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 BacTerial  infections  of  the central  nervous  system  BacTerial  infections  of  the central  nervous  system

BacTerial infections of the central nervous system - PowerPoint Presentation

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BacTerial infections of the central nervous system - PPT Presentation

Prof Ivo Ivić CNS Restricted space for expansion of the inflammatory edema I ncrease of intracranial pressure Tissue infarction Neurological sequelae Death located within the bony armor ID: 775204

csf brain meningitis signs csf brain meningitis signs blood bacterial abscess cns therapy meningeal neurological infection space disease symptoms

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Slide1

BacTerial infections of the central nervous system

Prof

. Ivo Ivić

Slide2

CNS

Restricted

space for expansion of the inflammatory edemaIncrease of intracranial pressureTissue infarction

Neurological sequelae

Death

located within the bony armor

protect

ed

against external

mechanical

injuries

Slide3

Meninges

3

layers of membranesDura mater (pachimeninges): firmly tied to boneArachnoid mater: loosely adheres to dura materPia mater Adheres to brain/spinal cordcontains blood vessels

leptomeninges

Slide4

3 spaces Epidural epidural abscessesSubdural subdural abscesses and effusionSubarachnoid contains CSF (purulent in bacterial meningitis)

almost pseudospaces

Meninges

Slide5

Chorioid pelxus

Production

of CSF by choriod plexus: 500 mL/dayCirculatin: ventiricles subarachnoid spaceReabsorption of CSFacrahnoid (pachioni) granules

CNS is floating in the 150 ml of CSF

Cerebrospinal fluid

(CSF)

Slide6

Chorioid pelxus

Bottlenecks

of CSF circulation inerventricular aperture cerebral aqueduct (Syilvii) lateral apertures (Luschka) median aperture (Magendi)

Inflammatiory adhesions

Hydocephalus

Obstructed straits of CSF circulation

Slide7

Blood-brain barrier (BBB)

Consisted of mutually tighly connected capillary endothelial cellsof the brain …………………… blood-brain barrierof the chorioid plexus: ………… blood-CSF barrierInflammation: disturbed permeability of CNS capillaries

Unified

name

Slide8

Arterial

side

Venous

side

M

ediates between arterial and venous circulation

Slide9

Blood Brain Barier functions

Maintaning constancy of the environment of CNSProtecton of CNS from endogenous and exogeonus toxins Intact BBB disables entry (from blood to CNS) of:Immunoglobulins, Complement ,Antibotics

Entry

is enabled

Infection

of

CNS

brekas

down

BBB

Slide10

Site of CNS infection: nomenclature

Infection

of

leptomeninges

Viral

aseptic

(

serous

) meningitis

Bacterial

-

purulent

meningitis

Infection

of

cerebral

matter

Viral

-

encephalitis

Bacterial

-

cerebritis

(

non

-

incapsulated

purulent

inflammation

)

Abscesses

(

incapsulated

pus

collection

)

Cerebral

:

usualy

within

cortex

Epidural

:

between

bone

and

dura mater

Subdural

:

between

dura

and

arachnoid

Slide11

Bacterial

meningitis

Slide12

Urgency

Life

threatenig

disease

Quick

diagnosis

and

therapy

are

mandatory

Maximum

30 min from suspicion to treatment

Diagnostic

lumbar

puncture

(LP) is

required

if

no

contraindication

is

present

Slide13

Etiology (in order of the incidence)

Community-acquiredStr. penumoniaeN. meningitidisH. influenzaeL. monocytogenesS.aureusGram-neg. bacilli

Nosocomial Gram-neg. bacilliStr.pneum. + other streptococci S. aureus

Immunocompetent

children

and

adults

Slide14

Etiology: causative agent

NeonatalE.coliStr. agalactiae (gr. B streptococcus) L. moncytogenes

Slide15

Epidemiology

Developed countries

steadily

decreasing

incidence

:

Hib

and

pneumococcal

vaccine

primarily disease of adults

Undeveloped

countries

10x

higher

incidence

Crowded

living

condition

,

lack

of

vaccination

Primarly

chilhood

disease

Slide16

The modes of spreading

Most

often

sporadic

diseases

Exception

:

meningococcus

A, C, W-135

S.pneumoniae

,

N.meningitidis

,

H.influenzae

Source

:

persons

with

nasopharyngeal

colonization

Modes

:

airborne

(

droplets

), close

contact

(

hands

)

L.moncytogens

Source

: animals

Mode:

ingestion

of

heavily

contaminated

food

Slide17

Nosocomial

Source

:

patinets

own flora,

hospital

bacteria

Mode:

contamination

during

neurosurgery

(VP

shunt

)

Neonatal

Source

:

mother

vaginal

flora

Mode:

ingestion

/

inhalation

during

labor

Slide18

The ways by which bacteria reach the meninges (subarchnoid space)

Blood borneFrom site of primary colonisation: naspoharynx, intestineinflamation: otitis media, penumonia, sinusitis, endocarditisVia blood (bacteremia)Large intracranial venous sinusesTo meninges

Slide19

Contigous

(per continuitatem)2a) via formation of brain abscess From site of primary infectionsinustis, otitis mediaSpread through the bone and meningesFormation of brain abscessesLeakage of pus to subaracnoid space

Slide20

2b)

via pathological communication on the skull base Consequences of head trauma cribriform plate fracture= nasoliquorrheatemporal bone pyramid fracture = otoliquorrheaAgents: nasopharinegal or middle ear bacteriatypically S.pneumoniaeentry into the CNS through pathological communication

Slide21

Multiplication of bacteria within CSFAttraction of neutrophils to kill bacteria Release of toxins and inflammtory cytokinesDamage of the the blood vessels

Inflammatory response within CNS

Slide22

Menigitis = inflammation in the subarachnoid space

Vasculitis of the blood vessel on the surface of the brain

brain

edemaincreased intracanial pressuredecreased blood flowhypoxiadamage of cortical neural cels

Slide23

Damaged permeability of BBBLeakage of serum proteins in to CSF elevated CSF proteins - proteinorrachia Altered glucose transportlowered CSF glucose – hypoglycorrachiaHypoxia -anerobic metabolismelevated lactate in CSF

Menigitis = inflammation in the subarachnoid space

Slide24

Other consequences:Damage of cranial nervesStatoacustic (VIII)Oculomotor (III)Abducens (VI)Hydrocephalusfibrin in inflammatory exudateadhesinosdisturbed circulatuion and absrobtion of CSF

Menigitis = inflammation in the subarachnoid space

long intracranial route

Slide25

Clinical features of bacterial meningitis

Slide26

Symptoms

(

anamnestic

or

heteroanamnestic

data)

Fever

Headake

Vomiting

Signs

(

physical

examiantion

)

Neck

stiffness

(

and

other

signs

of

meningeal

irritation

)

Altered

mental

status

Focal

neurological

signs

Slide27

Headake

(

meningeal

inflammation

+

increased

intracranial

pressure

)

T

he strongest that the patient had ever experienced

on a scale from 1 to 10

= p

atient

’s

rating

is100

O

ften

accompanied by

neck

pain and back

pain

C

ommon

analgesics

:

weak pain relief

Slide28

Meningeal irrition (meningismus, meningeal signs)

(meningeal inflammation + increased intracranial pressure)Neck stiffnesinability to flex the neck and to touch the sternum with chin sensitivity ≈ 30%

pain

Slide29

meningeal signs

inability of knee extension of semi flexed legsensitivity <10%

pain

Slide30

Tripod sign = inability to sit with extended legs and with hands in the front positionsensitivity <10%

Other meningeal signs

Slide31

Knee kiss sign- inability to kiss kneesitting position, leg is flexed at hip and kneesensitivity <10%amplification headache on sudden movement of the head = Head jolt signSensitivity > 95%

Other meningeal signs

Slide32

Altered consciousness

Quantitaive

:

Somnolece

-

early

Coma

- late,

poor

prognosis

Qualitative

:

Confusion

and

desorientaion

Behavioral

changes

Slide33

Glasgow Coma Score prognostic exam of brain injuryEye opening + Verbal response + Motor response range: 3-15 points ≤8 ponits ………. sever 9-12 points ……… moderate13-15 points ……… mild brain injury

Altered

consciousness

Slide34

Unilateral nerve palsyHemiparesis / hemiplegiaFocal cerebral attacks (seizures )Unilateral papiledema or cycloplegia

Focal neurological signs

Ominous signs

Space occupying lesion(abscess)

Neglected meningitis

Slide35

Other examinations/signs

Search for the rash, petechial: poor prognostic signMeningococcal infectionAsplenic patient: penumococcal or H.influenaze sepsisSearch for the source of infectionPneumoniaMiddle ear infectionSinustisInfective endocarditis

Pneumococci

- S.aureus

Slide36

Search

for

prediposing

factor

head

trauma- CSF

leakage

usually

precedes

meningitis

Pneumococcal

infection

no

leakage

during

meningitis

Slide37

Meningeal signs in elderly patients

Unreliable

,

often a stiff neck due to

Spondylosis

Previous

cerebrovascular

disease

Parkinson's disease

Altered

mental

status +

even

low

grade

fever

Lumbar

puncture

is

required

Slide38

Meningeal signs in neonates and very joung children (≤12 months)

absence of bony suture of scull (9-18 months)No neck stiffnes : sometimes bulgin fontanelleFever + irritationperform lumbar tap

Slide39

Diagnosis

Slide40

Diagnostic procedures

Fundoscopic

exam

Examination

of

CSF =

lumbar

puncture

(LP)

Appearance

Cytology

Biokemistry

Gram

stained

smears

Microbiology

Blood

culture

CSF

culture

Slide41

Slide42

LP

L4

L3

Cauda

equina

Slide43

Contraidications for LP: signs of space occupying process wthin CNS

Papiledema on fundoscopy: unilateral or bilateralFocal neurological signsImmunosupressed and HIV patientsfrequent space occupying processesRISK- incarcertion of medulla oblongata in to the foramen magnum:high intrcranial pressure from aboverelease of lumbar CSF by LPdownward moving of the brain= incarcerationsudden death or permanent neurological sequellae

Slide44

CSF appearance

Normal

clear

CSF

Slightly

clodyCSF

Grossly

clody

CSF

Slide45

CSF leukocytes (WBC)/mm3

Normal

: 5-7

Bacterial

meningitis

from several hundreds up to several thousand

s

>90% PMN

Exception

-

L.monocytogens

Elicit

mononuclear

respose

Lower

%

of

PMN

Slide46

CSF glucose level

Normal

:

2/3

of

blood

glucose

level

is maintained at the minimum 2.5

mmol

/L (45 mg/dL)

Bacterial

meningitis:

hypoglycorrachia

Below

40%

of

blood

glucose

level

Often

< 1.5

mmol

/L (25 mg/dL)

Slide47

Normal: 150 - 500 mg/L (15-50 mg/dL)Bacterial meningitis: proteinorracihaOften < 1500 mg/L

CSF protein level

Slide48

Normal: 1-2,5 mmol/L (10-25 mg/dL)Bacterial meningitis: >3 mmol/L (27 mg/dL)

CSF

lactate

level

Slide49

Gram stained smears of CSF

S.pneumoniae

G+ cocci, diplococci, coccci in chains

N.meningitidis

G-

diplococci

,

intra

and

extracellar

(PMN)

Slide50

Algorithm for supected bacterial meningitis

Papilledema and / or focal neurological sign

Yes

No

- Obtain blood culture- LP + CSF culture

Obtain blood culture

CSF examination=Bacterial meningitis

Gram stain of CSF sediment

Visible bacteria

No bacteria

Empiric atibiotic therapy

Focused atibiotic therapy

Empiric atibiotic therapy

CT of head

Mass lesion

Yes

No

Consult neurosurgeon

LP= meningitis

Continue antibiotic

30 min

Slide51

Tretament of bacterial meningitis

Slide52

Empiric therapy (pending culture results)

Determinats

of

empyrical

therapy

decision

:

Age

Immunological

status

Nosocomial

or

community

acquired

Maximum

dosage

of

antibiotic

(BBB)

Intravenous route + sometimes:

intrathecal route (IT) for Vancomycin

intraventricular

route

for VP

shunt

infection

Slide53

Age 3 months – 60 years

Moderetly ill patientCeftriaxon Severely ill patientCeftriaxon + Vancomycin penicillin resistant S.penumoniaeAnaphylactic allegry to penicillinVancomycin

S.pneumoniae

N.menigitidis

(

H.infunezae

b)

Slide54

Ceftriaxon + AmpicilinL.monocytogenesNeonates (0-30 days)see neonatal sepsis

Age 1-3 months and >60 years,

Slide55

Immunocompromised

patientCeftiaxon + Ampicilin + VacomycinNeurosurgery or VP shunt infectionVancomycin + Ceftazidime

MRSA,MRSE

Gram negative bacilli (including P.aeruginosa)

Slide56

PCN resistant S.pneumoniae

Intermediately

resitant

(MIC 0,1-

1

μ

g

/mL

)

High

dose

of

ceftriaxon

to

overcome

BBB

when

inflammation

stabilizes

Highly

resistant

(MIC >

2

μ

g

/mL

)

Vancomycin

+

Rifampin

possible

IT for

vancomycin

Repeated

LP

after

24-36

hours

of

therapy

Slide57

Antiinflammatory therapy of meningitis

Dexamethason :15 mg/kg IV for 4 daysreduces release of inflammatory cytokinesCSF pressure and brain edemaCSF protein levelincidece of deafness morataliyantibiotic permeability of BBB therefore short course - 4 days

30 min prior to antibiotic

Slide58

Other therapeutic measures

Controle of brain edema

and increased ICP

Manitol 20% IV, glycerol PO (children)

appropriate oxygenation

neither hyperventilation, nor hypoventialtion

CO

2

= vasodilatation, brain edema

 CO

2

= vasoconstriction, reduced perfusion

Control seisures

: diazepam

after first attac

not as prophylaxis

before

first attac

Slide59

PROGNOSIS and COMPLICATIONS

Slide60

Prognosis

D

epends

m

ostly

on early treatment

If started

within the first 24 hours of illness

full recovery

or minor curable complications

If started after 2 days of disease

serious complications are likely

Slide61

Mortality

Highest with:

L.monocytogenes

age

3 months and 65 years

immunocompromised patient

mortality

L-monocyitogenes ...... 26%

S.pneumoniae ............. 19%

N.meningitidis ............. 13%

H.influenzae ................ 3%

Slide62

Permanent neurological sequellae

from learning difficulties to mental retardation

from hearing impairment to deafness

seisure disorders

hydocephalus

cerebral

palsy

(

children

),

paresis

(adults)

cerebellar disfunction (adults)

Slide63

PREVENTION

Slide64

Vaccination

Prevents

invasive

(

bacteremic

)

infection

to

seed

CNS

H.influenzae

type

b

All

children

:

conjugated

polysaccharide

vacc

.

S.pneumoniae

All

children

: 13-valent

conjugated

polys.vaccine

Adults

: 23-valent

polysacchride

vaccine

Age

>65 y

Splenctomia

,

functional

asplenia

(

sickle

cell

disease

)

chronic

pulmonary

,

cardivascular

and

liver

disease

DM

Slide65

Vaccination

N.meningitidis

type

A

and

C

Polysacharide

vaccine

,

~

3years

of

protection

N.meningitidis

type

B

Obut 50%

of

childhood

invasive

meningococal

disease

No

vaccine

available

Under

development

, to

be expected in the near future

Slide66

Chemoprophylaxis

H.influenzae

:

Rifampin

/4

days

Within

6

day

of

contact

:

Household

contacts

if

at

least

1

child

aged

<2 y is

unvaccinated

Dycare

contact

children

aged

<2y ???

N.meningitidis

: single dose of Ciprofloxacin

Witin

5

days

of

contact

:

Hosehold

and

daycare

contacts

Slide67

Tuberculous

meningitis

Slide68

Pathogenis

Children

:

hematogenous

miliary

tb

(

primary

infection

)

Adults

:

miliary

tb

, or

rupture

of

tubercle

of

CNS (

previos

infection

)

Mostly basilar meninges are afected

Mononuclear inflammatory response

Slide69

Clinical feature: subacute course

1st

week

:

mostly

general +

scarse

menigneal

symptoms

fever (if low grade, may not be noticed)

insomia

,

loss

of

apetite,

headake

,

fotophobia

,

etc

.

2nd

week

:

meningeal

+

neurological

symptoms

fever

signs

meningeal

irritaion

,

painful

expression

somolence

,

disorientation

,

pathological

nerve

reflexes

kranial

nerve

palsy

(

oculomotors

)

other

focal

neurolgical

signs

(

epi

,

hemiplegia

,

etc

.)

Slide70

3rd

week

:

advanced

focal

neurological

signs

sopor

,

coma

death

within

5-8

weeks

Focal

neurological

signs

:

If

absent

:

beter

prognosis

, cure is

possible

typically

within

1st

week

of

disease

If

present

:

frequent

permanent

neurological

sequellae

Slide71

CSF examiantion: “viral cytology, bacterial biochemistry”

WBC

:

few

hundreds

/

mm

3

usualy

below

500

prevalence

of

lyphocytes

Proteins

:

elevated

usualy

over

1000mg/

mm

3

Glucose

:

lowered

below

2,5mmol/L (45 mg/dL)

Lactate

:

elevated

Over

3

mmol

/L

Slide72

Microbiological diagnosis

Microscopy

of

CSF

sedimet

smear

Ziehl

-

Neelsen

(

acid

fast

)

stain

aproximately1/3

positive

CSF

culture

Lage

samples

(

~

10ml)

PCR

~60%

sensitivity

high specificity

Slide73

Other diagnostic procedures

PPD-

usually

positive

Chest

X-

ray

positive

for

tb

almost

all

children

only

50%

adults

CT or MRI

of

brain

search

for

tuberculomas

Slide74

Therapy

ATD/12

monts

Pyrazinamide

+

Rifampin

+

Isoniazid

/2

months

Followed

by

Rifampin

+

Isoniazid

/10

months

Corticosteroids

/6-8

weeks

, to:

reduce

basilar

inflamation

,

and

prevent

hydocephalus

Slide75

(Infections of cerebral cortex)

BRAIN ABSCESS

Slide76

Pathogensis

Direct

(

contiogus

)

spred

:

F

rom

the adjacent inflammatory foci

chronic

otitis

media

/

mastioiditis

….

temporal

lobe,

cerebellum

sinusitis

, dental

infection

………….

frontal

lobe

Inoculation

by

penetrateing

wounds

Bulit

,

pencil

Neurosurgery

more

often

solitay

abscess

Slide77

Hematogenous

spread

from

:

Lung

abscess

and

empyema

Skin

infection

Abdominal

and

pelvic

infections

Bacterial

endocarditis

,

etc

.

Also freqently seen in patients with cyanotic hearth disease

More

frequently

multiple

absesses

Slide78

Pathology

Week1-2: cerebritisEarly:inflammatory edema without demarcationLate: development of inflammatory capsuleInhomgenous capsule and abscess content ring enhancment by contrast on CT/MRIdamaged BBB

Early

cerebritis

Late cerebritis

Slide79

Pathology

Week 2-3: foramtion of abscessliquefaction of affected tissue – isodens abscess content formation of isodense capsule (demarcation)no ring enhancement edema of the surrounding unaffected tissue

Slide80

MRI vs CT

MRI is

preferred

-

better

visualise

:

early

cerebritis

satelite

lesions

small

lesion

extent

of

necrosis

,

ring

enhancement

brain

edema

brain

steam

Slide81

Microbilogy: often mixed infections

Anaerobes, oral and intestinalAerobic gram positive cocci alpha-hemolytic (S.milleri)SA, etcGram negative rods - very rareImmunocompromised patients, possibility of: ToxoplasmaNocardia Fungi (Aspergilus, Cryptococcus, etc.)Cysticercus

Slide82

Clinical feature

Gradual

development

of

symptoms

Fever

:

only

in

50%,

frequenty

low

grade

Headake

and

vomiting

-

the

most

prominent

Meningeal

irritaion

-

rare

,

usualy

in

case

of

:

ruture

of

abscess

in

to

subarachnoid

space

large

abscesss

of

posterior

cranial

cavity

Slide83

Neurological symptoms

Reflect localisation of abscess, just as brain tumors motor and sensory deficitschanges in behavior are and personality, etc.Later symptoms:cranial nerve palsy (oculomotors)papiledemaseiszures

neurologyst/neurosurgeon most commonly establish diagnois

LP

Slide84

Therapy

IV antibiotics/ 6-8 weeks + NeurosurgeryAntibiotic selection: depending on origin of infetionOptimal combination of first choice:Metronidazol + Ceftriaxon

anaerobs

G+ cocci

Slide85

Pseudomonas

suspected

:

Ceftazidim

instead

of

Ceftriaxon

MSSA

suspected

:

head

trauma,

sepsis

add

Cloxacillin

(

Nafcillin

)

MRSA

suspected

:

neurosurgery

add

Vankomycin

Slide86

Corticosterids

If symptoms of edema are prominent

depressed

metal status,

etc

O

therwise

should be

avoide

d:

corticosteroids improve BBB funtion, and

affect

penetration

of

antibiotics

in

to CNS

Slide87

INTRACRANIAL EPIDURAL

AND SUBDURAL ABSCESS

Slide88

Epidural abscess

Originate from ostemyelitis associated with:neurosurgery, sinusitis (frontal), otitis/mastoiditisS.aureus most comon causative agent

Dura mater

Slide89

Symptoms

Epidural absces- slow progresivedura tightly adherent to scullSymptoms mimic brain abscessLocal symptoms of inflammation always presentswelling, erythema and pain

Slide90

Subdural

abscess: rapidly progressiveAcutely ill patients, high fever, headakeMeningeal irrtation presentRapid onset of focal neurolgical signswithin1-2 days

Slide91

Diagnosis and therapy(epi- and subdural abscess)

LP is

contraindicted

Urgent CT or MRI

Obtain hemoculture,

Introduce

high

dose

antibotic

IV

Consult neurosurgeon for urgent drainage

Slide92

SPINAL EPIDURAL ABSCESS

Slide93

Spine

canal: dura adheres lightly to vertebraeAnterior and posterior epidural space are formedConatin fat, vessels, nerve roots

Slide94

Pathogenesis

direct spred from spondylitis and/or discitisSA- most comon, followed by E.coli

Consequence

of

:Hematogenous spred from various sites,Neurosurgery

Slide95

Symptoms and management

Fever,

some patient are septic

Back

pain

,

spinous

processus

tenderness

Radicular

pain

Onset

of

lower

motor deficit (

praparesis

)

Compressed

spinal

cord

Urgent

CT/MRI-

drainge

is

necessary

24

hours

later

permanent

cord

damage

is

very

likely

Slide96

Therapy

Obtain

blood

culture

Introduce

antibiotic

according

to

pressumed

agent:

MSSA:

Cloxacillin

……………… (

community

acquired

)

MRSA:

Vancmycin

……………… (

nosocomial

)

G-negative :

Ciprofloxacin

…….. (UTI)

4-6

weeks

of

therapy

Consult

neurosurgen

Urgently

if

parparesis

present