Flashcards in H. Flu and Neisseria Meningitidis Deck (24):
Growth requirements for H. influenzae:
- Hemin or X factor.
- NAD or V factor.
- Heated blood agar (chocolate).
H. influenzae strains without capsule cause:
- Otitis media.
H. influenzae capsules are composed of:
Polyribitol phosphate. PRP.
H. influenzae strain that accounts for majority of invasive disease:
H. influenzae strains with a capsule cause:
H. influenzae colonization (6):
1. Outer membrane proteins (OMP) P2 and P5 promote bacterial binding to mucus.
2. LPS damages ciliated cells.
3. Adhesins and pili mediate direct adherence to non-ciliated epithelial cells.
4. IgA proteases cleave IgA.
5. Invasion into cells and subepithelial space.
6. Binding and uptake of iron and heme allow organisms to persist.
Encapsulated H. influenzae strains invade mucosa by:
Separating apical tight junctions of columnar epithelium and moving intercellularly.
Major H. influenzae virulence factor:
Severity of H. influenzae infection is related to:
Rate of clearance of bacteria.
Patients with higher risk for H. influenzae meningitis and epiglottitis (3):
- Pts with no anti-PRP antibodies.
- Complement deficiency.
Ages of highest risk of H. influenzae infection:
H. influenzae meningitis symptoms:
- Nonspecific signs and symptoms.
- 1-3 day history of mild upper respiratory disease.
- Irritability, fever, lethargy.
Older children may have:
H. influenzae arthritis:
- Leading cause of septic arthritis in children < 2.
- Most often affects single large joint.
- Due to bacteremic spread.
- Presents with fever, decreased ROM, warmth and swelling.
- Req's surgical drainage and IV antibiotic therapy.
H. influenzae stain:
Gram negative rods.
Staph aureus excretes NAD allowing H. flu to grow as small colonies.
H. influenzae treatment:
- 3rd gen cephalosporins for serious infections.
- PCN + beta-lactamase inhibitor.
Antibiotic prophylaxis for H. influenzae:
Neisseria meningitidis (5):
- Gram - diplococci with flattened sides.
- Complex growth req's: chocolate agar.
- Oxidize carbohydrates.
N. meningitidis virulence factors (6):
- Polysaccharide capsule.
- Porin proteins.
- IgA protease.
- Transferrin binding proteins.
N. meningitidis porin channel PorB (3):
- Interferes with degranulation of neutrophils.
- Facilitates invasion to epithelial cells.
- PIA antigen makes bacteria resistant to complement-mediated killing.
N. meningitidis LOS (4):
- Composed of lipid A and core oligosaccharide.
- Lacks the O-antigen polysaccharide of LPS.
- Lipid A possesses endotoxin activity.
- Neisseria release outer membrane blebs during rapid cell growth.
N. meningitidis transferrin binding proteins (2):
- Binds human transferrin.
- Allows bacteria to compete with host for iron.
N. meningitidis meningococcemia (4):
- Short hx of URI symptoms, fever and rash.
- Severe circulatory collapse with DIC and thrombosis of small blood vessels.
- Purpura and shock can occur within hours.
- Shock and DIC --> destruction of adrenal glands --> Friderichsen syndrome.