Meningitis - Acute and Chronic : Infection inflammatory Aseptic Drug Toxin Autoimmune Paraneoplastic

1. MENINGITIS
CHAIRPERSON- DR GAYATRI.B.H.
STUDENT-DR NATARAJ G S

2. DEFINATIONS
• MENINGITIS : Inflammation of the meninges.
• Encephalitis : Inflammation of the brain
parenchyma.
• Meningo encephalitis : Inflammation of
meninges and brain parenchyma.

3. • Meningitis is a clinical syndrome characterized by
inflammation of the meninges.
CAUSES:
1) INFECTIOUS
2) NON INFECTIOUS (MEDICATIONS AND CARCINOMATOSIS)
MAY BE CLASSIFIED AS
• 1) ACUTE MENINGITIS :HOURS TO DAYS
• 2) CHRONIC MENINGITIS :AT LEAST 4 WEEKS.

4. CLASSIFICATION
• 1)Acute bacterial meningitis.
• 2)Acute aseptic meningitis.
• 3)Chronic meningitis.
• 4)Others (depend on specific pathogen) fungal ,
parasitic

5. PATHOPHYSIOLOGY
• Three major pathways.
• Hematogenous (eg, from bacteremia, viremia,
fungemia).
• Retrograde neuronal pathway (eg, Naegleria
fowleri, rabies, HSV, VZV).
• Direct contiguous spread (eg, sinusitis, otitis media,
congenital malformations, trauma, direct inoculation
during intracranial manipulation).

6. PATHOPHYSIOLOGY

8. CLINICAL MANIFESTATIONS
• Fever , malaise
• Headache
• Vomiting
• Photophobia
• Hyperirritability
• Neck stiffness

9. • Changes in mental status Seizure (30% of patients.)
• Triad of fever, nuchal rigidity, and change in mental
status(2/3 of patients).
• Fever is the most common manifestation (95%),
while stiff neck and headache are less common.
• However, the negative predictive value of these
symptoms is high (ie, the absence of fever, neck
stiffness, or altered mental status eliminates the
diagnosis of meningitis .).

10. Meningeal irritation signs
1) Nuchal rigidity.
2) Kernig sign.
3) Brudzinsky sign .

12. PHYSICAL FINDING SENSITIVITY
FEVER 85%
NECK STIFFNESS 70%
ALTERED SENSORIUM 67%
ABSENCE OF ABOVE THREE 99% TO 100%
SPECIFIC EXAM
KERNIG SIGN 5%
BRUDZINSKI SIGN 5%
PHYSICAL EXAM
FINDING

13. Signs of increase ICP
1)Papilledema.
2) Cushing’s triad.
Bradycardia, Systolic Hypertension(widening of
pulse pressure) and Irregular decreased breathing.
3) Changes in pupils.
4) Focal neurological deficit.

14. Atypical presentation
• Elderly, especially with underlying
comorbidities (eg, diabetes, renal and liver
disease),
• Lethargy and an absence of meningeal
symptoms.
• Patients with neutropenia may present with
subtle symptoms of meningeal irritation.

15. Others
• Immuno compromised hosts,
• Including organ and tissue transplant
recipients.
• Patients with HIV and AIDS patients with
aseptic meningitis syndrome usually appear
clinically nontoxic with no vascular instability

16. Sexual contact and high-risk behavior
• HSV meningitis is associated with primary
genital HSV infection and HIV infection
• Exposure to a patient with a similar illness is
an important epidemiological clue when
determining etiology (eg, meningococcemia).

17. • Intake of unpasteurized milk predisposes to
brucellosis and L monocytogenes infection.
• Animal contacts rabies (lymohocytic
choriomeningitis) virus Leptospira.
• History of neurosurgery -ventriculo peritoneal
shunt cochlear implants.

18. •
Sinusitis or otitis suggests direct extension into the
meninges, usually with S pneumoniae and H
influenzae .
• Rhinorrhea / otorrhea suggests a CSF leak from a
basilar skull fracture, with meningitis most
commonly caused by S pneumoniae.
• Petechiae are seen in meningococcal disease with or
without meningitis .
• The presence of a murmur suggests infective
endocarditis with secondary bacterial seeding of the
meninges .

19. • Hepato splenomegaly and lymphadenopathy
suggest a systemic disease, including viral (eg,
mononucleosis like syndrome in EBV, CMV,
and HIV) and fungal (eg, disseminated
histoplasmosis) disease.
• Vesicular lesions in a dermatomal distribution
suggest varicella-zoster virus.
• Genital vesicles suggest HSV-2 meningitis

20. • Acute infections of the nervous system are
among the most important.
• clinical syndromes include
• 1) Acute bacterial meningitis,
• 2) Viral meningitis,
• 3)Encephalitis,
• 4) Focal infections such as brain abscess and
subdural empyema, and infectious
thrombophlebitis

21. Acute bacterial meningitis
• S. pneumoniae gram-positive cocci, colonize
at human nasopharynx.
• Most common bacterial cause of meningitis,
accounting for 47% of cases with mortality
rates 19-26%
• Mechanism: hematogenous or direct
extension from sinusitis or otitis media

22. Risk factor
• Basilar skull fracture and CSF leak.
• Patients with hyposplenism or splenectomy
hypogammaglobulinemia
• Multiple myeloma
• Glucocorticoids treatment
• Diabetes mellitus
• Renal insufficiency

23. • Alcoholism
• Malnutrition
• Chronic liver disease
• Pneumonia
• Sinusitis
• Endocarditis

24. MANAGEMENT
• Key goals of early management are to
emergently distinguish between these
conditions.
• Identify the responsible pathogen, and
initiate appropriate antimicrobial therapy.

25. • The first task is to identify whether an infection
predominantly involves the subarachnoid space
(meningitis) or
• whether there is evidence of either generalized or focal
involvement of brain tissue in the cerebral
hemispheres, cerebellum, or brainstem.
• When brain tissue is directly injured by a bacterial or
viral infection, the disease is referred to as encephalitis,
• whereas focal infections involving brain tissue are
classified as either cerebritis or abscess, depending on
the presence or absence of a capsule.

26. N. meningitidis
• Gram-negative diplococci in nasopharynx (10-
15%)
• Leading cause of bacterial meningitis in children
and young adults, accounting for 59% of cases.
• Meningococcal disease: purulent conjunctivitis,
septic arthritis, sepsis +/- meningitis.
• Risk factors: household crowding ,college
dormitories , military facilities chronic medical
illness corticosteroid use .

27. H. influenzae- small, pleomorphic,
gram-negative coccobacilli
• Frequently found as normal flora in the upper
respiratory tract of humans
• Spread by airborne droplets or direct contact with
secretions.
• Meningitis is caused by the encapsulated type B strain
It primarily affects infants younger than 2 years.
• Its isolation in adults suggests the presence of an
underlying medical disorder, including sinusitis, otitis
media, alcoholism, CSF leak following head trauma,
hyposplenism and hypogammaglobulinemia .

28. L. monocytogenes small gram-
positive bacillus
• One of the highest mortality rates (22%).
• Most human cases appear food-borne:
coleslaw, milk, cheese
• Risk factor: infants and children,
• Elderly (>60 y)
• Pregnant women
• Alcoholism Patients with CMI defect, immuno
compromised.

29. Aseptic meningitis syndrome
• Most common infectious syndrome affecting the CNS
• Acute onset of meningeal symptoms, fever, and
cerebrospinal pleocytosis (usually prominently
lymphocytic) with negative bacterial microbiologic
data.
• Most episodes are caused by a viral pathogen but they
can also be caused by bacteria, fungi, or parasites
Importantly, partially treated bacterial meningitis
accounts for a large number of meningitis cases with a
negative microbiologic workup.

30. Aseptic meningitis syndrome
• HERPES (HSV, HZV, EBV, CMV),
• ENTERO (Echo,Coxakie,Polio,Enterovirus etc.)
• ARBO (JEV, Tick-bite encephalitis virus)
• Adenovirus
• LCMV
• HIV

31. • VZV and CMV causes meningitis in immuno
compromised hosts.
• Lymphocytic chorio meningitis virus(LCMV)
transmit by aerosols and direct contact with
rodents. may be associated with orchitis,
arthritis, myocarditis, and alopecia.
• Mumps Meningitis usually follows the onset
of parotitis, which clinically resolves in 7-10
days

32. • HIV Aseptic meningitis may be the presenting
symptom in a patient with acute HIV infection
• Always suspect HIV as a cause of aseptic
meningitis in a patient with risk factors such as
intravenous drug use and in individuals who
practice high-risk sexual behaviors

33. Partially-treated bacterial meningitis
• L monocytogenes
• Brucella species
• Rickettsia rickettsii
• Ehrlichia species
• Mycoplasma pneumoniae
• Treponema pallidum
• Leptospira species
• Mycobacterium tuberculosis
• Nocardia species

34. Parasites
• N fowleri( brain eating amoeba)
• Acanthamoeba species
• Angiostrongylus cantonensis or rat lung
worm (commenest cause of eosinophilic
meningitis)
• Strongyloidiasis stercoralis (thread worm)
• Taenia solium (cysticercosis)

35. FUNGI
• Cryptococcus neoformans
• C immitis
• H capsulatum
• Candida species
• Aspergillus species

36. Chronic meningitis
• Signs and symptoms of meningeal irritation
associated with CSF pleocytosis that persists
for longer than 4 weeks.
• Bacterial
• Viral
• Fungal
• Aseptic (Lyme, syphillis)
• TB Other causes of aseptic meningitis

37. Tuberculous meningitis
• Acid-fast bacilli
• Patients generally have a prodrome of fever of
varying degrees, malaise, and intermittent
headaches
• Patients often develop central nerve palsies
(III, IV, V, VI, and VII) suggesting basilar
meningeal involvement

38. MRC STAGINGOF TB MENINGITIS
• Clinical staging of meningeal tuberculosis is based
on neurologic status
• Stage 1 - no change in mental function with no
deficits and no hydrocephalus.no definitive
neurological symptom.
• Stage 2 - confusion and with or without evidence
of neurologic deficit. signs of meningeal irritation.
• Stage 3 - stupor and lethargy. focal neurological
deficits and involuntary movements.(50 %to 70%)

40. INFARCTION IN TBM

41. TUBERCULOMA

42. BORDER ZONE ENCEPHALITIS IN
TBM

43. Spirochetal meningitis
• T pallidum modes of transmission:
• Sexual contact
• Direct contact with an active lesion passage
through the placenta blood transfusion (rare).
• Syphilitic meningitis usually occurs during the
primary or secondary stage.
• Its presentation is similar to other agents of
aseptic meningitis

44. Other CNS syphilitic syndromes
• Meningovascular syphilis
• Parenchymatous neurosyphilis
• Gummatous neurosyphilis and
• The symptoms are dominated by focal
syphilitic arteritis (ie, focal neurologic
symptoms associated with signs of meningeal
irritation)

45. Fungal meningitis C. neoformans
• An encapsulated yeast-like fungus that found in
high concentrations in aged pigeon droppings.
• 50-80% of cases occur in immunocompromised
hosts.
• The infection is characterized by the gradual
onset of symptoms, the most common of which is
headache.
• The onset may be acute, especially among
patients with AIDS.

46. Parasitic meningitis
• Free-living amoebas (ie, Acanthamoeba,
Balamuthia,Naegleria) infrequent but often
life-threatening illness.
• N fowleri is the agent of primary amebic
meningoencephalitis (PAM) .
• Infection occurs when swimming or playing in
the contaminated water invade the CNS
through the nasal mucosa and cribriform
plate.

47. Primary amebic meningo encephalitis
(PAM)
• An acute onset of high fever, photophobia, headache,
and change in mental status, similar to bacterial
meningitis with involvement of the olfactory nerves
sensation.
• Death occurs in 3 days in patients who are not treated.
• Subacute or chronic form, is an insidious onset of low-
grade fever, headache, and focal neurologic signs.
• Acanthamoeba and Balamuthia cause granulomatous
amebic encephalitis, which spreads hematogenously
from the primary site of infection (skin or lungs)

48. Helminthic eosinophilic meningitis
• Acantonensis cause eosinophilic meningitis
(pleocytosis with >10% eosinophils).
• Acquire the infection by ingesting raw
mollusks

49. • On rare occasions, the larva can migrate into
the CNS and cause eosinophilic meningitis.
• G spinigerum cause eosinophilic
meningoencephalitis acquire the infection
following ingestion of undercooked infected
fish and poultry.
• This is common in Southeast Asia, China, and
Japan

50. Differential diagnosis
• Encephalitis
• Brain Abscess.
• Noninfectious meningitis,
• Medication- induced meningeal inflammation
• Meningeal carcinomatosis
• Stroke
• CNS vasculitis
• Other causes of aseptic meningitis: malignancy
NSAID’s chemo

51. Lumbar puncture
• Lumbar puncture for CSF examination is urgently
warranted in individuals in whom meningitis is
clinically suspected.
• CSF for Chemistry (glucose & protein) cell count & diff
Gram stain ,AFB stain Culture for pathogens
• Other : India ink ,serology ,PCR ,Ag Identification
,cytology
• CSF Gram stain permits rapid identification of the
bacterial cause in 60-90% of patients with bacterial
meningitis.
• The presence of bacteria is 100% specific, but the
sensitivity for detection is variable

56. Lumbar puncture Contraindications
• Increase risk of herniation(suspected space
occupying lesion in CNS).
• Skin & soft tissue infection at area of tap.
• Bleeding disorder.
• Respiratory distress (positioning).

57. COMPLICATIONS
• Cerebral herniation.
• Post dural puncture headache .
• Traumatic tap ,Spinal trauma.
• Cerebral herniation following the lumbar tap
procedure is rare in individuals with no focal
neurologic deficits and no increased ICP.
• If it occurs, it usually happens within 24 hours
following the lumbar puncture and should always
be considered in the differential diagnosis if the
patient's neurologic status deteriorates

58. Laboratory investigation
• CBC
• Peripheral smear
• HIV
• Cultures from other possible sites of infection.
• The utility of these cultures is most evident in
cases when the performance of a lumbar
puncture is delayed by the need for head imaging
(risk for herniation in a patient with focal
neurologic deficit or coma) and when
antimicrobial therapy is rightfully initiated before
the lumbar puncture and neuroimaging tests.

59. Imaging study CT or MRI of the brain
• INDICATIONS:
• Focal neurologic deficit
• Increased ICP
• Suspicious for space-occupying lesions
• Suspected basilar fracture
• Diagnosis is unclear

60. • Helpful in the detection of CNS complications of
bacterial meningitis, such as hydrocephalus, cerebral
infarct, brain abscess, subdural empyema, and venous
sinus thrombosis.
• Do not aid in the diagnosis of meningitis.
• Some patients may show meningeal enhancement, but
its absence does not rule out the condition.
• CT scan of the brain may be performed prior to lumbar
puncture in some patient groups with a higher risk of
herniation newly onset seizures, moderate-to-severe
impairment in consciousness

61. Treatment : Bacterial meningitis
• Bacterial meningitis is a neurological emergency
that is associated with significant morbidity and
mortality.
• The initiation of empiric antibacterial therapy is
therefore essential for better outcome usually
based on the known predisposing factors and/or
initial CSF Gram-stain results.
• Delays in instituting antimicrobial treatment in
individuals with bacterial meningitis could lead to
significant morbidity and mortality Meningitis.

62. Treatment : Bacterial meningitis
• penicillins, certain cephalosporins (ie, third-
and fourth-generation cephalosporins), the
carbapenems, fluoroquinolones, and rifampin
provide high CSF levels
• Once the pathogen has been identified and
antimicrobial susceptibilities determined, the
antibiotics may be modified for optimal
targetted treatment Meningitis.

63. Antibiotics dosage
• Cefotaxime 12 g/day in divided doses 4h
• Ceftriaxone 4 g/day in divided doses 12h
• Gentamicin 7.5 mg/kq/day 8h
• Meropenem 3 g/day divided doses 8h
• Metronidazole 400 mg/day divided doses 8h
• Nafcillin 9-12 g/day divided doses 4h
• Penicillin G 20-24 million U/day 4h
• Vancomycin 2 g/day 12h

64. Use of corticosteroid
• The use of corticosteroids such as dexamethasone as
adjunctive treatment was significantly associated with
a reduction in case-fatality rate and neurologic
sequelae
• Strongly consider in patients with certain types of
bacterial meninigitis, such as H influenzae, tuberculous,
and pneumococcal meningitis
• Should be administered prior to or during the
administration of antimicrobial therapy May associate
with decreased penetration into the CSF of some
antimicrobials, such as vancomycin Dexamethasone
(0.15 mg/kg per dose q6h for 2-4 d)

65. Viral meningitis
• Most viral meningitis are benign and self-
limited. Often, they require only supportive
care and do not require specific therapy.
• In certain instances, specific antiviral therapy
may be indicated, if available Acyclovir (10
mg/kg IV q8h) for HSV-1 and HSV-2

66. • Ganciclovir (induction dose of 5 mg/kg IV q12h,
maintenance dose of 5 mg/kg q24h) and
foscarnet (induction dose of 60 mg/kg IV q8h,
maintenance dose of mg/kg IV q24h) for CMV
meningitis in immunocompromised hosts.
• Instituting highly active antiretroviral therapy
(HAART) may be necessary for patients with HIV
meningitis that occurs during an acute sero
conversion syndrome .

67. Tuberculous meningitis
• The demonstration of the acid-fast in the CSF is
difficult and usually requires a large volume of
CSF.
• The culture for Mycobacterium usually takes
several weeks and may delay definitive diagnosis.
• Nucleic acid amplification for M tuberculosis have
the advantage of a rapid, sensitive, and specific
• The need for mycobacterial growth in cultures
remains because this offers the advantage of
performing drug susceptibility assays.

68. • Isoniazid (INH) and pyrazinamide (PZA) attain
good CSF levels (approximate blood levels).
Rifampin (RIF) penetrates the BBB less
efficiently but still attains adequate CSF levels.
• Use the combination of the first-line drugs (ie,
INH, RIF, PZA, ethambutol, streptomycin. The
dosage is similar to what is used for
pulmonary tuberculosis(WEIGHT BAND).

69. • A treatment duration of 12 months is the
minimum, and some experts suggest a duration
of at least 2 years.
• The use of corticosteroids is indicated for
individuals with stage 2 or stage 3 disease (ie,
patients with evidence of neurologic deficits or
changes in their mental function).
• The recommended dose is 0.15 mg/d, which may
be tapered gradually during a span of 6 weeks.

70. Cryptococcal meningitis
• Diagnosis : identification of the pathogen in the CSF C neoformans
culture from CSF.
• India ink preparation : sensitivity of only 50%, but highly diagnostic
if positive
• CSF cryptococcal antigen : sensitivity of greater than 90%
• Blood cultures and serum cryptococcal antigen to determine if
cryptococcal fungemia is present
• In many cases, cryptococcal meningitis is complicated by increased
ICP

71. Cryptococcal meningitis in AIDS
• CD4<100/cu mm
• 2-7 cases/1000 with 89% CNS manifestation.
• 10,0000 cases world wide and 6,00000 death
annualy.
• Relapse rate is 30 -50%
• Spreads haematogenously from pulmonary
foci.

72. AIDS-related cryptococcal meningitis
• Induction therapy: amphotericin B ( 0.7 to 1 mg/kg/d
IV) for at least 2 weeks
• Consolidation therapy: fluconazole (400 mg/d for 8
wk).
• Itraconazole is an alternative Maintenance therapy:
Long-term antifungal therapy with fluconazole (200
mg/d)
• In case of increased ICP. Make an effort to reduce such
pressure by repeated lumbar puncture, a lumbar drain,
or shunt In many cases,
• cryptococcal meningitis is complicated by increased ICP

73. cryptococcal meningitis in patients
without AIDS
• Induction/consolidation: Administer
amphotericin B (0.7-1 mg/kg/d) plus flucytosine
(100 mg/kg/d) for 2 weeks.
• Then, administer fluconazole (400 mg/d) for a
minimum of 10 weeks.
• A lumbar puncture is recommended after 2
weeks to document sterilization of the CSF.
• If the infection persists, longer therapy is
recommended. Solid organ transplant recipients
require prolonged therapy.

74. Fungal meningitis C. immitis H
capsulatum Candida species
• Oral fluconazole (400 mg/d) or Itraconazole (
mg/d) Duration of treatment usually is life
long.
• H capsulatum Amphotericin B at0.7to 1
mg/kg/d to complete a total dose of 35 mg/kg
• Fluconazole (800 mg/d) for an additional 9-12
months may be used to prevent relapse.
• Candida species amphotericin B
(0.7mg/kg/d)+/- Flucytosine (25 mg/kg qid)

75. Syphilitic meningitis
• CSF SHOWS –
• Mild lymphocytic pleocytosis.
• Elevated CSF protein levels &
• Decreased glucose levels may be observed in 10-
70% of cases.
• Demonstrate the spirochete by using dark-field
or phase- contrast microscopy on specimens
collected from skin lesions (eg, chancres and
other syphilitic lesions).

76. • CSF VDRL : sensitivity of 30-70% (a negative result
does not rule out syphilitic meningitis) and a high
specificity (a positive test result suggests the
disease).
• serologic tests to detect syphilis : VDRL test ,FTA-
Abs ,TPHA
• Isolating T pallidum from the CSF is extremely
difficult and time consuming Always take care to
not contaminate the CSF with blood during spinal
fluid collection (eg, traumatic tap).

77. Syphilitic meningitis
• Penicillin G (2-4 million U/d IV q4h) for 14 days,
• Often followed with benzathine penicillin G 2.4
million U IM.
• Alternative : administer procaine penicillin G (2.4
million U/d IM) plus probenecid (500 mg PO qid)
for 14 days, followed by IM benzathine penicillin
G (2.4 million U).
• Repeat CSF examination : cell count , serologic
titers Because penicillin G is treatment of choice,
patients who are allergic to penicillin should
undergo penicillin desensitization .

78. • Lyme meningitis Neurologic complications of
Lyme disease (other than Bell palsy) ideally
require parenteral antibiotic administration.
• The drug of choice is ceftriaxone (2 g/d) for 14
to21 days. The alternative therapy is penicillin
G (20 million U/d) for14to 21 days.
• Doxycycline (100 mg PO/IV bid) for14to21
days or chloramphenicol (1 g qid) for14to 21
days has also been used.

79. Complications : Early increased
intracranial pressure (ICP)
• Venous sinus thrombosis.
• Subdural empyema.
• Brain abscess.
• Cranial nerve palsies cerebral infarction result
from impaired cerebral blood flow.
• Cranial nerve palsies and the effects of
impaired cerebral blood flow, such as cerebral
infarction, are caused by increased ICP.

80. Complications : Late Hearing impairment
Obstructive hydrocephalus.
Brain parenchymal damage

81. Further Inpatient Care
• Monitor the clinical course & response to
medical treatment.
• Surveillance for the development of
complications.
• Seizure precautions are indicated, especially
for patients with impaired mental function
Proper isolation precautions in cases of
invasive meningococcal disease

82. • Monitor patients for potential adverse effects
of medications,
• Such as hypersensitivity reactions, cytopenia,
or drug toxicity Drug-level monitoring for
some antibiotics such as vancomycin and
aminoglycosides.
• Liver dysfunction

83. Isolation – Meningococcemia
• Capable of transmitting organism up to 24
hours after initiation of appropriate therapy
• Droplet precautions x 24 hours, then no
isolation Incubation period days, usually <4
days

84. Meningococcemia - Prophylaxis
Rifampin
• <1 month 5 mg/kg PO Q 12 x 2 days
• >1 mo 10 mg/kg (max 600 mg) PO Q 12 x 2days.
• for adults 600mg 12 h for 2 days.or tab
ciprofloxacin 500mg once.
• Ceftriaxone
• <1m 125 mg IM x 1 dose
• >1m 125 mg IM x 1 dose
• >15y 250 mg IMx 1 dose

85. Prognosis viral meningitis usually
have a good prognosis for recovery.
• The prognosis is worse for patients at the extremes of
age (ie, <2 y, >60 y) and with significant comorbidities
and underlying immunodeficiency.
• Patients presenting with an impaired level of
consciousness are at increased risk for developing
neurologic sequelae or dying.
• A seizure during an episode of meningitis also is a risk
factor for mortality or neurologic sequelae.
• The presence of low-level pleocytosis (<20 cells) in
patients with bacterial meningitis suggests a poorer
outcome.

86. Meningococcemia - Prophylaxis
• Persons who have had “intimate contact” w/
oral secretions prior & during 1st 24 h of
antibiotics “Intimate contact” – HIGH RISK
• (kissing, eating/ drinking utensils, mouth-to-
mouth, suctioning, intubating).
• Treat within 24 hours of exposure
Chemoprophylaxis can be considered for
people in close contact with patients in the
endemic situation

87. CSF IN TB MENINGITIS
• (1) Elevated opening pressure,
• (2) Lymphocytic pleocytosis (10–500 cells/Μl)
• (3) Elevated protein concentration
• (4) Decreased glucose concentration in the
range of 20–40 mg/dL.

88. • Cultures of CSF take 4–8 weeks to identify the organism
and are positive in ~50% of adults.
• Culture remains the gold standard to make the diagnosis of
tuberculous meningitis.
• PCR for the detection of M. tuberculosis DNA should be
sent on CSF if available, but the sensitivity and specificity
on CSF have not been defined.
• CDC recommends the use of nucleic acid amplification tests
for the diagnosis of pulmonary tuberculosis.

89. • The combination of unrelenting headache,
stiffneck, fatigue, night sweats, and fever
• with a CSF lymphocytic pleocytosis
• and a mildly decreased glucose concentration
is highly suspicious for tuberculous meningitis.

90. • The last tube of fluid collected at LP is the best
tube to send for a smear for acid-fast bacilli
(AFB).
• If there is a pellicle in the CSF or a cobweb-like
clot on the surface of the fluid, AFB can best be
demonstrated in a smear of the clot or pellicle.
• Positive smears are typically reported in only 10–
40% of cases of tuberculous meningitis in adults.

91. CSF abnormalities in fungal meningitis
• A mononuclear or lymphocytic pleocytosis,
• an increased protein concentration,
• and a decreased glucose concentration.
• There may be eosinophils in the CSF in C. immitis
meningitis.
• Large volumes of CSF are often required to
demonstrate the organism on India ink smear or grow
the organism in culture.
• If spinal fluid examined by LP on two separate
occasions fails to yield an organism, CSF should be
obtained by high-cervical or cisternal puncture.

92. • The cryptococcal polysaccharide antigen test is a highly sensitive
and specific test for cryptococcal meningitis.
• A reactive CSF cryptococcal antigen test establishes the diagnosis.
• The detection of the Histoplasma polysaccharide antigen in CSF
establishes the diagnosis of a fungal meningitis
• But is not specific for meningitis due to H. capsulatum. It may be
falsely positive in coccidioidal meningitis.
• The CSF complement fixation antibody test is reported to have a
specificity of 100% and a sensitivity of 75% for coccidioidal
meningitis.

93. The diagnosis of syphilitic meningitis
• Reactive serum treponemal test (fluorescent
treponemal antibody absorption test [FTA-ABS] or
• Micro hemagglutination assay–T. pallidum
• [MHA-TP]) is associated with a CSF lymphocytic or
mononuclear
• Pleocytosis and an elevated protein concentration, or
when the CSF Venereal Disease Research Laboratory
(VDRL) test is positive.

94. • A reactive CSF FTA-ABS is not definitive
evidence of neurosyphilis. The CSF FTA-ABS
can be falsely positive from blood
contamination.
• A negative CSF VDRL does not rule out
neurosyphilis.
• A negative CSF FTA-ABS or MHA-TP rules out
neurosyphilis

95. TEST APPEAR
ENCE
PRESSURE WBC/
micro
lit
PROTEIN
mg/dl
Glucose
mg/dl
Chloridemeq/l
normal clear 90-180mm 0-8
lym
15-45 50-80 115-130
A. BACT
MEN
TURBID INCREASE
D
1000-
10000
100-500 <40 DECRESED
VIRAL CLEAR N ORMAL/
MODERAT
E
5-
300RA
RELY>
1000
N-
MILD>
NORMAL NORMAL
TB MEN COB
WEB
100-
600
MIXED
OR
LYM
50-300
due to
spinal
block
DECREASED DECREASED
FUNGAL CLEAR 40-400
mixed
50-300 decreased decreased
Ac
syphilitic
clear About
500ly
m
> But
<100
normal normal

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