Meningococcal Meningitis

Dr.T.V.Rao MD

MENINGITIS

Dr.T.V.Rao MD

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 evolving over 1-7days), or chronically (symptoms evolving over more than 1 week).
Dr.T.V.Rao MD 2

In Meningitis Meninges are infected and Inflamed

Dr.T.V.Rao MD

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 and

unvaccinated)
Streptococcus pneumoniae ( pneumococcus)
Dr.T.V.Rao MD 4

Etiology

gram-negative Coccus Neisseria species 13 serogroups groups A, B, C

Dr.T.V.Rao MD

Etiology
Other organisms
Neonates and infants at age 2-3 months
Escherichia coli B-hemolytic streptococci
Staphylococcus aureus Staphylococcus epidermidis Listeria Monocytogenes
Dr.T.V.Rao MD 6

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 first identified in the spinal fluid of patients by Weichselbaum in 1887.
Dr.T.V.Rao MD 7

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 well as perform other functions.
Dr.T.V.Rao MD 8

Transmission of Meninococcus
Transmission Primary mode is by respiratory droplet spread or by direct contact.
Dr.T.V.Rao MD 9

Pathogenicity
Meningococci are transmitted by droplet aerosol or secretions from the nasopharynx of colonized persons. The bacteria attach to and multiply on the mucosal cells of the nasopharynx. In a small proportion (less than 1%) of colonized persons, the organism penetrates the mucosal cells and enters the bloodstream
Dr.T.V.Rao MD

10

Pathogenesis
A offending bacterium from blood invades the leptomeninges. 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
Dr.T.V.Rao MD 11

Pathogenesis
The outer membrane is surrounded by a polysaccharide capsule that is necessary for pathogenicity because it helps the bacteria resist phagocytosis and complement-mediated lysis. The outer membrane proteins and the capsular polysaccharide make up the main surface antigens of the organism.
Dr.T.V.Rao MD 12

Serotyping of Meninococcus
Meningococci are classified by using serologic methods based on the structure of the polysaccharide capsule. Thirteen antigenically and chemically distinct polysaccharide capsules have been described.
Dr.T.V.Rao MD 13

Different Serotypes and Epidemiology

Almost all invasive disease is caused by one of five serogroups: A, B, C, Y, and W135. The relative importance of each serogroups depends on geographic location, as well as other factors, such as age. For instance, serogroups A is a major cause of disease in sub-Saharan Africa but is rarely isolated in the United States.
Dr.T.V.Rao MD 14

Systemic Spread of Meningococcal Infections

The bacteria spread by way of the blood to many organs. In about 50% of bacteremia persons, the organism crosses the bloodbrain barrier into the cerebrospinal fluid and causes purulent meningitis. An antecedent upper respiratory infection may be a contributing factor
Dr.T.V.Rao MD 15

N. meningitidis
Habitat: human nasopharynx (1025%) Similar to N. gonorrhea but less exacting ? Can grow in BA, Chocolate agar without selective media from CSF ? Id. CHO utilization: acid from glucose & maltose.
Dr.T.V.Rao MD

16

Meninges and spinal cord

Dr.T.V.Rao MD

17

How patients present with Meningitis

Meningitis ( inflammation of membrane covering brain) : Headache Photophobia (pain on looking at bright lights) Stiff Neck Convulsion Vomiting Septicemia (blood poisoning): Rash (pinpricks + bruises)
Dr.T.V.Rao MD 18

Clinical manifestation
Clinical manifestation of CNS
Increased intracranial pressure
Headache Projectile vomiting Hypertension Bradycardia Bulging fontanel Cranial sutures diastasis Coma Decerebrate rigidity Cerebral hernia
Dr.T.V.Rao MD 19

Clinical manifestation
Clinical manifestation of CNS
Conscious disturbance
Drowsiness Clouding of consciousness Coma Psychiatric symptom
Irritation Dysphoria dullness
Dr.T.V.Rao MD 20

Clinical manifestations
Prodromal period

Septic period Septic period

an abrupt onset chills high fever

Meningitic period Meningitic period

intracranial pressure headache vomiting restlessness Stiff neck Kernig (+) brudziski (+)

Headache
Petechias purpuras

Splenomegaly

Convalescent period
gradually disappears, recoversDr.T.V.Rao MD . Meningococcal meningitis to normal
21

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
Dr.T.V.Rao MD 22

Diagnosis
Isolation of the organism from CSF or blood.

Dr.T.V.Rao MD

23

Laboratory Findings
Other bacterial test
Blood cultivation Film preparation of skin petechiae and purpura Secretion culture of local lesion

Imageology examination
Dr.T.V.Rao MD 24

Pathogenicity
Meningococcal meningitis, as a spread from nasopharynx blood stream meninges in susceptible hosts. Direct spread to meninges Rash Adrenal hemorrhage (WaterhouseFriderchsen syndrome)
Dr.T.V.Rao MD 25

Clinical manifestations

Dr.T.V.Rao MD

Meningococcal meningitis

26

Death from Waterhouse-Friderichsen syndrome

Dr.T.V.Rao MD

27

Meningococcemia
Bloodstream infection May occur with or without meningitis Clinical findings fever petechial or purpuric rash hypotension multiorgan failure
Dr.T.V.Rao MD 28

Clinical examination and Important Signs

Dr.T.V.Rao MD

29

Diagnosing by Isolation and identification of Meninococcus

Invasive meningococcal disease is typically diagnosed by isolation of N. 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-negative diplococci strongly suggests meningococcal meningitis.
Dr.T.V.Rao MD 30

Diagnosis
Diagnostic methods
A careful evaluation of history A careful evaluation of infants signs and symptoms A careful evaluation of information on longitudinal changes in vital signs and laboratory indicators
Rout examination of cerebrospinal fluid (CSF)
Dr.T.V.Rao MD 31

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 streptococcus
Dr.T.V.Rao MD 32

Lumbar puncture for CSF Examination

Dr.T.V.Rao MD

33

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

Laboratory examination of CSF

Cerebrospinal fluid examination
(an important method to establish diagnosis) :

turbid

pressure WBC 10 /L >1000 protein

6

glucose sodium chloride

Dr.T.V.Rao MD

35

Diagnosis with Combination of Factors

Epidemic season, age and epidemic situations. Clinical features.
Manifestations of meningoencephalitis severe form in sepsis and

Increased

leukocytes and polymorph nuclear leukocytes predominantly in peripheral blood. Increased intracranial pressure and purulent changes in CSF.

Positive results in bacteriological examination.

Dr.T.V.Rao MD

36

USUAL MANAGEMENT OF SUSPECTED CASE Isolation Released once they have had their antibiotic treatment for 48 hours Intravenous Fluids Often ill and pyrexia Antibiotics Cefotaxime (+ Ciprofloxacin or rifampicin). Will be given former for first 24-48 hours even if diagnosis uncertain. Intensive care Not unusual - unfortunately
Dr.T.V.Rao MD 37

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 carriers of N. meningitidis, most strains of which are not pathogenic (i.e., strains that are not groupable).
Dr.T.V.Rao MD

38

Antibiotic Therapy
Course of treatment
7 days for meningococcal infection

1014 days for H influenza or S pneumoniae

infection

More than 21 days for S aureus or E coli infection

1421 days for other organisms
Dr.T.V.Rao MD 39

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
Dr.T.V.Rao MD 40

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 receive chemoprophylaxis. Different vaccines used: conjugate group C or ACW135Y polysaccharide vaccines. Limited immunity from polysaccharide vaccine: lifelong from conjugate vaccine Now there is vaccine available for

group B

Dr.T.V.Rao MD

41

Some countries (New Zealand, Cuba, Norway, and Chile) developed vaccines against local strains of B meningococci that use strain-specific outer membrane vesicle protein rather than capsular polysaccharide. Polyvalent serogroups B vaccine that contains multiple bacterial surface proteins believed to be found in most meningococcal B strains responsible for the disease globally being developed Dr.T.V.Rao MD

GROUP B VACCINES

42

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 some sequelae of the disease.
Dr.T.V.Rao MD 43

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
Dr.T.V.Rao MD 44

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 confirmed Public Health Practitioner, in consultation with clinician, considers meningococcal infection most likely cause POSSIBLE: no antibiotics or vaccine Public Health Practitioner, in consultation with clinician considers diagnoses other than meningococcal disease at least as likely

Dr.T.V.Rao MD

45

 Programme Created by Dr.T.V.Rao MD for Medical and Health care workers in the Developing World Email doctortvrao@gmail.com

Dr.T.V.Rao MD

46