Streptococci GBS Flashcards

You may prefer our related Brainscape-certified flashcards:
1
Q

characteristics of GBS

A

non motile, faculative anerobe, most b hemolytic, catalase neg, + cAMP and hip hydrous.

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

3 serological markers in GBS

A
  1. B antigen - group specific cell wall poly saccaride
  2. multiple type specific capsular poly sacc
  3. surface protein C (note: early onset in babies)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Epidemiology of GBS

A

asympt colonization of GU and URI and lower GI

no seasonal incidence

postpartum sepsis

certain neonates at risk

non prey people with DM cancer low complement and low ab or ETOH

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

neonatal early onset GBS

A

early onset, in utero or on delivery, abrupt onset, pneumonia, bacteremia, meningitis, low mortality

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

neonatal late onset GBS

A

insidious. poor feeding at first…. at 4-8 wks of life. organism must be at birth. meningitis (pus in CSF) and bacteremia, high survival

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

pregnant women GBS

A

UTI during or after delivery, NOOOOO bacteremia, endocarditis, meningitis, osteomylitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

characteristics of streptococcus pneumonia (SP)

A

slimy capsule. fac anerobe. oval or lancet shaped diplococci. pneumolysins, harder to grow bc needs special nutrients

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

how is SP alpha or beta hemolytic?

A

alpha if grown with O2, beta if not

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

pneumolyssin

A

in SP. necessary for alpha hemolysis

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

epidemiology of SP

A

common in nose and through of healthy people. children are colonized by 6 mo. more common in cooler season. caused by a distant place from colonized site in lungs sinus ears and meninges.

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

SP spread?

A

P2P droplet

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

SP increase risk?

A

inc risk if no cilia or impairment of anything that promotes bacterial clearance. other: COPD, URI, DM, CHF, ETOH

elderly and old at risk for meningitis

no spleen or sickle cell at risk for sepsis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

clinical dz in SP and what is each preceding event for all of them?

A

aspiration pneumonia s/p viral

sinusitis and OM s/p URI with PMN infection

meningitis - mostly peds

bacteremia with endocarditis

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

what is the virulence of SP dependent on?

A

the competency of the hosts immune system

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

where does SP colonize? and spread?

A

oropharynx to lung and tissue (local v. distal via blood)

CAPSULE IS ESSENTIAL FOR VIRULENCE

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

SP - 2 types of adhesins

A

F antigen and C polypeptide - both techoic

17
Q

what is required for autolysis in SP?

A

cholin and techoic acid (required by autolysin)

18
Q

what is secretory IgA protease?

A

prevents enveloping of bacteria by mucous so it can spread in SP

19
Q

pneumolysin

A

binds to cholesterol in host membrane forms pores. destroys ciliated epithelium and phagocytes. so it can spread — -then autolysin released. #1 VIRULENCE FACTOR

SP

20
Q

phiosphoryl choline

A

helps colonization in SP - binds plt activating factor, internalize and sequester bacteria and protects from opson

21
Q

what protects SP from oxidative burst?

A

capsule and pneumolysin - capsule poly sac can be soluble - and free - and bind opsin

22
Q

how is C5a produced and what activates the alternative compliment pathway and classic thereby increasing tissue destruction in SP?

A

techoic acid - alt (C5a)

pneumolysin - classic (releases C5 and C3a)

23
Q

E. facium and E. fecalis (EF)

A

also gram + cocci. faculative anerobe, non motile, nonspecific and nonhemolytic.

24
Q

EF AND EF epidemiology

A

not a threat unless in the hospital and/or you lack all normal flora. similar to staph epi.

colonize GI of human and animals.

spread P2P

NOOOOOO toxins

25
Q

EF and EF causes what dz.’s?

A

nosocomial UTI, wound infection, bacteremia, endocarditis

26
Q

cytolisin in EF

A

ruptures cells. bacteriocidin. inhibits other gram + from colonizing. local tissue damage. virulence similar to staph epi.

27
Q

gelatinase in EF

A

Gel-E. hydrolysis gelatin, collegin, and small molecules. mediates and binds aggregative factors. vanc resistent (VRE!!!!!!!!) and pheromones which attract neutrophils.