This document discusses central nervous system infections. It defines various types of CNS infections including meningitis, encephalitis, and brain abscesses. The key signs and symptoms of meningitis are headache, neck stiffness, and altered mental status. Diagnosis involves lumbar puncture to examine CSF for white blood cells, protein, and glucose. Treatment requires prompt intravenous antibiotics as well as supportive care to prevent neurological complications. The goals are to eradicate the infection and prevent long-term issues like hearing loss or seizures.

1. 1
Central Nervous
System Infections
Kassahun B.

2. Definition
2
 The term Central nervous system (CNS)
infections describes a variety of infections
involving the brain and spinal cord and
associated tissues, fluids, and membranes,
including:
 Meningitis
 Encephalitis
 Meningoencephalitis
 brain and meningeal abscesses
 shunt infections and
 Postoperative infections

3. Cont…
3
 Meningitis: is an inflammation (often the
result of infection) of the membranes of
the brain and spinal cord (meninges) and
the CSF in contact with these membranes,
whereas
 Encephalitis: is an inflammation of the
brain tissue.
 CSF flows through the subarachnoid
space, insulating and protecting delicate
CNS tissue.

4. Cont…
4
 CNS infections, such as meningitis, are
considered neurologic emergencies that
require prompt recognition, diagnosis, and
management to prevent death and residual
neurologic deficits.
 Neurologic impairment includes hearing
loss, hemiparesis, and learning
disabilities.
 Improperly treated, CNS infections are
associated with high rates of morbidity and
mortality.

5. Cont…
5
 Meningitis mortality rates: 20% to 30%
 Neurologic squeal:
 Seizures, sensorineural hearing loss,
hydrocephalus-30% to 50%
 Antimicrobial therapy and preventive
vaccines have revolutionized management
and improved outcomes of bacterial
meningitis and other CNS infections
dramatically.

6. The Meninges
6
Dura mater
The outer layer, is tough, white
fibrous connective tissue.
Arachnoid
The middle layer of meninges : a thin
layer resembling a cobweb with
numerous threadlike strands
attaching it to the innermost layer.
The space under the arachnoid, the
subarachnoid space, is filled with
cerebrospinal fluid and contains
blood vessels.
The pia mater
Is the innermost layer of meninges.
This thin, delicate membrane is tightly
bound to the surface of the brain and
spinal cord and cannot be dissected
away without damaging the surface.

7. Etiology
7
 CNS infections can be caused by bacteria, fungi,
mycobacteria, viruses, parasites, and non-
infectious agents such as chemical irritants.
 Bacterial meningitis is the most common cause
of CNS infections.
 The most common causes of bacterial meningitis
include:
 Streptococcus pneumoniae (G+ve)…….47%
 Neisseria meningitides(G-ve)…....………25%
 Listeria monocytogenes(G+ve) and……..8%
 Haemophilus influenzae(G-ve)…………...7%

8. Cont…
8
 Encephalitis may result from viral,
bacterial, parasitic, and other noninfectious
causes. Herpes simplex virus (HSV) is the
most common cause of encephalitis.
 Neurosurgical procedures may place
patients at risk for meningitis due to
bacteria (e.g., Staphylococcus
aureus,coagulase-negative staphylococci,
and gram-negative bacilli) acquired at the
time of surgery or in the postoperative
period.

9. Cont…
9
 In addition to bacteria, other pathogens
may cause meningitis in at-risk patients.
 Immunocompromised patients, such as
solid-organ transplant patients and patients
living with HIV infection, are at risk for
fungal meningitis with Cryptococcus
neoformans and encephalitis secondary to
Toxoplasma gondii.
 Tuberculosis can spread from pulmonary sites to
cause clinical disease in the CNS.

10. Cont…
10
 Because the treatments for different types
of CNS infections are often different, it is
important to pay close attention to patients’
risk factors when choosing empirical
antimicrobial therapy.
 Patients at extremes of age, those living in
close contact with others, and those with
immune defects are most susceptible to
meningitis.

11. Risk factors
11
Risk factors for CNS infections can be
classified as:
 Environmental: recent exposures (e.g.,
close contact with meningitis or respiratory
tract infection, contaminated foods), active
or passive exposure to cigarette smoke,
close living conditions.
 Recent infection in the patient: respiratory
infection, otitis media, sinusitis, mastoiditis

12. Cont…
12
 Immunosuppression: sickle cell disease,
alcoholism, cirrhosis, cancer, HIV/AIDS,
uncontrolled diabetes mellitus.
 Surgery: neurosurgery, CSF shunt,
cochlear implant
 Noninfectious causes of meningitis
include malignancy, medications (e.g.,
sulfonamides mainly Cotrimoxazole,
NSAIDs, IV immunoglobulin), autoimmune
disease (e.g., lupus), and head trauma.

13. Pathophysiology
13
 CSF is produced within the ventricles of
the brain and flows unidirectionally
downward through the spinal cord, serving
as a continuous flushing mechanism for
the CNS.
 The blood–brain barrier and blood–CSF
barrier are made of specialized tissue
capillaries that isolate the brain and CSF
from substances circulating in the blood
stream or colonizing nearby tissues.

14. Cont…
14
 To initiate a CNS infection, pathogens must
gain entry into the CNS by contiguous
spread, hematogenous seeding, direct
inoculation, or reactivation of latent
infection.
 Contiguous spread (the most common
mechanism), occurs when infections in
adjacent structures (e.g., sinus cavities or
the middle ear) invade directly through the
blood–brain barrier (e.g., Hib).

15. Cont…
15
 Hematogenous seeding occurs when a
more remote infection causes bacteremia that
seeds the CSF (e.g., pneumococcal
pneumonia).
 Reactivation of latent infection results from
dormant viral(HSV), fungal, or mycobacterial
pathogens in the spine, brain, or nerve tracts.
 Direct inoculation of bacteria into the CNS is
the result of trauma, congenital
malformations, or complications of
neurosurgery.

16. Cont…
16
 Once through the blood–brain barrier, pathogens
thrive and replicate due to limited host defenses
in the CNS.
 Neurologic tissue damage is the result of the
host’s immune reaction to bacterial cellular
components (e.g., lipopolysaccharide, teichoic
acid, and peptidoglycan), which triggers
cytokine production, particularly tumor
necrosis factor alpha (TNF-α) and interleukin 1
(IL-1), as well as other mediators of
inflammation.

17. Cont…
17
 Bacteriolysis resulting from antibiotic
therapy further contributes to the
inflammatory process.
 Cytokines increase permeability of the
BBB, allowing influx of neutrophils and
other host defense cells that contribute to
the development of cerebral edema and
increased intracranial pressure which
are characteristic of meningitis.

18. Cont…
18
 The increase in intracranial pressure is
responsible for the hallmark clinical signs
and symptoms of meningitis: such as
 Headache, neck stiffness, altered mental
status, photophobia, and seizures.
 Unaltered, these pathophysiologic changes
may result in cerebral ischemia and death.

19. 19

20. Clinical Presentation
20
 Clinical presentation varies with age, and,
generally, the younger the patient, the more
atypical and the less pronounced is the
clinical picture.
 Up to 50% of patients may receive antibiotics
before a diagnosis of meningitis is made,
delaying presentation to the hospital.
 Prior antibiotic therapy may cause the Gram
stain and CSF culture to be negative, but the
antibiotic therapy rarely affects CSF protein or
glucose.

21. Cont…
21
 Classic signs and
symptoms include:
 fever
 altered mental status
 nuchal rigidity
 Photophobia
 Severe headache.
 Chills
 Vomiting

22. Cont…
22
 Kernig’s and Brudzinski’s signs may be
present on 15-30% of patients but are
poorly sensitive and frequently absent in
children.
 Other signs and symptoms include
irritability, delirium, drowsiness, lethargy,
and coma.

23. Kernig’s and Brudzinski’s signs
23
BRUDZINSKI’S NECK SIGN
Elicitation: Flexing the patient’s
neck causes flexion of the patient’s
hips and knees.
KERNIG’S SIGN:
Elicitation: Flexing the patient’s hip 90
degrees then extending the patient’s knee
causes pain.

24. Cont…
24
 Clinical signs and
symptoms in young
children may include
bulging fontanelle,
apneas, purpuric rash,
and convulsions in
addition to those just
mentioned.
 Seizures occur more
commonly in children
(20% to 30%) than in
adults (0% to 12%).
Bulging
fontanelle

25. Differential Signs and Symptoms
25
 Purpuric and petechial skin lesions typically
indicate meningococcal involvement,
although the lesions may be present with H.
influenzae meningitis.
 Rashes rarely occur with pneumococcal
meningitis.
 H. influenza meningitis and meningococcal
meningitis both can cause involvement of
the joints during the illness.
 A history of head trauma with or without skull
fracture or presence of a chronically draining
ear is associated with pneumococcal
involvement.

26. Meningococcal Rash
26

27. Diagnosis
27
 Meningitis causes CSF fluid changes,
and these changes can be used as
diagnostic markers of infection
 Ideally, LP to obtain CSF for direct
examination and laboratory analysis, as
well as blood and CSF cultures, should be
obtained before initiation of antimicrobial
therapy.
 However, initiation of antimicrobial
therapy should not be delayed if a
pretreatment LP cannot be performed.

28. Laboratory Tests
28
 Several tubes of CSF are collected via
lumbar puncture for chemistry,
microbiology, and hematology tests.

29. Type Normal Bacterial Viral Fungal Tuberculosi
s
WBC
(cells/mm3)
<5 1000-5000 100-1000 40-400 100-500
Differential (%) >90a ≥ 80 PMNs 50b,c >50b >80b,c
Protein
(mg/dL)
<50 100-500 30-150 40-150 ≤ 40-150
Glucose
(mg/dL)
50-66%
simultaneous
serum value
<40 (<60%
simultaneous
serum value)
<30-70 <30-70 <30-70
aMonocytes.
bLymphocytes.
cInitial Cerebrospinal fluid (CSF), while blood cell (WBC) count may reveal a predominance of
polymorphonuclear neutrophils (PMNs).
29

30. Cont…
30
In acute bacterial meningitis
 the CSF is purulent, and turbid
 containing numerous WBCs (usually
>1000 cells/μL) with a predominance of
PMNs,
 CSF protein nearly always is elevated,
usually greater than 200 mg/dL, and
 CSF glucose concentration is low, either
less than 40 mg/dL or a CSF to serum
glucose ratio of ≤ 0.4.

31. Cont…
31
 In contrast, CSF obtained in viral and
fungal cases of meningitis usually is
 Clear
 Characterized by a much lower WBC
count (<100 cells/μL), with a
mononuclear or lymphocyte
predominance.
 Although the CSF protein concentration
often is elevated, it may be normal
 A variable effect is observed with CSF
glucose

32. Cont…
32
 The values for CSF glucose, protein, and
WBC concentrations found with bacterial
meningitis overlap significantly with those
for viral, tuberculous, and fungal
meningitis.
 CSF white blood cell (WBC) counts and
CSF glucose and protein concentrations
cannot always distinguish the different
etiologies of meningitis

33. Other Diagnostic Tests
33
 Blood and other specimens should be
cultured according to clinical judgment
because meningitis frequently can arise via
hematogenous dissemination or can be
associated with infections at other sites.
 A minimum of 20 mL of blood in each of
two to three separate cultures per each 24-
hour period is necessary for the detection
of most bacteremias.

34. Other Diagnostic Tests
34
 Gram stain and culture of the CSF are
the most important laboratory tests
performed for bacterial meningitis.
 When performed before antibiotic therapy
is initiated, Gram stain is both rapid and
sensitive and can confirm the diagnosis of
bacterial meningitis in 75% to 90% of
cases.

35. Other Diagnostic Tests
35
 Polymerase chain reaction (PCR)
techniques can be used to diagnose
meningitis caused by N. meningitidis, S.
pneumoniae, and H. influenzae type b
(Hib).
 PCR testing of the CSF is the preferred
method of diagnosing most viral
meningitis infections.
 Diagnosis of tuberculosis meningitis
employs acid-fast staining, culture, and
PCR of the CSF.

36. Desired Outcome
36
 The goals of treatment include:
 eradication of infection with amelioration
of signs and symptoms, and
 prevention of neurologic sequelae, such
as seizures, deafness, coma, and death.

37. Treatment Principles
37
 Fluids, electrolytes, antipyretics, analgesia,
anti-emetics and anticonvulsants are
supportive measures early in acute
bacterial meningitis.
 Surgical debridement should be
employed, if appropriate (as in
postneurosurgical infections and brain
abscess).

38. PRETREATMENT EVALUATION
38
If possible, the following historical information should be
obtained before antimicrobial therapy of presumed bacterial
meningitis is instituted.
 Serious drug allergies
 Recent exposure to someone with meningitis (eg, Neisseria
meningitidis)
 A recent or current sinusitis or otitis media (eg, S.
pneumoniae)
 Recent use of antibiotics (drug-resistant S. pneumoniae)
 Recent travel (eg, N. meningitidis)
 A history of recent injection drug use (eg, Staphylococcus
aureus)
 A progressive petechial or ecchymotic rash (eg, N.
meningitidis)
 A history of recent or remote head trauma (eg, S.
pneumoniae)
 HIV infection or risk factors (eg, S. pneumoniae, Listeria
monocytogenes, Cryptococcus neoformans)

39. Pharmacologic Treatment
39
 Prompt initiation of IV, high-dose,
bactericidal antimicrobial therapy directed
at the most likely pathogen(s) is essential
due to the high morbidity and mortality
associated with CNS infections.
 Empiric antimicrobial therapy should be
instituted as soon as possible to eradicate
the causative organism.

40. Cont…
40
 Antibiotic doses for treatment of CNS
infections must be maximized to optimize
penetration to the site of infection.
 Continued therapy should be based on the
assessment of clinical improvement,
cultures, and susceptibility testing results.
 Once a pathogen is identified, antibiotic
therapy should be tailored to the specific
pathogen.

41. Cont…
41
 With increased meningeal inflammation,
there will be greater antibiotic penetration.
 Problems of CSF penetration may be
overcome by direct instillation of antibiotics
by intrathecal, or intraventricular routes
of administration

42. Penetration of Antimicrobial Agents
Into the Cerebrospinal Fluid (CSF)
Therapeutic levels in CSF with or without
inflammation
42
 Chloramphenicol
 Pyrazinamide
 Cycloserine
 Rifampin
 Ethionamide
 Sulfonamides
 Isoniazid
 Trimethoprim
 Metronidazole

43. Therapeutic levels in CSF with
inflammation of meninges
Ceftazidime
Mezlocillin
Ceftizoxime
Moxifloxacin
Ceftriaxone
Nafcillin
Cefuroxime
Ofloxacin
Ciprofloxacin
Penicillin G
Colistin
43
 Acyclovir
 Ganciclovir
 Ampicillin ±
sulbactam
 Imipenem
 Aztreonam
 Levofloxacin
 Carbenicillin
 Linezolid
 Cefotaxime
 Meropenem
 Piperacillin
 Pyrimethamine
 Ethambutol
 Quinupristin/dalfopristi
n
 Fluconazole
 Ticarcillin ± clavulanic
acid
 Flucytosine
 Vancomycin
 Foscarnet
 Vidarabine
 Daptomycin

44. Non-therapeutic levels in CSF with or
without inflammation
44
 Aminoglycosides
 Amphotericin B
 Cefoperazone
 Cephalosporins (first-
generation)
 Cephalosporins
(second-generation)a
 Clindamycin b
 Itraconazole c
 Ketoconazole
a Cefuroxime is an exception.
b Achieves therapeutic brain tissue concentrations.
c Achieves therapeutic concentrations for Cryptococcus neoformans therapy.

45. Cont…
45
 An adequate duration of therapy is
required to treat meningitis successfully.
 Parenteral (IV) therapy is administered
for the full course of therapy for CNS
infections to ensure adequate CSF
penetration throughout the course of
treatment.
 Antimicrobial therapy should last at least
48 to 72 hours or until the diagnosis of
bacterial meningitis can be ruled out.

46. Duration of antibiotics
46
 Meningitis caused by N. meningitidis
usually can be treated with a 7-day course.
 Meningitis caused by S. pneumoniae is
successfully treated with 10 to 14 days of
antibiotic therapy.
 A longer course, ≥21 days, is
recommended for patients infected with L.
monocytogenes .
 Therapy should be individualized, and
some patients may require longer courses.

47. Dexamethasone as an Adjunctive
Treatment for Meningitis
47
 In addition to antibiotics, dexamethasone
is a commonly used therapy for the
treatment of meningitis.
 Dexamethasone causes
 a significant improvement in CSF
concentrations of proinflammatory cytokines,
glucose, protein, and lactate as well as
 significantly lower incidence of neurologic
sequelae commonly associated with bacterial
meningitis.
 However, there are conflicting results.

48. Cont..
48
 Dexamethasone should be administered
prior to the first antibiotic dose or together
and not after antibiotics have already been
started.
 Serum hemoglobin and stool guaiac
should be monitored for evidence of GI
bleeding.

49. Cont…
49
 The benefit of dexamethasone in developing regions is
less clear than for developed countries.
 In regions with high HIV prevalence, high rates of
malnutrition, and delayed clinical presentation such as
Africa, there does not appear to be any clinical benefit to
the administration of dexamethasone.
 In other regions, we suggest administering
dexamethasone in patients who have bacterial meningitis
confirmed by Gram stain or a rapid diagnostic test.
 We suggest the regimen used in the Vietnamese trial (0.4
mg/kg every 12 hours for four days) starting before the
first dose of antibiotics.
 Dexamethasone should only be continued if the CSF
Gram stain and/or the CSF or blood cultures reveal S.
pneumoniae. Reference- UpToDate,2022

50. 1. Community acquired,
bacterial etiology unknown
50
First line
 Ceftriaxone, 4g/day, I.V., divided in 2
doses for 10-14 days or Cefotaxime 2gm
IV every 4-6 hrs
PLUS
 Where Penicillin resistance is common
(particularly S.pneumoniae), Empiric
treatment should include:
 Vancomycin, 15-20 mg/kg IV every 8-12
hrs for 10-14days

51. Cont…
51
Alternative
 Benzyl penicillin, 20-24 million IU/day I.V. in 4-6
divided doses for 7 –10 days. PLUS
 Chloramphenicol, 500mg I.V. QID. In severe
infections, up to 100mg/kg/day in 4 divided
doses, may be used for 7 days
If >50 y or alcoholic: for Listeria monocytogens
 Ampicillin, 2g IV q4h
OR (if beta-lactam allergic)
 Trimetoprime/Sulphamethoxazole, 20mg/kg
per day divided Q6-12 should be added

52. 2.Community Acquired Etiology
known
52
N.meningitides and S. pneumonia
 Benzyl penicillin, 20-24 MU/day I.V. in 4-6
divided doses for 7-10 days.
H. influenzae:
 Chloramphenicol, 100 mg/kg/day I.V. in 4
divided doses for the first 48-72 hours,
then 50 mg /kg/day for 7-10 days.

53. Cont…
53
 For resistant strains of N.meningitides,
S. pneumonia and H. influenzae:
First line
 Ceftriaxone, 4 g/day I.V. divided in 2
doses for at least 10-14days.
Alternative
 Cefotaxime, 8-12 g/day I.V. in 4 divided
doses, 6 hourly

54. 3. Hospital acquired meningitis,
etiology unknown
54
 Empiric treatment, hospital acquired
meningitis, particularly related to post-
neurosurgery ventriculostomy/lumbar catheter,
ventriculoperitoneal (atrial) shunt or penetrating
trauma without basillar skull fracture
First line
 Vancomycin, 15-20 mg/kg IV Q8h
PLUS
 Ceftazidime, 2g IV q8h or Cefepime – 2 g IV
q8h or Meropenem – 2 g IV q8h

55. 4. Hospital acquired, etiology known
55
Staphylococcus aureus methicillin
sensitive
 Cloxacillin, 9-12 g/day I..V, in 4 divided
doses. For 2-3 weeks
For methicillin-resistant Staph aureus,
 Vancomycin, 1 g I.V. BID for 2 - 3 weeks
PLUS
 Rifampicin, 600 mg P.O. QD for 3 weeks.

56. Cont…
56
Pseudomonas aeruginosa
First Line
 Ceftazidime , 8-12 g/day I.V. in 4 divided
doses for 10 - 14 days. PLUS
 Gentamicin, 3-5 mg/kg/day I.V. in 3 divided
doses for 7-10 days.
Alternative
 Ceftriaxone, 4 g/day I.V. divided in 2 doses
for 7 – 10 days. PLUS
 Gentamicin, 3-5 mg/kg/day I.V. in 3 divided
dose for 7-10 days

57. Cont…
57
Enterobacteriaceae
First Line
 Ceftriaxone, 4 g/day I.V. divided in 2
doses for 7-10 days.
Alternative
 Cefotaxime, 8-12 g/day I.V. in 4 divided
doses, QID.

58. Cryptococcal Meningitis
58
Non-drug treatment:
 If CSF opening pressure greater than 250
H2O mm, drain 20-30ml of CSF daily until
less than 200 mm H2O.

59. Cont…
59
Drug treatment:
First Lline
 Amphotericin B, 0.7-1.0mg/kg/day I.V. for
2 weeks
PLUS
 Flucytosine, 25mg/kg P.O. QID for 14
days

60. 60
5. Immunosuppressed (HIV positive,
uncontrolled diabetes, patients
taking high dose corticosteroids)
 Vancomycin, 15-20 mg/kg IV Q8h PLUS
 Ampicillin, 2g IV q4h PLUS
 Cefepime – 2 g IV every 8 hours or Meropenem – 2
g IV every 8 hours.
 Acyclovir 10mg/kg (infuse over 1h) Q8h for 14-21d
 (This is added in a situation where HSV-1 encephalitis is
likely. Early diagnosis and treatment are imperative.
Mortality is reduce from >70% to <20% with IV acyclovir
treatment).
 If meropenem is used, initial treatment with ampicillin is not
required, as meropenem has activity against Listeria.

61. Cont…
61
 Adjuvant Therapy: Consider steroids in
all bacterial meningitis prior to organism
identification. Treatment must start before
or with first dose of antibiotics to derive any
benefit.
 This treatment has been shown to reduce
neurologic disability and mortality by
about 50% particularly in patients with S.
pneumoniae meningitis and & GCS 8–11.

62. AGE
COMMONLY
AFFECTED
MOST LIKELY
ORGANISMS
EMPIRICAL
THERAPY
RISK FACTORS
FOR ALL AGE
GROUPS
Newborn–1
month
Streptococcus
agalactiae
Ampicillin plus
cefotaxime or
Ampilcillin plus
aminoglycoside
Respiratory tract
infection
Escherichia coli, Otitis media
Mastoiditis
Listeria
monocytogenes
Head trauma
Alcoholism
High-dose
steroids
1 month–23
month
S. pneumoniae Vancomycin and
cefotaxime or
ceftriaxone
Splenectomy
N. meningitidis Sickle cell
disease
H. Immunoglobulin
Most Likely and Empirical Therapy for Bacterial
Meningitis by Age Group

63. Most Likely and Empirical Therapy for
Bacterial Meningitis by Age Group
Age Commonly
Affected
Most Likely
Organisms
Empirical Therapy Risk
Factors for
All Age
Groups
2–50 years S. pneumoniae Vancomycin and
cefotaxime or
ceftriaxone
N. meningitidis
>50 years S. Pneumoniae
and N.
meningitidis
Vancomycin plus
ampicillin plus
cefotaxime or
ceftriaxone
Aerobic Gram-ve
bacili
L.
monocytogenes
A fourth-generation cephalosporin, cefepime, has been shown to be a safe and
therapeutically equivalent to ceftriaxone and cefotaxime when broad activity
against both pneumococcus and gram-negative bacteria, such as P. aeruginosa,

64. Meningitis Caused by Type of Organisms
Organism Antibiotic of First
Choice
Alternative
Antibiotics
duation of
Therapy
Gram-positive - streptococcus pneumoniae 10–14 days
Penicillin
susceptible
• Penicillin G or
• ampicillin
• Cefotaxime
• ceftriaxone,
• chloramphenicol
Penicillin
intermediate
• Cefotaxime or
• ceftriaxone
• Cefepime,
• meropenem,
• moxifloxacin,
• linezolid
Penicillin
resistant
• Vancomycin plus
cefotaxime or
ceftriaxone
• Cefepime ,
• meropenem
• moxifloxacin,
• linezolid
Group B
Streptococcus
• Penicillin G or
ampicillin ± gentami
cin
• Cefotaxime
• ceftriaxone
• chloramphenicol
14–21 days

65. Organism Antibiotic of
First Choice
Alternative
Antibiotics
Recommended
Duration of
Therapy
Gram-positive
Staphylococcus aureus 14–21 days
Methicillin
susceptible
Nafcillin or
oxacillin
Vancomycin,
meropenem
Methicillin
resistant
Vancomycin Trimethoprim-
sulfamethoxaz
ole, linezolid
Staphylococcu
s epidermidis
Vancomycin Linezolid 14–21 days
Listeria
monocytogene
s
Penicillin G or
ampicillin ± g
entamicin
Trimethoprim-
sulfamethoxaz
ole),
meropenem
21 days

66. ORGANISM ANTIBIOTIC
OF FIRST
CHOICE
Alternative Antibiotics Recommended
Duration of Therapy
NEISSERIA MENINGITIS 7 days
Penicillinsuscepti
ble
Penicillin G or
ampicillin
Cefotaxime, ceftriaxone,
chloramphenicol
Penicillin
resistant
Cefotaxime or
ceftriaxone
Chloramphenicol, meropenem
fluoroquinolone
HAEMOPHILUS INFLUENZAE 7 days
Beta-Lactamase
negative
Ampicillin Cefotaxime, ceftriaxone,
chloramphenicol, cefepime,
fluoroquinolone
Beta-Lactamase
positive
Cefotaxime or
ceftriaxone
Cefepime , fluoroquinolone,
chloramphenicol
Enterobacteriace
ae
Cefotaxime or
ceftriaxone
Cefepime, fluoroquinolone,,
meropenem, aztreonam
21 days
Pseudomonas
aeruginosa
Cefepime or
ceftazidime
± tobramycin
Ciprofloxacin, meropenem,
piperacillin plus tobramycin, colistin
sulfomethate, aztreonam
21 days