Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

ID Week 3 > ICL 2.9: Staphylococci > Flashcards

ICL 2.9: Staphylococci Flashcards

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
Q

what are superantigens?

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what do the different cytolytic toxins of s. aureus do?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what does exfoliative toxin A do?

A

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
Q

what do enterotoxins A-I do?

A

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
Q

what does TSST-1 do?

A

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
Q

how is s. aureus spread?

A
  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
Q

what populations are more likely to be colonized with s. aureus?

A
  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
Q

what is CA MRSA?

A

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
Q

what are the risk factors for CA-MRSA?

A
  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
Q

what does the clinical disease of s. aureus depend on?

A
  1. adherence
  2. immune evasion
  3. penetration into tissue
  4. inoculum size
  5. host immune status
35
Q

how does s. aureus adherence work?

A

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

  1. traumatized or broken skin

coagulase degrades fibrinogen –> fibrin (clot)

  1. endothelial surfaces

teichoic acids bind fibronectin

36
Q

how does s. aureus perform immune evasion?

A
  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
Q

disease by S. aureus is a result of what combination of things?

A
  1. toxin action
  2. localized infection (pyogenic disease)
  3. systemic infection (disseminated infection; bacteremia)
38
Q

what are the clinical diseases caused by s. aureus?

A
  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
Q

what is SSSS?

A

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
Q

what is staph food poisoning?

A

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
Q

what is TSS?

A

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

  1. menstrual = young women age 15-25 using tampons during menses
42
Q

how do you treat TSS?

A

remove source of the Staph (removes toxin production): abscesses, fluid collections, tampons

supportive measures, immunoglobulins, antibiotics

43
Q

what are some of the cutaneous infections you can get from staph?

A
  1. impetigo
  2. folliculitis
  3. furuncles
  4. carbuncles
  5. hidradenitis suppurativa
  6. cellulitis
  7. lymphagitis
44
Q

what is impetigo?

A

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
Q

what is osteomyelitis?

A

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
Q

how do you diagnose s. aureus infections?

A
  1. Pus contains few bacteria
  2. Culture from base of abscess
  3. Blood sample should be cultured, not stained
  4. rapid test = staphaurex
47
Q

how does staphaurex work?

A

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
Q

how do you treat s. aureus infections?

A

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
Q

how would you treat MSSA?

A

MSSA = methicillin sensitive s. aureus

good drug choices are β-lactams = nafcillin, oxacillin, cefazolin

50
Q

how would you treat hospital acquired MRSA?

A

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
Q

how would you treat CA-MRSA?

A

clindamycin, doxycycline, trim-sulfa (Bactrim), linezolid, vancomycin good initial choices if CA-MRSA suspected

rifampin resistance occurs rapidly and combination therapy is useful

52
Q

what causes VRSA?

A

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
Q

which staph bacteria are coagulase negative?

A
  1. s. epidermidis
  2. s. lugdunensis
  3. s. saphrophyticus
  4. s. hemolyticus
54
Q

how do coagulase negative staphylococci work?

A

they typically produce polysaccharide slime layer that aids in attachment to surfaces (e.g. catheters, shunts, prosthetic joints)

55
Q

what is the microbiology of s. epidermidis?

A

coagulase negative

catalase positive

γ hemolysis = white color on agar

56
Q

what is s. epidermidis?

A

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
Q

what is s. lugdunensis associated with?

A

native valve endocarditis

58
Q

what is the microbiology of s. lugdunensis?

A

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
Q

what is s. saprophyticus associated with?

A

UTIs

infection occurs in healthy young women in an outpatient setting

60
Q

what is the microbiology of s. saprophyticus?

A

catalase positive

coagulase negative

γ-hemolytic on blood agar

novobiocin resistant

61
Q

what is s. hemolyticus associated with?

A

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
Q

what is the microbiology of s. hemolyticus?

A

catalase positive

coagulase negative

non-hemolytic on blood agar

63
Q

FLASHCARD: microbiology, pathology, epidemiology, clinical, diangnosis and treatment of staphylococcus aureus

A

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
Q

FLASHCARD: s. epidermidis

A

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
Q

FLASHCARD: s. lugdunensis

A

β hemolytic;

PYR test positive

native valve endocarditis

treat with vanc + gent + rifampin

66
Q

FLASHCARD: s. saprophyticus

A

Υ-hemolytic

novobiocin resistant

UTIs

treat with fluoroquinolones or bactrim (trimethoprim-sulfamethoxazole)

67
Q

FLASHCARD: s. hemolyticus

A

Υ-hemolytic; resident on skin

line infections, septicemia

less frequent UTI, wound infections, bone and joint infections

ID Week 3 (25 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions