Bacterial Meningitis Flashcards
Infections of the Brain
brain parenchyma = encephalitits, abcess
meninges = meningitis
spinal cord = myelitis
Meningitis - Definition
- inflammation of the meninges
- exudative response seen in CSF
Meningitis - Categories
- infectious causes
- bacteria, viruses, fungi
- non-infectious causes
Bacterial Meningitis - Risk Factors
- age - v. young and v. old
- immunocompromised
- basal skull fracture, head trauma, post-neurosurgery, cerebrospinal fluid shunt
Causes of Bacterial Meningitis in the US
- Streptococcus Pneumoniae (adults)
- Neisseria Meningitides (teens, colleges)
- Group B Streptococcus (newborns!)
- Haemophilus Influenzae Type B* (infants!)
- Listeria Monocytogenes
*Hib is the most common cause of bacterial meningitis in the developing world where children are not vaccinated.
Causes of Bacterial Meningitis by AGE
Newborn
- **Gp B Strep, **E. Coli, Listeria Monocytogenes
Infants
- Neisseria Meningitidis, Hib, Strep Pneumoniae
Children
- Neisseria Meningitidis*, Strep Pneumoniae
- *teens, colleges, etc
Adult
- **Strep Pneumoniae, **N. Meningitidis, mycobacteria
Bacterial Meningitis - Pathogenesis
- Hematogenous delivery of bacteria to SAS.
- Host immune response.
- Edema, increased intracranial pressure.
- Decreased cerebral bloodflow.
- Damage, seizures, herniation.
Injury and direct delivery of bacteria is less common.
Bacterial Meningitis - Symptoms
In neonates - temperature instability and lethargy.
Sudden onset…
- fever
- headache
- stiff neck
Often accompanied by…
- nausea, vomiting
- photophobia
- altered mental status, confusion
Bacterial Meningitis - Diagnosis
Examination of CSF via
- cell count
- gram stain
- antigen tests
- *culture - gold standard
CSF Findings in Acute Bacterial Meningitis
WBCs >1,000/mm3 (very high)
Cells PMNs (note - lymphocytes in viral, fungal)
Protein mild to marked elevation
Glucose normal to marked decrease
Streptococcus Pneumoniae
- ID
- Causes?
- Virulence
- Vaccine?
- Gm + diplococci, lancet-shaped
- catalase –
- alpha hemolytic
- optochin sensitive
- bile soluble
pneumonia, bacteremia, meningitis, otitis media
virulence - capsule, multiple types
vaccine - 13 valent conjugate, 23 valent polysaccharide only
Neisseria Meningitidis - Morphology & ID
Gm – diplococci (only one!)
Oxidase +
- cytochrome C oxidase reduces dye to **blue color **
Aerobic, grows on chocolate agar w/ hemin, NAD+
- glistening colonies = capsule!
Neisseria Meningitidis - **Key **Virulence
antiphagocytic capsule
- interferes w/ complement deposition
- prevents C3b-mediated uptake of meningococci by phagocytes
Recall that N. meningitidis is gm –. Ab deposition in presence of complement can also lead to cell lysis in addition to phagocytosis.
12 serogroups/types
- US - Gp B and C
(type B capsule cross-reacts w/ E. coli K-1 capsule)
- Africa - Gp A and W-135
Neisseria Meningitidis - Other Virulence
LOS (as opposed to LPS)
- released blebs of lipid A + sugar are toxic
Protease that cleaves sIgA1 (secretory IgA)
Capsule, IgA protease, and serum resistance allow it to survive in the bloodstream. Pili allow it to attach to the BBB; LOB causes BBB inflammation and mediates entry into CNS.
Neisseria Meningitidis - Clinical Signs and Symptoms
MOST COMMON CAUSE IN TEENS, COLLEGES
- 5-10% are asymptomatic pharyngeal carriers (esp in closed populations, ie. military barracks)
-
meningococcemia (meningococci in blood)
- petechiae, purpura
- Waterhouse-Friderichsen Syn (shock, DIC, bilateral destruction adrenal glands)
- meningitis
- chronic recurring meningococcal disease
Neisseria Meningitidis - Pathogenesis
Exposure -> colonize URT -> evades PMNs -> invades mucosa -> meningococcemia ->
- no clinical manifestations -> recovery
- Waterhouse-Friedrichsen Syn -> recovery, death
- meningitis and/or cutaneous manifestations -> recovery, death
Neisseria Meningitidis - Epidemiology
Spread = human to human
Age = greatests in 6 mo to 3 yrs unvaccinated
Serogroups - incidence varies with serogroup and location.
*Gp A causes epidemics in less developed nations.
US - Gp B > Gp C (we have a Gp C vaccine, we are just getting a Gp B vaccine)
Neisseria Meningitidis - Vaccine
MenACWY-D or MenACWY-CRM
- tetravalent conjugate vaccine
- contains capsular polysaccharide from A, C, Y, and W135 conjusted to diphtheria toxoid
- @ age 11-12 yrs, 1 dose (1 booster recommended if first dose given before 16 yrs)
MCV4 (multivalent) recommended for
- v. young or v. old at risk
- microbiologists
- college freshmen, military recruits
- travelers
- persons with complement deficiency
Group B Strep (GBS) (aka Streptococcus agalactiae)
Clinical Course and Prevention
MOST COMMON CAUSE IN NEONATES
- Why? Normal flora in gut and transient vaginal flora in 10-30% of pregnant (and non-pregnant) women.
- Can cause respiratory tract infections or septicemia that can progress to meningitis.
- Prolonged labor after rupture of membranes increases transmission risk.
- Also causes meningitis in pregnant or post-partum adults due to bacteremia.
- Can also occur in non-pregnant adults; usually elderly or individuals with chronic disease.
Prevent via administration of penicillin G I.V. during labor.
Group B Streptococci (GBS) - Morphology and ID
- Gm + cocci in chains, catalase –
- beta-hemolytic (GAS or GBS)
- bacitracin insensitive (v. GAS)
- CAMP test positive (v. GAS)
- confirm via detection of gp-B specific antigen
Listeria Monocytogenes - Clinical Course
Food-borne pathogen (e.g. soft cheese, lunch meaths, hot dogs) that can cause
- miscarriage and stillbirth in pregnant women
- severe systemic disease in immunosuppressed
- occasionally, gastroenteritis in healthy persons
Listeria Monocytogenes – Morphology & ID
widely distributed in nature
psychrophilic – grows in cold temps
mesophilic – grows in moderate temps
Gm + rod, motile, catalase +, beta-hemolytic, CAMP +
facultative intracellular pathogen
Listeria Monocytogenes – Virulence, Pathogenesis
Facultative Intracellular Pathogen
- Produces listerolysin (LLO) that promotes release of the bacteria from phagosomes into the cytoplasm, responsible for hemolytic phenotype.
- Multiplies in the cytoplasm; moves w/in cell by a mechanism involving host actin polymerization mediated by ActA produced by L. monocytogenes.
- Spreads directly from cell to cell via actin tails without entering extracellular space.
*Infections are terminated by a cell-mediated immune response.
