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Bacterial Meningitis

Bacterial Meningitis

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Bacterial Meningitis

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  1. Bacterial Meningitis Ziad Elnasser, MD, Ph.D

  2. Anatomical considerations • CNS parts. • Blood brain barrier. • CSF and its circulation. • Hydrocephalus.

  3. Routes of infection • Blood borne. • Occult or overt. • Remote focus. • Venous spread. • Direct. • Congenital. • Surgery complications.

  4. Neisseria meningitidis

  5. General characteristics • G –ve diplococci, size variations. • Polysaccharides capsule. • Colonial morphology. • Growth conditions and media. • Carbohydrates fermentation. • Oxidase positive. • Significance of iron.

  6. Antigenic structure • Capsular polysaccharides. • Quellung reaction, group A and C. • 13 serotypes: A, B, C, D, X, Y, Z, E, W135, H, I, K and L. • A, B, C, X, Y, Z, W135, and L has been purified. • Group C divided into Neuraminidase R or S. • Serogrouping and antibiotics resistance? • Group B not immunogenic.

  7. Noncapsular Cell wall Antigens • Like other G –ve bacteria. • Lipo-oligosaccharide (12 serotypes). • Similar to human Glycosphingolipid Antigens. • Lipo-oligosaccharides as future vaccines. • OMP typing. • Classification based on Serotyping, OMP and Lipo-oligosaccharides.

  8. Pili • Phase and antigenic variation. • Attachment to nasopharyngeal cells. • Colonies of Piliated and nonpiliated are the same not as that of Gonococci.

  9. Pathogenesis • Nasopharyngeal surface. • Ciliated or nonciliated. • Mucus. • Pili and attachment to MCPs (CD46). • Opa and Opc role. • Only non encapsulated strains invade? • Actin rearrangement and porin protein. • IgAase and Pil C role and BB barrier.

  10. Immune response

  11. Immune response • Group A antigen and Bacillus pumilis. • E. coli K1 antigen and Group B. • Neonatal tissue and group B. • Some times not protective. • IgAase only in pathogenic strains.

  12. Carrier state • Presence of the meningococci in healthy individuals. • Parameningococci. • Carrier state and epidemic status, >20%. • Carrier to carrier via respiratory route. • Normal flora role. • Group B is the most common (9.6months). • Invasion and newly infected patients. • Upper respiratory tract infection and carriage.

  13. Epidemiology • Worldwide epidemics. • 5 – 19 years old during epidemic. • Fatality rate 2 – 10% and in septicemia up to 70%. • Low socioeconomic status and poverty. • Serotypes and different epidemic potential. • School children, military recruits and medical personnel.

  14. Clinical manifestations • Ranges from mild fever to septicemia and fulminant death. • Bacteremia without sepsis, upper respiratory tract infection. • Meningococcemia, leukocytosis, skin rash, headache and hypotention. • Meningitis with or without septicemia. • Meningoencephalitic manifestation. • Children vs adults.

  15. Laboratory Diagnosis • CSF and Blood. • Synovial, pleural, petechial skin and mucosal lesions and pericardial. • Chemical and cytological examination. • CIE, latex agglutination, coagglutination. • Lactate dehydrogenase and neuraminidase detection. • PCR value if antibiotics were used.

  16. Treatment • Antibiotics reduced mortality and supportive care improved prognosis. • Sulfonamides. • Penicillin. • Chloramphenicol. • First generation cephalosporins?. • Second and third generation cephalosporins. • Value of early treatment.

  17. Supportive care • Treat complications caused by LPS. • TNF alpha and other cytokines as indicators of shock. • Complement level. • Recombinant proteins. • Steroids? Low dose. • Heparin? • Plasmin activator with fibrinolysis for DIC.

  18. Chemoprophylaxis • Sulfonamides reduced the carrier state. • Penicillin proved to be ineffective. • Rifampin and minocycline. • Ciprofloxacin. • Ceftriaxone. • House hold contacts, medical personnel, nursery schools, military barracks

  19. Immunoprophylaxis • Capsular polysaccharides A and C. • Erythema and irritability in some. • Not effective before 24 months of age. • Day care centers. • Hyporesponsiveness. • Now quadrivalent of A, C, Y and W135 is avialable. • Detoxified LOS and OMP, Capsule protein conjugate, anti-idiotype antibodies.

  20. CRYPTOCOCCOSIS • Cryptococcus neoformans. • Yeast , large capsue unique, polysaccharide • Urease positive. • Bacterial like colonies. • Pigeon and birds droppings in soil. • No human to human transmission.

  21. PATHOGENESIS • Inhalation of yeast or conidia. • Minimal signs and symptoms. • CNS is the primary target. • Common complication of AIDS. • Phagocytosis? • Humoral and CMI role.

  22. CLINICAL MANIFESTATIONS • Meningitis, skin, pneumonia. • Slow insidious onset. • Headache, irritability, dizziness and behavioural changes. • Seizures, cranial nerves, papillidema, and dementia. • In AIDS 5 - 15% becomes infected.

  23. DIAGNOSIS • CSF pleocytosis, lymphocytes predominance, Sugar, protein. • Microscopy, negative staining. • Culture, urease. • Serology.

  24. TREATMENT • Amphotericin B + Flucytosine. • Fluconazole. • Relapse is a problem, chronic. • Residual neurological damage.

  25. Viral Meningitis • Self limiting to severe. • Meningitis vs encephalitis and clinical course. • Viral infections in the immune suppressed. • Slow viral infections. • Unconventional infections.

  26. Aetiological agents • Acute Aseptic Meningitis Syndrome • Mumps. • Coxsakie. • Echo. • HSV-2 • HIV • Polio • Lymphocytic choriomeningitis virus.

  27. Acute lymphocytic pleocytosis in the CSF. • No involvement of the brain paranchyma. • Normal sugar and slight protein increase. • Clinical course is usually mild. • Trimethoprim, Ibubrufin, Carbamazipine. • IV Immunoglobulin injection. • Treatment is supportive.

  28. Acute encephalitides • Parenchymal affection. • Like viral meningitis but more severe symptoms, seizures to coma. • Togaviruses, mosquitoes, summer to fall. • St. Louis encephalitis. • Eastern Equine Encephalitis. • Western Equine Encephalitis. • California Encephalitis. • Supportive care.

  29. HSV-2 some times HSV-1. • Acute widespread necrotizing infection of the newborne. Cervical infection and the baby. • Very high mortality or sever retardation. • HSV-1 and cold sores, frontal and temporal. • Acyclovir is effective mortality drops from 70 to 40%. • Steroids use.

  30. Viral infections in the immune suppressed • PML and the JC virus. • Chronic demyelinating disease. • Hodgkin's, Lymphoma, Leukemia and HIV. • CSF studies are completely normal. • HIV and AIDS. • Opportunistic infections. • Double infection.

  31. Slow Viral diseases • SSPE and mealses. • PRPE and Rubella. • Unconventional Agents: • Cretzfeldt-Jacob disease (prog. Dementia). • Kuru. • Gerstmann–Straussler-Scheinker Syndrome. • Familial Fatal Insomnia. • Bovine Spongiform encephalopathy. • Scrapie, Transmissible Mink encephalopathy, chronic wasting disease.