBCs per cubic mm with 10% 
segs, 80% lymphs, and 10% monos, glucose 75, 
protein 59.  The Gram stain shows no organisms.  
These clinical and laboratory findings are most 
consistent with which of the following possibilities:
     Aseptic meningitis
     Bacterial meninigitis
     Tuberculous meninigitis
     Viral encephalitis
     Brain abscess
     Cerebrovascular accident
     Shaken infant syndrome

     The CSF analysis is consistent with aseptic 
meningitis, but since this is usually a benign clinical 
entity, this child who is very sick, is not likely to have 
just aseptic meningitis.  Bacterial meningitis is not likely 
(practically not possible) given this CSF analysis.  
Tuberculous meningitis is possible, but the clinical 
course is too acute for this.  Viral encephalitis is the 
most likely since the CSF analysis suggests a viral 
picture and the patient's poor neurological status is 
consistent with an acute encephalitis.  Additionally, the 
skin lesions on the patient's face may be herpes 
simplex lesions.  Brain abscess is another possibility 
which needs to be ruled out by imaging.  
Cerebrovascular accident cannot be ruled out, but it is 
less likely.  Shaken infant syndrome is usually 
associated with CSF which is grossly bloody.  Brain 
imaging studies will help to obtain a more definitive 
diagnosis.  A CT and a MRI are performed.

View her CT scan.

     The CT scan without contrast demonstrates (upper 
two images) some hypodensity in the thalami and 
temporal lobes, indicative of bilateral cortical and 
subcortical edema.  After the administration of IV 
contrast (lower two images), there is meningeal 
enhancement at the margins of the abnormal 
parenchyma, as well as mild central enhancement. This 
is consistent with a breach in the blood-brain barrier 
following vasculitis.  There is no evidence of herniation.

View her MRI scan.

     The areas of increased signal intensity in the MRI 
scan indicate the presence of abnormal water, 
consistent with the CT scan findings of 
cortico-medullary edema in the bilateral 
temporoparietal lobes. There is also meningeal 
enhancement over the affected areas of the brain.
     The above findings are compatible with bilateral 
temporoparietal lobe meningoencephalitis.

What additional tests would you request?

     The CSF sample is positive for  herpes simplex virus 
(HSV) DNA by polymerase chain reaction (PCR) 
although the viral culture of the CSF is negative.
     Her EEG is abnormal.  It is diffusely slow for her 
age.  These results are compatible with a diffuse 
encephalopathic process.  In addition, there are some 
sharp waves emanating from the right frontotemporal 
and right frontal central regions, consistent with seizure 
foci in the affected areas shown on her brain CT and 

     What is the classic presentation for an infant with 
HSV encephalitis?  What is the relationship between 
HSV encephalitis and the presence of mucocutaneous 
skin lesions?  What is the prognosis for HSV 

     Encephalitis is an infection of the parenchyma of the 
brain (in contrast to meningitis, an infection of the 
meninges).  The most common cause of viral meningitis 
is enterovirus infection, whereas one of the more 
common causes of viral encephalitis is HSV.  The major 
manifestations of viral meningitis include fever, 
headache, irritability, mild lethargy or drowsiness, and 
some degree of nuchal rigidity.  On the other hand, 
encephalitis often presents with significant neurologic 
signs and symptoms in addition to an acute febrile 
illness.  In the usual case of viral meningitis, the 
disease is relatively benign and self-limiting.  
Encephalitis, however, is a disease which can be 
associated with significant morbidity and mortality (1).  
It is not unusual for encephalitis and meningitis to 
coexist in the same patient as meningoencephalitis.  
     Encephalitis must also be distinguished from 
cerebritis.   Cerebritis is a highly destructive 
inflammatory condition of the brain, which may be 
bacterial in origin, often leading to abscess formation.  
Encephalitis is most commonly viral in nature and the 
extent of parenchymal damage is variable.
     Arboviruses are the most common cause of episodic 
viral encephalitis.  Two of the most common forms of 
arboviral encephalitis are:  1) St. Louis encephalitis, 
which is mainly found in urban areas around the 
Mississippi River, and 2) California encephalitis, which 
is principally found in rural areas of the northern 
Midwest and East.  Eastern equine encephalitis is one 
of the most severe causes of arboviral encephalitis, but 
it is uncommon (mostly in the New England area).  
Western equine encephalitis is most prevalent in the 
rural areas west of the Mississippi (2).  The arboviruses 
tend to have a seasonal preference for the summer and 
early fall months because they are largely transmitted 
via arthropod vectors.
     HSV is the most common cause of sporadic viral 
encephalitis in the United States, accounting for 
approximately 10 to 20 percent of all cases.  It is 
estimated that about 2 persons per million per year will 
suffer from HSV encephalitis.   HSV-1 is acquired more 
frequently and earlier in life than HSV-2.  By the fifth 
decade of life, more than 90 percent of adults will be 
HSV-1 seropositive.  It has been also estimated that 
about 22 percent of the adults in the United States are 
HSV-2 seropositive.  HSV-1 accounts for more than 95 
percent of all cases of HSV encephalitis (3). Unlike 
other sources of viral encephalitis, HSV encephalitis 
has no seasonal pattern.  HSV encephalitis is most 
prevalent in the neonatal, 5 to 30, and over 50 age 
       Neonates (infants less than 6 weeks old) have the 
highest incidence of HSV visceral and/or CNS infection 
among all age groups.  Untreated, neonatal herpes 
infection disseminates or invades the CNS in greater 
than 70 percent of cases.  In contrast to childhood/adult 
HSV encephalitis, 70 percent of neonatal HSV infection 
is caused by HSV-2, acquired from contact with 
infected genital secretions at time of birth (3).   The 
incidence is about 1:3500-5000 deliveries, with signs 
and symptoms manifesting 4-11 days after delivery (4).  
The herpes virus can also be acquired postnatally from 
contact with immediate family members who may be 
shedding virus from a symptomatic or asymptomatic 
oral-labial infection.
     Varicella-zoster virus causes a deadly encephalitis 
in immunocompromised patients and has an incidence 
of 1:2000 infected persons.  Toxoplasma 
encephalopathy is prevalent among HIV+ patients.  
Measles is responsible for two types of encephalitis, 
post-infectious, with an incidence of 1:1000 infected 
persons, and subacute sclerosing panencephalitis, with 
an incidence of 1:100,000 infected persons.  Rabies 
accounts for 0-3 cases of encephalitis yearly in the US.  
      The most common form of encephalitis outside the 
US is Japanese encephalitis, which affects persons in 
Japan, SE Asia, China, and India (2).
     Arboviruses require a mosquito or tick vector (hence 
the name "arthropod borne" virus).  In general, the virus 
replicates outside the CNS and gains entry by 
hematogenous spread.  
      The herpes simplex virus (HSV) is a 
double-stranded DNA virus which can infect 
mucocutaneous surfaces, the central nervous system, 
and, less commonly, visceral organs.   The virus may 
remain latent in neuronal ganglia and may 
subsequently be reactivated, resulting in viral 
replication.  HSV is usually transmitted via contact with 
active ulcerative lesions.  However, individuals with 
subclinical disease may also shed infectious virus.  
Subclinical transmission of HSV may partially account 
for the continued rise in worldwide seroprevalence.  
     HSV gains entry at mucosal surfaces or abraded 
skin and replicates within the epidermis and dermis.  
Often, the primary infection is subclinical.  However, 
sufficient numbers of virus may still be present to infect 
peripheral sensory or autonomic nerve endings.  Once 
inside the neuron, the virus travels intraaxonally to the 
nerve cell bodies in ganglia, where replication occurs.  
The virus can also migrate to other tissues either 
proximally, by contiguous spread, or distally through a 
neuronal network.  After the primary infection has 
resolved, the herpes simplex virus can no longer be 
found in the ganglia.  However, about 10 to 50 percent 
of ganglion cells in the area of the initial infection may 
harbor viral DNA.  Approximately 1 percent of these 
cells possess latency-associated transcripts of RNA.  
The molecular mechanisms of latency and reactivation 
are not well understood.  Factors linked to reactivation 
include: ultraviolet light, immunosuppression, and 
trauma to the skin or ganglia.  The maintenance of 
latency, the frequency of reactivation, and the severity 
of illness ultimately depend upon the host immune 
response (3). 
     The exact pathogenesis of HSV encephalitis is not 
well known.  One hypothesis is that the virus gains 
entry into the CNS directly from a peripheral route via 
either the trigeminal or olfactory nerve.  HSV 
encephalitis is the result of a primary infection in about 
1/3 of cases (4).  In children and in adults, HSV 
encephalitis is generally localized to the inferior and 
medial regions of the temporal lobe and the orbital gyri 
of the frontal lobes.  In neonates, brain involvement 
tends to be more diffuse.  The disease is necrotizing 
and often hemorrhagic in the most severely affected 
regions (5).
     In general, a patient with encephalitis presents with 
diffuse or focal neurologic signs and symptoms, 
including an altered mental state and level of 
consciousness, behavioral or personality changes, 
nuchal rigidity, photophobia, and generalized or focal 
seizures.  Depending upon the type of virus, the patient 
may present with additional signs and symptoms.  For 
example, patients with varicella zoster or measles 
encephalitis will typically have a rash, 
lymphadenopathy, hepatosplenomegaly, and parotid 
enlargement.  Patients with St. Louis encephalitis will 
present with dysuria and pyuria (2).
     In the case of HSV encephalitis, the patient will 
generally present with an altered state of 
consciousness, an abnormal mental state, and focal 
neurologic signs and symptoms, in addition to the acute 
febrile illness characteristic of viral meningitis.  The 
level of consciousness may vary from mild lethargy to a 
comatose state.  The patient is not mentally alert and is 
often confused, delirious, or disoriented.  The patient 
may also suffer hallucinations and exhibit personality 
and/or behavioral changes, sometimes escalating into 
frank psychosis.  Focal neurologic changes depend 
upon the site of infection within the brain.  Common 
neurologic abnormalities include:  aphasia, ataxia, 
cranial nerve deficits, hemiparesis, hyperactive tendon 
reflexes, and involuntary movements, such as 
myoclonic jerks (1).  Prolonged seizures, or status 
epilepticus, which are refractory to anticonvulsants are 
also common in the presentation of encephalitis.  
     In children and adults, there is no relationship 
between the presence of mucocutaneous lesions and 
HSV encephalitis (4).  In fact, only about 10% of 
patients have a positive history of prior labial herpes 
(5).  Thus, the presence or absence of such lesions is 
of no diagnostic value.  
      By contrast, neonates often have pathognomonic 
lesions.  Neonates with HSV encephalitis may present 
with lethargy, poor feeding, irritability, tremors, 
seizures, temperature instability, a bulging fontanelle, 
and pyramidal tract signs.  With disseminated disease, 
the neonate may present with systemic signs and 
symptoms such as jaundice, shock, bleeding, or 
respiratory distress (4).
     Once the diagnosis of encephalitis is suspected, the 
patient should be given intravenous acyclovir 
immediately.  The cause of the encephalitis is assumed 
to be HSV until proven otherwise.  HSV encephalitis 
has specific antiviral chemotherapy and the patient's 
prognosis relies heavily upon the expediency of this 
     The clinician must be wary of non-viral causes of 
encephalopathy, including infectious and non-infectious 
agents.  Among the non-viral infectious etiologies are 
abscesses, as well as bacterial, fungal, parasitic, 
rickettsial, and tuberculous infections.  Non-infectious 
causes of encephalopathy include tumors, hematomas, 
vascular insults, toxic encephalopathy, and systemic 
lupus erythematosus.  
     Hundreds of  viruses have been implicated in viral 
encephalitis and it is difficult to clinically distinguish 
HSV encephalitis from the other viral forms.  Therefore, 
confirmation of HSV encephalitis depends upon 
laboratory work-up; however, this should not delay the 
immediate initiation of  acyclovir treatment.  The CSF 
profile in viral encephalitis mimics that of viral 
meningitis, with a lymphocytic pleocytosis, an elevated 
protein content, and a normal glucose level.  The 
lymphocytic pleocytosis is found in more than 95 
percent of patients with viral encephalitis.  Thus, given 
an immunocompetent patient, the absence of a 
pleocytosis should raise the suspicion of a non-viral 
cause of the encephalopathy.  Similarly, a decreased 
glucose level should also prompt the search for a 
non-viral cause.  About 20 percent of patients with 
encephalitis will have RBCs in their CSF profile 
following a non-traumatic tap, indicating a hemorrhagic 
encephalitis such as that associated with HSV, 
Colorado tick fever virus, and sometimes California 
encephalitis virus (1). 
     PCR amplification of viral nucleic acid in the CSF is 
a sensitive (75-98%) and specific (100%) test for HSV 
encephalitis within the first 25-45 hours (2).  PCR 
analysis of the CSF is less invasive and less costly 
than the traditional brain biopsy, and is therefore 
becoming the diagnostic test of choice.  A brain biopsy 
does have the advantage, however, of potentially 
identifying alternative causes of the encephalopathy 
(1). The PCR test for HSV is not routinely done on CSF 
samples and must be specifically requested.  Results 
are usually available within 24 hours (4).  The initial 
result may return negative and should be redone if 
clinical suspicion remains high (6,7).
     HSV antibody detection in the CSF yields the best 
results after a week into the illness.  Thus, its 
usefulness is limited to a retrospective confirmation of 
HSV infection rather than for acute diagnostic 
purposes.  CSF culture for HSV is unreliable and is 
invariably negative in cases of HSV-1 encephalitis (1).
     CT, MRI, and EEG are helpful to identify or exclude 
alternative diagnoses and in determining whether the 
disease is focal or widespread.  Such tests for HSV 
encephalitis tend to yield focal abnormalities, such as:  
1) periodic focal spikes and slow-wave or periodic 
sharp wave patterns over the temporal lobes on EEG; 
2) areas of low absorption, mass effect, and contrast 
enhancement in the temporoparietal regions of the 
brain on CT; 3) areas of increased signal intensity in 
the frontotemporal, cingulate, or insular regions on 
T2-weighted spin-echo MRI images.  The 
aforementioned findings, however, are not pathognomic 
for HSV encephalitis (1,4).
     MRI is a more sensitive test than CT.  However, CT 
is fast and is useful to rule out other causes of 
encephalopathy, such as acute hemorrhage, shaken 
infant syndrome, brain tumor, or some conditions that 
requires immediate neurosurgery.   Many authorities 
recommend performing a CT scan of the head, with and 
without contrast, prior to obtaining a lumbar puncture 
     A patient with encephalopathy should be evaluated 
and treated for shock or hypotension.  The clinician 
may place the patient on prophylactic anticonvulsant 
medication and also consider airway protection in 
patients with altered states of consciousness.  For 
patients with signs of hydrocephalus and increased 
intracranial pressure, coughing and straining should be 
controlled.  If the patient is stable, the head should be 
elevated and neurologic status should be monitored.  
When aggressive intervention is required, the clinician 
may consider the use of diuretics (if the patient's 
circulatory volume is protected) or hyperventilation in 
an emergency situation.  Cerebral edema can also be 
controlled with steroids, but the use of steroids in HSV 
encephalitis is controversial (4).  Intracranial pressure 
monitoring is also controversial (2).
     In general, with the exception of HSV and varicella 
zoster virus, the viral encephalitides lack specific 
treatment (Cytomegalovirus and toxoplasma 
encephalitis do have specific treatments, but they are 
not usually initiated in the ED) (2).
     The consensus report on the diagnosis of HSV 
encephalitis published in 1996 recommends that 
intravenous acyclovir be given to the patient as soon as 
the diagnosis is suspected, since early intervention is 
key (6).  Even if the CSF PCR returns negative for 
HSV, treatment with acyclovir should continue if 
clinicial suspicion remains high, since the drug is 
relatively non-toxic, with the major side-effect being 
transient renal insufficiency (8).  Acyclovir should be 
given at a dose of 10 mg/kg every 8 hours (for a total of 
30 mg/kg per day) for 14 days (Acyclovir should be 
infused slowly over one hour to minimize the risk of 
renal insufficiency. The dose of 30 mg/kg per day is 
double that for mucocutaneous/visceral infections 
because CSF levels of acyclovir only reach 30-50 
percent of plasma levels).  The dosage should be 
adjusted for patients with existing renal dysfunction (3). 
     For HIV+ patients, foscarnet (Foscavir), may be a 
suitable substitute for acyclovir, given the increased 
incidence of acyclovir-resistant strains of HSV (2).
     Patient prognosis is dependent upon several host 
factors as well as the virulence of the virus.  For 
example, rabies, eastern equine encephalitis, and 
Japanese encephalitis are associated with significant 
mortality and morbidity, including severe neurologic 
sequelae.  California encephalitis and western equine 
encephalitis tend to be milder diseases (2). 
     Mortality in untreated patients with HSV encephalitis 
is about 70%, and many survivors are left with 
neurologic abnormalities (4).  According to National 
Institute of Allergy and Immune Diseases-Collaborative 
Antiviral Study Group (NIAID-CASG) trials, of 32 
acyclovir treated patients, 81 percent survived.  Among 
the survivors, 46 percent suffered little or no neurologic 
sequelae, 12 percent were moderately impaired, and 
42 percent were severely impaired, requiring 
continuous supportive care (1).  5-10 percent of 
surviving patients relapse days to weeks after 
completion of treatment (4).
     Factors important in the prognosis of HSV 
encephalitis are the timeliness of intervention, the age 
of the patient, and the level of consciousness at the 
initiation of therapy.  For example, patients with a 
Glasgow coma score of less than or equal to 6, either 
died or suffered severe neurologic sequelae.  Acyclovir 
can reduce neonatal death by 25 percent, but the rate 
of morbidity, especially with HSV-2 infections, is still 
very high (1,3).  40-60 percent of neonatal survivors 
have developmental abnormalities after 2 years of 
follow-up care (4).

     1. HSV is the most common cause of viral 
encephalitis in the United States, accounting for 10 to 
20 percent of all cases.
     2. Neonates (infants less than 6 weeks old) have the 
highest incidence of HSV visceral and/or CNS infection 
among all age groups.
     3. Individuals with subclinical disease may still shed 
infectious virus.
     4. In children and adults, there is no relationship 
between the presence of mucocutaneous lesions and 
HSV encephalitis.  Thus, the presence or absence of 
such lesions is of no diagnostic value.  For neonates, 
however, pathognomonic lesions have positive 
predictive value.
     5. Neonates often present with disseminated 
disease and thus may have signs and symptoms of 
jaundice, shock, bleeding, or respiratory distress
     6. PCR amplification of viral nucleic acid in the CSF 
is a sensitive and specific test for HSV encephalitis, 
and is becoming the diagnostic test of choice.  The 
PCR test for HSV is not routinely done on CSF samples 
and must be specifically requested. 
     7. The initial PCR result may return negative and 
should be redone if clinical suspicion remains high.
     8. MRI is the preferred imaging study for HSV 
encephalitis, especially T2 weighted and FLAIR 
     9. Intravenous acyclovir should be given to the 
patient as soon as the diagnosis of HSV encephalitis is 
suspected (ie., prior to confirmation).
     10. Even if the CSF PCR returns negative for HSV, 
treatment with acyclovir should continue if clinicial 
suspicion remains high, since the drug is relatively 

     1.  Tyler KL.  Aseptic Meningitis, Viral Encephalitis, 
and Prion Diseases.  In: Fauci AS, Braunwald E, 
Isselbacher KJ, Wilson JD, Martin JB, Kasper DL, 
Hauser SL, Longo DL (eds).  Harrison's Principles of 
Internal Medicine, 14th edition.  USA, McGraw-Hill, 
1998, pp. 2440-2445.
     2.  Lazoff M.  Encephalitis.  
www.emedicine.com/emerg/topic163.htm (no date, 
reviewed online September 2000).
     3.  Corey L.  Herpes Simplex Viruses.  In: Fauci AS, 
Braunwald E, Isselbacher KJ, Wilson JD, Martin JB, 
Kasper DL, Hauser SL, Longo DL (eds).  Harrison's 
Principles of Internal Medicine, 14th edition.  USA, 
McGraw-Hill Co., Inc., 1998, pp. 1080-1084.
     4.  Pritz T.  Herpes Simplex Encephalitis.  
www.emedicine.com/emerg/topic247.htm (no date, 
reviewed online September 2000).
     5.  Girolami UD, Anthony DC, Frosch MP.  The 
Central Nervous System.  In: Cotran RS, Kumar V, 
Collins T (eds).  Robbins Pathologic Basis of Disease, 
6th edition.  Pennsylvania, W.B. Saunders Co., 1999, 
pp. 1317-1319.
     6.  Coren ME, Buchdahl RM, Cowan FM, Riches 
PG, Miles K, Thompson EJ.  Imaging and laboratory 
investigation in herpes simplex encephalitis.  Journal of 
Neurology, Neurosurgery, and Psychiatry 
     7.  Spuler A, Blaszyk H, Parisi JE, Davis DH.  
Herpes simplex encephalitis after brain surgery:  case 
report and review of the literature.  Journal of 
Neurology, Neurosurgery, and Psychiatry 
     8.  Carlini ME, Shandera WX.  Infectious Diseases: 
Viral and Rickettsial.  In:  Tierney LM, McPhee SJ, 
Papadakis MA (eds).  Current Medical Diagnosis and 
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Lange, 1999, pp. 1256-1259.   

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Web Page Author:
Loren Yamamoto, MD, MPH
Professor of Pediatrics
University of Hawaii John A. Burns School of Medicine