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Pyogenic Gam Positive Cocci Flashcards

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1
Q

three genera of pathogenesis in pyogenic Gram-Positive Cocci

A

Staphylococcus, Streptococcus and Enterococcus

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2
Q

4 infections associated with Pyogenic Gram Positive Cocci (GPC)

A

1) Skin and soft tissue infections, 2) Toxic Shock Syndrome (TSS), 3) Bone and joint infections and 4) Endocarditis

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3
Q

What is the genera of Gram Positive Cocci (GPC) that cluster and are catalase positive?

A

Staphylococcus

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4
Q

What is the Gram Positive Cocci Genera that is in chains and is catalase negative?

A

Streptococcus and Enterococcus

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5
Q

The most virulent Staphylococcus

A

Staphylococcus Aureus (S. aureus)

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6
Q

Only coagulase positive Staphylococcus

A

S. aureus

*Coagulase is a protein enzyme produced by several microorganisms that enables the conversion of fibrinogen to fibrin.

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7
Q

ATTRIBUTES OF STAINING of S. aureus (GPC staphylococcus family)?

A
  • catalase + (has the enzyme catalase which converts H2O2 into water and gas)
  • coagulase + (Coagulase is a protein enzyme produced by several microorganisms that enables the conversion of fibrinogen to fibrin.)
  • colonies yellow
  • usually B-hemolytic
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8
Q

How is S. aureus (GPC staphylococcus family) transmitted? Where do they normally live?

A

transmitted: person to person, direct or indirect (via fomite)
normally: common superficial flora on skin/mucosa– especially in the nose (25%), hand (25%), skin (10-20%), vagina (5%)

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9
Q

path of the invasion and spread of S. aureus (GPC Staphylococcus family)

A

Superficial colonization that gets in via epithelial damage. The colony invades which leads to tissue damage. Sometimes, s aureus is further spread in the blood and lymph

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10
Q

what does it mean to be coagulase positive?

A

Coagulase is a protein enzyme produced by several microorganisms that enables the conversion of fibrinogen to fibrin, and therefore increases clotting

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11
Q

What does it mean to be catalase positive

A

catalase is an enzyme that degrades H2O2 into water and O2 gas

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12
Q

How does S. aureus escape the host?

A

Protein A– a surface protein that binds the Fc domain of IgG blocks the host antibody from opsonizing bacterium

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13
Q

Damage to the hosts from s aureus is caused by

A
  1. the bacteria entering sterile sites

2. toxin production (eg food poisoning)

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14
Q

3 virulence factors present in most S aureus what they do

A
  1. Cytolytic toxins (hemosysins, leukocidins)– attack membranes of host cells damaging tissue, (particularly alpha toxin) and killing WBCs
  2. enzymes that degrade host tissue (fibrinolysin, lipases, DNAase, hyaluronidase– cleave/destroy host structures, damaging host tissue and promoting invasion of bacteria
  3. coagulase (cell bound and free forms)– converts fibrinogen to fibrin forming clots. Might have a role in abcess formation or protection from immune system
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15
Q

alpha, beta, delta, gamma toxins and Panton-Valentine leukocidin

A

exotoxins common to almost all S. aureus

cause tissue destruction and immune evasion by attacking cell membranes/killing WBCs

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16
Q

The three virulence factors associated with specific manifestations of S. aureus

A
  1. Enterotoxins
  2. Exfoliative Toxins 1 and 2
  3. Toxic-shock-syndrome-toxin- 1 (TSST-1)
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17
Q

Enterotoxins:

  • come from:
  • result in:
  • virulence category:
  • Mechanism:
A

Enterotoxins:

  • come from: S. aureus
  • result in: food poisoning
  • virulence category: superantigens
  • Mechanism: superantigen– but not well understood
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18
Q

Exfliative toxins 1 & 2

  • come from:
  • result in:
  • virulence category:
  • Mechanism:
A
  • come from: S. aureus
  • result in: SSSS, bullous impetigo
  • virulence category: tissue destruction
  • Mechanism: enzymatically degrade desmoglein-1, a protein which mediates adhesion between keratinocytes of the superficial dermis
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19
Q

Toxic Shock Syndrome Toxin 1-come from:

  • result in:
  • virulence category:
  • Mechanism:
A
  • come from: S. aureus
  • result in: Toxic shock
  • virulence category: Superantigen
  • Mechanism: binds to conserved region of TCR (V-beta), leading to over stimulationof T-cells and cytokine production
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20
Q

how does S aureus cause food poisoning?

A

S. aureus grows in improperly stored food (room temp) and secretes an enterotoxin which are eaten. 1-6 hours later, the person has nausea, vomiting and diarrhea.

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21
Q

why aren’t Abx helpful for food poisoning from S aureus

A

because it’s caused by intoxication– a person ingests the toxin, not the bacteria

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22
Q

intoxication

A

the ingestion of a toxin made by a bacteria, but not the bacteria itself

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23
Q

Osteomyelitis– what is it? What are most cases caused by?

A

bacterial infection of the bone– over 50% caused by S aureus

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24
Q

Septic Arthritis- what is it, and what is it usually caused by?

A

bacterial infection of a joint. Neisseria gonorrhoeae and S aureus are the most common causes

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25
Q

Endocarditis– what is it and what causes it?

A
  • infection of any part of the endocardium, but usually means a part of the heart valves
    S. aureus causes about 1/3 of the cases
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26
Q

6 diseases associated with S. Aureus

A
  1. Skin and soft tissue damage
  2. Toxic Shock Syndrome (TSS)
  3. Staphylococcal food poisoning (enterotoxins)
  4. Bone and Joint Infections (osteomyelitis and Septic arthritis)
  5. Endocarditis (particularly valve disease)
  6. pneumonia (rare but destructive lobar pneumonia)
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27
Q

Cell Wall Synthesis Inhibitors (3 types of Abx)

A
  1. penicillin
  2. Methicillin
  3. Vancomycin
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28
Q

Txt for S. Aureus

A

cell wall synthesis inhibitors are first-line agents:

  1. 90% of isolates are resistant to penicillin
  2. txt with Methicillin– but Methicillin resistance is increasingly common
  3. txt with vancomycin (vancomycin resistance is rare but it exists)
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29
Q

MRSA

A

Mithicillin Resistance Staphylococcus Aureus– can generally be treated with Vancomycin

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30
Q

most common Coagulase Negative Staphylococci

A

Staphylococcus epidermidis

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31
Q

S. saprophyticus is identified as…

A
  • coagulase negative staphylococci
  • Gram positive
  • novobiocin resistance
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32
Q

S. saprophyticus is a common cause of…

because it is found…

A

UTI… as a commensal on the skin/mucosa/in the rectum

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33
Q

where are coagulase negative staphylococci like S. epidermidis and S. saprophyticus found?

A

commensals found on the mucosa/skin (and saprophyticus is found in the rectum)

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34
Q

How do coagulase negative staphylococci damage the host?

A

they’re low virulence orgs.

- S. saprophyticus adheres to uroepithelial cells, which allows it to infect the urinary tract

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35
Q

Diseases causes by coagulase negative gram positive staphylococci (ie S saprophyticus and S. epidermidis)

A
  1. infections associated with foreign bodies (IV ctheters, prosthetic health valves, CSF shunts, etc)
  2. skin and soft tissue infections (but less frequently than S aureus)
  3. S. saprophyticus is the second most common cause of UTI (after Escheria coli) in young, sexually active women
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36
Q

which medication should you use for coagulase negative gram positive staphylococci?

A

Try vancomycin– they’re frequently resistant to penicillin and methilicillin.

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37
Q

are streptococci catalase positive or catalase negative?

A

catalase negative

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38
Q

streptococci are gram positive cocci that grow in…

A

chains

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39
Q

beta-hemolytic streptococci

A

cause complete hemolysis (a clear zone in the agar around the streptococcus colony)

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40
Q

Group A streptococci

A

Streptococcus pyogenes

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41
Q

Group B streptococci

A

Streptococci agalactiae

42
Q

alpha-hemolytic streptococci

A

cause incomplete hemolysis (a green zone in the agar around the colony)

43
Q

the most important alpha-hemolytic streptococci

A

streptococcus pneumonia (which is not grouped in the lancefield system)

44
Q

gamma-hemolytic streptococci

A

non-hemolytic streptococci– they don’t lyse RBCs

45
Q

viridians group streptococci

A

all alpha hemolytic streptcocci except strep pneumoniae plus all non-hemolytic (gamma-hemolytic) strep

46
Q

Group D streptococci

A

non-hemolytic (gamma-hemolytic) or alpha-hemolytic streptococci

47
Q

For each species or group, note the lancefield group and the hemolysis:

  1. S. pyogenes
  2. S. agalactiae
  3. S. pneumoniae
  4. Viridians-group streptococci
A
  1. S. pyogenes: Lancefield group A, beta-hemolytic
  2. S. agalactiae: lancefield group B, beta-hemolytic
  3. S. pneumoniae: no lancefield group, alpha-hemolytic
  4. Viridians-group streptococci: lancefield group D, all alpha hemolytics (except S. pneumoniae) and gamma (aka non)-hemolytics
48
Q

two ways S. pyogenes can be identified

A
  1. susceptibility to bacitracin in culture (A disk)

2. serological grouping (Lancefield grp A)

49
Q

How is S. pyogenes spread to people

A

through droplets (it’s a common commensal found in mucosa of upper resp sys and sometimes on skin)

50
Q

How does S. pyogenes escape host defenses (2 way)?

A
  1. surface M protein: reduces phagocytsis by bocking complement activation and binding host fibrinogen. M protein comes in many serotypes so it can escape M protein specific Antibodies
  2. a capsule of hyuluronic acid that resembles “self” to the host: poor host antibody response
51
Q

3 virulence factors of S. pyogenes (all exotoxins)

A
  1. Streptolysin O (oxygen labile) and Streptolysin S (oxygen stable): attack membranes of host cells, damagin tissue and killing leukocytes
  2. Enzymes that degrade host tissue (streptokinase, DNAase, hyaluronidase): destroy host tissue and promote bacterial invasion
  3. Streptococcal pyogenic exotoxins: superantigens that bind to conserved portions of T cell receptor to over stimulate T-cells and cytokine production
52
Q

What do the virulence factors Streptolysin O (oxygen labile) and Streptolysin S (oxygen stable) do in S pyogenes?

A
  1. Streptolysin O (oxygen labile) and Streptolysin S (oxygen stable): attack membranes of host cells, damagin tissue and killing leukocytes
53
Q

What do virulence factors such as streptokinase, DNAase, hyaluronidase do in S pyogenes?

A

these are all Enzymes that destroy host tissue and promote bacterial invasion

54
Q

what do Streptococcal pyogenic exotoxins do during S. pyogenes infection?

A

Streptococcal pyogenic exotoxins: superantigens that bind to conserved portions of T cell receptor to over stimulate T-cells and cytokine production

55
Q

what is the most common bacterial cause of pharyngitis (>95% of cases)

A

S. pyogenes

56
Q

symptoms of Streptococcal pharyngitis and population most frequently affected

A

symptoms: sore throat, fever, malaise and exudate (pus) on tonsils
most frequently affected population: school age children

57
Q

what antibodies are used to diagnose recent S. pyogenes infection?

A

antistreptolysin-O (ASLO) antibodies, which bind to the exotoxin streptolysin O (an oxygen labile streptolysin that attacks membranes of host cells, damaging tissues and killing leukocytes)

58
Q

what are the sequelae (pathological consequences) of streptococcal pyogenes (6)?

A
  1. suppurative (pus forming) sequelae
  2. scarlet fever
  3. acute rheumatic fever/rheumatic heart disease
  4. Poststreptococcal acute glomerulonephritis (PAG)
  5. skin and soft tissue infections (ie impetigo, cellulitis, erysipelas, necrotizing fascia)
  6. Toxic Shock Syndrome (TSS)
59
Q 
suppurative sequelae:
pathogenesis:
manifestation:
time of onset:
preventable with antibiotics:
A

pathogenesis: S. pyogenes spreads from the pharynx to adjacent sites
Manifestations: an abcess (peritonsillar, retropharyngeal)/other local infection (sinusitis/otitis media)
Time of onset: around time of pharyngitis or soon after
Preventable with Abx: yes

60
Q 
scarlet fever--
Pathogenesis:
manifestation:
time of onset:
preventable with Abx?
A

Pathogenesis: pyrogenic exotoxin from S pyogenes (which binds to the constant region of a TCR, overstimulating T-cells and cytokine production)

Manifestation: red, rough (sandpaper texture) rash on the trunk and extremities (not palms or soles), circumoral pallor: The face is flushed except around the mouth, “white” or “red strawberry tongue”

Time of onset:1-2 days post pharyngitis

Preventable with Abx?” prevent rare severe sequelae

61
Q 
Acute rheumatic Fever (ARF)--
Pathogenesis:
manifestation:
Time of onset:
Preventable with Abx:
A

Pathogenesis: unknown, possibly immune mediated
manifestations: migrating polyarthritis (75%), pancarditis (40-50%), chorea- involuntary movements (15%), skin nodules/rash (<10%)
time of onset: 1-5 wks after initial infection
preventable with Abx: yes, prophylaxis to prevent recurrence

62
Q

manifestations of Acute Rheumatic Fever (ARF)

A
  1. migrating polyarthritis
  2. pancarditis (inflammation of the heart, and particularly of the aortic or mitral valves)
  3. involuntary movements called “chorea”
  4. skin nodules or rash (<10%)
63
Q

what is the result of untreated Acute Rheumatic Fever (ARF) brought on by untreated streptococcal pharyngitis

A

rheumatic heart disease– permanent scarring and damage to the affected heart valves. this sometimes causes heart failure (but rarely) and predisposes the patient to infection of the valves (endocarditis)

64
Q

rheumatic heart disease

A

permanent scarring and damage to the aortic or mitral valves caused by untreated streptococcal pharyngitis

65
Q

How can acute rheumatic fever (ARF) be prevented?

A

prompt treatment of initial infection with antibiotics, and since ARF tends to recur, long term antibiotic prophylaxis is given

66
Q

Poststreptococcal acute glomerulonephritis (PAG) is caused by which bacteria? and what is the mechanism of damage

A

caused by: uncommon strains of S. pyogenes (which means it’s generally rare, but it happens in 10-15% of cases of infections with the specific S. pyogenes strain)

Mechanism of pathogenesis: an immune complex (formed by an antibody and the streptococcal antigen) is trapped in the filtering apparatus of the glomeruli, causing inflammation and renal damage

67
Q

physiologic manifestations of Poststreptococcal acute glomerulonephritis (PAG)

A
  1. urine output is love
  2. high levels of protein in urine
  3. edema from fluid retention
  4. mild hypertension from fluid retention
68
Q

Is poststreptococcal acute glomerulonephritis (PAG) damage permanent?

A

no– most people recover and recurrence is rare

69
Q

what does suppurative mean?

A

“suppurative” means pus forming

70
Q 
Poststreptococcal acute glomerulonephritis (PAG)--
pathogenesis:
manifestations:
time of onset:
preventable with Abx?"
A

pathogen: probably immune complex deposition in renal glomeruli
manifestations: reduced urine output, proteinuria, edema and mild hypertension from fluid retention
time of onset: 10 days after pharyngitis, 3 weeks after pyoderma
preventable with Abx: no

71
Q

first line drug for S pyogenes?

A

penicillin– all S. pyogenes are sensitive to penicillin so far

72
Q

Pt with S. pyogenes who are allergic to penicillin should use what for txt?

A

macrolides (erythromycin and azithromycin)

73
Q

Source and spread of Viridans-group streptococci

A

source: commensals found in mouth, intestinal tract and vagina
spread: person to person via contact

74
Q

Viridans-group streptococci evasion of host response and damage to host

A

generally low-virulence organisms which cause disease when they grow in a normally sterile site
some species/strains produce dextram which allows them to adhere to damaged heart valves (frequently caused by rheumatic heart disease) and cause endocarditis

75
Q

Endocarditis is commonly caused by…

A

viridans-group streptococci, particularly in people with heart valve damage (ie those with a H/O rheumatic heart disease)

76
Q

diseases caused by Viridans-group streptococci

A
  1. endocarditis

2. rarely: meningitis and pneumonia

77
Q

Txt of viridan grp streptococci

A
  1. all isolates are sensitive to vancomycin
  2. often resistant to penicillin and cephalosporins but these agens can be used if the organism is demonstrated to be sensitive in vitro
78
Q 
Enterococci:
gram stain:
catalase positive or negative
how do they grow?
cell wall antigen:
A
  • gram positive
  • catalase negative
  • grow in pairs in short chains
  • have the same cell wall antigen as group D streptococci, but are not streptococci
79
Q

how can you tell streptococci from enterococci?

A

enterococci:

  1. grow in the presence of a high salt broth
  2. hydrolize esculin in the presence of high concentration bile
  3. produce pyrrolidonyl arylamidase (PYR test)
  4. is alpha hemolytic
  • note that some streptococci strands do some of these things, but none should do all of these things
80
Q

source and spread of enteroccoci

A

source: commensals of the colon
spread: person-person contact

81
Q

enterococci evasion of host response and damage to host

A

enteroccoci are low-virulence orgs which cause disease when they grow in a normally sterile site
damage is increased bc they’re highly abx resistant

82
Q

Diseases caused by enterococci

A
  1. UTI (esp in people with urinary catheters)
  2. Enterococci faecalis cause 5-15% of endocarditis cases (usually with a previously abnormal heart valve)
  3. mixed infections of the abdomen and pelvis
83
Q

Why is treatment of enterococci so difficult?

A

because they’re resistant to most Abx

84
Q

why are enterococci resistant to Beta-lactam ABx (penicillin and cephalosporins)

A

bc the target of these abx are penicillin binding proteins (PBRs), and the PBRs on enteroccoci have low binding affinity for the Beta-lactam ring on Beta-lactam Abx

85
Q

why are enterococci resistant to vancomycin when most gram-positive organisms are not?

A

because vancomycin resistant enterococci have alternative structures in their cell walls that have a lover affinity for the drug

86
Q

most skin and soft tissue infections caused bystaphylococcus and streptococcus are caused by

A
  1. S. aureus
  2. coagulase negative staphylococci
  3. s. pyogenes
87
Q

Staphylococcal scalded skin syndrome (SSSS or Ritter’s disease)–

  1. manifestation:
  2. cause
  3. who
A
  1. manifestation: the loss of superficial epidermis (desquamation) over most of the body
  2. cause: localized S. aureus infection releases exfoliative toxins that spread through the whole body
  3. who: usually children who lack anti-toxin Ab
88
Q

Bullous impetigo–

  1. manifestation
  2. cause
A
  1. manifestation: local desquamation which leads to large blisters (bullae)
  2. an adjacent S. aureus infection
89
Q

Folliculitis, furuncles and carbungles

  1. manifestations
  2. cause
A

manifestions: all are superficial, pyogenic (pus forming) infections that start in hair follicles.
folliculitis stays in the follicle
furuncles: extend out of the follicle to form a local abcess
carbuncles: complex, interconnected abcesses
cause: S aureus (>90%)

90
Q

impetigo (without bullae)–
manifestation:
cause:

A

manifestation: infection of the epidermis with oozing lesions and honey-colored crust
cause: S aureus and S. pyogenes

91
Q

cellulitis–
manifestation:
cause:

A

manifestation: bacterial infection of the subcutaneous tissue that causes swelling and redness
cause: S. aureus and S. pyogenes

92
Q

erysipelas–
manifestation:
cause:
prompt txt is necessary because:

A

manifestation: infection of the dermis and dermal lymphatics. Very painful red area with a sharply demarcated, raised border, generally on the legs or face
cause: S. pyogenes
prompt txt to: prevent spread of infection/sepsis

93
Q

Necrotizing fascitis is commonly caused by

A

S pyogenes

94
Q

what is necrotizing fascitis

A

infection of the sub-q tissues, including the fascia. It occurs most often in the legs, it is usually proceeded with trauma and begins with fever, painful, red and tender swelling. If untreated, it turns grey-purple skin with bullae within days and then becomes gangrenous

95
Q

two types of necrotizing fascitis

A

type I: multimicrobial with obligate anaerobes mixed with facultative anaerobes (S pyogenous, S. aureus or E coli)
Type II: monomicrobial and caused by S pyogenes (most often) and sometimes S. aureus

96
Q

txt for necrotizing fascitis?

A

Abx and surgical removal of dead tissue

97
Q

Toxic Shock Syndrome (TSS)

A

a systemic illness caused by localized infection with S. aureus or (less often) S. pyogenes that secrete a superantigen toxin (Toxic-shock syndrome toxin-1 (TSST-1))

98
Q

pathogenesis of TSS

A

infection with S. aureus or (less often) S. pyogenes that secrete a superantigen toxin (Toxic-shock syndrome toxin-1 (TSST-1)). This causes the overstimulation of T cells which release cytokines (IL-1, IL-2, TNF-alpha, and IFN-gamma)

99
Q

manifestations of TSS include

A

fever, shock, rash (including palms and soles) and organ failure

100
Q

increased susceptibility to TSS is linked to

A

lack of Ab to TSST-1

Microbiology (11 decks)

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