streptococci Flashcards

1
Q

gram stain and catalase status/ oxidase status of streptococci

A

gram positive cocci in chains or pairs, catalase negative, oxidase negative, aerotolerant bacteria that ferment carbs to produce lactic acid

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

list the members of the streptococci family

A

Streptococcus pyogenes (group A), S. agalactiae (group B), S. equinus (Group D), viridians streptococci, and S. pneumoniae (pneumococcus)

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

Describe the classification system of streptococci based on visible hemolysis on sheep blood agar.

A

Some strains of streptococci can hemolyze red blood cells.

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

alpha hemolysis and strep groups

A

Incomplete destruction of erythrocytes, resulting in a green coloration of the medium surrounding the colonies. The green pigment is due to biliverdin and other heme compounds. Many of the oral streptococci and S. pneumoniae are alpha hemolytic.

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

beta hemolysis and strep groups

A

Complete lysis of RBCs results in a distinct clear zone around the colonies. Beta hemolysis usually is visualized better under reduced oxygen tension (i.e., by stabbing the organisms into the agar) because of the oxygen lability of the hemolysin. Lancefield groups A, B and C streptococci usually are beta-hemolytic.

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

gamma hemolysis

A

conventional designation for strains which produce no hemolysis effect on sheep blood agar. The term “nonhemolytic streptococci” is more precise

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

Describe Lancefield classification of streptococci and the antigens involved in classification

A

Beta hemolytic strep can be classified into 21 serological groups (A-U) based on antigen differences in cell wall carbohydrates. Certain alpha and nonhemolytic groups can also be classified this way. Group A strep antigen is the M protein of the cell wall. For S. pneumoniae it is the capsular polysaccharide

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

Assign the common streptococci species to the correct Lancefield groups.

A

A (bacitracin sensitive): S. pyogenes (beta hemolytic). B (Camp test positive): S. agalactiae (beta hemolytic or none). D (Bile-Esculin hydrolysis positive and 6.5% NaCl tolerance): Enterococcus faecalis, Non-typable: S. Salivarius, S. sanguis

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

Describe the structure of streptococci

A

Contains outer capsule > cell wall (M, T, R antigens) > carbohydrates > peptidoglycan > cytoplasmic membrane. And teichoic acids (lipotechoic acids associated with M protein). M proteins project from the cell surface

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

hyaluronic acid capsule

A

surrounds Group A strep- anti phagocytic.

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

M protein

A

The major virulence determinant of S. pyogenes. Prevents interaction of bacteria with complement. Phagocytes kill strains without M-protein.
Antibody against M-protein allows killing to occur.
80 different M-protein serotypes- vary at the N terminalThe major virulence determinant of S. pyogenes. Prevents interaction of bacteria with complement. Phagocytes kill strains without M-protein.
Antibody against M-protein allows killing to occur.
80 different M-protein serotypes- vary at the N terminalThe major virulence determinant of S. pyogenes. Prevents interaction of bacteria with complement. Phagocytes kill strains without M-protein.
Antibody against M-protein allows killing to occur.
80 different M-protein serotypes- vary at the N terminal

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

lipoteichoic acid

A

Virulence factor for group A strep which mediates initial adherence of the streptococci to mucosal cells. M protein aids by binding to LTA in correct orientation

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

T and R antigens

A

Cell wall proteins on Group A strep- not virulence factors

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

List extracellular products produced by S. Pyogenes

A

Streptolysin O, Streptolysin S, pyrogenic exotoxins A, B and C, Spreading factors (streptokinase, hyaluronidase, DNAse and proteinase)

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

Streptolysin O functions

A

hemolysin- binds cholesterol in RBCs and Causes hemolysis by inserting as a pore. Does not lyse neutrophils. Cardiotoxic. Inhibited by oxygen and inactivated by cholesterol. Anti-streptolysin O antibody increases after infection

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

Streptolysin S functions

A

hemolytic and cytotoxic

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

Pyrogenic exotoxins functions

A

pyrogenic, immunosuppressive, enhance host susceptibility to endotoxin shock. Rash (scarlet fever)

18
Q

streptokinase functions

A

Activates human plasminogen which cleaves fibrin and fibrinogen. Facilitates spread.

19
Q

Hyaluronidase functions

A

Breaks down CT and allows spread

20
Q

DNAses functions

A

digests DNA, especially in pus.

21
Q

Suppurative Group A strep infections

A

Pus forming- pharyngitis, pneumonia, osteomyelitis, cellulitis (bacteria gain access to subcutaneous tissues and spread rapidly), impetigo (superficial skin infection from break in skin), scarlet fever (fever, red rash, strawberry tongue, pyrogenic exotoxins)

22
Q

List non suppurative Group A strep complications

A

Acute rheumatic fever and post-streptococcal glomerulonephritis

23
Q

Acute rheumatic fever onset, mechanisms

A

3-6 weeks after S. pyogenes infection (pharyngitis). Inflammation of heart valve, skin, joints and CNS plus fever. Damage to heart valves may occur. Most likely model is autoimmune disease. Prevention possible by therapy of acute infection.

24
Q

Post-streptococcal glomerulonephritis onset, mechanism

A

Inflammation of glomerulus 2-4 weeks after strep pyogenes infection of skin or throat. May cause acute renal failure. Most likely model is immune complex disease. Immune complexes get trapped in glomerular basement membrane resulting in complement deposition and neutrophil recruitment/ damage to kidney. Prevention most likely not possible with therapy of acute infection

25
Q

autoimmune model of acute rheumatic fever

A

Abs against Goup A strep develop which are cross reactive with heart tissue (sarcolemmal sheaths of myofibers and glycoprotein of heart valves)

26
Q

additional mechanisms proposed in pathogenesis of ARF

A
  1. Cardiotoxic effects of streptolysin O causing initial heart damage. 2. L forms of streptococci may directly infect the heart. 3. rehumatogenic strains of strep such as M18 and M3. 4. genetically determined variation in immune response to streptococci.
27
Q

Protection against Group A strep

A

M type specific- there are over 80 serotypes but few are rheumatogenic

28
Q

Group B strep structure

A

C- carbohydrate is major component of cell wall but is different from group A strep. LTA mediate adherence. Polysaccharide capsule. Group B strep does NOT have M, T or R antigens.

29
Q

Group B strep capsule functions

A

Capsular types Ia, Ib, II and II. The capsule confers resistance to phagocytosis and anticapsular antibody mediates phagocytosis by promoting activation of alternative complement pathway.

30
Q

Group B strep extracellular products

A

Virulence factors: Neuraminidase (cleaves sialic acid from polysaccharide/ glycoprotein substrates), proteases, beta-hemolysin (weak hemolysis), hyaluronidase and CAMP factor (enhances hemolysis of staph aureus)

31
Q

What is used to identify group B strep

A

CAMP factor

32
Q

Describe the pathogenesis of group B streptococci infections, particularly the role of the capsule.

A

Group B strep causes neonatal pneumonia and sepsis (many healthy women have GBS in rectum/vagina). All capsular types can cause early onset, but all late onset dz is due to type III. ARF and PSGN do not occur after GBS infection

33
Q
  1. Differentiate enterococci and group D streptococci.
A

Enterococci share the group D antigen (lipotechoic acid in the cell membrane). Identified by ability to grow in 6.5% NaCl, 40% bile and to hydrolyze exculin. They are resistant to penicillins. Group D strep have the group D antigen, can grow in 40% bile and utilze esculin. Group D strep CANNOT grow in 6.5% NaCl and ARE sensitive to penicillins.

34
Q

list common enterococci and group D streptococci

A

enterococci: Main pathogens are E faecalis and E faecium. Group D strep: S. Bovis and S. equinus

35
Q

Group D strep and enterococci infections

A

Both are normal flora of the upper respiratory tract, gastrointestinal tract, genitourinary tract, and skin. These organisms are opportunistic pathogens and secondarily invade damaged tissue. They are frequent causes of urinary tract infections, and cause intra-abdominal infections, endocarditis and infection of IV catheters

36
Q

enterococcus resistance

A

Inherent resistance to cephalosporins, penicillin, aminoglycosides, tmp/smx, clindamycin. Inducible vancomycin resistance (VRE)

37
Q

viridians streptococci features

A

alpha hemolytic, do not contain group specific antigens so they don’t belong to a Lancefield group. Normal flora in pharynx

38
Q

List important viridians streptococci

A

S. salivarius, S. pyogenes sanguis, S. mitis and S. mutans

39
Q

Describe common infections due to viridans streptococci.

A

Dental caries (S. mutans- produce dextrans and adhere to tooth surface) and endocarditis (adhere to previously damaged heart valves)

40
Q

Group G streptococci features

A

similar to group A- produce streptolysin O and streptokinase, have several M proteins. Uncommon cause of pharyngitis. ARF does NOT occur but PSGN has been seen

41
Q

Group C streptococci features

A

Can cause pharyngitis. Produces streptolysin O. ARF does not occur but PSGN can be seen