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Cardio > Staph Micro Lecture 1 > Flashcards

Staph Micro Lecture 1 Flashcards

1
Q

Staphlococcus tend to form (clusters, chains)

A

clusters

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2
Q

Streptococci tend to form (clusters, chains)

A

chains

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3
Q

How to gram - and gram + stain with gram stain

A

gram + = blue

gram - = red

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4
Q

What are the structural differences between gram + and gram -? (cell membrane, walls, what is in the cell wall, perimplasmic space, etc)

A

gram - have 2 cell membranes
gram + have one cell membrane

gram + have a thick peptidoglycan cell wall and gram - have a thin peptidoglycan layer

gram - have a periplasmic space, gram + do not

gram - make lipoploysaccharide
gram + male liooteichoic acid

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5
Q

Why do gram ___ have a greater exposure to our immune system?

A

+
bc when they die, the cell wall fragments get everywhere (since they have bigger cell walls, they have more shit to activate immune cells)

gram + also has LPS which is a potent TLR agonist

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6
Q

Gram + cell wall must be very strong due to _______

A

high turgor pressure

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7
Q

Describe the structure of the peptidoglycan cell wall.

A

NAG and NAM polymers that are cross linked with peptide cross bridges

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8
Q

What is the basis of penicillin?

A

disrupt/inhibit formation of peptide cross bridges

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9
Q

What is the advantage to using phage lysins to kill bacteria

A

they do not have to be growing (i.e biofilms)

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10
Q

What is the MOA of phage lysins?

A

PlyC is a lysin derived from a bacteriophage that degrades the peptide cross bridge by chopping off

  1. the lactyl moitety from NAM and
  2. the L-Ala off of the pentapeptide

*target gram +, and are very specific to the genus they target

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11
Q

What are the 2 basic types of teichoic acids?

A 
lipoteichoic acid (LTA)
wall teichoic acid (WTA)
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12
Q

Describe the structures of LTA and WTA.

Similarities and differences

A
  • Both have long poly-glycerolphosphate (PGP) chains that are very negatively charged (due to PO4)
  • this is neutralized by the addition of D-ala (which has a + charge)
  • LTA possesses a diglucosyldiacylgycerol moiety (2FA) on the end embedded in the cell wall then a couple of hexoses and then the long PGP backbone
  • WTA is a PGP without the diaglycerol (no FA) and are attached to the wall at the ends of peptide crossbridges
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13
Q

If gram + bacteria are unable to add D-ala to LTA, then they are _______

A

much less virulent

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14
Q

What is a common target in teichoic acids for antimicrobials?

A

dec D-ala available to bacteria (no D-ala attached to PGP, the less virulent they are)

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15
Q

pus filled abcesses

A

S. aureus

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16
Q

indwelling medical devices

A

S. epidermis

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17
Q

UTIs

A

S. saprophyticus

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18
Q

What type of respiration do Staphlycocci use?

A

faculative aerobes (grow in O2, prefer low O2)

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19
Q

Where on our body does S. aureus tend to colonize?

A

nasal cavity, axilla, perineum

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20
Q

Where on our body does S. epidermis tend to colonize?

A

skin

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21
Q

Where on our body does S. saprophyticus tend to colonize?

A

GI, perineum

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22
Q

Is staph an extracellular or intracellular pathogen

A

mainly extracellular (i.e they do not invade other cells)

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23
Q

Why is a capsule considered a virulence factor?

A

it can sterically block phagocytosis by neutrophils and macrophages
*blocks access of FcR to complement or deposited Abs

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24
Q

Produces a capsule called “slime”

A

S. epi

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25
Q

Staph species that produces a variety of extracell toxins (as virulence factor)

A

S. aureus

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26
Q

T or F: S. aureus can produce a capsule, but it is minor

A

T

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27
Q

What does it mean for a bacteria to be pyrogenic?

A

pus forming

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28
Q

What test can be used to distinguish staph from strep and enterococci?

A

Catalase test

**ALL staph make catalase

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29
Q

Of the staphlococci, only S. ___ make coagulase.

What does coagulase do?

A

aureus

activates prothrombin in plasma (converted fibrin to fibinogen –> clotting)

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30
Q

What does catalase do? Why would a bacteria want to be able to make catalase?

A

breaks down H2O2 into H2O and O2

**degrades one of the enzymes phagocytes use to kill bacteria

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31
Q

What test can distinguish S. aureus from S. epi?

A

coagulase test

  • S. aureus is coag +
  • S. epi is coag -
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32
Q

T or F: S. aureus can spread to clothing and infect other individuals

A

T

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33
Q

What is a community acquired infection?

A

carriers of disease infecting people they come into contact with
***this is the most common way staph is spread

34
Q

Who suffers from more severe infections: staph carriers or non-carriers

A

non-carriers

probably an adaptive immunity thing

35
Q

Healthcare Acquired infections of staph usually follow _____

A

some sore of invasive procedure in which the skin was “breached”

36
Q

What are the 3 exotoxins S aureus makes?

A

alpha toxin: cytolytic toxin = beta-barrel pore forming

Panton-Valentine Leukocdin (PVL): beta toxin that also forms pores

exfoliatin:

  • epidermolytic exotoxin that causes scalded skin syndrome (SSS)
  • protease that degrades desmoglein-1 (cadherin in desmosomes)
37
Q

PVL gene was transferred to S. aureus from a phage, why is this important?

A

horizontal gene transfer = may virulence factors can be passed around = bacteria become more resistant to abx

38
Q

Cause of enhanced virulence in CA-MRSA

A

PVL

*low prevalence in HA-MRSA and methicillin-sensitive S. aureus

39
Q

seen in kids younger than 5 and is caused by extracellular toxin, _____, produced by S. aureus

A

exofoliatin

Scalded skin syndrome

40
Q

Exfolative toxin A genes are found on _____

Exfolative toxin B genes are found on _____

A

A: on the chromosome
B: on a plasmid

41
Q

In SSS, the skin separates at a relatively superficial layer, between _____ and _____. How can SSS lead to death?

A

stratum granulosum and stratum spinosum

large amts of fluid can be lost –> dehydration

42
Q

SSS reaction in older children is usually less severe and may only cause _____

A

bullous impetigo

43
Q

toxin than separates desmosomes

A

exfolatin

44
Q

2 ways the skin be breached

A
  1. disruption in skin layer (burns, bites, cuts)

2. shit gets in thru ducts and pores of sweat glands

45
Q

What are SAg toxins? How are they bad? Who makes them?

A

made by some S. aureus strains (10%)

they are superantigens that have specificity for both MHC II and TCR and will bind both to cause a polyclonal expansion of up to 20% of T cell population –> cytokine storm = bad

46
Q

What enterotoxins does S. aureus make?

A

SEA, SEB

47
Q

causes food poisoning (most commonly)

A

SEB

48
Q

MOA and effects that enterotoxins have on body

A

very stable proteins (can hand around even after bacteria dies) that act like SAgs –> stimulates a GI reflex transmitted to medullary emetic centers via vagus N

a few hrs after exposure –> vomiting and intestinal cramping

49
Q

Surface bound S. aureus virulence factor

A

adhesins

50
Q

MSCRAMM , what is it?

A

microbial surface components recognizing adhesive matrix molecule
~ to adhesin, general term for things on microbial surface that binds host cell receptors

51
Q

Sortase

A

enzyme that anchors MSCRAMMs to cell wall

52
Q

Describe sortase mechanism of anchoring MSCRAMMS

A
  1. protein to be anchored has signal sequence that gets protein to PM
  2. if protein has LPXTG aa moteif at C term, the sortase will clip between the T and G
  3. sortase then covalently anchors the T of the protein to a G of a peptidoglycan peptide crossbridge
53
Q

aids in the spread of infection within tissues be degrading hyaluronic acid

A

hyaluronidase

54
Q

cell wall components that are potent stimulators of TLRs (on monocytes and machrophages/innate immune system) –> excessive cytokine secretion

A

PAMPs

55
Q

_____ is very important for the development and dispersal of biofilms

A

quorum sensing

56
Q

Describe the regulation of virulence factor expression

A

TIGHTLY REGULATED via QUORUM SENSING:

Big colony –>inc AIPs –> AIPs bind AgrC and activate it –> AgrA is P and activated –> AgrA + SarA activate RNA III promoter –> more AIPs, toxins, adhsins, and polysaccharide matrix made

57
Q

Order these VF in the sequence they would be made

polysaccharide matrix
adheins
cytolysins

A

adhesins –> cytolysins –> polysaccharide matrix

58
Q

Why are biofilms difficult to eradicate?

A

they are less susceptible to abx

  • abc cannot penetrate the extracellular polysaccharide matrix around the colonies
  • bacteria are not growing so cell wall abx dont work
59
Q

What are the phases of biofilm development?

A
  1. adhesion
  2. colonization
  3. microcolony formation
    - quorum sensing at work
    - begin to make polysacchride matrix
  4. maturation
  5. dispersal (–> nidus)

**this happens with catheters and other indwelling devices

60
Q

Folliculitis

A

S. aureus infection of skin (specifically hair follicles which serve as the point of entry)

usually does not leave skin/not systemic

61
Q

another term for boils

A

furuncles

*pus just beneath the epidermis

62
Q

bunches of boils

A

carbuncle

**start to have systemic symptoms!

63
Q

symp assc with carbuncle

A

fever, chills

64
Q

What is infected with external styes?

A

sebaceous glands or sweat glands

65
Q

What is infected with internal styes?

A

Meibomian (or tarsal) glands

66
Q

blistering vesicles that crust over

What S. aureus toxin causes these?

A

bullous impetigo

exfoliatin

67
Q

T or F: pneumonia caused by Strep pneumoniae has a worse prognosis than pneumonia caused by staph aureus

A

F: staph aureus worse than strep bc staph forms necrotizing abscesses!

68
Q

S. aureus pneumonia is freqently secondary to ______

A

influenza infections

69
Q

What are risk factors for pneumonia?

A

CF, alcoholism, and DM

70
Q

Staphylacoccal TSS is caused by _____

A

TSST-1

71
Q

Where is the gene for TSST-1 found?

A

within a pathpgenicity island in S. aureus chromosome

**mobile genetic element

72
Q

Signs and symptoms of Staphylacoccal TSS is caused by TSST-1

A

high fever, vomiting, diarrhea, sore throat, and erythematous skin rash that blanches when pressure is applied, hypotension (<90), multisystem involvement (hepatic, renal, CNS)

73
Q

Does strep or staph TSS have a worse prognosis?

A

strep is worse than staph TSS

74
Q

A pt has symptoms and Hx consistent with TSS, would you expect blood culture to be positive for S. aureus?

A

not necessarily

75
Q

A pt has symptoms and Hx consistent with TSS, would you expect a serology test for TSST-1 to be positive?

A

yes

76
Q

T or F: Staphyloccocal food poisoning is intoxication not infection

A

true (is self-limiting)

77
Q

What lab findings are consistent with Dx of S. aureus infection

A
  • Gram + bacteria in clusters (blue)
  • Beta-hemolysis on BAP (agar clears completely around coloies)
  • golden appearence of colonies due to carotenoid pigment
  • Catalase +/coagulase +
78
Q

infections with ___ became a problem with the rise in use of indwelling devices

A

S. epi

79
Q

What are the 2 major virulence factors of S. epi?

A
  1. colonize forgein bodies

2 form bioflims

80
Q

What are the coag negative staph?

A

S. epi and S. saprophyticus

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