Micro - Pneumococcus Flashcards

1
Q

S. pneumoniae: (G+, G-), (shape)

A

G+ lancet-shaped diplococci

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2
Q

Pneumococcus is non-typable, meaning:

A

Can’t be speciated from other types of strep via reactions with Lancefield antigen

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3
Q

S. pneumoniae is the most common cause of:

A

CAP
Meningitis (if not epidemic)
Otitis media
Sinusitis

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4
Q

Diseases caused by pneumococcus

A
CAP
Meningitis
Otitis media
Sinusitis
Endocarditis
Sepsis
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5
Q

(T/F): Pneumococcus can commonly colonize people without causing disease

A

True - up to 60% of healthy kids and 30% of adults

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6
Q

3 outcomes of pneumococcus carriage:

A
  1. Clear it
  2. Asymptomatic persistence
  3. Progression to disease
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7
Q

Where would you most likely culture S. pneumoniae from in a healthy individual?

A

Nasal cavity

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8
Q

Primary vector of pneumococcus

A

Kids

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9
Q

List the 10 virulence factors of S. pneumoniae

A
  1. Polysaccharide capsule
  2. Pneumolysin
  3. Hyaluronidase
  4. Neuraminidase
  5. Pili
  6. Peptidoglycan and techoic acids
  7. Choline binding protein
  8. Competence protein
  9. Autolysin
  10. Lipoproteins
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10
Q

Most important virulence factor of pneumococcus? What does it do?

A

Polysaccharide capsule - antiphagocytic

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11
Q

When is a polysaccharide capsule not effective as a virulence factor?

A

In presence of anti-capsule Abs which opsonize the capsule

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12
Q

How can capsular types be identified?

A

Quellung reaction - anti-capsule Abs bind capsule and stabilize it so it’s more visible; the Ab identifies which capsule is present

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13
Q

What does pneumolysin do?

A

Pore forming toxin that binds to cholesterol in host cell membranes causing cell lysis; contributes to inflammation by recruiting PMNs and lymphocytes as well as direct interaction with TLR4 to stimulate cytokine production

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14
Q

What role does pneumolysin play in diagnosing S. pneumoniae?

A

It causes partial lysis of RBCs, called alpha-hemolysis, giving characteristic green zone on BAP

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15
Q

What does hyaluronidase do?

A

Facilitate spread of pneumococcus in tissues with hyaluronic acid

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16
Q

What does neuraminidase do?

A

Cleaves N-acetylneuaminic acid on cell surface glycoproteins which either causes direct damage or unmasks binding sites for the bacteria

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17
Q

Neuraminidase is a particularly important virulence factor for what disease process?

A

Otitis media - spread of pneumococcus up Eustachian tube

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18
Q

Function of pili? How are the formed?

A

Attachment to epithelial cells; sortase mechanism

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19
Q

How do lipoproteins contribute to virulence?

A

Take in iron + other functions

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20
Q

Two types of techoic acid? What is unique about pneumococcal TA?

A

WTA, LTA

The negatively-charged phosphate groups in S. pneumoniae are neutralized by CHOLINE instead of D-ala like other G+ spp.

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21
Q

How do peptidoglycan and TA contribute to virulence?

A

They bind together to from C-polysaccharide, which when bound by CRP activates the alternative complement pathway. C-polysaccharide can also stimulate PRRs to release cytokines.

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22
Q

High levels of CRP are predictive of:

A

Heart disease

almost as predictive as hypercholesterolemia!!

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23
Q

Common feature of all choline binding proteins?

A

Bound to cell wall by choline of WTA/LTA

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24
Q

What do the different choline binding proteins do?

A
  1. Hydrolytic enzyme that causes release of inflammatory mediators, like autolysin
  2. Bind to nasopharyngeal/lung epithelium, causing release of PspA and PspC that inhibit phagocytosis by binding complement factor H
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25
Q

What does competence protein do?

A

Acquires DNA from env. –> drug resistance and ability to form capsules

26
Q

What is the historical significance of competence protein?

A

S. pneumoniae used in early experiments proving DNA was the transforming factor/heritable material

27
Q

What does autolysin do?

A

Disrupts bacterial cell wall, releasing inflammatory components of wall

28
Q

Direct spread of pneumococcus infects:

A

Middle ear, lungs, trachea, sinuses, bronchi

29
Q

Hematogenous spread of pneumococcus infects:

A

Meninges, pleural cavity, bones, peritoneal cavity, joints, heart valves

30
Q

Pathogenesis of pneumococcal pneumonia

A

Pneumococcus replicates in alveoli –> Fluid accumulates and facilitates spread –> Few PMNs initially but leaky capillaries allow RBCs to provide Fe2+ to bugs –> Bugs recruit PMNs, activate complement, and cause cytokine production –> Exudative fluid and WBCs accumulate

31
Q

Predisposing factors to pneumococcal pneumonia:

A
Smoking
COPD
CHF
Diabetes
EtOH
Viral infx
32
Q

Two ways pneumococci can cause meningitis

A
  1. Hematogenous spread (most commong)

2. Direct extension from otitis media/sinusitis

33
Q

Progression to otitis media

A

Nasal congestion –> Eustachian tube –> middle ear (neuraminidase!!)

34
Q

Complication of otitis media

A

TM rupture (usually heals once treated)

35
Q

Predisposing factors to pneumococcal sinusitis:

A

Viral infx

Allergen/pollutant exposure

36
Q

Most common causes of pneumococcal sepsis

A

Seeding from pneumonia or meningitis

37
Q

Sepsis from pneumococcus is rare in the absence of predisposing factors, which are:

A

Asplenia/splenectomy
Recent surgery
Immunocompromised states

38
Q

6 common sx of pneumococcal pneumonia

A

Fever, chills, SOB, sweats, cough, fatigue

39
Q

How can differentiate pneumococcal pneumonia from other types just off of signs?

A

Pt will look gray and anxious

40
Q

Characteristic findings of pneumococcal pneumonia

A

Rust-colored sputum
Shaking chills
Gray, anxious pt

41
Q

Appearance of pneumococcal pneumonia on CXR

A

One of more segments of consolidation in a single lobe

42
Q

Pneumococcal vs. staph aureus pneumonia

A

S. pneumoniae doesn’t cause abscesses so lungs can return to normal

43
Q

What causes the symptoms of pneumococcal pneumonia?

A

Host’s immune response

44
Q

Complication of host’s immune response to pneumococcal pneumonia?

A

Alveoli filled and fluid and consolidated –> pt suffocates

45
Q

Sx of pneumococcal meningitis

A

HA, seizures, loss of consciousness, stiff neck, photophobia, bulge over fontanelle in babies
(sx caused by increased pressure on brain)

46
Q

When does pneumococcal colonization increase?

A

Mid-winter

47
Q

Who usually gets pneumococcal disease?

A

Newborns/infants and elderly

48
Q

Primary organ that clears unopsonized bacteria?

A

Spleen

49
Q

Primary risk factor for developing pneumococcal infections?

A
Ab deficiency
(remember they have capsules that can't be phagocytosed but can be opsonized by anti-capsule Abs)
50
Q

Why do CHF, DM, EtOH abuse, and chronic lung disease cause predisposition to pneumococcal infection?

A

Cause poorly functioning PMNs

51
Q

Besides asplenia, disease reducing clearance of pneumococcus

A

Sickle cell

52
Q

Good sputum sample for pneumococcus

A

Few epithelial cells, many G+ lancet-shaped rods, many PMNs

53
Q

___% of pneumococcal pneumonia results in bacteremia

A

25%

so - culture not always helpful

54
Q

4 characteristics of pneumococcus on BAP:

A
  1. alpha hemolysis
  2. Catalase -
  3. Optochin sensitive
  4. Bile salt sensitive
55
Q

Tx of otitis media/sinusitis

A

1st - amoxicillin/clavulanic acid

2nd - ceftriaxone

56
Q

Tx outpatient pneumococcal pneumonia

A

1st - macrolide, doxy, amox, or quinolone

2nd - Adjust if not improved

57
Q

Tx inpatient pneumococcal pneumonia

A

Penicillin, amoxicillin, ceftriaxone

58
Q

Pneumococcal pneumonia mortality reduced by ____. Why?

A

Beta-lactam + macrolide

Macrolide doesn’t cause release of cell wall components = anti-inflammatory effects

59
Q

Pneumovax vs prevnar 13

A

Pneumovax has 23 capsular proteins; prevnar 13 has 13 capsular proteins + DIPHTHERIA TOXIN

60
Q

Standard length of Abx tx for pneumococcal pneumonia

A

10-14 days