PEREZ, Patricia Marie E.

2H-2
Comparative Microbiology: MENINGITIS AND ENCEPHALITIS

INFECTION/ KEY FEATURES/

ETIOLOGY DIAGNOSIS TREATMENT PREVENTION
INTOXICATION MANIFESTATIONS

MENINGITIS

1. Aseptic / Viral  Echoviruses and  fever, headache,nuchal rigidity To obtain a definitive diagnosis of If possible, antibiotic therapy should Universal administration of S
coxsackieviruses A and B  maculopapular rashes and meningitis, it is necessary to be delayed until blood and CSF pneumoniae and H influenzae
 Human simplex virus type 2 conjunctivitis (commonly seen perform a lumbar puncture. samples have been collected. If not type b vaccines to infants has been
(HSV-2) when caused by an echovirus) and possible, performing the lumbar tap shown to dramatically
 Varicella-zoster virus (VZV) lethargy but with clear mentation After lumbar puncture, empiric within 30 minutes after beginning reduce the number of cases of
 Epstein-Barr virus (EBV) and no focal neurologic findings antimicrobial therapy can be antibiotic therapy increases the acute bacterial meningitis in
 cytomegalovirus (CMV)  tinnitus, vertigo, chest and initiated in most cases. likelihood of culturing the CSF for children.
 Human abdominal pain, and paresthesia bacterial causes of meningitis
immunodeficiency virus In certain cases, a CT scan should Administering the N meningitidis
(HIV) be performed before lumbar vaccine to college
puncture to ensure that no Aseptic meningitis students who plan to stay in
2. Infant intracerebral masses are present Patients should be given empiric dormitories and to military
 Poor feeding, vomiting, paradoxic in patients with focal neurologic antibiotics pending results of CSF recruits also has been shown to
irritability (i.e., quiet when deficits (i.e., dilated fixed pupils, culture, blood cultures, and follow- reduce the number of these
 Viral: Enteroviruses, Herpes
stationary, cries when held), or Cheyne-Stokes respiration, up lumbar puncture. infections.
simplex virus, Varicella-
high-pitched cry decerebrate posturing,
zoster virus,
 Respiratory distress, apnea, and hemiplegia); Acute bacterial meningitis To protect neonates from
Cytomegalovirus
cyanosis. patients with an abnormal level of Once samples of blood and CSF meningitis caused by S agalactiae
 Bacterial: Escherichia coli,
 Bulging fontanelle. consciousness (i.e., coma); patients are obtained, intravenous (group B streptococcus), vaginal
Streptococcus agalactiae,
 Hypotonia with a history of CNS disease empiric therapy based on the most and rectal swab samples should be
Listeria monocytogenes
 Jaundice or rash (i.e., petechial, (e.g., mass lesion, stroke, or focal likely cause of the patient’s obtained from the pregnant
 Parasitic: Toxoplasma
vesicular, macular,mucosal) infection); patients with meningitis should begin woman (at 35–37 weeks’
gondii
 Seizures or subdural effusions papilledema; patients who have immediately. gestation). If cultures are positive
 Syndrome of inappropriate had seizures within 1 week before for S agalactiae, administration of
antidiuretic hormone presentation; or If the cause of penicillin intrapartum can
(SIADH)secretion (hyponatremia immunocompromised patients. acute bacterial meningitis is known, significantly reduce neonatal
and hypovolemia of blood and specific therapy can then be infections.
inappropriately elevated urine initiated.
osmolality). Symptoms can include The following tests on the CSF will Pregnant women with a history of
nausea, vomiting, irritability, help in determining a Empiric Treatment genital herpes should be
seizures, and stupor or coma. diagnosis: assessed before delivery, and a
Preterm to <1 month: cesarean section should be
3. Acute CSF clarity, protein concentration, Ampicillin +cefotaxime performed if herpetic lesions or
Bacterial  Upper respiratory tract infection glucose concentration (compare Ampicillin +gentamicin prodromal symptoms are present
(e.g., sore throat, rhinorrhea, and with blood glucose), and white during labor rather than delivering
nasal congestion) or ear infection blood cell 1 month to 50 years: the fetus vaginally.
 Headache, fever, nuchal rigidity, count Cefotaxime or ceftriaxone +
Community-Acquired
and altered mental status vancomycin + dexamethasone Pregnant women with no history of
(neurologic findings). The CSF should also be smeared VZV infection should avoid
 Neonates (Preterm to <1
 Less than 50% of patients with on a glass slide and Gram stained Age >50 years, alcoholism, exposure to patients with clinically
 month of age): Escherichia acute bacterial meningitis have and cultured impaired cell-mediated immunity: apparent signs of this viral infection
coli, Streptococcus the classic triad of fever, nuchal Cefotaxime or ceftriaxone + (e.g., chickenpox, zoster). They
agalactiae , Listeria rigidity, and change in mental ampicillin + vancomycin + should also avoid contact with cat
monocytogenes status If certain bacterial pathogens are dexamethasone litter boxes (Toxoplasma gondii)
 Persons 1 month to 50 years suspected (e.g., S pneumoniae, S and uncooked or undercooked
of age: Streptococcus Other signs and symptom agalactiae, N meningitidis, E coli Specific Antimicrobial Therapy meats (T gondii and Listeria)
pneumoniae, Neisseria associated with acute K1), the CSF can be tested for Streptococcus pneumoniae:
meningitidis bacterialmeningitis bacterial capsular antigens by Penicillin G or vancomycin (for
 Persons older than 50 years  Evidence of otitis media. latex agglutination. resistant strains)
of age, alcoholics, and  Pharyngeal inflammation.
impaired cell-mediated  Purulent nasal discharge If certain bacterial pathogens are Neisseria meningitidis: Penicillin G
immunity: Streptococcus  Diastolic heart murmur suggests suspected (e.g., S pneumoniae, or chloramphenicol
pneumoniae, Listeria endocarditis S agalactiae, N meningitidis, E coli
monocytogenes:  Nonblanching petechiae or K1), the CSF can be tested for Listeria monocytogenes: Ampicillin
purpura are usually due to bacterial capsular antigens by + gentamicin
Nosocomial Neisseria meningitidis infection. latex agglutination.
 Patients with severe N Staphylococcus aureus: Methicillin-
 Following endocarditis: meningitidis infection may Other tests used to determine the sensitive S aureus (MSSA) Nafcillin
Staphylococcus aureus experience endotoxic shock with cause of chronic meningitis include or oxacillin + rifampin
 Following ventricular shunt vascular collapse. a chest radiograph and a
replacement:  Hemorrhage into the adrenals tuberculin skin test, which may aid Methicillin-resistant S aureus
Staphylococcus epidermidis, can result in Waterhouse- in the diagnosis of meningitis due (MRSA) : Vancomycin + rifampin
Staphylococcus aureus, Friderichsen syndrome. to M tuberculosis (also used to treat Staphylococcus
Enterococcus sp, Bacillus  Acute adrenal gland insufficiency epidermidis)
subtilis, Corynebacterium sp and shock occur in 50% of CT scan of the brain, with and
patients with N meningitidis CNS without contrast, or MRI may Enterobacteriaceae: Ceftriaxone +
infections. show calcifications if the cause is gentamicin (intrathecal and
 Ocular effects include lateral gaze CMV, toxoplasmosis, rubella, or systemic)
palsy (abducens, or 6th, cranial HSV, whereas Staphylococcus
nerve) and photophobia. aureus, Citrobacter diversus, Infant meningitis
 NOTE: Papilledema, asymmetric Proteus mirabilis, and other Because the causative agent usually
response to light, and unilateral bacteria can cause abscesses, is not known at presentation, all
cranial deficits are rare in acute which will have a well-defined newborns or infants with meningitis
bacterial meningitis and are more border with a less opaque center. should be treated aggressively, and
4. Chronic common in space-occupying antibiotics should be given to
lesions in the brain. protect against the most common
bacterial causes of meningitis.

 Manifestations of chronic Antibiotics should be administered

meningitis due to M tuberculosis until all bacterial cultures have been
 Mycobacterium tuberculosis include fever, unremitting negative for at least 72 hours.
 Cryptococcus neoformans headache, nausea, nuchal rigidity,
and drowsiness, which can Empiric therapy for infants who
progress to stupor and coma are preterm or younger than 1
 Manifestations of chronic month of age includes ampicillin
meningitis due to Cryptococcus plus cefotaxime or gentamicin. If
neoformans progress slowly in HSV infection is likely, acyclovir
immunocompetent patients with should also be given.
symptoms such as headache,
nuchal rigidity, and a fever that
tends to wax and wane. Antibiotics specific for identified
bacterial agents are the
same as those administered to
patients with acute bacterial
meningitis.

However, chloramphenicol should

NOT be administered to infants or
to women who are pregnant or
breastfeeding because fetuses and
neonates lack the liver enzymes
necessary to metabolize this drug.
Drug toxicity can cause gray baby
syndrome (e.g., hypotension,
cyanosis, and frequently death).

Chronic meningitis
Tubercular, or tuberculous,
meningitis is a severe bacterial
meningitis caused by M
tuberculosis; it is fatal if not treated
within 5–8 weeks of symptom
onset. A regimen of isoniazid,
rifampin, pyrazinamide, and
ethambutol should be administered
for 12 months.

Patients who have fungal meningitis

should be given amphotericin B plus
flucytosine until they are afebrile
and cultures are negative; then
treatment with amphotericin B plus
flucytosine should be stopped and
treatment with fluconazole should
be given for 8–10 weeks.
ENCEPHALITIS HUMAN-TO-HUMAN Encephalitis Encephalitis Encephalitis Preexposure prophylaxis for rabies
ENCEPHALITIS Lumbar puncture to assess the Treatment of encephalitis is Veterinarians and others who may
Common manifestations include CSF and CT scan or MRI with supportive, usually resulting in be exposed to rabid animals
HSV-1 is the most common severe headache, meningeal contrast to rule out brain abscess, hospitalization, intravenous fluids, should receive rabies vaccination.
cause irritation (headache and nuchal stroke, or another structural respiratory support, and prevention
rigidity), sensory or motor deficits disorder such as hematoma, of secondary infections for patients The most commonly used
Others: VZV, HSV-2 (seen similar to ataxia, and grand mal or aneurysm, or tumor. with severe disease. vaccine is produced in human
almost exclusively in focal seizures. diploid cell cultures and may be
neonates), CMV, influenza Viral culture can be performed on administered either intradermally or
virus, and HIV Patients with encephalitis may the CSF and on swab samples Ribavirin in high doses and intramuscularly into the
(i.e., HIV encephalopathy or experience visual or auditory obtained from the throat. Even interferon alpha-2b has some deltoid muscle.
AIDS dementia) hallucinations. with these tests, a specific activity against West Nile virus in
microorganism is identified less vitro, but no controlled studies have Postexposure prophylaxis for rabies
ZOONOTIC ENCEPHALITIS They may perform peculiar higher than 50% of the time. been completed on the use of these For patients who have not been
motor functions such as continuous medications in treating West immunized against rabies, the
Arbovirus (arthropodborne buttoning and unbuttoning of a shirt Tests for the detection of viral Nile virus encephalitis. rabies vaccine should be given on
viruses) or the rabies virus or placing their underwear over antigens in the CSF or days 0, 3, 7, 14, and 28.
their outerwear. identification When HSV encephalitis cannot be
of agents by reverse transcriptase ruled out, acyclovir must Rabies immunoglobulin should be
Viral encephalitis can cause polymerase chain reaction (RT- be started promptly, before the administered into the tissues
personality changes, confusion, and PCR) are available for some patient lapses into coma, and surrounding the wound.
sleepiness and can progress to coma viruses, and the CSF profile is continued for at least 10 days to
and death. similar to that seen in aseptic achieve maximal therapeutic If more immunoglobulin remains, it
meningitis. benefit. can be infused into the wound area
Rabies by injecting the remainder
Patients who develop manifestations The CSF can also be assayed for Sometimes the initial lumbar intramuscularly at a site distant
of rabies virus encephalitis virus-specific IgM and IgG using puncture does not disclose from the vaccination site.
experience an abrupt onset of paired acute and convalescent a cellular pleocytosis, so treatment
hydrophobia. samples. with acyclovir should not be Patients who have been immunized
delayed when the clinical picture is against rabies should
When attempting to drink water, Diagnosis of West Nile virus compatible with HSV encephalitis. receive two intramuscular doses of
the pharynx spasms, spreading to encephalitis is based on clinical rabies vaccine on days 0 and
the respiratory muscles and causing suspicion and positive results of The lumbar puncture should be 3, and rabies immunoglobulin
shallow quick respirations and specific laboratory tests. West Nile repeated 24 hours later. should not be administered.
possibly hyperactivity. virus or other arboviral diseases Lymphocytosis is usually observed
such as St. Louis in the second CSF sample. Prevention of arboviral encephalitis
Seizures with coma usually follow encephalitis should be strongly When outdoors, protective clothing
these manifestations. Patients often considered in adults older Rabies should be worn and
experience pituitary dysfunction than age 50 who develop Following an animal bite, the insect or tick repellent should be
resulting in diabetes insipidus or unexplained encephalitis or wound should be cleaned by applied.
inappropriate antidiuretic hormone meningitis in summer or early fall. allowing it to bleed, and then it
secretion. The most efficient diagnostic should be washed with soap and Outdoor activity should be avoided
method is detection of IgM water. at dusk and dawn when
Cardiac arrhythmias and autonomic antibody to West Nile virus in mosquitoes prefer to feed.
dysfunction are also common. Death serum collected 8–14 days All pets should be immunized.
usually occurs within 1–2 weeks. after onset of illness or CSF Contact with bats and wild animals Habitat for mosquitoes should be
The manifestations of rabies begin collected within 8 days of onset that are not behaving normally reduced by removing objects that
10–240 days after exposure; of illness. Identification of West should be avoided. collect water (e.g., old tires, garden
however, the usual incubation period Nile virus genome in CSF by RT- containers).
is 30–90 days. PCR.
Habitat for ticks should be reduced
The three clinical phases of the by removing brush and weeds from
disease are prodromal, excitation, Herpes encephalitis is clinically around the home.
and paralytic similar to other viral
encephalitides Pets should be protected with
but is strongly suggested by repellent so that ticks are not
repeated seizures occurring brought into the home.
early in the course of the disease
and by signs indicating temporal Ticks should be removed as soon as
lobe involvement. possible after returning
from the outdoors.
An electroencephalogram usually
demonstrates electrical spikes in
the region of the infected
temporal
lobe.

Erythrocytes in the CSF after an

atraumatic lumbar tap also
suggests HSV.

PCR can detect HSV DNA in the

CSF;
however HSV is rarely isolated
from the CSF.

Rabies
The animal vector should be
euthanized and its brain examined
for signs of rabies.

Pets (e.g., dogs, cats, ferrets)

that do not appear sick may be
confined and observed by a
veterinarian for 10–14 days.

If the pet remains healthy, it is

considered to be free of rabies
infection.

Patients should not begin

therapy unless the confined pet
begins to show symptoms.

If an animal shows signs of

sickness, postexposure prophylaxis
 should begin immediately.

If the animal cannot be tested and

if prodromal signs of
rabies exist, tests can be
performed on human patients.

RT-PCR to detect rabies viral

RNA can be performed on saliva
or a skin biopsy can be taken
from the posterior region of the
neck at the
hairline.

Biopsies of the neck skin can be

tested for viral antigen
by immunofluorescent staining.
Serum and CSF can be tested
for antibodies to rabies by indirect
immunofluorescence and
virus neutralization tests.

If no vaccine or rabies immune

serum has been given, the
presence of antibody to rabies
virus in the serum is diagnostic
and tests of CSF are unnecessary.

Antibody to rabies virus in the

CSF, regardless of immunization
history,
suggests a rabies virus infection.

Reference: Harrison's Principles of Internal Medicine (19th Ed) pages 81 - 94