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Staph Flashcards

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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
What type of pathogens are Staph generally?
Mainly extra-cellular
26
What kind of capsule do S. aureus produce?
A polysaccharide capsule (usually minor)
27
What kind of capsule does S. epi produce?
A heavy capsule called Slime
28
What else does S. aureus produce?
A variety of extracellular toxic substances
29
What is meant by pyogenic, suppurative, purulent?
Bacteria that cause pus
30
What are capsules considered to be in Staphlococci?
A virulence factor
31
Why are capsules considered virulence factors?
1. Can sterically block phagocytosis 2. Can act as adhesive factor 3. Can be shed and activate the immune system
32
What compound do ALL staphylococci make?
Catalase
33
Of all the staphylococci what do S. aureus make?
Coagulase
34
What does coagulase do?
Activates prothrombin in plasma which converts fibrinogen to fibrin causing clotting. Called clotting factor.
35
Are S. epi and S. saprophyticus coagulase positive?
NO. S. epi and S. saprophyticus are known as CoaggNS
36
What are CA infections?
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
What are HA infections?
Healthcare acquired S. Aureus infections usually caused by a single strain that passes around the facility. Usually follows some sort of invasive procedure
38
What kind of toxins do S. Aureus make?
Exotoxins
39
What is a prime example of S. aureus exotoxin?
alpha-toxin which is a cytolytic toxin that creates a large pore in the cell membrane
40
What is (PVL) Panton-Valentine Leukocidin?
- 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
How is alpha toxin secreted?
As subunits which then assemble into multimers in the Eukaryotic cell membrane
42
What class of toxins does Alpha toxin belong to?
Pore-forming, beta-barrel toxin family
43
Who does Alpha toxin cause the death of cells?
Cells die due to the loss of critical monovalent and Divalent ions through the pores
44
What skin infection usually found in children younger than 5 is caused by S. aureus?
Scalded Skin Syndrome
45
What is the cause of the symptoms of SSS?
Exfoliatin an epidermolytic exotoxin
46
What is Exfoliatin?
A protease that degrades desmoglein-1, a cadherin involved in desmosome formation
47
What does the SSS infection cause in Older children?
A limited infection and blisters (bullous impetigo)
48
Where are the toxin genes located for exfoliatin?
Toxin genes are on the chromosome (exfoliative toxin A; eta) or on a plasmid (exfoliative toxin B, etb)
49
When are these toxin active?
The toxins are not active till they reach the skin
50
Where does the skin separate??
At a relatively superficial layer between the stratum granulosum and stratum spinosum
51
How can SSS lead to death?
Extensive loss of fluids
52
What are Superantigen exotoxins?
These antigen bridge MHC class II molecules and T-Cell receptors resulting in Polyclonal T cell activation and massive cytokine release
53
What percentage of S. aureus make superantigens?
10%
54
What are enterotoxins?
A subdivision of the exotoxins
55
What are the most common causative agents of food poisoning?
Staph enterotoxin B (SEB)
56
What do enterotoxins cause?
Emesis and intestinal cramping
57
What is peculiar of enterotoxins?
1. Are extremely stable proteins | 2. Bacteria that produced it can be dead and you will still have the symptoms of food poisoning
58
How do enterotoxins work?
Stimulates a GI reflex transmitted to medullary emetic centers via the vagus nerve
59
Are enterotoxins superantigen?
YES
60
What warfare applications may SEB have?
Its stable enough to allow it to be aerosolized
61
How long before the onset of SEB symptoms?
2-3 hours
62
Do the enterotoxins get into the blood?
No they stay in the GI tract
63
What is the function of Adhesins in Staphlococcus?
They are a virulence factor that facilitate adhering of bacteria to cells or tissues
64
What are some of the targets of Adhesins?
1. Fibronectin 2. Type IV collagen 3. Laminin
65
What does the term MSCRAMM mean
Microbial surface components recognizing adhesive matrix molecules
66
What molecule anchors MSCRAMMs and other surface proteins to the cell wall?
Sortase
67
What is the protein sequence common to all proteins achored by sortase?
L-P-X-T-G amino acid sequence motif near their C termininal and the sortase clips it between the T and G
68
What does Sortase do?
Covalently links the T to G peptidoglycan crossbridges
69
What molecule is considered a virulence "enhancer"?
Hyaluronidase
70
What function does hyaluronidase serve to S. aureus?
It degrades hyaluronic acid in the connective tissue spaces and thus makes bacterial spreading easier
71
What are PAMPs
Pathogen Associated Molecular patterns
72
What are the functions of PAMPs?
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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