"Respiratory" Bacteria (Legionella, Haemophilus, Pseudomonas) Flashcards

1
Q

Legionnaire’s disease: classic S/S?

A

severe atypical (unilateral/lobar) pneumonia; rigors; dry non-productive cough; hyponatremia; GI/CNS symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

incubation period of Legionnaire’s disease

A

2-10d

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

incubation period of Pontiac Fever

A

1-2d

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

S/S Pontiac Fever

A

mild flu-like

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

habitat of Legionella

A

environmental water supplies (lakes, hot water tanks, ACs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

pathogenesis of Legionella

A
  • invades alveolar Macrophages via the C3b receptor; – - - inhibits lysosome binding, replicates;
  • releases degradative enzymes to kill the macrophages at time of release
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

habitat of Pseudomonas aeroginosa

A

ubiquitous in moist areas (sinks, soap bars, cut flowers, respiratory/dialysis equipment)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

transmission of Legionella

A

aerosols from the environmental water source (NOT person to person)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

detection of Legionella

A

urine antigen (warm 1st AM urine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

treatment of Legionella

A

macrolides, quinolones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

pathogenesis of P.aeroginosa

A

pili adhere to respiratory epithelia, capsule adheres to tracheal => biofilm formation, toxins released

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

5 toxins of P. aeroginosa

A
Phospholipase C (degrades cell membranes)
Endotoxin (fever, shock)
Exotoxin A (ADP-ribosylation of eEF-2)
Endotoxin exoenzyme S (prevents phagocytosis)
Pigments (pyocyanin, pyoverdine: color + ROS)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

P. aeroginosa morphology (4 easy-to-remember points)

A

1-3 flagella;
grape candy odor;
greenish-blue colonies (pyocyanins);
aerobic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

10 manifestations of P. aeroginosa

A

SKIN: burn wound infections, hot tub folliculitis, ecthyma gangrenosum
EAR: otitis externa, malignant external otitis
EYE: keratitis
LUNGS: CF/COPD bronchopneumonia
NOSOCOMIAL: UTIs in cath’d patients
BONES: Osteomyelitis
DIFFUSE: sepsis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Ecthyma gangrenosum (P. aeroginosa)

A

P. aeroginosa. Rapidly progressing necrotic cutaneous lesions. Common in i-comp, especially leukemia/neutropenia/hematologic malignancies.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Hot tub folliculitis (P. aeroginosa)

A

P. aeroginosa. Infection of the apocrine sweat glands (nipples, areolas, external ear)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Malignant otitis externa (P. aeroginosa)

A

When otitis externa gets out of control. EAC pussy discharge, pain, swelling. Can lead to CNS damage or sepsis. Often mistaken for mastoiditis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Osteomyelitis (P. aeroginosa)

A

Clasically, puncture wound in sweaty sneakers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Pneumonia (P. aeroginosa)

A

Diffuse bilateral bronchopneumonia, classic infection in CF patients (biofilm!)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Burn wound infections (P. aeroginosa)

A

Very moist environment with limited immune surveillance. Bacteria causes vascular damage and necrosis, can spread to bloodstream and cause sepsis.

21
Q

Nosocomial infections (P. aeroginosa)

A

UTIs in cath’d patients– biofilm does well on plastics.

22
Q

Keratitis (P. aeroginosa)

A

Usually a fulminating cornea injury, associated with contact lens wearers. Can cause panophthalmitis

23
Q

morphology of Haemophilus: Gram status, aerobicity

A

Gram negative; aerobic but facultatively anaerobic

24
Q

morphology of Legionella: Gram status

A

Gram negative (but poor Gram staining)

25
Q

morphology of Pseudomonas: Gram status, aerobicity

A

Gram negative; aerobic

26
Q

special culture requirements for Haemophilus (look at its name!)

A

Hemin (Factor X) and/or NAD (Factor V) on chocolate agar; or, add S. aureus on blood agar to produce the Factor V through hemolysis

27
Q

Haemophilus influenzae: capsulated or not?

A

Some are, some aren’t (Hib is capsulated)

28
Q

Virulence factor of Hib

A

IgA protease

29
Q

6 manifestations of H.influenzae

A

1) Epiglottitis
2) Meningitis
3) Otitis media (most common)
4) Pneumonia (2nd most common)
5) Cellulitis
6) Arthritis

30
Q

Epiglottitis (H. influenzae)

A

Ages 2-4; pharynx pain, swollen epiglottis (cherry red on endoscope + “thumb sign” on neck XR), inspiratory stridor

31
Q

Meningitis (H. influenzae)

A

Infants (3-18m); rare because of vaccine; preceded by URI

32
Q

Otitis media (H. influenzae)

A

Most common manifestation; kids & adults; preceded by URI, causes fever, pain, irritability

33
Q

Pneumonia (H. influenzae)

A

Elderly, asplenic, complement deficient patients; may or may not have a preceding URI; consolidated lower lobe infiltrate, abrupt high fever, bloody sputum, chest pain, rigors, productive cough

34
Q

Cellulitis (H. influenzae)

A

Young kids; in buccal mucosa, spreads to face/neck. Classic blue-red patches, fever, swelling

35
Q

Arthritis (H. influenzae)

A

<2 years; single large joint (especially the hip)

36
Q

Prevention of H. influenzae

A

1) Hib vaccine (given several times under 2 years old): conjugate of Hib capsule with the diphtheria toxin
2) Rifampin prophylaxis

37
Q

Treatment of H. influenzae

A

Mucosal infections: amoxi + clavu

Meningitis: ceftriaxone

38
Q

Morphology of Bordetella pertussis (Gram status, aerobicity, site)

A

Gram negative, aerobic, grows intracellularly

39
Q

5 virulence factors of B. pertussis

A
  1. Pertussis exotoxin
  2. Hemagglutinin
  3. Adenylate cyclase toxin
  4. Tracheal cytotoxin
  5. Endotoxin
40
Q

Action of the pertussis exotoxin

A

Inhibits G proteins, raising cAMP levels => fluid loss, mucus secretion, lymphocytosis

41
Q

Action of hemagglutinin in B. pertussis

A

Affects coagulation, vascular permeability

42
Q

Action of adenylate cyclase toxin in B. pertussis

A

Increases cAMP

43
Q

Action of tracheal cytotoxin in B. pertussis

A

Damages ciliated tracheal cells; key to the pertussis cough reaction!

44
Q

How is B. pertussis transmitted?

A

Fine respiratory droplets

45
Q

Risk populations for B. pertussis

A

1) Unvaccinated (babies < 2m) or wanted immunity

2) I-suppressed adults

46
Q

B. pertussis disease stages

A

7-10 day incubation
Stage 1: Catarrhal (“bad cold”, runny nose, low fever, mild cough, highly infectious). 1-2 weeks.
Stage 2: Paroxysmal (coughing fits with vomiting/broken ribs/exhaustion from the cough). 1-10 weeks.
Stage 3: Convalescent (less coughing, susceptible to RIs). 2-3 weeks.

47
Q

Prevention of B. pertussis

A

Vaccine (acellular or inactivated)

Macrolide prophylaxis

48
Q

Treatment of B. pertussis

A

Macrolides. Can’t treat symptoms, maybe can minimize contagious period