meningitis meningitis meningococcal meningitis

7/29/2019 Meningitis MENINGITIS Meningococcal Meningitis

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MENINGITIS

Meningococcal MeningitisDr.T.V.Rao MD

Dr.T.V.Rao MD 1


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Introduction

Bacterial meningitis is an inflammation of

the leptomeninges, usually causing by

bacterial infection. Bacterial meningitis may present acutely

(symptoms evolving rapidly over 1-24

hours), sub acutely (symptoms evolvingover 1-7days), or chronically (symptoms

evolving over more than 1 week).

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In Meningitis Meninges are infected

and Inflamed

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Etiology

Causative organisms vary with patient age, with

three bacteria accounting for over three-quarters

of all cases:

Neisseria meningitidis (Meninococcus)

Haemophilus influenza (if very young andunvaccinated)

Streptococcus pneumoniae ( pneumococcus)

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Etiologygram-negative CoccusNeisseria species13 serogroupsgroups A, B, C

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Etiology

Other organisms

Neonates and infants at age 2-3

months Escherichia coli

B-hemolytic streptococci

Staphylococcus aureus

Staphylococcus epidermidis

Listeria MonocytogenesDr.T.V.Rao MD 6


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Knowing about Meningococcal

Disease Meningococcal disease is an acute, potentially

severe illness caused by the bacterium

Neisseria meningitidis. Illness believed to be

meningococcal disease was first reported in

the 16th century. The first definitive

description of the disease was by Vieusseux in

Switzerland in 1805. The bacterium was firstidentified in the spinal fluid of patients by

Weichselbaum in 1887.

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Characteristics of N. meningitides

N. meningitidis, or Meninococcus, is an

aerobic, gram-negative diplodocus, closely

related to N. gonorrhea, and to several

nonpathogenic Neisseria species, such as N.

lactamica. The outer membrane contains

several protein structures that enable the

bacteria to interact with the host cells as wellas perform other functions.

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Transmission of Meninococcus

Transmission

Primary mode is

by respiratorydroplet spread

or by direct

contact.

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Pathogenicity

Meningococci are transmitted by droplet

aerosol or secretions from the

nasopharynx of colonized persons. Thebacteria attach to and multiply on the

mucosal cells of the nasopharynx. In a

small proportion (less than 1%) ofcolonized persons, the organism

penetrates the mucosal cells and enters

the bloodstream Dr.T.V.Rao MD 10


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Pathogenesis

A offending bacterium from blood invades theleptomeninges.

Bacterial toxics and Inflammatory mediators are

released.

Bacterial toxics

Lipopolysaccharide, LPS

Teichoic acid

Peptidoglycan

Inflammatory mediators

Tumor necrosis factor, TNF

Interleukin-1, IL-1

Prostaglandin E2, PGE2

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Pathogenesis

The outer membrane is surrounded by a

polysaccharide capsule that is necessary

for pathogenicity because it helps thebacteria resist phagocytosis and

complement-mediated lysis. The outer

membrane proteins and the capsularpolysaccharide make up the main surface

antigens of the organism.

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Serotyping of Meninococcus

Meningococci are

classified by using

serologic methods

based on the structureof the polysaccharide

capsule. Thirteen

antigenically and

chemically distinctpolysaccharide capsules

have been described.

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Different Serotypes and Epidemiology

Almost all invasive disease is caused by

one of five serogroups: A, B, C, Y, and W-

135. The relative importance of eachserogroups depends on geographic

location, as well as other factors, such as

age. For instance, serogroups A is a majorcause of disease in sub-Saharan Africa

but is rarely isolated in the United States.

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Systemic Spread of Meningococcal

Infections

The bacteria spread by way of the blood

to many organs. In about 50% of

bacteremia persons, the organismcrosses the bloodbrain barrier into the

cerebrospinal fluid and causes purulent

meningitis. An antecedent upperrespiratory infection may be a

contributing factor

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N. meningitidisHabitat: human nasopharynx (10-

25%)

Similar to N. gonorrhea but lessexacting ?

Can grow in BA, Chocolate agar

without selective media from CSF ?

Id. CHO utilization: acid from glucose

& maltose. Dr.T.V.Rao MD 16


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Meninges and spinal cord

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How patients present withMeningitis

Meningitis ( inflammation of membranecovering brain) :

Headache

Photophobia (pain on looking at bright

lights)

Stiff Neck

Convulsion

Vomiting

Septicemia (blood poisoning):

Rash (pinpricks + bruises)

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Clinical manifestation

Clinical manifestation of CNS

Increased intracranial pressure

Headache

Projectile vomiting Hypertension

Bradycardia

Bulging fontanel

Cranial sutures diastasis Coma

Decerebrate rigidity

Cerebral hernia

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Clinical manifestation

Clinical manifestation of CNS

Conscious disturbance

Drowsiness Clouding of consciousness

Coma

Psychiatricsymptom

Irritation

Dysphoria

dullness

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Dr.T.V.Rao MD

Clinical manifestations

Meningococcal meningitis

Septic period

an abrupt onset

chills high fever

Headache

Petechias

purpuras

Splenomegaly

Meningitic period

intracranial pressure

headache

vomiting restlessness

Stiff neck

Kernig (+)

brudziski (+)

gradually disappears,

recovers to normal.

Prodromal period

Septic period Meningitic period

Convalescent period

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MENINGOCOCCAL INFECTION

Neisseria meningitidis: gram

negative intracellular

diplococci.

Groups A, B, C, W135 and Y.

Septicaemia, meningitis or

bacteraemia.

Incubation period of 2 to 7

days.

Spread by droplets from

asymptomatic carriers.

Case fatality of 10% (meningitis)and 20% (septicaemia).

Affects young children

predominately

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Diagnosis

Isolation of the organism

from CSF or blood.

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Laboratory Findings

Other bacterial

test

Blood cultivation

Film preparation of skin

petechiae and purpura

Secretion culture of local

lesion

Imageology examination

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Pathogenicity

Meningococcal meningitis, as a spreadfrom nasopharynx blood stream

meninges in susceptible hosts.

Direct spread to meninges

Rash

Adrenal hemorrhage (Waterhouse-Friderchsen syndrome)

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Dr.T.V.Rao MD

Clinical manifestations

Meningococcal meningitis 26


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Death from Waterhouse-Friderichsen

syndrome

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Meningococcemia

Bloodstream infection

May occur with or without meningitis

Clinical findings fever

petechial or purpuric rash

hypotension

multiorgan failure

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Clinical examination and

Important Signs

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Diagnosing by Isolation and

identification of Meninococcus

Invasive meningococcal disease is typically

diagnosed by isolation ofN. meningitidis

from a normally sterile site. However,

sensitivity of bacterial culture may be low,

particularly when performed after initiation of

antibiotic therapy. A Gram stain of

cerebrospinal fluid showing gram-negativediplococci strongly suggests meningococcal

meningitis.

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Diagnosis

Diagnostic methods

A careful evaluation of history

A careful evaluation of infant

s signs andsymptoms

A careful evaluation of information on

longitudinal changes in vital signs andlaboratory indicators

Rout examination of cerebrospinal fluid (CSF)

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Laboratory Findings

Especial examination of CSF

Specific bacterial antigen test

Countercurrent immuno-electrophoresis

Latex agglutination

Immunoflorescent test

Neisseria meningitidis (Meninococcus)

Haemophilus influenza

Streptococcus pneumoniae ( pneumococcus)

Group B streptococcusDr.T.V.Rao MD 32


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Lumbar puncture for CSF

Examination

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INVESTIGATION

1. Blood culture (sp)

2. Naso-pharyngeal

swab (both)

3. Lumbar puncture(mg)

4. PCR serum (sp)

5. PCR CSF (mg)6. Serology

7. Bleb aspirate (sp)

8. Skin scrapings (sp) Dr.T.V.Rao MD 34


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Dr.T.V.Rao MD

Laboratory examination of CSF

Cerebrospinal fluid examination

(an important method to establish diagnosis) :

pressure glucose

WBC sodium

protein chloride

M

turbid

>1000106/L

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Dr.T.V.Rao MD

Diagnosis with Combination of Factors

Epidemic season, age and epidemic situations.

Clinical features.Manifestations of severe form in sepsis and

meningoencephalitis

Increased leukocytes and polymorph nuclear

leukocytes predominantly in peripheral blood.

Increased intracranial pressure and purulent changes

in CSF.

Positive results in bacteriological examination.

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USUAL MANAGEMENT OF SUSPECTED CASE

Isolation

Released once they have had their antibiotictreatment for 48 hours

Intravenous Fluids

Often ill and pyrexiaAntibiotics

Cefotaxime (+ Ciprofloxacin or rifampicin).Will be given former for first 24-48 hours even

if diagnosis uncertain.Intensive care

Not unusual - unfortunately

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Epidemiology

Occurrence Meningococcal disease occurs worldwide in

both endemic and epidemic form.

Reservoir

Humans are the only natural reservoir of

Meninococcus. As many as 10% of adolescents

and adults are asymptomatic transient carriersofN. meningitidis, most strains of which are

not pathogenic (i.e., strains that are not

groupable). Dr.T.V.Rao MD 38


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Antibiotic Therapy

Course of treatment

7 days for meningococcal infection

1014 days for H influenza or S pneumoniaeinfection

More than 21 days for S aureus or E coli infection

1421 days for other organisms

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PREVENTION: CHEMOPROPHYLAXIS

Gets rid of bacteria from carriers (and cases)

Does not prevent infection

Given to those who, in 7 days before symptoms:

* Lived in same house* Kissed case on lips

* Gave mouth to mouth

resuscitation.Options: Ciprofloxacin, Rifampicin, Ceftriaxone.

Can be given up to 28 days after contact with case

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PREVENTION:

VACCINATION IN RESPONSE TO CASE

Available for groups A, C, W135 or Y.Only used once group is confirmed

Given to same group who receivechemoprophylaxis.

Different vaccines used: conjugate groupC or ACW135Y polysaccharide vaccines.

Limited immunity from polysaccharide

vaccine: lifelong from conjugate vaccineNow there is vaccine available forgroup B

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GROUP B VACCINESSome countries (NewZealand, Cuba, Norway,and Chile) developedvaccines against localstrains of B meningococcithat use strain-specific outer

membrane vesicle proteinrather than capsularpolysaccharide.

Polyvalent serogroups Bvaccine that contains

multiple bacterial surfaceproteins believed to befound in mostmeningococcal B strainsresponsible for the disease

globally being developed Dr.T.V.Rao MD 42


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Prognosis

Appropriate antibiotic therapy reduces the

mortality rate for bacterial meningitis in

children, but mortality remain high.

Overall mortality in the developed

countries ranges between 5% and 30%.

50 percent of the survivors have somesequelae of the disease.

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Public Health Importance

Challenges:-Educating public

-Timely reporting and records keeping

-Updating information daily.-Alleviating public anxiety and concerns

-Collaborating with health partners

Opportunities:-Educating public

-Communication

-Strengthening partnerships

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PUBLIC HEALTH RESPONSE: CASE DEFINITIONS

CONFIRMED: antibiotics +/- vaccine

Clinical diagnosis of meningitis or septicaemia

Confirmed microbiologically as due to Neisseria meningitidis

PROBABLE: antibiotics +/- vaccine

Clinical diagnosis of meningitis or septicaemia

Not microbiologically confirmedPublic Health Practitioner, in consultation with clinician,considers meningococcal infection most likely cause

POSSIBLE: no antibiotics or vaccine

Public Health Practitioner, in consultation with clinicianconsiders diagnoses other than meningococcal disease atleast as likely

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Programme Created by Dr.T.V.Rao MD for

Medical and Health care workers in the

Developing World

Email

[email protected]

meningitis meningitis meningococcal meningitis

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