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CV Module > Staph > Flashcards

Staph Flashcards

1
Q

How to Staph tend to grow?

A

Tend to form CLUSTERS!

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2
Q

What are some of the basic features of Gram + bacteria?

A
  1. Stain dark bluish due to cell wall trapping the Gram stain
  2. Have 1 cell membrane
  3. Have a thick peptidoglycan Wall
  4. No periplasmic space
  5. Make lipoteichoic acid
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3
Q

What is the cause for the dark blue stain of Gram + bacteria?

A

The much thicker cell wall.

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4
Q

What is the major component of the Gram + cell wall?

A

Peptidoglycan

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5
Q

Which antibiotic therapy exposes the immune system to more cell wall fragments for processing and building immunity?

A

Cell wall active antibiotics such as penicillin

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6
Q

What are the Gram + counterparts to LPS?

A

Teichoic and Lipoteichoic acids

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7
Q

What is the reason for the strength of the Gram positive cell wall?

A

Turgor pressure. Up to 300 psi.

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8
Q

What is the basic structure of peptidoglycan?

A

NAG linked to NAM crosslinked by peptides

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9
Q

Which of the Peptidoglycan subunits are cross linked in three dimensions by peptide crossbridges which provide strength?

A

NAM molecules

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10
Q

When do Antibiotics like Penicillin fail to work?

A

When bacteria are NOT growing as in Biofilms

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11
Q

What currently developing class of Antiobiotics appear to kill bacteria even when they’re not growing?

A

Phage Lysins

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12
Q

What is the active ingredient in phage Lysins?

A

PlyC

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13
Q

How does PlyC work?

A

PlyC degrades the crossbridge by cleaving between the lactyl moiety of NAM and the L-Ala of the pentapeptide Ala-Glu-Glu-Lys-Ala

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14
Q

What is the limiting factor of Phage lysins?

A

They are very specific i.e one that would work against S.pyogenes wouldn’t affect group B strep

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15
Q

What are the two types of teichoic acids?

A

Lipoteichoic acids and Wall Teichoic acid

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16
Q

What is the structure of LTA and WTA?

A

Both have long polyglycerophosphate chains that are very negatively charged (due to phosphate) the negative charge is neutralized by the addition of D-Ala

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17
Q

What is the consequence of bacteria being unable to add D-Ala?

A

They are much less virulent

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18
Q

What is the association with S. aureus infection?

A

Pus-filled abscess

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19
Q

What is the association with S. epidermidis infection?

A

Indwelling medical devices

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20
Q

What is the association with S. Saprophyticus infection?

A

Urinary tract infections

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21
Q

What are the general characteristics of Staphylococci?

A
  1. Facultative aerobes
  2. Can survive weeks or days on linens
  3. Part of our normal microbiota
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22
Q

Where do S. aureus frequently colonize?

A
  1. Nasal cavity
  2. Axilla
  3. Perineum
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23
Q

Where do S epidermis usually colonize?

A

Always present on the skin

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24
Q

Where do S. saprophyticus usually colonize?

A

GI tract

Perineal area

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25
Q

What type of pathogens are Staph generally?

A

Mainly extra-cellular

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26
Q

What kind of capsule do S. aureus produce?

A

A polysaccharide capsule (usually minor)

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27
Q

What kind of capsule does S. epi produce?

A

A heavy capsule called Slime

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28
Q

What else does S. aureus produce?

A

A variety of extracellular toxic substances

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29
Q

What is meant by pyogenic, suppurative, purulent?

A

Bacteria that cause pus

30
Q

What are capsules considered to be in Staphlococci?

A

A virulence factor

31
Q

Why are capsules considered virulence factors?

A
  1. Can sterically block phagocytosis
  2. Can act as adhesive factor
  3. Can be shed and activate the immune system
32
Q

What compound do ALL staphylococci make?

A

Catalase

33
Q

Of all the staphylococci what do S. aureus make?

A

Coagulase

34
Q

What does coagulase do?

A

Activates prothrombin in plasma which converts fibrinogen to fibrin causing clotting. Called clotting factor.

35
Q

Are S. epi and S. saprophyticus coagulase positive?

A

NO. S. epi and S. saprophyticus are known as CoaggNS

36
Q

What are CA infections?

A

Community Acquired infections (S. aureus) from carries ifected by the strain they carry or infecting other people they come in contact with. sometimes due to poor hygiene

37
Q

What are HA infections?

A

Healthcare acquired S. Aureus infections usually caused by a single strain that passes around the facility. Usually follows some sort of invasive procedure

38
Q

What kind of toxins do S. Aureus make?

A

Exotoxins

39
Q

What is a prime example of S. aureus exotoxin?

A

alpha-toxin which is a cytolytic toxin that creates a large pore in the cell membrane

40
Q

What is (PVL) Panton-Valentine Leukocidin?

A
  • A pore formin Beta toxin
  • The PVL gene is in a virus prophage that incorporated into the S. aureus chromosome
  • PVL contributes to the enhanced virulence of CA-MRSA
41
Q

How is alpha toxin secreted?

A

As subunits which then assemble into multimers in the Eukaryotic cell membrane

42
Q

What class of toxins does Alpha toxin belong to?

A

Pore-forming, beta-barrel toxin family

43
Q

Who does Alpha toxin cause the death of cells?

A

Cells die due to the loss of critical monovalent and Divalent ions through the pores

44
Q

What skin infection usually found in children younger than 5 is caused by S. aureus?

A

Scalded Skin Syndrome

45
Q

What is the cause of the symptoms of SSS?

A

Exfoliatin an epidermolytic exotoxin

46
Q

What is Exfoliatin?

A

A protease that degrades desmoglein-1, a cadherin involved in desmosome formation

47
Q

What does the SSS infection cause in Older children?

A

A limited infection and blisters (bullous impetigo)

48
Q

Where are the toxin genes located for exfoliatin?

A

Toxin genes are on the chromosome (exfoliative toxin A; eta) or on a plasmid (exfoliative toxin B, etb)

49
Q

When are these toxin active?

A

The toxins are not active till they reach the skin

50
Q

Where does the skin separate??

A

At a relatively superficial layer between the stratum granulosum and stratum spinosum

51
Q

How can SSS lead to death?

A

Extensive loss of fluids

52
Q

What are Superantigen exotoxins?

A

These antigen bridge MHC class II molecules and T-Cell receptors resulting in Polyclonal T cell activation and massive cytokine release

53
Q

What percentage of S. aureus make superantigens?

A

10%

54
Q

What are enterotoxins?

A

A subdivision of the exotoxins

55
Q

What are the most common causative agents of food poisoning?

A

Staph enterotoxin B (SEB)

56
Q

What do enterotoxins cause?

A

Emesis and intestinal cramping

57
Q

What is peculiar of enterotoxins?

A
  1. Are extremely stable proteins

2. Bacteria that produced it can be dead and you will still have the symptoms of food poisoning

58
Q

How do enterotoxins work?

A

Stimulates a GI reflex transmitted to medullary emetic centers via the vagus nerve

59
Q

Are enterotoxins superantigen?

A

YES

60
Q

What warfare applications may SEB have?

A

Its stable enough to allow it to be aerosolized

61
Q

How long before the onset of SEB symptoms?

A

2-3 hours

62
Q

Do the enterotoxins get into the blood?

A

No they stay in the GI tract

63
Q

What is the function of Adhesins in Staphlococcus?

A

They are a virulence factor that facilitate adhering of bacteria to cells or tissues

64
Q

What are some of the targets of Adhesins?

A
  1. Fibronectin
  2. Type IV collagen
  3. Laminin
65
Q

What does the term MSCRAMM mean

A

Microbial surface components recognizing adhesive matrix molecules

66
Q

What molecule anchors MSCRAMMs and other surface proteins to the cell wall?

A

Sortase

67
Q

What is the protein sequence common to all proteins achored by sortase?

A

L-P-X-T-G amino acid sequence motif near their C termininal and the sortase clips it between the T and G

68
Q

What does Sortase do?

A

Covalently links the T to G peptidoglycan crossbridges

69
Q

What molecule is considered a virulence “enhancer”?

A

Hyaluronidase

70
Q

What function does hyaluronidase serve to S. aureus?

A

It degrades hyaluronic acid in the connective tissue spaces and thus makes bacterial spreading easier

71
Q

What are PAMPs

A

Pathogen Associated Molecular patterns

72
Q

What are the functions of PAMPs?

A

These cell wall components such as peptidoglycan, lipoteichoic acid and teichoic acid are potent stimulators of TLRs on monocytes and Macrophages causing excessive cytokine secretion

CV Module (24 decks)

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