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SKin Bacterial infections Flashcards

(59 cards)

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1
Q

most common cause of acne

A

propionibacterium acnes

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2
Q

microscopic appearance of p. acnes

A

Gram + rod

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3
Q

oxygen requirement of propionibacterium acnes

A

anaerobic aerotolerant

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4
Q

virulence factors that p acnes has

A

neuraminidase
hyaluronidase

break down molecules to help create a local inflammatory response

lipases- breaks down lipids for food

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5
Q

tx for propionibacterium acnes

A

benzoyl peroxide, salicylic acid
retinoids
antibiotics

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6
Q

Impetigo info

lesion characteristic*

A

Very contagious superficial skin infection in children
lesions on face and extremities
with characteristic golden appearance*

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7
Q

impetigo caused by what bacteria

A

Staph Aureus
or
Streptococcus Pyogenes (GAS)

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8
Q

How do you determine between Staph and Strep initially

whats the next step

A

Catalase test
Staph: catalase +
Strep: Catalase -

place Strep them in blood agar to determine rate of hemolysis

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9
Q

Blood agar B hemolysis

and Bacitratrin

A

Bacitracin sensitive: Strep pyogenes

non sensitive: Other B hemolytic

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10
Q

Blood agar A hemolysis

Optochin

A

Optochin sensitive: strep pneumoniae

non sensitive: other alpha hemolytic

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11
Q

bullous impetigo

characteristic*

A

more serious form of impetigo- vesicles enlarge and fill with clear yellow fluid—

which leave a thin brown crust when they rupture*
seen on trunk with fewer lesions*
(staph or strep)

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12
Q

Echthyma

characteristic*

A

ulcerative form of impetigo
usually due to a scratch/ insect bite
lesions extend deep into the dermis

Punched out ulcers- with yellow crust and violet colored margins* (due to strep pyogenes only )

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13
Q

two complications from strep

A

post streptococcal glomerulonephritis

rheumatic fever

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14
Q

How do you diagnose S. Aureus (plating/ chemical tests?)

A

Mannitol salt agar to isolate for staph

then hemolysis
MSSA: B hemolyitc
MRSA: non B hemolytic

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15
Q

S aureus exotoxins

A

exfoliative toxins A n B

- serine proteases that cleave desmosomal cahderins in superficial epidermis

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16
Q

TX for strep v staph impetigo

A

strep: penicillin
Staph: penicilinnase resistant penicillin or 1 generation cephalosporins

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17
Q

folliculitis/ furuncles carbuncles caused by

A

Staph aureus

normal flora of skin un 20%

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18
Q

what is a carbuncle

A

large painful group of contiguous furuncles ( boils)

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19
Q

who is at risk for recurrent furunculosis

A

someone that has been colonized with staph in their nose — SO they need to be decolonized*

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20
Q

what is Erypselas

aka

A

an ACUTE
SUPERFICIAL skin infection: upper dermis and superficial lymphatics

that DIFFERS from cellulitis

st. anthonys fire

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21
Q

Erypselas caused by

A 
Streptococcus Pyogenes 
Gram + cocci in chains
catalase negative
Bacitracin sensitive
B hemolitic
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22
Q

how is erypselas different from cellulitis

A

erypselas is ACUTE v cellulitis is slow onset
Erypselas is superficial v cellulitis that is deeper infection
Erypselas lesions are RAISED with CLEAR demarcations
erypselas is often associated with fever

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23
Q

Specific characteristics of erypselas*

A

Butterfly involvement of the face

Milians ear sign

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24
Q

DD for erypselas

say its rapid progressive reddening with signs of systemic toxicity

Study These Flashcards
A

severe infection
-necrotizing fasciitis
gas gangrene
- toxic shock syndrome

25
Cellulitis caused by? (2 main) + rest
B hemolytic strep ( ABCGF)* and staph aureus * ``` H. Influenzae o Clostridia o Non spore forming anaerobes o Pneumococcus o Meningococcus ```
26
Characteristics of cellulitis
Infections develop as bacteria enter via breaches in skin (similar to erysipelas) Involves deeper dermis and subcutaneous fat SLOWER course of disease with localized sx developing over a few days +/- purulent drainage or exudate Unilateral involvement of lower extremities
27
2 main etiologic agents of cellulitis have what? | what does it do?
Staph aureus and b hemolytic strep act as super antigens causes a NON specific interaction - activate a ton of Cells -- which causes massive activation of immune system but NOTHING gets done
28
tx for cellulitis staph v strep
staph aureus- clyndamycin and vancomycin b hemolytic strep- clyndamycin and b lactam
29
staph TSS risk due to? is bacteria needed to diagnose?*
could be due to leaving tampons in for a long time Bacteria are NOT * needed to diagnose since they aren't recovered in all cases
30
What does it mean if you can find toxin producing S. | aureus but NOT antibody to the toxin?
Highly suggestive of TSS- helpful in retrospective diagnosis of cases suspicious for TSS The toxin did its job: act as a super Ag
31
Tx of staph TSS
``` tRACS Remove toxin Alleviate symptom Cultura nad antibiotic susceptibility Treat for colonization ```
32
When should you suspect Staph TSS
rapid onset of shock sx in healthy ppl Such as high fever, rash, hypotension, multi-organ failure (involving at least 3 systems) and desquamation (peeling of skin, even on palms and sores), severe myalgia, vomiting, diarrhea, HA and nonfocal neuro abnormalities
33
when should you suspect Step TSS
Pt presents from community in shock but cant find a reason for it ``` History or recent trauma Severe pain Isolation of GAS from a usually sterile site (blood, CSF) Hypotension ```
34
if no other etiology is established and you isolate GAS at a non sterile site what do you assume? What do you do?
Strep TSS treat right away!: clyndamicin and beta lactam (even without culture results)
35
Scarlet fever caused by
a complication of Strep throat S. pyogenes
36
characteristics of scarlet fever*
diffuse erythematous rash that has "SANDPAPER" quality to skin rash blanches with pressure and has circumorally pallor accompanied by a STRAWBERRY TONGUE pastias lines
37
Pastias lines
also a characteristic of scarlet fever | linear petechiae in folds: antecubilat fossa and pressure points) due to exotoxin of bacterium
38
is scarlet fever contagious where does it start
FUCK YES IT IS usually starts in groin/ armpits and then expands to trunk and then eventually peels
39
SSSS aka
Staphylococcal scalded skin syndrome ritter disease staph epidermal necrolysis
40
SSSS is due to Is seem more in.
acute exfoliation of skin due to Staph Aureus' exfoliative toxins common in kiddos adult higher mortality ( underlying disorder)
41
SSSS Characteristics*
red sandpaper like rash and separation of epidermis beneath granular layer, then ill defined bullae form and DIFFUSE SHEET LIKE DESQUAMATION OCCURS* wrinkly lookin
42
how do the exfoliative toxins of S. aureus act*
they trigger proteolysis of desmoglein -1 (Dg-1) | which is an important keratinocyte that provides cell to cell attachment in superficial epidermis
43
why do lil kids show increased frequency of sSSS
because they have reduced renal clearance capability ( exotoxins released thru pee) and maternal antibodies though to be partially protective
44
do the bullae in SSSS have stuff>
no. they sterile
45
nikolsky sign:
gentle stroking of skin causes it to separate at epidermis
46
how do you differentiate SSSS from TEN
in SSSS the mucous membranes are spared | in toxic epidermal necrosis they are NOT
47
how do you treat SSSS
no steroids- worsen immune function fluid rehydration topical wound care
48
Two types of necrotizing fasciitis
I: Polymicrobial ( 1 facultative anaerobe and one anaerobe) II: GAS (Strep pyogenes), or MRSA or aeromonas or vibrio
49
when should you suspect necrotizing fasciitis
superficial cellulitis fails to respond to standard and therapy progresses rapidly and results in systemic toxicity PAIN IS OUT OF PROPORTION* from exam findings: too painful or not painful at all muscle groups cannot be distinctly palpated changes in skin color: red to patches of blue gray
50
Frank cutaneous gangrene
advanced of necrotizing facts now lacks sensation because thrombosis of small blood vessels and destruction of superficial nerves
51
difference between scarlet fever and measles and rubella
SF: rash first seen on neck and spreads downward, more pronounced on flexures of joints measles begins on forehead and spreads down: fades in a week rubella: rash fades w/i 24 h
52
surgical findings of necrotizing fasciitis
foul dishwater pus gray friable necrotic fascia does not resist blunt dissection
53
Type I necrotizing fasciitis
poly microbial GAS: G + Staph aureus: G+ enterobacteriade: G - rod bacteorides : gram - rod clostridia: g + rod
54
tx for necrotizing fasciitis
iv antibiotics | surgical debridement
55
Gas Gangrene caused by aka
Clostridium perfingens (90%) aka clostridial myonecrosis - they are gas producing
56
clostridium perfingens characteristics
Gram + rod spore forming anaerobic
57
pathogenesis of c. perfingens
theta toxin destroys PMNS | - therefore there is little host inflammatory response
58
findings of gas gangrene
sudden onset of pain severe extreme tenderness brownish skin discoloration with bullae: that ave "mousy" sweet odor Crepitant bullae: BC of the gas they make
59
how do you diagnose gas gangrene
Gram + rod absence of PMN cells* ITS A SURGICAL EMERGENCY

Microbio (7 decks)

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