H. Flu and Neisseria Meningitidis

Question 1

Growth requirements for H. influenzae:

Answer 1

• Hemin or X factor.
• NAD or V factor.
• Heated blood agar (chocolate).

Question 2

H. influenzae strains without capsule cause:

Answer 2

Mucosal infections:

• Otitis media.
• Sinusitis.
• Bronchitis.
• Pneumonia.

Question 3

H. influenzae capsules are composed of:

Answer 3

Polyribitol phosphate. PRP.

Question 4

H. influenzae strain that accounts for majority of invasive disease:

Answer 4

Hib

Question 5

H. influenzae strains with a capsule cause:

Answer 5

Invasive infections:

• Meningitis.
• Epiglottitis.
• Etc.

Question 6

H. influenzae colonization (6):

Answer 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.

Question 7

Encapsulated H. influenzae strains invade mucosa by:

Answer 7

Separating apical tight junctions of columnar epithelium and moving intercellularly.

Question 8

Major H. influenzae virulence factor:

Answer 8

Polysaccharide capsule.

Question 9

Severity of H. influenzae infection is related to:

Answer 9

Rate of clearance of bacteria.

Question 10

Patients with higher risk for H. influenzae meningitis and epiglottitis (3):

Answer 10

• Pts with no anti-PRP antibodies.
• Complement deficiency.
• Post-splenectomy.

Question 11

Ages of highest risk of H. influenzae infection:

Answer 11

6-18 months.

Question 12

H. influenzae meningitis symptoms:

Answer 12

Younger children:
- Nonspecific signs and symptoms.
- 1-3 day history of mild upper respiratory disease.
- Irritability, fever, lethargy.
Older children may have:
- HA. 
- Photophobia.
- Meningismus.

Question 13

H. influenzae arthritis:

Answer 13

• 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.

Question 14

H. influenzae stain:

Answer 14

Gram negative rods.

Question 15

Satellite phenomenon:

Answer 15

Staph aureus excretes NAD allowing H. flu to grow as small colonies.

Question 16

H. influenzae treatment:

Answer 16

• 3rd gen cephalosporins for serious infections.

- PCN + beta-lactamase inhibitor.

Question 17

Antibiotic prophylaxis for H. influenzae:

Answer 17

Rifampin.

Question 18

Neisseria meningitidis (5):

Answer 18

• Non-motile.
• Aerobic.
• Gram - diplococci with flattened sides.
• Complex growth req’s: chocolate agar.
• Oxidize carbohydrates.

Question 19

N. meningitidis virulence factors (6):

Answer 19

• Polysaccharide capsule.
• Pili.
• Porin proteins.
• LOS.
• IgA protease.
• Transferrin binding proteins.

Question 20

N. meningitidis porin channel PorB (3):

Answer 20

• Interferes with degranulation of neutrophils.
• Facilitates invasion to epithelial cells.
• PIA antigen makes bacteria resistant to complement-mediated killing.

Question 21

N. meningitidis LOS (4):

Answer 21

• 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.

Question 22

N. meningitidis transferrin binding proteins (2):

Answer 22

• Binds human transferrin.

- Allows bacteria to compete with host for iron.

Question 23

N. meningitidis meningococcemia (4):

Answer 23

• 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.

Question 24

N. meningitidis diagnosis (2):

Answer 24

• Microscopy: readily seen in CSF.

- Culture = gold standard for diagnosis.