ICL 2.9: Staphylococci Flashcards

(67 cards)

1
Q

what’s the microbiology of staphylococci?

A

gram (+) coccus

nonmotile

non-spore forming

grape-like clusters

clinical specimens can be clusters, single, paired, or chained cocci

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

are staphylococci catalase positive or negative?

A

catalase positive

H2O2 –> H2O + O2

this is what differentiated staph from strep!! strep is catalase negative

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

are staphylococci anaerobes or aerobic?

A

facultative anaerobes

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

how strong/resistant are staphylococci?

A

hardy bacteria; not fastidious

can withstand heat, drying, high salt concentrations

this is due to their capsule

antibiotic resistance is a worsening problem….

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

what are the two general groups of staphylococci?

A
  1. coagulose-positive staphylococci

2. coagulase-negative staphylococci

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

what are coagulase postitive staphylococci?

A

coagulase does fibrinogen –> fibrin

so it allows bacterial aggregation/clumping or clot formation

β-hemolytic

ex. S. aureus

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

what are coagulase negative staphylococci?

A

part of the normal skin flora!

most have low virulence and are non-hemolytic

but slime layers allow for adherence to catheters, prosthetic valves and joints

ex. S. epidermidis, S. haemolyticus, S. hominis,
S. lugdunensis

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

which staph bacteria is coagulase positive?

A

s. aureus

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

which staph bacteria are coagulase negative?

A

S. epidermidis,

S. haemolyticus,

S. hominis,

S. lugdunensis

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

what color is staphylococcus aureus in cultures? why?

A

gold! aureus duh

comes from production of carotenoids

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

what type of hemolysis do stephylococcus aureus do?

A

B-hemolytic

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

what are the important cell wall components of staphylococcus aureus?

A
  1. polysaccharide capsule
  2. peptidoglycan
  3. teichoic acids
  4. protein A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what are the characteristics of the capsule of s. aureus?

A

polysaccharide capsule

11 capsule serotypes

inhibits phagocytosis by PMNs

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

what are the characteristics of the PG of s. aureus?

A

thick because gram (+) bactiera

immunostimulatory

methicillin resistance and penicillin resistance due to PBP2’ which blocks penicillin binding

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

what are the characteristics of the teichoic acids of s. aureus?

A

parts of the cell wall

bound to PG NAM or cytoplasmic membrane (lipoteichoic acids)

binds fibronectin for adhesion

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

what are the characteristics of the protein A of s. aureus?

A

binds Fc portion of IgG1, IgG2, IgG4

inhibits Ab-mediated clearance

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

what is the structure of the PG of s. aureus?

A

alternating NAG-NAM backbone = very stable

side chains (tetrapeptide) are linked to NAM and crosslinked by a pentaglycine bridge = staph specific*

PG is a target for B-lactam and glycopeptide antibiotics

PG is immunostimulatory!!!**

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

how is PG of s. aureus immunostimulatory?

A
  1. IL-1 production from monocytes
  2. attracts PMNs
  3. activates complement
  4. has some endotoxin-like activity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what are the important virulence enzymes of s. aureus?

A
  1. coagulase

2. catalase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what is the function of coagulase in s. aureus?

A

s. aureus is coagulase (+) and it’s a virulence enzyme for it

it stimulates the reaction fibrinogen –> fibrin which allows for clumping/aggregation of bacteria

activation of the clotting cascade occurs with sepsis

fibrin bound to S. aureus inhibits phagocytosis!!

there is either bacterial-associated (bound coagulase) or extracellular (free coagulase)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what is the function of catalase in s. aureus?

A

it’s a virulence enzyme

it catalyzes the reaction H2O2 –> H2O + O2

this is important because PMNs release H2O2 to kill pathogens but then catalase just breaks it down

**catalase production is also used to differentiate Staph (+) from Strep (-)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

how can you differentiate staph from strep?

A

staph is catalase positive

strep is catalase -

so staph will form bubbles with the catalase test!

H2O2 –> H2O + O2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what are the s. aureus toxins?

A
  1. 5 cytolytic toxins
  2. 2 exfoliative toxins
  3. 8 enterotoxins
  4. toxic shock syndrome toxin-1
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

which s. aureus toxins are superantigens?

A

exfoliative toxin A

all 8 enterotoxins

toxic shock syndrome toxin-1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
what are superantigens?
they bind MHC II on macrophage to *force* interaction with T cell TCR macrophages release IL-1β (fever) + TNFα (hypotension, shock) T cells release IL-2, IFNγ, TNFβ (hypotension, shock)
26
what do the different cytolytic toxins of s. aureus do?
α toxin = forms pores that allow loss of osmoregulation β toxin = cleaves lipids in membranes of RBC, fibroblasts, leukocytes, macrophages 𝛿 toxin = has detergent-like qualities that disrupt membranes of many cells γ and PV toxin = forms pores in leukocytes
27
what does exfoliative toxin A do?
it's an s. aureus toxin that's a superantigen* causes staphylococcal scaled skin syndrome (SSSS) = exfoliative dermatitis (literally pealing baby skin) exfoliative toxins are proteases that cleave desmoglein 1, which disrupts cell-to-cell adhesion in epidermis Ab can neutralize toxin! less than 5-10% of strains contain these toxins
28
what do enterotoxins A-I do?
A = food poisoning, usually ham* all are superantigens!! also all are heat stable and acid-resistant 30-50% of S. aureus strains carry enterotoxins
29
what does TSST-1 do?
TSST-1 = toxic shock syndrome toxin-1 = toxin of s. aureus it's a superantigen --> stimulates cytokines leading to hypovolemia and shock damages many cells, including endothelial cells, leading to vascular leakage
30
how is s. aureus spread?
1. person-to-person 2. fomites 30% chronically colonized, 50% intermittently colonized, 20% never colonized s. aureus can survive on dry surfaces because of PG and capsule
31
what populations are more likely to be colonized with s. aureus?
1. vaginal carriage of S. aureus occurs in 10% of women 2. hospital personnel have high rates of colonization (50% - 90%) 3. wounds or foreign body penetration (catheters, prosthetic valve/joints)
32
what is CA MRSA?
CA MRSA strain(s) carry the Panton-Valentine leukocidin (PVL) toxins* association of PVL toxin in CA-MRSA with skin and soft tissue infections and severe necrotizing pneumonia with sepsis
33
what are the risk factors for CA-MRSA?
1. skin trauma 2. high BMI 3. cosmetic body shaving 4. prison residence 5. physical contact with a person who has a draining lesion or is a carrier of MRSA 6. sharing equipment that is not cleaned or laundered between users 7. tattoo recipient 8. military
34
what does the clinical disease of s. aureus depend on?
1. adherence 2. immune evasion 3. penetration into tissue 4. inoculum size 5. host immune status
35
how does s. aureus adherence work?
s. aureus can adhere to: 1. mucosal cells/nasal epithelial cells teichoic acids on bacterial cell wall bind fibronectin to allow adherence to mucosal cells coagulase allows bacterial clumping/aggregation 2. traumatized or broken skin coagulase degrades fibrinogen --> fibrin (clot) 3. endothelial surfaces teichoic acids bind fibronectin
36
how does s. aureus perform immune evasion?
1. Protein A binds antibodies to limit clearance 2. Polysaccharide capsule inhibits PMN phagocytosis 3. Catalase limits toxic effects of PMN H2O2 4. Cytolytic toxins lyse a variety of immune cells
37
disease by S. aureus is a result of what combination of things?
1. toxin action 2. localized infection (pyogenic disease) 3. systemic infection (disseminated infection; bacteremia)
38
what are the clinical diseases caused by s. aureus?
1. SSSS 2. staph food poisoning 3. toxic shock syndrome 4. cutaneous infections (pyogenic disease) 5. bacteremia/endocarditis 6. pneumonia 7. osteomyelitis 8. septic arthritis
39
what is SSSS?
SSSS = staph scalded skin syndrome primarily in newborns toxins act on the dermis --> staph secretes exfoliative toxins systemically abrupt perioral erythema --> 2 days later whole body --> skin detaches easily --> may form bullae --> usually self-resolving in 7-10 days but may administer anti-Staph antibiotics or local wound care antibodies neutralize toxins
40
what is staph food poisoning?
ingestion of preformed enterotoxin (usually enterotoxin A or B; superantigen); food appears normal common with processed meats, especially ham* there's abrupt onset of nausea/vomiting, abdominal pain, diarrhea 2 - 6 h after ingestion; symptoms may last 24 h usually occurs in community outbreaks but it's self limiting! Abs develop and are cross-protective
41
what is TSS?
TSS = toxic shock syndrome associated with staph strains producing TSST-1 (superantigen) abrupt onset of fever, hypotension, diffuse rash, vomiting, diarrhea, myalgia rash progresses to desquamation of palms and soles** (unique) CNS, GI, liver, blood, musculature, renal systems involved 2 scenarios: 1. non-menstrual = usually 48 hours after a surgical procedure; patient looks septic but wound looks good 2. menstrual = young women age 15-25 using tampons during menses
42
how do you treat TSS?
remove source of the Staph (removes toxin production): abscesses, fluid collections, tampons supportive measures, immunoglobulins, antibiotics
43
what are some of the cutaneous infections you can get from staph?
1. impetigo 2. folliculitis 3. furuncles 4. carbuncles 5. hidradenitis suppurativa 6. cellulitis 7. lymphagitis
44
what is impetigo?
superficial infection of the skin, face, and limbs young children begins as a vesicular lesion (macule; flat and red) --> pustule (pus-filled) --> crusty erosion 80% of impetigo are Staph; 20% Group A Strep
45
what is osteomyelitis?
one of the possible disease outcomes of s. aureus Hematogenous spread to bone or area adjacent to trauma in children, affects long bones (rapid growth and highly vascularized) in adults, affects vertebral column Brodie abscess = foci of Staph
46
how do you diagnose s. aureus infections?
1. Pus contains few bacteria 2. Culture from base of abscess 3. Blood sample should be cultured, not stained 4. rapid test = staphaurex
47
how does staphaurex work?
rapid test; latex agglutination for s. aureus infection S. aureus bound coagulase binds fibrinogen that is bound to latex beads S. aureus Protein A binds Fc region on rabbit IgG that is bound to latex beads Latex beads and S. aureus clump together
48
how do you treat s. aureus infections?
remove foreign bodies or drain pus duration of therapy depends on the type of infection bone, foreign body, endocarditis require at least 4 weeks of antibiotics
49
how would you treat MSSA?
MSSA = methicillin sensitive s. aureus good drug choices are β-lactams = nafcillin, oxacillin, cefazolin
50
how would you treat hospital acquired MRSA?
most frequently due to altered penicillin binding proteins (PBP2a)- mecA gene Vancomycin best choice because it's resistant to more drugs than CA-MRSA
51
how would you treat CA-MRSA?
clindamycin, doxycycline, trim-sulfa (Bactrim), linezolid, vancomycin good initial choices if CA-MRSA suspected rifampin resistance occurs rapidly and combination therapy is useful
52
what causes VRSA?
VRSA = MRSA that is Vancomycin intermediate-sensitive or resistant this is due to thickened PG or vanA gene from Enterococci (modified PG) consider linezolid or Synercid or daptomycin
53
which staph bacteria are coagulase negative?
1. s. epidermidis 2. s. lugdunensis 3. s. saphrophyticus 4. s. hemolyticus
54
how do coagulase negative staphylococci work?
they typically produce polysaccharide slime layer that aids in attachment to surfaces (e.g. catheters, shunts, prosthetic joints)
55
what is the microbiology of s. epidermidis?
coagulase negative catalase positive γ hemolysis = white color on agar
56
what is s. epidermidis?
normal resident bacteria on skin, mucous membranes antibiotic resistance encoded by plasmids; can easily transfer within or between genus/species nearly all infections are hospital acquired usually caused by infection after “hardware” is introduced into body or “line sepsis” specially artificial valves* common cause of artificial valve endocarditis (40% S. epi) requires aggressive treatment with Vancomycin + gent + rifampin and removal of the valve
57
what is s. lugdunensis associated with?
native valve endocarditis
58
what is the microbiology of s. lugdunensis?
β hemolytic on blood agar coagulase negative PYR) positive [rapid test] --> most staph are negative!! requires aggressive treatment with vancomycin + gent + rifampin and removal of valve
59
what is s. saprophyticus associated with?
UTIs infection occurs in healthy young women in an outpatient setting
60
what is the microbiology of s. saprophyticus?
catalase positive coagulase negative γ-hemolytic on blood agar novobiocin resistant
61
what is s. hemolyticus associated with?
opportunistic infections it's a normal resident bacteria on skin, mucous membranes infections similar to S. epidermidis = line infections, endocarditis, septicemia, etc. 2nd most common cause of coag neg Staph infections
62
what is the microbiology of s. hemolyticus?
catalase positive coagulase negative non-hemolytic on blood agar
63
FLASHCARD: microbiology, pathology, epidemiology, clinical, diangnosis and treatment of staphylococcus aureus
MICROBIOLOGY: Gram + cocci; clusters; β-hemolytic; catalase positive; coagulase (clumping factor) positive; carbohydrate capsule inhibits phagocytosis PATHOLOGY: PG immunostimulatory; teichoic acid binds fibronectin (adhesion); Protein A binds antibody; coagulase (clumping factor); catalase; hyaluronidase; fibrinolysin; nuclease; toxins (cytolytic, exfoliative, enterotoxins, TSS1; superantigens) EPIDEMIOLOGY: colonized at birth; fomites; person-to-person; vaginal colonization; wounds CLINICAL: Toxin-mediated (food poisoning, Scalded Skin Syndrome [SSSS], Toxic Shock Syndrome [TSS]); Cutaneous (impetigo, folliculitis, carbuncles, furuncles, sweat glands, wound infections); Bacteremia, endocarditis; Pneumonia; DIAGNOSIS: Culture from abscess, blood, nasopharynx (SSSS), vagina (TSS); rapid disease (food poisoning); Staphaurex; PCR or PFGE TREATMENT: Culture susceptibility; nafcillin, oxacillin, cefazolin; MRSA = vanc; CA-MRSA = clindamycin, doxy, bactrim, linezolid, vanc
64
FLASHCARD: s. epidermidis
Υ-hemolytic resident on skin hospital acquired infection; cath infections; artificial valve endocarditis >80% methicillin-res; >50% resistant to erythromycin, clindamycin, chloramphenicol, tetracyclines; treat with vanc, rifamin, or cipro
65
FLASHCARD: s. lugdunensis
β hemolytic; PYR test positive native valve endocarditis treat with vanc + gent + rifampin
66
FLASHCARD: s. saprophyticus
Υ-hemolytic novobiocin resistant UTIs treat with fluoroquinolones or bactrim (trimethoprim-sulfamethoxazole)
67
FLASHCARD: s. hemolyticus
Υ-hemolytic; resident on skin line infections, septicemia less frequent UTI, wound infections, bone and joint infections