Meningitis Meningococcal Meningitis

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Meningitis Meningococcal Meningitis

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Meningitis Meningococcal Meningitis

  1. 1. MENINGITISMeningococcal Meningitis Dr.T.V.Rao MD Dr.T.V.Rao MD 1
  2. 2. 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
  3. 3. In Meningitis Meninges are infected and Inflamed Dr.T.V.Rao MD 3
  4. 4. 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
  5. 5. Etiology◆ gram-negative Coccus◆ Neisseria species◆ 13 serogroups◆ groups A, B, C Dr.T.V.Rao MD 5
  6. 6. 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
  7. 7. 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
  8. 8. 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
  9. 9. Transmission of Meninococcus• Transmission• Primary mode is by respiratory droplet spread or by direct contact. Dr.T.V.Rao MD 9
  10. 10. 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
  11. 11. 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
  12. 12. 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
  13. 13. 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
  14. 14. 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 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
  15. 15. 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 blood–brain 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
  16. 16. N. meningitidisHabitat: human nasopharynx (10- 25%)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
  17. 17. Meninges and spinal cord Dr.T.V.Rao MD 17
  18. 18. How patients present with Meningitis•Meningitis ( inflammation of membranecovering brain) :•Headache•Photophobia (pain on looking at brightlights)•Stiff Neck•Convulsion•Vomiting•Septicemia (blood poisoning):•Rash (pinpricks + bruises) Dr.T.V.Rao MD 18
  19. 19. 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
  20. 20. Clinical manifestation• Clinical manifestation of CNS – Conscious disturbance • Drowsiness • Clouding of consciousness • Coma • Psychiatric symptom – Irritation – Dysphoria – dullness Dr.T.V.Rao MD 20
  21. 21. Clinical manifestations Prodromal periodSeptic periodSeptic period Meningitic period Meningitic period ▲ an abrupt onset ▲ intracranial pressure ▲ chills high fever ▲ headache ▲ Headache ▲ vomiting ▲ restlessness ▲ Petechias ▲ Stiff neck ▲ purpuras ▲ Kernig (+) ▲Splenomegaly ▲ brudziski (+) Convalescent period ▲ gradually disappears, ▲ recovers to normal. Meningococcal meningitis Dr.T.V.Rao MD 21
  22. 22. MENINGOCOCCAL INFECTION•Neisseria meningitidis: gramnegative intracellulardiplococci.•Groups A, B, C, W135 and Y.•Septicaemia, meningitis orbacteraemia.•Incubation period of 2 to 7days.•Spread by droplets fromasymptomatic carriers.•Case fatality of 10% (meningitis)and 20% (septicaemia).•Affects young childrenpredominately Dr.T.V.Rao MD 22
  23. 23. Diagnosis• Isolation of the organism from CSF or blood. Dr.T.V.Rao MD 23
  24. 24. 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
  25. 25. PathogenicityMeningococcal meningitis, as a spread from nasopharynx blood stream meninges in susceptible hosts.Direct spread to meningesRashAdrenal hemorrhage (Waterhouse- Friderchsen syndrome) Dr.T.V.Rao MD 25
  26. 26. Clinical manifestations Dr.T.V.Rao MD Meningococcal meningitis 26
  27. 27. Death from Waterhouse-Friderichsen syndrome Dr.T.V.Rao MD 27
  28. 28. 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
  29. 29. Clinical examination and Important Signs Dr.T.V.Rao MD 29
  30. 30. 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
  31. 31. Diagnosis• Diagnostic methods – A careful evaluation of history – A careful evaluation of infant’s 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
  32. 32. 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
  33. 33. Lumbar puncture for CSF Examination Dr.T.V.Rao MD 33
  34. 34. INVESTIGATION1. Blood culture (sp)2. Naso-pharyngeal swab (both)3. Lumbar puncture (mg)4. PCR serum (sp)5. PCR CSF (mg)6. Serology7. Bleb aspirate (sp)8. Skin scrapings (sp) Dr.T.V.Rao MD 34
  35. 35. Laboratory examination of CSF Cerebrospinal fluid examination(an important method to establish diagnosis) : turbid ● pressure ● glucose ● WBC ×10 /L >1000 6 ● sodium ● protein chloride Dr.T.V.Rao MD 35 M
  36. 36. Diagnosis with Combination of Factors ⒈ Epidemic season, age and epidemic situations. ⒉ Clinical features. ⒊Manifestations of severe form in sepsis and meningoencephalitis⒋Increased leukocytes and polymorph nuclear leukocytes predominantly in peripheral blood. ⒌ Increased intracranial pressure and purulent changes in CSF.⒍ Positive results in bacteriological examination. Dr.T.V.Rao MD 36
  37. 37. 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
  38. 38. 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
  39. 39. Antibiotic Therapy• Course of treatment – 7 days for meningococcal infection – 10~14 days for H influenza or S pneumoniae infection – More than 21 days for S aureus or E coli infection – 14~21 days for other organisms Dr.T.V.Rao MD 39
  40. 40. 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
  41. 41. 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 polysaccharidevaccine: lifelong from conjugate vaccine• Now there is vaccine available forgroup B Dr.T.V.Rao MD 41
  42. 42. GROUP B VACCINES•Some countries (NewZealand, Cuba, Norway,and Chile) developedvaccines against localstrains of B meningococcithat use strain-specific outermembrane vesicle proteinrather than capsularpolysaccharide.•Polyvalent serogroups Bvaccine that containsmultiple bacterial surfaceproteins believed to befound in mostmeningococcal B strainsresponsible for the diseaseglobally being developed Dr.T.V.Rao MD 42
  43. 43. 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
  44. 44. Public Health ImportanceChallenges: -Educating public -Timely reporting and records keeping -Updating information daily. -Alleviating public anxiety and concerns -Collaborating with health partnersOpportunities: -Educating public -Communication -Strengthening partnerships Dr.T.V.Rao MD 44
  45. 45. 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 clinicianconsiders diagnoses other than meningococcal disease atleast as likely Dr.T.V.Rao MD 45
  46. 46. • 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

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