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HMS IDD > Common Cutaneous Infections > Flashcards

Common Cutaneous Infections Flashcards

1
Q

Major components of the normal skin flora

A

Aerobic cocci (Staphylococci and Streptococci)

Corynebacteria

Gram negative bacteria

Yeast (Malassezia)

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2
Q

Appearance of Staphylococcal lesions

A
  • Usually appear as pustules, furuncles, or erosions with honeycolored crusts
  • Bullae, widespread erythema and desquamation, or vegetating pyodermas may also indicate Staphylococci
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3
Q

Commensal Staphylococci

A
  • Anterior nares of 20-40% of adults
  • MAy also reside on hands and perineum
  • Individuals usually infected via the nasopharyngeal route with their own Staphylococci
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4
Q

MRSA Risk Factors

A
  • Exposure to children
  • Prior antibiotic therapy
  • Age >65
  • Exposure to others with MRSA history
  • Crowded housing
  • Chronic skin disease
  • Contact sports
  • Pets
  • Recent hospitalization for chronic illness
  • HIV/AIDS
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5
Q

Treatment for Staphylococcal Infection

A
  • First line treatment: Cephalexin (1st generation cephalosporin)
  • For community-acquired infections withour MRSA risk factors, clindamycin, trimethoprim/sulfamethoxazole, doxycycline, or oral linezolid.
  • MRSA Presumed without testing in patients with substantial risk factors
  • IV Vancomycin or Linezolid for MRSA
  • The underlined do not cover group A streptococci and should be perscribed with penicillin if coinfection is suspected. Clindamycin alone is sufficient to treat both.
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6
Q

Staphylococcal folliculitis

A
  • May affect eyelashes, axilla, pubis, thighs
  • Pubic follicultis may be sexually transmitted
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7
Q
A

Staphylococcal folliculitis of the pubis

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8
Q
A

Furuncle = boyle (acute, round, tender, circumscribed, perifollicular abcess that ends in central suppuration)

Carbuncle = two or more furuncles

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9
Q

Staphylococcal furunculosis

A
  • Begins in hair follicles, continues by autoinoculation
  • Often undergo necrosis and rupture, spilling out pussy necrotic discharge
  • Usually begins with skin lesion, often from shaving
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10
Q

Impetigo contagiosa

A
  • May be staphylococcal, streptococcal, or combined (70% staph aureus, rest GAS or combination, Group B streptococci common in newborn impetago)
  • Characterized by discrete, thin-walled vesicles that rapidly become pustular and then rupture
  • complication of pediculosis capitis
  • Spread around the body via fingers or towels contaminated with discharge
  • More common in hot humid weather
  • May complicate other inflammatory skin conditions or skin infections
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11
Q

Diseases that impetigo may immitate

A
  • Ringworm infection
  • Toxicodendron dermatitis
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12
Q

Treatment of Impetago contagiosa

A
  • Systemic antibiotics and topical treatment combination recommended
  • Since most are staphylococcal, semisynthetic penicillins and 1st generation cephalosporines recommended
  • Soak off crusts frequently to prevent autoinfection, and follow soaking with topical antibiotics
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13
Q

Bullous impetago

A
  • Caused by bacteriophage 71- or 55-infected S. aureus
  • Usually occurs in newborns (starts 4-10 days after birth)
  • Neonatal type highly contagious and often affects family and nurses
  • Often starts on hands and face, appear as large fragile bullae
  • Rupture to leave impetigo circinata, which are circinate, weepy, crusted lesions
  • Weakness and fever present as a late symptom
  • Diarrhea or green stool, pneumonia, bacteremia, meningitis
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14
Q
A

Bullous impetago

(impetago circinata also visible)

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15
Q

Erysipelas

A
  • aka St. Anthony’s Fire
  • Streptococcal infection (Usually GAS, sometimes goup C or G, often B in infants)
  • Intense local redness, heat, swelling, with a raised, indurated border (may develop secondary features like bullae, vesiculation, sometimes with associated gangrene)
  • Often, but not always, preceded by malaise and fever, headache, vomitting, joint pain
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16
Q

Complications of Erysipelas

A

Septicemia, deep cellulitis, necrotizing fasciitis, abcess development

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17
Q

Erysipelas is often confused with. . .

A

Contact dermatitis

Angioneurotic edema

The major distinguishing features are the absence of itchiness and the presence of fever

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18
Q

Treatment for erysipelas

A
  • Systemic penicillin very effective
  • General constitution improves within 24-48 hr, but skin may take longer to heal
  • Treat w/ antibiotics for at least 10 days
  • ice bags/cold compress locally
  • Leg involvement and bullae may require hospitalization and monitoring with IV antibiotics
  • Recurrence may occasionally occur, in which case long-term antibiotic prophylaxis is recommended
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19
Q

Cellulitis

A
  • suppurative infammation involving the subcutaneous tissue
  • Usually follows some discernable wound
  • Mild local erythema and tenderness, malaise, fever, chills may be present at onset
  • Spreads outward from central wound
  • Pits upon pressure
  • Central part may become vesicular or necrotic
  • May be followed by gangrene, metastatic abscesses, and severe sepsis
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20
Q

Diagnosing cellulitis

A
  • Usually made on clinical grounds
  • uncommon for blood studies, including cultures, and skin biopsies or aspirates to be positive
  • If, however, an open wound is present, there is a high probability of a culture being positive
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21
Q

Causes of cellulitis

A
  • Streptococci ~75% of cases
  • Remainder mostly staphylococci
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22
Q
A

Cellulitis

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23
Q

Intertrigo

A
  • Superfcial infammatory dermatitis occurring where two skin surfaces are in apposition
  • As a result of friction, heat, moisture, the affected fold becomes erythematous, macerated, and secondarily infected
  • may be erosions, fssures, and exudation, with symptoms of burning and itching
    *
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24
Q

Risk factors for intertrigo

A
  • Heat, humidity
  • Obesity
  • Extremes of age
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25
Q

Organisms which may cause the secondary infection associated with intertrigo

A
  • Streptococcus
  • Staphylococcus
  • Pseudomonas
  • Corynebacterium
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26
Q

Maceration

A

Maceration occurs when skin is in contact with moisture for too long. Macerated skin looks lighter in color and wrinkly. It may feel soft, wet, or soggy to the touch. Skin maceration is often associated with improper wound care

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27
Q

How skin microbiota protect us

A
  • Provide ecological competition for potentially infectious agents
  • Produce free fatty acids, which are toxic to many bacteria, from triacylglycerols
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28
Q

The most common cause of orolabial Herpes infection

A

HSV-1

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29
Q

__% of individuals infected with HSV-1 at some point will develop skin lesions

A

50% of individuals infected with HSV-1 at some point will develop skin lesions

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30
Q

Most persons with HSV-2 infection are . . .

A

Most persons with HSV-2 infection are symptomatic, but the majority do not recognize that their symptoms are caused by HSV

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31
Q

First episode

A

As opposed to primary infection, first episode refers to the first observed instance of disease manifestation, which may be due to primary infection or a recurrence

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32
Q

Tzanck smear

A
  • Nonspecific method for diagnosing an alpha group Herpesvirus
  • Scrape of the base of an ulcer or skin lesion and staining
  • Screening for multinuclear epidermal giant cells which are characteristic of alpha Herpesvirus infection
  • Accuracy 60-90%, false positive rate 3-13%
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33
Q

Methods for diagnosing an alpha Herpesvirus infection

A
  • Tzanck smear (only gives you alpha Herpesvirus, not which kind, and requires an acute vesicular lesion)
  • Direct Fluorescent Antibody Test (specific to type of virus)
  • Viral culture (specific and relatively quick)
  • PCR
  • Histology
  • Immunohistochemistry
  • Serology not that helpful
    *
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34
Q

Orolabial Herpes

A
  • Virtually always HSV-1
  • Prodrome of 24 hours of itchiness or irritation common
  • Major presentation is cold sore, blisters on lips or gingival mucosa with erythematous base
  • Herpetic gingivostomatitis in <1% of infected, usually young adults or adolescents
  • Accompanied with fever, malaise, regional lymphadenopathy
  • May develop to pharyngitis with ulceration or exudation
  • May recur in cheeks, eyelids, earlobes, hard palate
  • UV light a common cause of recurrence
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35
Q

Treatment for Orolabial Herpes

A
  • Untreated, lasts 1-2 weeks
  • If severe, IV acyclovir 5 mg/kg 3 times per day recommended
  • For more mild cases, oral acyclovir 15 mg/kg 5x daily for 7 days or valacyclovir 1g 2x daily for 7 days will reduce duration by 50%
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36
Q

Genital Herpes

A
  • Usually caused by HSV-2
  • HSV-1 represents 50% of cases in women under 25
  • Spread by skin-skin contact, often as STI, lesions are infectious
  • Incubates ~5 days before appearing, prodromal itching or discomfort, presentation of skin lesion lasts 1-3 weeks
  • Risk of transmission in partners is 5-10% annually
  • grouped blisters on an erythematous base, with initial episode lasting 10-14 days and subsequent episodes shorter
  • Fever, flulike symptoms, inguinal lymphadenopathy bilaterally
  • Virtually all those infected have recurrence at some point
  • Psychological stigma a big part of the disease, must be addressed
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37
Q

Treatment for Genital Herpes

A
  • Oral acyclovir 200 mg 5x daily or 300 mg 3x daily
  • Famcicyclovir or valacyclovir similar regimens
    *
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38
Q

__% of “initial” clinical episodes of genital herpes are actually recurrence

A

25% of “initial” clinical episodes of genital herpes are actually recurrence

39
Q

Eczema herpeticum

A
  • aka Kaposi varicelliform eruption
  • Occurs when dermatitis patients are infected with HSV
  • Associated with more severe AD, higher IgE levels, elevated eosinophil count, food and environmental allergies, onset of AD <5 years of age
  • Higher risk of Staph. aureus and Molluscum contagiosum infection
  • May present as large skin lesions or small papules
  • Often there is coinfection with bacteria or yeast
40
Q

Risk factors for eczema herpeticum

A
  • Some form of dermatitis
  • Topical calcineurin inhibitors
  • Bath or hot tub exposure
41
Q

Treatment of Eczema herpeticum

A
  • Given the limited toxicity of systemic antiviral therapy, it should be started immediately, IV or oral
  • Coinfections should be addressed with topical antibiotics
42
Q

Ways HSV hides from the immune system

A
  • Inhibits TLR2
  • Decreases CD1d expression
  • Blocks TAP to prevent MHC Class I loading with self peptides
  • Prevents complement activation
  • Destabilizes TNF mRNA
  • Induces Fas-ligand expression on monocytes and macrophages, resulting in death-receptor activation in T cells
43
Q

Zoster

A
  • Caused by VZV
  • Latent virus hides in dorsal root ganglia and is reactivated by immunosuppression (age and TNF inhibition most common stimuli)
  • Dermatomal distribution
  • In order of likelihood, Thoracic > Cranial > Lumbar > Sacral
  • May appear in mouth from V2/V3 dermatome, may appear in vagina from S2/S3 dermatomes
  • Usually preceded by 1-2 days of pain in affected area
  • Skin lesion initially presents as erythematous papules and plaques, progress to blisters within hours, gradually become pustous over a couple days, crust, then heal
  • May become hemorrhagic, nercrotic, or bullous
  • Lasts for 1-6 weeks (shorter for younger patients), new lesions appear for first 1-5 days
44
Q

Risk factors for Zoster

A
  • Family history (some genetic component)
  • Immunosuppression (TNF inhibitors or age most commonly)
  • Malignancy, especially blood-borne
  • Statins
  • 1/3 unvaccinated persons with a history of Varicella will develop Zoster
45
Q

Neonatal Zoster

A
  • May be seen in children <1 year of age
  • Can result from intrauterine exposure to VZV or exposure during the first few months of life (prior to adaptive immune system development)
  • Maternal antibodies fight off Varicella, but may be naive or gone by the time Zoster appears
46
Q

Diagnosing Zoster

A
  • Clinical manifestation can only really be confused with other alpha Herpesviruses
  • Direct fluorescence antibody can easily distinguish
47
Q

Treating Zoster

A
  • May be prevented with Zoster vaccination (halves incidence)
  • Recommended for all 60 and older
  • Since the vaccine is a live virus, antiviral medications must be stopped 24 hours before taking if the patient is on any
  • Acyclovir and related antivirals help relieve symptoms
48
Q

Molluscum contagiosum

A
  • Caused by 4 closely related groups of Poxviridae
  • MCV-1 most common, but varies with geography
  • MCV-2 most common in patients with HIV
  • Spread by skin-skin contact, may be spread as STI, bathing/swimming also easy way to transmit
  • Most lesions smooth-surfaced, frm, dome-shaped, pearly papules, averaging 3–5 mm in diameter with central umbilication, may develop to pus-filled or crusted lesions
  • “Giant” lesions may be up to several centimeters in diameter
  • When MC is restricted to the genital area in a child, sexual abuse must be considered.
49
Q

Risk factors for molluscum contagiosum

A
  • Swimming/bathing
  • Sexual activity
  • Foot lesions
  • Pubic hair removal by shaving, clipping, or waxing
  • Atopic dermatitis (here lesions tend to be confined to dermatitic skin)
50
Q

Treatment of Molluscum contagiosum

A
  • May depend on situation
  • If there are few lesions, topical tretinoin works well\
  • If there are many, topicals may be impractical and one might consider systemic therapy. But, systemic therapies can be harsh, cause scarring, and be emotionally traumatic.
  • Spontaneous resolution is virtually a certainty, with the total course lasting 2 years or less
  • Continuous application of surgical tape to each lesion daily after bathing for 16 weeks led to cure in 90% of children
51
Q

Candidiasis

A
  • Candida albicans, typically commensal but can become pathogenic
  • intertriginous areas are frequently affected (warmth, moisture, maceration of skin)
52
Q

Candidiasis risk factors

A
  • Immunosuppression
  • Warmth and moisture
  • Free niche (ex, antibiotic therapy removes many competing bacteria)
  • High skin pH (from baby diapers, panty liners, other occlusive products)
  • Diabetes
53
Q

Treatment of Candidiasis

A
  • Topical acidic buffers may be helpful as preventative measure for recurrence and have no side effects
  • Topical anticandidal ointments are effective
54
Q

Candidal intertrigo

A
  • pruritic intertriginous eruptions caused by C. albicans
  • pink to red, intertriginous moist patches surrounded by thin, overhanging fringe of somewhat macerated epidermis
  • Tiny, superficial, white pustules may be seen adjacent to patches
55
Q

Why can diabetes predispose to candidiasis?

A
  • Chronic hyperglycemia leads to acidosis and decreased immune effector cell function
  • Glycosylation of C3
  • Candida albicans expresses a glucose-inducible protein homologous to mammalian phagocyte complement receptor that when activated promotes adhesion in the yeast and subverts phagocytosis by the host
  • Glycosylation end products lead to neuropathy and decreased sensation, decreased blood flow
  • In general, bacteria and yeast thrive in glucose rich environment
56
Q

Human beta-Defensins

A
  • Released by keratinocytes
  • HBD-1 constitutively expressed in epidermis
  • HBD-2 and HBD-3 expressed in response to bacterial infection
57
Q

Cathelicidins

A
  • Secreted by keratinocytes
  • Induce pro-inflammatory cytokine secretion
  • Chemoattractant to PMNs, T cells and monocytes
  • Reduced in patients with Th2 disorders
58
Q

Dermicidin

A
  • Constitutively expressed in sweat
  • Potent antibiotic and antifungal (esp staph aureus and candida)
  • Reduced in patients with Th2 disorders
59
Q

Impetigo infection usually occurs at sites of . . .

A

. . . minor trauma

60
Q
A

Gingivostomatitis due to HSV-1

61
Q
A

Orolabial HSV-2 infection

62
Q
A

Recurrent genital herpes in male

63
Q
A

Recurrent genital herpes on female

64
Q
A

Primary genital herpes on female

65
Q
A

Eczema herpeticum

66
Q
A

Herpes Zoster (bullous example)

67
Q
A

Herpes Zoster (dusky purple indicates older vesicles)

68
Q
A

Herpes Zoster (later stage, pus-filled vesicles)

69
Q
A

Zoster of V1 (Ophthalmic branch of Trigeminal)

70
Q
A

Herpes Zoster (early stage, pre-vesicular)

71
Q
A

Herpes Zoster (vesicular)

72
Q
A

Impetigo

73
Q
A

Erysipelas

74
Q
A

Herpes Simplex (HSV-2)

Particularly bad case. This particular patient also suffers from AIDS, complicating the infection

75
Q
A

Herpes Zoster

(This particular lesion is necrotic. May be related to age-dependent immunosuppression)

76
Q
A

Herpes Varicella

Classic presentation

77
Q
A

Herpes Zoster

classic presentation

78
Q
A

Herpes Zoster

with facial nerve entanglement, Bell’s Palsy of the left facial nerve.

79
Q
A

Molluscum contagiosum

80
Q
A

Molluscum contagiosum

Particularly bad case involving AIDS patient

81
Q
A

Genital molluscum contagiosum

82
Q
A

Staphylococcal abscess

(no real way to tell it is Staph)

83
Q
A

Staphylococcal folliculitis

84
Q
A

Impetigo

85
Q
A

Impetigo

early childhood

86
Q
A

Bullous impetigo

87
Q
A

Erysipelas

88
Q
A

Erysipelas

89
Q
A

Cellulitis

90
Q
A

Eczema herpeticum

91
Q
A

Molluscum contagiosum

92
Q
A

Molluscum contagiosum

Particularly bad case, this one complicated by atopic dermatitis

93
Q

Impetago is usually caused by a ___ strain of ___, while abscesses are usually caused by a ___ strain of ___.

A

Impetago is usually caused by a foreign strain of Staphylococcus aureus, while abscesses are usually caused by a native strain of Staphylococcus aureus.

94
Q

Satellite papules and pustules around intertrigo are a good call for ___ over ___.

A

Satellite papules and pustules around intertrigo are a good call for Candida albicans over bacterial intertrigo.

HMS IDD (28 decks)

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