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Microbiology > Skin Infections Cards > Flashcards

Skin Infections Cards Flashcards

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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
Q

What organism most likely causes cellulitis in diabetes patients?

A

Pseudomonas aeruginosa or fungal infection

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26
Q

What two organisms most likely cause cellulitis after animal bites?

A

Pasteurella multocida, Capnocytophagia canimorsus

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27
Q

What organism most likely causes cellulitis in IV drug users?

A

S. aureus, including MRSA

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28
Q

How do we treat impetigo (local and extensive)?

A

Local: topical mupirocin 2% and carefully wash lesions to avoid lancing bullae; Extensive: beta-lactam

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29
Q

Are blood cultures helpful in diagnosing erysipelas or cellulitis?

A

No. Blood culturese are positive in

30
Q

How is S. aureus infection of internal hardware treated?

A

Remove the hardware! Hardware that cannot be removed (spinal pins) are essentially never-ending infections.

31
Q

Where and how would you actively decolonize patients with S. aureus?

A

Decolonization with chlorhexidine; most commonly used in the ICU setting

32
Q

What is the most common location for necrotizing fasciitis?

A

Extremities

33
Q

Two weeks of IV antibiotic therapy is necessary for what kind of staphylococcus infection?

A

Uncomplicated bacteremia

34
Q

What gene confers S. aureus resistance to methicillin?

A

MecA

35
Q

What causes most of the symptoms of a dermatophyte infection?

A

Host response to fungal metabolic products; fungal infections rarely invade past stratum corneum

36
Q

What is the usual mode of transmission of a dermatophyte?

A

Fomite transmission (fallen hair, desquamated skin in a variety of locations)

37
Q

What is the clinical presentation of ringworm?

A

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
Q

What stain visualizes dermatophytes? What do they look like under this stain?

A

KOH stain; septate hyphae fungi

39
Q

What type of dermatophyte infection requires systemic therapy?

A

Tinea capitis

40
Q

What are the common systemic antifungal agents, and how long is each therapy?

A

Griseofulvin (6-12 weeks), terbafine (2-4 weeks), or oral azoles (itraconazole, fluconazole for 2-4 weeks)

41
Q

What is the treatment for tinea corporis, cruris, or pedis?

A

Topical aoles, topical terbinafin for > two weeks. Avoid simultaneous topical steroid use. Cannot use nystatin.

42
Q

What is the treatment for tinea unguium?

A

Topical azoles, terbinafine, nail lacquers; or, systemic treatment. Therapy requires months.

43
Q

What organism causes tinea versicolor?

A

Malassezia furfur yeast; NOT a dermatophyte fungus.

44
Q

What is the treatment of tinea versicolor?

A

Topical azoles, selenium sulfide shampoo

45
Q

What is the common presentation of onychomycosis?

A

Chronic, painless thickening of the nail plate with debri in the nail bed.

46
Q

What are the six major childhood exanthems?

A

Measles, Scarlet Fever, Rubella, 4th disease (not considered a separate disease in modern medicine), Slapped Cheek/erythema infectiosum, Roseola

47
Q

What is the clinical exanthem of measles?

A

Erythematous macules and papules, starting on the face/trunk and spreading to limbs

48
Q

What is the clinical prodrome of measles?

A

Flu-like symptoms with congestion, coryza, conjunctivitis

49
Q

What is the clinical enanthem of measles?

A

Kopllik spots (blue-white dots on oral buccal mucosa) present 2 days BEFORE the exanthem

50
Q

What is the etiology of scarlet fever?

A

S. pyogenes producting pyrogenic exotoxin A

51
Q

What is the clinical exanthem of scarlet fever?

A

Sandpaper rash on neck spreading to extremities, circumoral pallor, with desquamation

52
Q

What is the clinical enanthem of scarlet fever?

A

Strawberry or raspberry tongue, prominent swollen papillae with desquamation

53
Q

How is scarlet fever diagnosed?

A

Throat culture and rapid antigen test detects S. pyogenes

54
Q

What is the clinical exanthem of rubella?

A

Pink-red macules on face, spreading FAST (within 24 hours) to trunk and extremities.

55
Q

What is the clinical enanthem of rubella?

A

Petichiae on palate and uvula (Forchheimer’s sign) is seen in 20% of rubella cases.

56
Q

What is the clinical prodrome of rubella?

A

Fever, headache, pharyngitis, conjunctivitis, cough, and lymphadenopathy may occur 1-2 days before the rash

57
Q

Why is rubella dangerous to pregnant women?

A

Congenital rubella may cause deafness, cataracts, heart defects, and mental retardation

58
Q

What organism causes “slapped cheek” disease?

A

Parvovirus B19

59
Q

When is “slapped cheek disease” most contagious?

A

Prior to the appearance of a rash.

60
Q

What cell is infected in erythema infectiosum? (And what sequelae can that lead to?)

A

Parvovirus B19 infects erythrocyte precursors. That may lead to anemia.

61
Q

What is the clinical exanthem of “slapped cheek”?

A

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
Q

What is the clinical enanthem of “slapped cheek”?

A

None!

63
Q

In what populations is “slapped cheek” particularly dangerous?

A

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
Q

What organism causes roseola?

A

HHV6 and HHV7

65
Q

What is the clinical exanthem of roseola?

A

Blanching non-pruritic pink macules/papules, beginning on trunk and spreading; sudden onset after high fever.

66
Q

What is the prodrome of roseola?

A

High fevers (104F/40C) with possible febrile seizures for multiple days

67
Q

What is the clinical enanthem of roseola?

A

Nagayama spots (red papules in the soft palate and uvula)

68
Q

What is the best way to distinguish a morbiliform drug-reaction rash from a morbiliform viral exanthem?

A

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
Q

What is the clinical presentation of Kawasaki disease?

A

Unexplained fever for longer than 5 days + 4 of these findings (polymorphous rash, enanthem, conjunctivitis sparing the iris, extremity erythema, cervical lymphadenopathy)

70
Q

What is the enanthem of Kawasaki disease?

A

Cracked lips, strawberry tongue, bulbar conjunctivitis

71
Q

What is the pathogenesis and common sequalae of Kawasaki?

A

Medium-size vasculitis; sequelae are mostly CV including CA aneurysm, myocarditis, MI, peripheral artery occlusion.

72
Q

What is the treatment for Kawasaki, and why should you be 100% sure of your diagnosis before giving it?

A

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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