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Bacteriology (mine) > Stapholococci > Flashcards

Stapholococci Flashcards

1
Q

What’s the division pattern of Staph?

A

divide along three planes - resulting in grape-like clusters (can also be seen singularly or in pairs, but most often clusters)

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2
Q

How do streptococcus species divide? (different from staph)

A

divide along a single plane that is perpendicular to long axis of cells - resulting in formation of chains or pairs of cells (diplococci)

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3
Q

What is this?

A

staph aureus

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4
Q

What is this?

A

strep pneumoniae

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5
Q

Explain the catalase test.

A

catalase - breakdown of hydrogen peroxide (H2O2) -> water + O2

take a colony -> drop 3% H2O2 onto colony-> positive test will show bubbling over region (from oxygen!)

staph = positve

strep = neg

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6
Q

Explain the coagulase test.

A

coagulase converts fibrinogen-> fibrin

plasma inoculated with bacteria -> incubate specimen at 37OC -> positive will see clotting of plasma sample

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7
Q

Explain the mannitol salt agar test.

A

Positive: changes the pH indicator from red to yellow - meaning mannitol was fermented and acid formed as end product (lowering the pH and causing this change in color)

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8
Q

What is the link between staph aureus and coagulase?

A

hallmark positive test!

allows staph aureus to wall itself from the immune defenses via promotion of abscess formation (walls off from immune responses AND prevent antibiotics penetration)

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9
Q

What is the siginificance of staph aureus ability to ferment mannitol?

A

mannitol provides the main carbon source

indication that S. aureus can live happily on the surface of skin despite salt, dry environment containing sebaceous, anti-microbial peptides

test serves as both selective and differential for S. aureus

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10
Q

What is seen on blood agar plate with S. aureus?

A

gold pigment from production of anti-oxidant pigment staphyloxanthin

(keep in mind is hallmark of the bacteria but not all strains will have this golden pigment)

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11
Q

What is hemolysis?

A

destruction of RBCs around colony

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12
Q

Where do we find staph aureus?

A

part of normal/transient flora in human and animals

particularly found on skin (axilla), nasopharynx, nares, groin (perineum)

risk of nosocomial infections!

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13
Q

What is the significance of adherance factors?

A

helps staph aureus stick to a lot of surfaces

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14
Q

What’s the importance of the antimicrobial resistance factors?

A

allows staph aureus to bcome resistant to many drugs

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15
Q

How does beta-lactamase work?

A

cuts off the active part of the antibiotics that allow S. aureus to have immunity

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16
Q

What is the order of virulence factor expressions for S. aureus?

A

early on we have adherence -> then immuno-evasion and invasiveness -> then exotoxins

makes sense if think about what pathogen needs to invade

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17
Q

Are s. aureus able to make biofilms?

A

yes! (staph epidermidis can as well)

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18
Q

What is the sigfinicance of biofilms?

A

makes it hard for antibiotics to get to is - also, hard to eradicate with phagocytes when they’re imbedded in this biofilm

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19
Q

What are the invasins virulence factors of S. aureus?

A

hyaluronidase, staphylysin, leukocidin, leukotoxin, coagulase, staphylokinase

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20
Q

What do leukotoxin and leukocidin do?

A

kill WBCs

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21
Q

What are the functions of hyaluronidase and staphylokinase?

A

spreading factors - promote tissue destruction that allows the bacteria to disseminate throughout the tissue

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22
Q

What are the adherence factors of Staph Aureus?

A

Fbe (fibrinogen adhesions), AtlE (vitronectin adhesion), GehD (collagen adhesion), Embp (fibronectin adhesion)

aka MSCRAMMs (microbrial surface components recognizing adhesive matrix molecules)

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23
Q

What is significant about the adherence pattern of Staph Aureus?

A

will bind our own proteins (fibrin, fibronectin) and has predilection for adhering to damaged tissues

gives bacteria ability to adhere to SEVERAL diff surfaces and initiate biofilm formation

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24
Q

What are the exotoxin damage / superantigens of staph aureus?

A

TSST (toxic shock syndrome toxin), EFT (exfoliative toxins), SE AG (staphylococcal enterotoxin)

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25
Q

What are superantigens?

A

molecules that can cross-circuit (nonspecific activation) of the T-cell receptors to APCs -> non-specific activation of immune system -> produce hurricane of cytokines with variety of neg consequences

cytokines (IL-1 and TNF) -> fever

capillary permeability -> desquamation

generation of gamma interferon and others (IL-2) -> nausea, vomitting, diarrhea, and shock

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26
Q

What are the biofilm forming virulence factors of S. aureus?

A

PIA (polysaccharide intercellular adhesion); Aap (accumulated associated protein)

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27
Q

How do biofilms allow for avoidance of antibiotics?

A

changing the bacteria replication pattern so antibiotics can no longer recognize

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28
Q

How do bacteria conserve energy in regards to virulence factors?

A

not all virulence factors are produced at once - made as needed

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29
Q

What conditions predisposes to infection with S. aureus?

A
  1. breach in skin
  2. immunological defects (chemotaxis, opsonization, PMNs functional defects i.e. chronic granulomatous disease and leukocyte adhesion deficiency)
  3. presence of foreign bodies (catheters, prosthetic joints)
  4. sharing of fomites, contact sports, close quarters, hospital stay, hygiene
  5. previous tissue damage (scar tissue, endocarditis)
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30
Q

What makes it easy to have Staph Aureus infections?

A

can survive in environment for substantial periods of times - easy community spread!

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31
Q

What’s important about protein A?

A

since it binds to Fc receptor of IgG molecule -> blocks the binding site of PMNs and macrophages on IgGs for opsonization and prevents phagocytosis of the organism

so microcapsule has an anti-phagocytic disease

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32
Q

Define abscess.

A

collection of pus usually around a hair follicle

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33
Q

How do we treat abscesses?

A

incise, drain, and surgically remove foreign body

34
Q

What gives pus the yellow/green color?

A

myeloperoxidase found in neutrophils

35
Q

What are furuncles?

A

abscess into subcutaneous tissue

PAINFUL (bc sensors are in this layer)

36
Q

How do we treat furuncles?

A

incise, drain, doxycycline

(mupirocin to nares + bleach baths)

37
Q

Define carbuncles.

A

multiple contiguous abscesses

found commonly in areas where people may not clean much

38
Q

How do we treat carbuncles?

A

drainage +/- antibiotic therapy depending on severity

39
Q

When is antibiotics not needed?

A

simple abscesses -> simple drainage of all pus pockets then packing the incisied area will suffice

40
Q

What is this?

A

abscess

41
Q

What is this?

A

furuncle

42
Q

What is this?

A

carbuncle

43
Q

What are hemolysins?

A

exotoxin virulence factors that lead to tissue damage at site of infection

44
Q

Name some hemolysins.

A

alpha-toxin, gamma toxin, phenol-soluble modulins

beta-toxin and delta toxin

all cytotoxins

45
Q

What’s the most important exotoxin for Staph Aureus?

A

alpha-toxin

46
Q

What’s the significance of alpha toxin?

A

major pore-forming toxin causing the disease of S. aureus infection - cause of hemolysis and skin necrosis

the pore provides an easy entry route for further S. aureus infection - easy dissemination into blood stream

will aos insert into membranes of PMNs and cause lysis

47
Q

What bacteria likes to adhere to stitches?

A

staph aureus

48
Q

How does staph aureus infection lead to cellulitis?

A

staphylokinase + hyaluronidase aid in the spread along the subcutaneous fascial plane

49
Q

How do we treat the staph aureus induced cellulitis?

A

antibiotics

50
Q

What virulence factors of staph aureus are involved in formation of corneal ulcers?

A

alpha, beta, delta, gamma toxins; coagulase, nuclease, lipase, and hyaluronidase

51
Q

What are the host factors involved in corneal ulcer?

A

influx of PMNs into the infected region

52
Q

Describe what it clinically seen in patients with corneal ulcers.

A

ppthalamic emergency!

  1. moderate to marked stromal cellular infiltration
  2. moderate to marked anterior chamber reacton (hypopyon)
  3. well-demarcated infiltrate: yellow-white (pus)
  4. satellite lesions may be present

“wake up in the morning with eyes glued shut”

53
Q

What Staph infections cause impetigo?

A

Staph Aureus and Staph Pyogenes

54
Q

How do we treat corneal ulcers?

A

best outcome: topical antibiotics

worst outcome: cornea perforates and transplant necessary

55
Q

Describe the transmission of impetigo.

A

very contagious -> spreading quickly through preschools or grade schools

scratching/picking at sores -> contact with others -> SPREAD

56
Q

Describe the progression seen in impetigo.

A

small scartch or barely perceptible lesion -> vesicles -> pustules -> crust over to become honey-colored and flakey

57
Q

What form if impetigo is specific for Scalded Skin Syndrome?

A

bullous impetigo - burn-like blisters but pus filled (NOT clear liquid seen in real burns)

58
Q

How do we treat impetigo?

A

topical and oral antibiotics (bc no single, focal lesion to be excised and drained)

59
Q

How does staph aureus cause food contamination?

A

secretes enterotoxins (SEA, SEB, SEC1, etc)

60
Q

SEA is ____ - encoded

A

phage

61
Q

SED is _____ - encoded

A

plasmid

62
Q

In food poisoning, super-antigen effects result in excess what?

A

IL-2

63
Q

What treatment is needed for Staph Aureus food poisoning?

A

supportive treatment - symptoms abate within a day or two

64
Q

What causes Scalded Skin Syndrome?

A

skin lifted and filled with fluid from destruction of desmoglein-1 via epidermolyitc exotoxins (exfoliatin A and B - both are proteases)

65
Q

What layers do desmoglein-1 hold together?

A

granulosum and spinosum

66
Q

What is clinically seen in Scalded-Skin Syndrome?

A

fever, large bullae, erythematous macular rash

  1. skin slough, serous fluid exudes, electrolytic imbalance - possible secondary infections
  2. hair and nails lost
  3. recovery usu within 7-10 days
67
Q

How do we treat SSS?

A

treat like a burn!

treat open skin with antibiotics to prevent further infection

68
Q

What toxin is secreted by Staph Aureus to elicit toxic shock syndrome?

A

TSST-1: toxic shock syndrome toxin-1 (becomes absorbed and acts as super-antigen)

69
Q

What is seen clinically in toxic shock syndrome?

A

initially fever, nausea, vomitting, and diarrhea followed by rash and exfoliation

can be deadly: pressure drops, multiple organ system failure

70
Q

How do we treat toxic shock syndrome?

A

antibiotics, remove colonized item, supportive care

71
Q

Describe “trojan horse” method of dissemination.

A

Staph aureus can hijack neutrophils during phagocytosis - prevents bacteria from being effectively killed by antibiotics

PMN goes on to spread infection systemically

72
Q

What is one of the causes for chronic infective endocarditis?

A

coagulase negative staph - bc their virulence factors do not attract the immune system as quickly

73
Q

What is PVL?

A

panton-valentine leukocidin: newer toxin related to S. aureus

74
Q

What’s the link between PVL and pneumonia?

A

forms pores in cells lining alveolar spaces allowing fluid to accumulate inside the tissues

activates PMNs and macrophages causing IL-8 release (attracting more PMNs)

PMNs destroy the cells lining alveolar space -> hemorrhaging

lungs = hemorrhagic, necrotic pneumonia

75
Q

Describe the virulence factors associated with Staph Epidermidis.

A

Not as prominent as S. aureus but have lots of adhesins -> making easy to stick to plastics (like lines in ICU patients)

76
Q

Who gets infected by Staph Epidermidis?

A

sickest of the sick (ICU patients), septicemia, endocarditis

77
Q

What is seen in blood agar with Staph Epidermidis?

A

small white non-hemolytic colonies

78
Q

What is seen on the blood agar of Staph saprophyticus?

A

large white to yellow non-hemolytic colonies

79
Q

How do we treat staph saprophyticus?

A

amoxicillin or bactrim/sulfa-trimethoprim (same as community acquired E. coli)

80
Q

What is seen on blood agar infected with staph aureus?

A

golden yellow

Bacteriology (mine) (6 decks)

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