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Microbiology > Skin Infections Cards > Flashcards

Skin Infections Cards Flashcards

1
Q

How does a necrotizing soft tissue infeciton spread?

A

Via subcutaneous fascial planes

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2
Q

What are early stage signs and symptoms of necrotizing fasciitis?

A

Pain out of proportion to exam, warmth, erythema

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3
Q

What are intermediate stage signs and symptoms of necrotizing fasciitis?

A

Systemic fever/malaise, edema, bullae

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4
Q

What are late-stage signs and symptoms of necrotizing fasciitis?

A

Hemorrhagic bullae, ecchymosis, crepitus, anesthesia of skin, septic shock

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5
Q

What are the two most common organisms causing necrotizing fasciitis or cellulitis after fresh-water exposure?

A

Virbio species, Aeromonas hydrophilia

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6
Q

What organism most commonly causes necrotizing fasciitis and is commonly associated with blunt trauma?

A

Strep pyogenes (Group A strep)

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7
Q

What organisms often cause perineal necrotizing fasciitis?

A

Clostridium perfringes, Bacteroides, and other mixed aerobe/anaerobe infections

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8
Q

What clinical features are associated with mixed anaerobe/aerobe necrotizing fasciitis?

A

Grey discharge, foul odor, crepitus, and often perineal location

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9
Q

How does hyaluronidase contribute to necrotizing fasciitis pathogenesis?

A

Hyaluronicase breaks down tissue via proteolysis and causes ischemia

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10
Q

How does streptolysin contribute to necrotizing fasciitis pathogenesis?

A

Streptolysin causes vessel thrombosis, leading to bullae development

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11
Q

How does TNF-alpha contribute to necrotizing fasciitis pathogenesis?

A

TNF-alpha increases capillary permeability, causing warmth, edema, and erythema

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12
Q

What factor of Strep pyogens causes T cell activation?

A

Pyrogenic endotoxin, causing fever, tachycardia, and a WBC increase. May lead to toxic shock syndrome.

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13
Q

What is the treatment of necrotizing soft tissue infections?

A

Surgical emergency! May have post-surgical care with antibiotics and supportive care.

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14
Q

What is the eagle effect?

A

In a large infection with high #s of bacteria, growth may be stationary. Use Clindamycin to kill stationary growth bacteria via ribosomes; the remaining bacteria begin to grow/proliferate again and are now susceptible to beta-lactams.

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15
Q

What antibiotic reduces endotoxin production?

A

Clindamycin

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16
Q

What is the most common microbiologic etiology of abscesses?

A

S. aureus

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17
Q

What is the most common microbiologic etiology of “hot tub” folliculitis?

A

Pseudomonas aeruginosa

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18
Q

Contrast a furuncle and a carbuncle

A

Furuncle: dermal abscess associated with hair follicles. Carbuncle: coalescence of furuncles into sinus tracts

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19
Q

What is the treatment of an furucle or carbuncle?

A

Warm compress (if small), surgical drainage (if large), culture w/ sensitivities and antibiotics if severe

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20
Q

What four antibiotics can be used for MRSA outpatient therapy?

A

TMP-SMX, doxycycline, minocycline, clindamycin

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21
Q

What manifests as pustules with “honey-colored crust” on the face?

A

Non-bullous impetigo, caused largely by S. aureus

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22
Q

What is the microbiological etiology of bullous impetigo?

A

S. aureus

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23
Q

What manifests as well-demarcated erythematous lesions involving superficial dermis and lymphatics?

A

Eryseiplas, caused by beta-hemolytic streptococcus (Strep pyogenes)

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24
Q

What manifests as flat erythema involving deep dermis and subcutaneous fat?

A

Cellulitis, often caused by beta-hemolytic streptococcus

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25
What organism most likely causes cellulitis in diabetes patients?
Pseudomonas aeruginosa or fungal infection
26
What two organisms most likely cause cellulitis after animal bites?
Pasteurella multocida, Capnocytophagia canimorsus
27
What organism most likely causes cellulitis in IV drug users?
S. aureus, including MRSA
28
How do we treat impetigo (local and extensive)?
Local: topical mupirocin 2% and carefully wash lesions to avoid lancing bullae; Extensive: beta-lactam
29
Are blood cultures helpful in diagnosing erysipelas or cellulitis?
No. Blood culturese are positive in
30
How is S. aureus infection of internal hardware treated?
Remove the hardware! Hardware that cannot be removed (spinal pins) are essentially never-ending infections.
31
Where and how would you actively decolonize patients with S. aureus?
Decolonization with chlorhexidine; most commonly used in the ICU setting
32
What is the most common location for necrotizing fasciitis?
Extremities
33
Two weeks of IV antibiotic therapy is necessary for what kind of staphylococcus infection?
Uncomplicated bacteremia
34
What gene confers S. aureus resistance to methicillin?
MecA
35
What causes most of the symptoms of a dermatophyte infection?
Host response to fungal metabolic products; fungal infections rarely invade past stratum corneum
36
What is the usual mode of transmission of a dermatophyte?
Fomite transmission (fallen hair, desquamated skin in a variety of locations)
37
What is the clinical presentation of ringworm?
Pigmented patch with an inflammatory border and central clearing, with scale. Ringworm is another name for tinea corporis, or dermatophyte infection of the body.
38
What stain visualizes dermatophytes? What do they look like under this stain?
KOH stain; septate hyphae fungi
39
What type of dermatophyte infection requires systemic therapy?
Tinea capitis
40
What are the common systemic antifungal agents, and how long is each therapy?
Griseofulvin (6-12 weeks), terbafine (2-4 weeks), or oral azoles (itraconazole, fluconazole for 2-4 weeks)
41
What is the treatment for tinea corporis, cruris, or pedis?
Topical aoles, topical terbinafin for > two weeks. Avoid simultaneous topical steroid use. Cannot use nystatin.
42
What is the treatment for tinea unguium?
Topical azoles, terbinafine, nail lacquers; or, systemic treatment. Therapy requires months.
43
What organism causes tinea versicolor?
Malassezia furfur yeast; NOT a dermatophyte fungus.
44
What is the treatment of tinea versicolor?
Topical azoles, selenium sulfide shampoo
45
What is the common presentation of onychomycosis?
Chronic, painless thickening of the nail plate with debri in the nail bed.
46
What are the six major childhood exanthems?
Measles, Scarlet Fever, Rubella, 4th disease (not considered a separate disease in modern medicine), Slapped Cheek/erythema infectiosum, Roseola
47
What is the clinical exanthem of measles?
Erythematous macules and papules, starting on the face/trunk and spreading to limbs
48
What is the clinical prodrome of measles?
Flu-like symptoms with congestion, coryza, conjunctivitis
49
What is the clinical enanthem of measles?
Kopllik spots (blue-white dots on oral buccal mucosa) present 2 days BEFORE the exanthem
50
What is the etiology of scarlet fever?
S. pyogenes producting pyrogenic exotoxin A
51
What is the clinical exanthem of scarlet fever?
Sandpaper rash on neck spreading to extremities, circumoral pallor, with desquamation
52
What is the clinical enanthem of scarlet fever?
Strawberry or raspberry tongue, prominent swollen papillae with desquamation
53
How is scarlet fever diagnosed?
Throat culture and rapid antigen test detects S. pyogenes
54
What is the clinical exanthem of rubella?
Pink-red macules on face, spreading FAST (within 24 hours) to trunk and extremities.
55
What is the clinical enanthem of rubella?
Petichiae on palate and uvula (Forchheimer's sign) is seen in 20% of rubella cases.
56
What is the clinical prodrome of rubella?
Fever, headache, pharyngitis, conjunctivitis, cough, and lymphadenopathy may occur 1-2 days before the rash
57
Why is rubella dangerous to pregnant women?
Congenital rubella may cause deafness, cataracts, heart defects, and mental retardation
58
What organism causes "slapped cheek" disease?
Parvovirus B19
59
When is "slapped cheek disease" most contagious?
Prior to the appearance of a rash.
60
What cell is infected in erythema infectiosum? (And what sequelae can that lead to?)
Parvovirus B19 infects erythrocyte precursors. That may lead to anemia.
61
What is the clinical exanthem of "slapped cheek"?
Bright red cheecks, which fades, replaced by a lacy/reticulated rash on the trunk and extremities. Adolescents may have a "papular-purpuric glove and socks syndrome" instead.
62
What is the clinical enanthem of "slapped cheek"?
None!
63
In what populations is "slapped cheek" particularly dangerous?
Pts with hemoglobinopathies (e.g. sickle cell) are more likely to have prolonged anemia. In pregnant women, erythema infectiosum causes 10% fetal death due to hydrops fatalis secondary to severe fetal anemia.
64
What organism causes roseola?
HHV6 and HHV7
65
What is the clinical exanthem of roseola?
Blanching non-pruritic pink macules/papules, beginning on trunk and spreading; sudden onset after high fever.
66
What is the prodrome of roseola?
High fevers (104F/40C) with possible febrile seizures for multiple days
67
What is the clinical enanthem of roseola?
Nagayama spots (red papules in the soft palate and uvula)
68
What is the best way to distinguish a morbiliform drug-reaction rash from a morbiliform viral exanthem?
Age: in adults, morbiliform rashes are more likely due to drug reactions; in children, viral infection is more likely. (Additionally, drug reactions are more likely to be pruritic.)
69
What is the clinical presentation of Kawasaki disease?
Unexplained fever for longer than 5 days + 4 of these findings (polymorphous rash, enanthem, conjunctivitis sparing the iris, extremity erythema, cervical lymphadenopathy)
70
What is the enanthem of Kawasaki disease?
Cracked lips, strawberry tongue, bulbar conjunctivitis
71
What is the pathogenesis and common sequalae of Kawasaki?
Medium-size vasculitis; sequelae are mostly CV including CA aneurysm, myocarditis, MI, peripheral artery occlusion.
72
What is the treatment for Kawasaki, and why should you be 100% sure of your diagnosis before giving it?
Treatment of Kawasaki = aspirin. This is the only time you give a child with a fever aspirin. Aspirin in children may cause Reye's syndrome, which causes swelling in the liver and brain (seizures, loss of consciousness, vomiting, paralysis)

Microbiology (9 decks)

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