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Streptococcus Flashcards

Gram-positive cocci

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1
Q

Streptococcus
pyogenes (group A streptococcus) causes

A
  • pharyngitis and cellulitis
  • impetigo, necrotizing
    fasciitis, & streptococcal toxic shock syndrome.
  • rheumatic fever & acute glomerulonephritis.
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2
Q

Streptococcus
agalactiae (group B streptococcus) causes

A

neonatal sepsis and meningitis.

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3
Q

Enterococcus faecalis causes

A

hospital-acquired urinary tract infections
and endocarditis.

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4
Q

Viridans group streptococci causes

A

endocarditis

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5
Q

Streptococcus
bovis (S. gallolyticus) causes

A

endocarditis (uncommon)

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6
Q

Important properties

A
  • spherical gram + cocci arranged in chains or pairs
  • catalase negative

Type of hemolysis
1) a-Hemolytic streptococci
2) B-Hemolytic streptococci
3) Nonhemolytic streptococci (γ-hemolysis).

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7
Q

1) a-Hemolytic streptococci

A
  • form green zone around
    their colonies-> incomplete lysis of rbcs.
  • green color formed when hydrogen peroxide produced by bacteria oxidizes hemoglobin
    (red color) to biliverdin (green color)
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8
Q

2) B-Hemolytic streptococci

A
  • form clear zone around
    their colonies-> complete lysis of rbcs
  • production of enzymes (hemolysins) called streptolysin O & S
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9
Q

2 important antigens of β-hemolytic streptococci

A

(1) C carbohydrate
(2) M protein

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10
Q

(1) C carbohydrate

A
  • determines group of β-hemolytic streptococci.
  • located in cell wall
  • specificity determined by amino sugar.
  • Group A β-hemolytic streptococci (S. pyogenes) distinguished from Group B β-hemolytic streptococci (S. agalactiae) because of different C carbohydrate.
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11
Q

(2) M protein

A
  • virulence factor of S. pyogenes.
  • protrudes from outer cell surface, blocks phagocytosis (antiphagocytic).
  • inactivates C3b (component of complement that opsonizes bacteria prior to phagocytosis.
  • Strains of S. pyogenes do not produce M protein-> nonpathogenic.
  • determines type of group A β-hemolytic streptococci.
  • 100 serotypes based on M protein-> multiple
    infections with S. pyogenes can occur.
  • Antibody to M
    protein-> type-specific immunity.
  • Strains of S. pyogenes produce certain M protein
    types are rheumatogenic (rheumatic fever)
  • strains of S. pyogenes produce other M
    protein types are nephritogenic (acute
    glomerulonephritis).
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12
Q

Classification of Streptococci

A
  • B-Hemolytic Streptococci
  • Non–B-Hemolytic Streptococci
  • Peptostreptococci
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13
Q

B-Hemolytic Streptococci

A
  • arranged into Lancefield groups A–U -> antigenic differences in C carbohydrate.
  • Groups C, E, F, G, H, K–U infrequently cause disease.
  • precipitin tests with specific antisera or by
    immunofluorescence.
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14
Q

Group A streptococci (S. pyogenes)

A
  • pharyngitis & skin infections.
  • adhere to pharyngeal epithelium via
    pili composed of lipoteichoic acid and M protein.
  • have a hyaluronic acid antiphagocytic capsule.
  • growth of S. pyogenes inhibited by antibiotic bacitracin (diagnostic criterion)
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15
Q

Group B streptococci (S. agalactiae)

A
  • colonize genital
    tract
  • neonatal meningitis
    & sepsis.
  • bacitracin-resistant
  • hydrolyze (break down) hippurate (diagnostic
    criterion).
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16
Q

Group D streptococci

A

Enterococci (E. faecalis
& E.faecium)

Nonenterococci (S. bovis)

hemolytic reaction of is variable most are α-hemolytic, some
β-hemolytic, & others nonhemolytic.

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17
Q

Enterococci (E. faecalis
& E.faecium)

A

Enterococci
- normal flora of colon
- urinary, biliary, & cardiovascular infections.
- grow in hypertonic (6.5%) saline or in bile & not killed by penicillin G.

  • synergistic combination of penicillin & aminoglycoside
    (gentamicin) required to kill enterococci.
  • vancomycin used, but vancomycin-resistant enterococci (VRE) emerged -> life-threatening nosocomial infections.
  • More strains of E. faecium are vancomycin-resistant than E. faecalis.
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18
Q

Nonenterococci (S. bovis)

A
  • cause similar infections
  • inhibited by 6.5% NaCl & killed by penicillin G
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19
Q

Non–B-Hemolytic Streptococci

A

Some no hemolysis; others
α-hemolysis.

α-hemolytic organisms ->
S. pneumoniae (pneumococci) & viridans group (S. mitis, S. sanguinis,
and S. mutans).

Viridans streptococci part of normal flora of human pharynx & reach bloodstream-> infective endocarditis.

S. mutans synthesizes
polysaccharides (dextrans) found in dental
plaque -> dental caries.

S. intermedius & S. anginosus -> α-hemolytic or nonhemolytic, some isolates β-hemolytic.

  • mouth & colon
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20
Q

Non–B-Hemolytic Streptococci: Pneumococci & viridans
distinguished in laboratory by 2 main criteria:

A

(1) growth of pneumococci inhibited by optochin; growth of viridans not inhibited

(2) colonies of pneumococci dissolve when exposed to bile (bile-soluble); viridans do not dissolve.

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21
Q

Peptostreptococci

A
  • grow under anaerobic or microaerophilic conditions
    & produce variable hemolysis.
  • normal flora of gut, mouth, & female
    genital tract & participate in mixed anaerobic infections (caused by anaerobes & facultatives).
  • most common bacteria
    found in brain, lung, abdominal, and pelvic abscesses

peptostreptococci & viridans, members of oral flora found in brain
abscesses after dental surgery

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22
Q

Transmission

A
  • produce disease when
    gain access to tissues or blood.
  • Viridans & S. pneumoniae found in oropharynx
  • S. pyogenes found on skin & oropharynx
  • S. agalactiae in vagina & colon
  • Enterococci & anaerobic
    in colon.
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23
Q

Group A streptococci (S. pyogenes) cause disease by three
mechanisms

A

(1) pyogenic inflammation
- induced locally at site

(2) exotoxin production
- cause widespread systemic symptoms
in areas of body where no organisms

(3) immunologic
- antibody against
component of organism cross-reacts with normal tissue or forms immune complexes that damage normal tissue.
- cause inflammation; no organisms in lesions.

24
Q

S.pyogenes hyaluronic acid capsule

A
  • antiphagocytic.
  • Antibodies not formed
    against capsule as hyaluronic acid is normal
    component of body & humans are tolerant to it.
25
Q

Group A streptococci produce 3 inflammation-related enzymes:

A

(1) Hyaluronidase (spreading factor)
- degrades hyaluronic acid (ground substance of subcutaneous tissue).
- facilitates spread of S. pyogenes in skin infections (cellulitis).

(2) Streptokinase (fibrinolysin) activates plasminogen to form plasmin dissolves fibrin in clots, thrombi,
and emboli.
- used to lyse thrombi in coronary arteries of heart attack patients.

(3) DNase (streptodornase) degrades DNA in exudates
or necrotic tissue.
- Antibody to DNase B develops during
pyoderma (diagnostic criteria).

26
Q

Group A streptococci produce 5 toxins & hemolysins:

A

(1) Erythrogenic toxin
(2) Streptolysin O
(3) Streptolysin S
(4) Pyrogenic exotoxin A
(5) Exotoxin B

27
Q

(1) Erythrogenic toxin

A
  • rash of scarlet fever.
  • mechanism of action similar to TSST of S. aureus (superantigen)
  • produced by strains of S. pyogenes lysogenized by bacteriophage carrying gene for toxin.
  • injection of skin test dose of erythrogenic toxin (Dick test) gives a positive result -> lacking antitoxin (susceptible persons).
28
Q

(2) Streptolysin O

A
  • hemolysin inactivated by
    oxidation (oxygen-labile).
  • causes β-hemolysis when colonies grow under the surface of a blood agar plate.
  • antigenic & antibody (ASO) develops after infections.
  • titer of ASO used in rheumatic fever diagnosis.
29
Q

(3) Streptolysin S

A
  • hemolysin not inactivated
    by oxygen (oxygen-stable). - not antigenic; responsible
    for β-hemolysis when colonies grow on surface of a blood agar plate.
30
Q

(4) Pyrogenic exotoxin A

A
  • toxin responsible for
    streptococcal toxic shock syndrome.
  • same mode of action as staphylococcal TSST (superantigen causes release of large amounts
    of cytokines from helper T cells and macrophages)
30
Q

(5) Exotoxin B

A
  • protease rapidly destroys tissue & produced in large amounts by strains of
    S. pyogenes “flesh-eating” -> necrotizing fasciitis.
31
Q

Pathogenesis by group B streptococci (S. agalactiae)

A
  • ability of organism to induce inflammatory
    response.
  • antiphagocytic polysaccharide capsule & anticapsular antibody is protective.
32
Q

Pathogenesis by S. pneumoniae & viridans streptococci

A
  • uncertain-> no exotoxins or tissue-destructive
    enzymes demonstrated.
  • S. pneumoniae virulence factor-> antiphagocytic polysaccharide
    capsule.
  • Strains of viridans streptococci cause endocarditis produce glycocalyx enables
    organism to adhere to heart valve
33
Q

Streptococcus pyogenes (Group A) causes 3 types of diseases:

A

(1) pyogenic diseases (pharyngitis & cellulitis)

(2) toxigenic diseases (scarlet fever & toxic shock
syndrome)

(3) immunologic diseases (rheumatic
fever & acute glomerulonephritis (AGN)).

34
Q

(1) pyogenic diseases (pharyngitis & cellulitis)

A

S. pyogenes -> pharyngitis (sore throat).

S.pharyngitis (strep throat) ->throat pain & fever. inflamed throat
& tonsils, with yellowish exudate, & tender cervical lymph nodes.
- untreated-> spontaneous recovery in 10 days, but rheumatic fever may occur

Untreated pharyngitis may extend to middle ear (otitis media), sinuses (sinusitis), mastoids (mastoiditis), or meninges (meningitis).

Continuing inability to swallow indicate a peritonsillar or retropharyngeal abscess.

Impetigo (pyoderma)->
superficial skin infection-> “honeycolored” crusted lesions.

Forearm Lymphangitis associated with hand infection.

35
Q

(2) toxigenic diseases (scarlet fever & toxic shock
syndrome)

A

Infecting streptococci produce erythrogenic toxin
& host lacks antitoxin-> scarlet fever
- strawberry tongue lesion

S.pyogenes -> TSS
- recognizable site of pyogenic inflammation & positive blood cultures
- staphylococcal TSS
no pyogenic inflammation & negative blood cultures.

36
Q

(3) immunologic diseases (rheumatic
fever & acute glomerulonephritis (AGN)).

A

Endometritis (puerperal
fever), pregnant women sepsis.

Immune-mediated poststreptococcal AGN following skin infections caused by certain
M protein types of S. pyogenes.

37
Q

Group B streptococci clinical findings

A
  • neonatal sepsis & meningitis.
  • prolonged (>18 hours) membrane rupture in women colonized by organism.
  • Children born prior to
    37 weeks’ gestation have increased risk & whose mothers lack antibody & born without transplacentally
    acquired IgG have higher rate of neonatal sepsis.
  • neonatal pneumonia
  • pneumonia, endocarditis, arthritis, cellulitis, & osteomyelitis in adults.
  • Postpartum endometritis

Diabetes-> predisposing factor for adult group B
streptococcal infections.

38
Q

Viridans streptococci clinical findings
(S. mutans, S. sanguinis, S.
salivarius, & S. mitis)

A
  • infective endocarditis.
  • enter bloodstream (bacteremia) from oropharynx after dental surgery.
  • Signs of endocarditis: fever, heart murmur, anemia, & embolic events (splinter hemorrhages, subconjunctival
    petechial hemorrhages, & Janeway lesions).
  • heart murmur -> vegetations on heart valve ->100% fatal unless treated with antimicrobial agents.
  • 10% caused by enterococci; any organism causing bacteremia settle on deformed valves.
  • 3 blood cultures necessary to recover organism

S. anginosus, S. milleri,
& S. intermedius-> brain abscesses with mouth anaerobes
- Dental surgery -> predisposing factor to brain abscess -> provides portal for viridans & mouth anaerobes to enter bloodstream (bacteremia) & spread to brain.

  • involved in mixed aerobic–anaerobic infections (lung abscesses, abdominal abscesses,
    liver abscesses).
39
Q

Enterococci clinical findings

A
  • urinary tract infections
    in hospitalized patients.
  • Indwelling urinary catheters & urinary tract instrumentation -> predisposing
    factors.
  • endocarditis-> gastrointestinal or urinary
    tract surgery or instrumentation.
  • intraabdominal
    & pelvic infections
    with anaerobes.
40
Q

Streptococuss bovis (nonenterococcal
group D streptococcus) clinical findings

A
  • endocarditis in
    patients with carcinoma of colon.
  • patients with S. bovis, bacteremia, or endocarditis should be investigated for presence of colonic carcinoma.
41
Q

Poststreptococcal (Nonsuppurative)
Diseases

A
  • local infection of group A followed weeks later (length of time it takes to produce sufficient antibodies) by inflammation in organ not infected by streptococci-> immunologic (antibody) response to streptococcal M proteins that cross-react with human tissues.
  • nephritogenic strains of S. pyogenes -> AGN
  • rheumatogenic strains of S. pyogenes -> acute rheumatic fever.
42
Q

Acute Glomerulonephritis (AGN)

A
  • 2 to 3 weeks after skin infection by group A in children (M protein type49)
  • hypertension, face edema (periorbital edema), ankles edema, smoky urine (rbcs).
  • recover completely
  • Reinfection rare -> recurrence of glomerulonephritis.
  • initiated by antigen–antibody complexes
    on glomerular basement membrane.
  • Complement activated & C5a attracts neutrophils secrete enzymes damage glomerular capillaries endothelium.
  • prevented-> early eradication of nephritogenic streptococci from skin colonization sites - not by administration
    of penicillin after onset of symptoms.
43
Q

Acute Rheumatic Fever

A
  • 2 weeks after pharyngitis infection
  • children age 5 to 15 years
  • fever, migratory polyarthritis, & carditis (damages myocardial & endocardial tissue in mitral & aortic valves-> vegetations on valves).
  • Uncontrollable, spasmodic movements
    of limbs or face (chorea)

ASO titers & erythrocyte sedimentation rate elevated.

  • group A streptococcal skin infections do not
    cause rheumatic fever.
  • immunologic crossreaction
    between antibodies formed against M proteins of S. pyogenes & proteins on surface of joint, heart and brain tissue.
  • autoimmune disease-> recurrence of infections.
  • If streptococcal
    infections treated within 8 days of onset, rheumatic
    fever prevented.
  • After heart-damaging attack of rheumatic fever, reinfection prevented by longterm prophylaxis.
44
Q

Laboratory Diagnosis:
Microbiologic
Group A

A

Gram-stained smears-> useless; viridans are normal flora & cant distinguish from pathogenic S. pyogenes.

  • stained smears from skin
    lesions or wounds reveal streptococci are diagnostic.
  • Cultures from pharynx or lesion -> small, translucent β-hemolytic colonies in 18 to 48 hours.
  • inhibited by bacitracin disk-> likely to be group A streptococci.
45
Q

Laboratory Diagnosis:
Microbiologic
Group B

A
  • hydrolyze hippurate & produce protein -> enhanced hemolysis on sheep blood agar when
    combined with β-hemolysin of S. aureus (CAMP test).
46
Q

Laboratory Diagnosis:
Microbiologic
Group D

A
  • hydrolyze esculin in presence of bile (produce black pigment on bile-esculin agar).
  • Enterococci -> grow in hypertonic (6.5%) NaCl
  • Nonenterococci don’t.
47
Q

Laboratory Diagnosis:
Microbiologic
Rapid Test

A
  • culturing results not available for 18 hours-> beneficial to know while patient in office if antibiotics prescribed.
  • rapid tests -> diagnosis in
    10 minutes-> detects bacterial antigens in a throat swab specimen extracted with enzymes & reacted with antibody to these antigens bound to latex particles.
  • Aggultination of coloured latex particles occurs-> group A
  • Test specificity is high;
    sensitivity is low (false-negative results occur).
  • Result is negative but clinical suspicion of streptococcal
    pharyngitis is high, culture done.
  • available for group B
    in vaginal & rectal samples. - detects organism DNA, results -> 1 hour.
48
Q

Laboratory Diagnosis:
Microbiologic
Viridans

A
  • form α-hemolytic colonies
    on blood agar & must be distinguished from S. pneumoniae(pneumococci)-> also α-hemolytic.
  • resistant to lysis by bile, grow optochin presence; pneumococci wont.
  • biochemical tests used to classify species of viridans.
49
Q

Laboratory Diagnosis:
Microbiologic
Serologic

A
  • ASO titers high after group A infections.
  • suspected rheumatic
    fever-> elevated ASO titer -> evidence of previous infection -> throat culture negative with rheumatic
    fever.
  • anti-DNase B titers high in group A skin infections -> previous infection in suspected AGN.
50
Q

Treatment Group A

A
  • penicillin G or amoxicillin, - rheumatic fever nor
    AGN patients benefit from penicillin treatment after the onset of the two diseases.
  • mild ->oral penicillin V
  • penicillin allergic->
    erythromycin or azithromycin or Clindamycin
  • erythromycin-resistant strains of S. pyogenes-> limit effectiveness.

S. pyogenes-> not resistant to penicillins.

51
Q

Treatment Group B

A
  • penicillin G or ampicillin
  • higher doses of penicillin G or combination of
    penicillin G & aminoglycoside
52
Q

Treatment Viridans

A
  • Endocarditis -> prolonged penicillin treatment.
53
Q

Treatment Group D

A
  • enterococcal endocarditis penicillin or vancomycin combined with aminoglycoside.

Enterococci resistant -> penicillins, vancomycin,
aminoglycosides
VREs -> nosocomial infections; no reliable antibiotic therapy
- linezolid (Zyvox) & daptomycin (Cubicin) used for VREs.

Nonenterococcal (S. bovis)
- not highly resistant
- penicillin G

54
Q

Treatment Peptostreptococci

A
  • penicillin G.
55
Q

Prevention

A
  • Rheumatic fever -> group A treatment with penicillin G or oral penicillin V.
  • prevent recurrence of the disease.
  • no evidence patients who had AGN require penicillin prophylaxis.
  • damaged heart valves & undergo invasive dental procedures-> viridans endocarditis prevented using amoxicillin perioperatively.
  • amoxicillin prophylaxis only high risk endocarditis consequences (prosthetic heart valves or previous infective endocarditis) & high-risk dental procedures (manipulation
    of gingival tissue).

not recommended-> gastrointestinal or genitourinary tract
procedures receive prophylaxis.

Oral ampicillin -> group B vaginal carriers not eradicate organism.
- Rapid tests for antigens in
vaginal specimens -> insensitive
- neonates born of
antigen-negative women have neonatal sepsis.

  • group B infections declined -> prophylactic measures
  • E. coli neonatal infections -> increased.

no vaccines available against any streptococci
except S. pneumoniae.

56
Q

Incidence of group B neonatal sepsis reduced by a two-pronged approach:

A

(1) All pregnant women 35 to 37 weeks’ gestation screened -> vaginal & rectal cultures.
- cultures positive, penicillin G (or ampicillin)
administered intravenously at delivery time.

(2) patient not done cultures, penicillin G (or
ampicillin) administered intravenously at delivery time to women who experience prolonged (>18 hours) rupture of membranes, labor
begins before 37 weeks’ gestation, fever at time of labor.

Allergic to penicillin-> cefazolin or vancomycin.

Medical Microbiology (29 decks)

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