Pyogenic Gam Positive Cocci

Question 1

three genera of pathogenesis in pyogenic Gram-Positive Cocci

Answer 1

Staphylococcus, Streptococcus and Enterococcus

Question 2

4 infections associated with Pyogenic Gram Positive Cocci (GPC)

Answer 2

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

Question 3

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

Answer 3

Staphylococcus

Question 4

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

Answer 4

Streptococcus and Enterococcus

Question 5

The most virulent Staphylococcus

Answer 5

Staphylococcus Aureus (S. aureus)

Question 6

Only coagulase positive Staphylococcus

Answer 6

S. aureus

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

Question 7

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

Answer 7

• 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

Question 8

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

Answer 8

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%)

Question 9

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

Answer 9

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

Question 10

what does it mean to be coagulase positive?

Answer 10

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

Question 11

What does it mean to be catalase positive

Answer 11

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

Question 12

How does S. aureus escape the host?

Answer 12

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

Question 13

Damage to the hosts from s aureus is caused by

Answer 13

1. the bacteria entering sterile sites

2. toxin production (eg food poisoning)

Question 14

3 virulence factors present in most S aureus what they do

Answer 14

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

Question 15

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

Answer 15

exotoxins common to almost all S. aureus

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

Question 16

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

Answer 16

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

Question 17

Enterotoxins:

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

Answer 17

Enterotoxins:

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

Question 18

Exfliative toxins 1 & 2

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

Answer 18

• 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

Question 19

Toxic Shock Syndrome Toxin 1-come from:

• result in:
• virulence category:
• Mechanism:

Answer 19

• 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

Question 20

how does S aureus cause food poisoning?

Answer 20

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.

Question 21

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

Answer 21

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

Question 22

intoxication

Answer 22

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

Question 23

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

Answer 23

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

Question 24

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

Answer 24

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

Question 25

Endocarditis-- what is it and what causes it?

Answer 25

- 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

Question 26

6 diseases associated with S. Aureus

Answer 26

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)

Question 27

Cell Wall Synthesis Inhibitors (3 types of Abx)

Answer 27

1. penicillin 2. Methicillin 3. Vancomycin

Question 28

Txt for S. Aureus

Answer 28

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)

Question 29

MRSA

Answer 29

Mithicillin Resistance Staphylococcus Aureus-- can generally be treated with Vancomycin

Question 30

most common Coagulase Negative Staphylococci

Answer 30

Staphylococcus epidermidis

Question 31

S. saprophyticus is identified as...

Answer 31

- coagulase negative staphylococci - Gram positive - novobiocin resistance

Question 32

S. saprophyticus is a common cause of... | because it is found...

Answer 32

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

Question 33

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

Answer 33

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

Question 34

How do coagulase negative staphylococci damage the host?

Answer 34

they're low virulence orgs. | - S. saprophyticus adheres to uroepithelial cells, which allows it to infect the urinary tract

Question 35

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

Answer 35

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

Question 36

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

Answer 36

Try vancomycin-- they're frequently resistant to penicillin and methilicillin.

Question 37

are streptococci catalase positive or catalase negative?

Answer 37

catalase negative

Question 38

streptococci are gram positive cocci that grow in...

Answer 38

chains

Question 39

beta-hemolytic streptococci

Answer 39

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

Question 40

Group A streptococci

Answer 40

Streptococcus pyogenes

Question 41

Group B streptococci

Answer 41

Streptococci agalactiae

Question 42

alpha-hemolytic streptococci

Answer 42

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

Question 43

the most important alpha-hemolytic streptococci

Answer 43

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

Question 44

gamma-hemolytic streptococci

Answer 44

non-hemolytic streptococci-- they don't lyse RBCs

Question 45

viridians group streptococci

Answer 45

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

Question 46

Group D streptococci

Answer 46

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

Question 47

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

Answer 47

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

Question 48

two ways S. pyogenes can be identified

Answer 48

1. susceptibility to bacitracin in culture (A disk) | 2. serological grouping (Lancefield grp A)

Question 49

How is S. pyogenes spread to people

Answer 49

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

Question 50

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

Answer 50

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

Question 51

3 virulence factors of S. pyogenes (all exotoxins)

Answer 51

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

Question 52

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

Answer 52

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

Question 53

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

Answer 53

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

Question 54

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

Answer 54

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

Question 55

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

Answer 55

S. pyogenes

Question 56

symptoms of Streptococcal pharyngitis and population most frequently affected

Answer 56

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

Question 57

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

Answer 57

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)

Question 58

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

Answer 58

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)

Question 59

``` suppurative sequelae: pathogenesis: manifestation: time of onset: preventable with antibiotics: ```

Answer 59

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

Question 60

``` scarlet fever-- Pathogenesis: manifestation: time of onset: preventable with Abx? ```

Answer 60

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

Question 61

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

Answer 61

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

Question 62

manifestations of Acute Rheumatic Fever (ARF)

Answer 62

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%)

Question 63

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

Answer 63

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)

Question 64

rheumatic heart disease

Answer 64

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

Question 65

How can acute rheumatic fever (ARF) be prevented?

Answer 65

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

Question 66

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

Answer 66

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

Question 67

physiologic manifestations of Poststreptococcal acute glomerulonephritis (PAG)

Answer 67

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

Question 68

Is poststreptococcal acute glomerulonephritis (PAG) damage permanent?

Answer 68

no-- most people recover and recurrence is rare

Question 69

what does suppurative mean?

Answer 69

"suppurative" means pus forming

Question 70

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

Answer 70

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

Question 71

first line drug for S pyogenes?

Answer 71

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

Question 72

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

Answer 72

macrolides (erythromycin and azithromycin)

Question 73

Source and spread of Viridans-group streptococci

Answer 73

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

Question 74

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

Answer 74

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

Question 75

Endocarditis is commonly caused by...

Answer 75

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

Question 76

diseases caused by Viridans-group streptococci

Answer 76

1. endocarditis | 2. rarely: meningitis and pneumonia

Question 77

Txt of viridan grp streptococci

Answer 77

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

Question 78

``` Enterococci: gram stain: catalase positive or negative how do they grow? cell wall antigen: ```

Answer 78

- gram positive - catalase negative - grow in pairs in short chains - have the same cell wall antigen as group D streptococci, but are not streptococci

Question 79

how can you tell streptococci from enterococci?

Answer 79

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

Question 80

source and spread of enteroccoci

Answer 80

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

Question 81

enterococci evasion of host response and damage to host

Answer 81

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

Question 82

Diseases caused by enterococci

Answer 82

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

Question 83

Why is treatment of enterococci so difficult?

Answer 83

because they're resistant to most Abx

Question 84

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

Answer 84

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

Question 85

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

Answer 85

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

Question 86

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

Answer 86

1. S. aureus 2. coagulase negative staphylococci 3. s. pyogenes

Question 87

Staphylococcal scalded skin syndrome (SSSS or Ritter's disease)-- 1. manifestation: 2. cause 3. who

Answer 87

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

Question 88

Bullous impetigo-- 1. manifestation 2. cause

Answer 88

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

Question 89

Folliculitis, furuncles and carbungles 1. manifestations 2. cause

Answer 89

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%)

Question 90

impetigo (without bullae)-- manifestation: cause:

Answer 90

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

Question 91

cellulitis-- manifestation: cause:

Answer 91

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

Question 92

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

Answer 92

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

Question 93

Necrotizing fascitis is commonly caused by

Answer 93

S pyogenes

Question 94

what is necrotizing fascitis

Answer 94

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

Question 95

two types of necrotizing fascitis

Answer 95

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

Question 96

txt for necrotizing fascitis?

Answer 96

Abx and surgical removal of dead tissue

Question 97

Toxic Shock Syndrome (TSS)

Answer 97

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))

Question 98

pathogenesis of TSS

Answer 98

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)

Question 99

manifestations of TSS include

Answer 99

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

Question 100

increased susceptibility to TSS is linked to

Answer 100

lack of Ab to TSST-1