Bacterial Meningitis Flashcards
Conditions that Predispose Patients to Bacterial Meningitis
- Age-very young; very old
- Immunocompromised state
- Basal skull fracture
- Head trauma, post neurosurgery
- Cerebrospinal fluid shunt
Most Frequent Causes of Bacterial Meningitis in the US:
Streptococcus pneumoniae 58% Group B streptococcus 18% Neisseria meningtides 14% Haemophilus infuenzae 7% Listeria monocytogenes 3%
pathogenesis & clinical presentation of bacterial meningitis
- Hematogenous delivery of bacteria to subarachnoid space
- Host immune response
- Edema
- Increased intracranial pressure
- Decreased cerebral blood flow
- Damage, seizures, herniation
- Clinical Presentation
- Headache ≥ 90
- Fever ≥ 90
- Meningismus ≥ 85
- Altered sensorium > 80
- Kernig’s sign ≥50
- Brudzinski’s sign ≥ 50
General diagnosis of bacterial meningitis
CSF: *White blood cell count ≥1,000 per mm3 Cell differetial Mostly PMNs Protein Mild to marked elevation CSF-to-serum glucose ratio Normal to marked decrease
Diagnosis of Meningococcal Meningitis
- meningococci in blood.
- May occur with or without:
- petechiae and/or purpura
- Waterhouse-Friderichsen syndrome
- chronic recurring meningococcal disease.
- Gram-negative cocci
- Oxidase Positive
Diagnosis of Group B streptococcal Meningitis
- Gram-positive cocci
- catalase negative
- Usually beta hemolytic
- bacitracin insensitive
- group B-specific cell wall antigen
Diagnosis of Listeria monocytogenes Meningitis
Gram positive aerobic rod.
General traits of Neisseria species
- Morphology: Gram-negative cocci occur in pairs
- Oxidase positive – have cytochrome C oxidase
- measured by reduction of a dye to a blue color
- All are aerobic but will multiply under microaerophilic conditions
- Sugar Reactions Determines Species of Nesseria
Traits of Listeria monocytogenes
- Gram positive aerobic rod.
- Grows at cold temperatures or mesophilic (moderate temps)
- Widely distributed in nature.
- Facultative intracellular pathogen
- Produces listerolysin (LLO)
- promotes release of bacteria from phagosomes into cytoplasm
Epidemiology of various serogroups of Neisseria meningitidis in the U.S. vs the developing world
-Spread: human to human.
*Asymptomatic carrier = focus of infection.
Age: incidence greatest b/t 6 months & 3 years in unvaccinated
-Serogroup- incidence varies w/ serogroup & location of outbreak.
-Serogroup A causes epidemics in less developed nations
-In US, Groups B and C most often cause meningitis
-Africa, group A and W-135.
Serogroup A=one clonal serotype and that serogroups B and C have multiple serotypes.
Virulence Factors of Neisseria meningitidis
- Capsules are Key Virulence Determinants
- Antiphagocytic: interfere w/ complement deposition
- prevent C3b-mediated uptake of meningococci by phagocytes.
- 12 serogroups: Antibodies to type B capsule cross-react with E. coli-1 capsule
- Antibodies against capsular polysaccharide are bactericidal in the presence of complement
- LOS (lipooligosaccharide): toxic properties of the meningococcus reside in its LOS
Virulence factor in Group B streptococci
capsules = virulence factor
Virulence Factors for Listeria monocytogenes
- Listeriolysin O: required to escape vacuole & multiply in cytoplasm of cells
- promotes release of bacteria from phagosomes into cytoplasm
- LLO responsible for hemolytic phenotype of L. monocytogeneson blood agar plates
meningococcal vaccines
- Tetravalent conjugate vaccine licensed for use in the US in 2005
- Called MCV4: capsular polysaccharide from A, C, Y, & W135
- each conjugated to diphtheria toxoid.
- Two dose of MCV4 is recommended for all 11-16 year-olds
- Vaccination with MCV4 also recommended for unimmunized persons (ages 2-55) who are at increased risk
- college freshmen living in dormitories
- microbiologists routinely exposed to isolates of N. meningitids
- military recruits
- travelers/residents of countries where N. meningitidis epidemic
- persons with terminal complement component deficiencies
- anatomic or functional asplenia.
Describe how L. monocytogenes moves from cell to cell
After bacteria escape from phagosomes, multiply in cytoplasm
- Move w/in cells by a mechanism that involves host actin polymerization meditated by ActA
- Bacteria then spread directly from cell to cell without re-entering the extracellular space.
- Actin acts as ‘rocket tail’ allowing it to propel to next cell w/o entering extracellular space