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Meningitis Meningococcal Meningitis

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  • 1.MENINGITISMeningococcal Meningitis Dr.T.V.Rao MDDr.T.V.Rao MD1

2. Introduction Bacterial meningitis is an inflammation ofthe leptomeninges, usually causing bybacterial infection. Bacterial meningitis may present acutely(symptoms evolving rapidly over 1-24hours), sub acutely (symptoms evolvingover 1-7days), or chronically (symptomsevolving over more than 1 week).Dr.T.V.Rao MD2 3. In Meningitis Meninges are infected and Inflamed Dr.T.V.Rao MD3 4. Etiology Causative organisms vary with patient age, withthree bacteria accounting for over three-quartersof all cases: Neisseria meningitidis (Meninococcus) Haemophilus influenza (if very young andunvaccinated) Streptococcus pneumoniae ( pneumococcus)Dr.T.V.Rao MD 4 5. Etiology gram-negative Coccus Neisseria species 13 serogroups groups A, B, CDr.T.V.Rao MD 5 6. Etiology Other organismsNeonates 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. Knowing about MeningococcalDisease Meningococcal disease is an acute, potentiallysevere illness caused by the bacteriumNeisseria meningitidis. Illness believed to bemeningococcal disease was first reported inthe 16th century. The first definitivedescription of the disease was by Vieusseux inSwitzerland in 1805. The bacterium was firstidentified in the spinal fluid of patients byWeichselbaum in 1887. Dr.T.V.Rao MD 7 8. Characteristics of N. meningitides N. meningitidis, or Meninococcus, is anaerobic, gram-negative diplodocus, closelyrelated to N. gonorrhea, and to severalnonpathogenic Neisseria species, such as N.lactamica. The outer membrane containsseveral protein structures that enable thebacteria to interact with the host cells as wellas perform other functions.Dr.T.V.Rao MD8 9. Transmission of Meninococcus Transmission Primary mode isby respiratorydroplet spreador by directcontact.Dr.T.V.Rao MD 9 10. Pathogenicity Meningococci are transmitted by dropletaerosol or secretions from thenasopharynx of colonized persons. Thebacteria attach to and multiply on themucosal cells of the nasopharynx. In asmall proportion (less than 1%) ofcolonized persons, the organismpenetrates the mucosal cells and entersthe bloodstream Dr.T.V.Rao MD 10 11. Pathogenesis A offending bacterium from blood invades theleptomeninges. Bacterial toxics and Inflammatory mediators arereleased. Bacterial toxics Lipopolysaccharide, LPS Teichoic acid Peptidoglycan Inflammatory mediators Tumor necrosis factor, TNF Interleukin-1, IL-1 Prostaglandin E2, PGE2Dr.T.V.Rao MD 11 12. Pathogenesis The outer membrane is surrounded by apolysaccharide capsule that is necessaryfor pathogenicity because it helps thebacteria resist phagocytosis andcomplement-mediated lysis. The outermembrane proteins and the capsularpolysaccharide make up the main surfaceantigens of the organism.Dr.T.V.Rao MD12 13. Serotyping of Meninococcus Meningococci areclassified by usingserologic methodsbased on the structureof the polysaccharidecapsule. Thirteenantigenically andchemically distinctpolysaccharide capsuleshave been described. Dr.T.V.Rao MD 13 14. Different Serotypes and Epidemiology Almost all invasive disease is caused byone of five serogroups: A, B, C, Y, and W-135. The relative importance of eachserogroups depends on geographiclocation, as well as other factors, such asage. For instance, serogroups A is a majorcause of disease in sub-Saharan Africabut is rarely isolated in the United States.Dr.T.V.Rao MD14 15. Systemic Spread of MeningococcalInfections The bacteria spread by way of the bloodto many organs. In about 50% ofbacteremia persons, the organismcrosses the bloodbrain barrier into thecerebrospinal fluid and causes purulentmeningitis. An antecedent upperrespiratory infection may be acontributing factor Dr.T.V.Rao MD 15 16. N. meningitidisHabitat: 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 MD16 17. Meninges and spinal cord Dr.T.V.Rao MD 17 18. How patients present withMeningitisMeningitis ( inflammation of membranecovering brain) :HeadachePhotophobia (pain on looking at brightlights)Stiff NeckConvulsionVomitingSepticemia (blood poisoning):Rash (pinpricks + bruises)Dr.T.V.Rao MD 18 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. Clinical manifestation Clinical manifestation of CNS Conscious disturbance Drowsiness Clouding of consciousness Coma Psychiatric symptom Irritation Dysphoria dullnessDr.T.V.Rao MD 20 21. Clinical manifestationsProdromal periodSeptic periodSeptic periodMeningitic 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 MD21 22. MENINGOCOCCAL INFECTIONNeisseria 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. Diagnosis Isolation of the organismfrom CSF or blood.Dr.T.V.Rao MD 23 24. Laboratory Findings Other bacterialtest Blood cultivation Film preparation of skin petechiae and purpura Secretion culture of local lesion Imageology examinationDr.T.V.Rao MD 24 25. PathogenicityMeningococcal meningitis, as a spread from nasopharynx blood streammeninges in susceptible hosts.Direct spread to meningesRashAdrenal hemorrhage (Waterhouse- Friderchsen syndrome)Dr.T.V.Rao MD25 26. Clinical manifestations Dr.T.V.Rao MD Meningococcal meningitis 26 27. Death from Waterhouse-FriderichsensyndromeDr.T.V.Rao MD27 28. Meningococcemia Bloodstream infection May occur with or without meningitis Clinical findings fever petechial or purpuric rash hypotension multiorgan failureDr.T.V.Rao MD28 29. Clinical examination and Important SignsDr.T.V.Rao MD29 30. Diagnosing by Isolation andidentification of Meninococcus Invasive meningococcal disease is typicallydiagnosed by isolation of N. meningitidisfrom a normally sterile site. However,sensitivity of bacterial culture may be low,particularly when performed after initiation ofantibiotic therapy. A Gram stain ofcerebrospinal fluid showing gram-negativediplococci strongly suggests meningococcalmeningitis. Dr.T.V.Rao MD30 31. Diagnosis Diagnostic methods A careful evaluation of history A careful evaluation of infants signs andsymptoms A careful evaluation of information onlongitudinal changes in vital signs andlaboratory indicators Rout examination of cerebrospinal fluid (CSF)Dr.T.V.Rao MD 31 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 MD32 33. Lumbar puncture for CSFExamination Dr.T.V.Rao MD33 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. Laboratory examination of CSFCerebrospinal fluid examination(an important method to establish diagnosis) : turbid pressure glucose WBC 10 /L >10006 sodium protein chlorideDr.T.V.Rao MD35 M 36. Diagnosis with Combination of Factors Epidemic season, age and epidemic situations. Clinical features.Manifestations ofsevere form in sepsis and meningoencephalitisIncreasedleukocytes 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 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 - unfortunatelyDr.T.V.Rao MD37 38. Epidemiology Occurrence Meningococcal disease occurs worldwide inboth endemic and epidemic form. Reservoir Humans are the only natural reservoir ofMeninococcus. As many as 10% of adolescentsand adults are asymptomatic transient carriersof N. meningitidis, most strains of which arenot pathogenic (i.e., strains that are notgroupable).Dr.T.V.Rao MD 38 39. 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 40. PREVENTION: CHEMOPROPHYLAXISGets rid of bacteria from carriers (and cases)Does not prevent infectionGiven to those who, in 7 days before symptoms:* Lived in same house* Kissed case on lips* Gave mouth to mouthresuscitation.Options: Ciprofloxacin, Rifampicin, Ceftriaxone.Can be given up to 28 days after contact with case Dr.T.V.Rao MD40 41. PREVENTION: VACCINATION IN RESPONSE TO CASEAvailable for groups A, C, W135 or Y.Only used once group is confirmedGiven 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 BDr.T.V.Rao MD 41 42. GROUP B VACCINESSome countries (NewZealand, Cuba, Norway,and Chile) developedvaccines against localstrains of B meningococcithat us

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