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MICRO > Skin & soft tissue infections > Flashcards

Skin & soft tissue infections Flashcards

1
Q

what is the epidermis?

A

thin layer portion consisting of several layers of epithelial cells
- when unbroken, an effective physical barrier against microbes

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2
Q

what is the dermis?

A

thick inner layer portion; provides strength and flexibility and supports growth of the epidermis
- blood vessels, nerve endings, hair follicles, sweat an oil glands
- follicles an glands can serve as passageways for microorganisms

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3
Q

in what part of the body does the normal flora change?

A

when its warm and moist

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4
Q

what is the benefit of the microbiome?

A

microbial antagonism

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5
Q

what is the risk of the microbiome?

A

entry into tissues

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6
Q

normal flora must be resistant to what?

A

drying and high salt concentrations

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7
Q

concentration of microbes vary with available nutrients, moisture, pH, temp, salt and sebum levels. T or F

A

T

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8
Q

90% of normal skin flora is which microbe?

A

staphylococcus epidermidis

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9
Q

what other bacteria is also present in normal skin flora?

A

cutibacterium acnes, proprionibacteria)

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10
Q

when does normal skin flora become pathogenic?

A

when skin barrier is broken or invaded (catheterization)

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11
Q

how can the skin have microbial growth in hospital environment?

A

covered in salt, sweat and sebum which contains antimicrobials

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12
Q

what is a bullae?

A

is a large vesicle (>5mm), will rupture easily to tough, fluid is clear

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13
Q

what is a skin rash?

A

a vesicle forms from accumulation of fluid under the epidermis
- any change in colour or texture

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14
Q

what is a palpule?

A

a raised lesion resulting from accumulation of material, infectious or otherwise, in the dermis.

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15
Q

what is plaque?

A

is a large raised area that forms a plateau

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16
Q

what is enanthem?

A

rash on mucous membranes accompanied by systemic symptoms such as fever, malaise and headache

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17
Q

what is exanthem?

A

skin rash accompanied by systemic symptoms, fever, malaise and headache

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18
Q

what is a macule?

A

is a flat lesion that cannot be palpated, like a freckle

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19
Q

what is a wheal?

A

is a raised, itchy area of the skin that is almost always an overt sign of allergy

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20
Q

what is a nodule?

A

is a large papule that travels deeper into the skin

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21
Q

what is a skin rash most commonly associated with?

A

an infection

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22
Q

why does a rash form?

A

reaction to a toxin produced by the bacteria, damage to the skin by a pathogen, immune response to a pathogen BUT… can also be associated with drug reactions, allergy, autoimmune diseases

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23
Q

what is an ulcer?

A

is an open sore often caused by initial abrasion

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24
Q

what is an ulcer maintained by?

A
  1. inflammation, 2. infection, 3. medical conditions that impede healing
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25
Q

what is a pustule?

A

a pus filled raised lesion on the skin, usually the result of a buildup of the cellular debris of inflammatory cells, with or without microorganisms, under the epidermis

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26
Q

what sampling techniques are available?

A
  • skin scraping
  • biopsy and needle aspiration
  • swabs are only useful is sample contains suspected pathogen
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27
Q

what do swabs collect?

A

swabs only sample surface and collect a small amount of fluid

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28
Q

where should samples be stored?

A

in a sterile container for immediate transport

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29
Q

the skins normal flora will interfere with what?

A

sampling
- normal flora will colonize the wound and different than bacteria deeper in the wound which are true pathogens

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30
Q

skin infections arise from what 3 things?

A
  • exogenous penetration
  • hematogenous spread
  • superficial structures of skin (hair follicles)
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31
Q

what is exogenous penetration?

A

animal and insect bites, surgery, trauma (skin abrasions, etc)

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32
Q

what is hematogenous spread?

A

disseminated infection (eg. gonococcal infections)

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33
Q

is group A streptococci gram neg or pos?

A

beta-hemolytic, gram pos cocci, catalase negative

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34
Q

what does group A streptococci colonize?

A

colonizer of skin and nasopharynx

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35
Q

what diseases can group A streptococci cause?

A

skin an soft tissue infections, bone an joint infections, strep, scarlet fever, rheumatic fever, bacteremia and glomerulonephritis

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36
Q

is staphylococcus aureus gram neg or pos?

A

gram pos cocci, catalase positive, coagulase positive

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37
Q

what does staphylococcus aureus colonize?

A

colonizes nasopharynx, axillae, rectum, skin

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38
Q

what diseases can staphylococcus aureus cause?

A

skin an soft tissue, bone, joint, heart valves, kidneys, lungs, brain, bacteremia, food poisoning

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39
Q

what is folliculitis?

A

localized infection of the hair follicle (red, swollen an pus filled), lesions vary in size and may scar

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40
Q

what are the manifestations of folliculitis?

A

pain, tenderness and localized edema at site of infection

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41
Q

when does folliculitis resolve?

A

1 - 2 weeks

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42
Q

what is carbuncle (folliculitis)?

A

cluster of boils, often hard round and deep infection of multiple hair follicles
- associated with fever and are slower to heal

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43
Q

where does carbuncle usually appear?

A

often occurs on back of knees, neck, shoulders or thighs (especially in men where skin is thick)

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44
Q

what are furuncles (folliculitis)?

A

large, painful, raised nodular lesion - extension of folliculitis into surrounding hypodermis

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45
Q

how is furuncles different from carbuncle?

A

grows larger an more painful (5-7 days) before it develops a yellow white tip that then ruptures an drains

46
Q

what are the 3 causative pathogens of folliculitis?

A
  • Staphylococcus aureus
  • Pseudomonas aeruginosa
  • Candida albicans
47
Q

what are the 4 treatments for folliculitis?

A
  • antibacterial soap to area, warm compress
  • clean an drain abscess of pus, if possible
  • multiple lesions: topical mupriocin
  • severe multiple lesions: oral dicloxacillin
48
Q

what is Staphylococcal scalded skin syndrome?

A

some strains of S.aureus produce exfoliative exotoxins, skin falls away within 2 days of symptom onset and resolves within 7-10 days

49
Q

how does Staphylococcal scalded skin syndrome occur? (patho)

A

exotoxin travels from site of infection through the bloodstream causing widespread epidermal response to the exotoxin. toxins cause cells within the outer epidermis to separate from each other an from underlying tissues - systemic effect (toxemia)

50
Q

how does Staphylococcal scalded skin syndrome typically appear?

A

redness an wrinkling problem of the skin commonly appears first on the mouth then spreads across entire body followed by the formation of clear, fluid filled blisters

51
Q

what is the Tx for Staphylococcal scalded skin syndrome?

A
  • IV naficillin
  • oxacillin therapy
52
Q

what is impetigo/pyoderma?

A

small, flattened, red patches on face an limbs an develop into thin-walled vesicles an pustules that rupture an crust over (golden brown, sticky crust)

53
Q

is impetigo/pyoderma contagious?

A

lesions are highly contagious an itchy until healed

54
Q

who is impetigo/pyoderma most common in?

A

common in children 2-5 years, peaks in summer months

55
Q

when does impetigo/pyoderma resolve?

A

1-2 weeks

56
Q

what are the causative pathogens of impetigo/pyoderm?

A

s. pyogenes (20%), s.aureus (80%)

57
Q

what are the Tx for impetigo/pyoderma?

A
  • limited lesions: topical mupirocin
  • multiple severe lesions: PO clindamycin or doxycycline
58
Q

what is erysipelas?

A

acute infection of the dermis and dermal. often preceded by impetigo/streptococcal pharyngitis an concomitant fever

59
Q

who is erysipelas most common in?

A

most common in children an elderly (face arms legs)

60
Q

signs/symptoms of erysipelas:

A
  • ERYTHEMA!
  • risk of bacteremia
  • increased WBC
  • pain, fever, chills
  • swollen lymph nodes
61
Q

5% of pt with erysipelas, develop what?

A

bacteremia which carries high rate of mortality

62
Q

how does erysipelas usually appear on the face?

A

often presents as a “butterfly wing” lesion

63
Q

what is erythema caused by in erysipelas?

A

pyrogenic toxins

64
Q

what is the Tx for erysipelas?

A

PO or IV penecillin therapy

65
Q

what is cellulitis?

A

acute spreading infection of the skin involving SQ fatty tissues an can lead to bacteremia

66
Q

what can cellulitis develop in to?

A

sepsis

67
Q

what are the causative pathogen of cellulitis?

A

streptococcus pyogenes, s. aureus

68
Q

how long for cellulitis to resolve?

A

1-2 weeks, can reoccur

69
Q

what are risk factors of cellulitis?

A
  • previous infection
  • chronic venous stasis
  • diabetes
70
Q

what is the treatment for cellulitis?

A

oral or IV antibiotic therapy (in complicated cases)

71
Q

what are clinical signs of cellulitis?

A

malaise, chills, fever, warmth, pain, erythema, edema

72
Q

what is necrotizing fasciitis?

A

life threatening infection located deep fascia and necrosis of SQ tissue

73
Q

what is type 1 (polymicrobial) necrotizing skin infection?

A

mixed infection associated with anaerobic, aerobic and facultative anaerobic bacteria which fuel a cycle of bacterial colonization an inflammatory tissue necrosis

74
Q

what is type 1 (polymicrobial) necrotizing skin infection associated with?

A

post surgical setting an previously ill patients

75
Q

what is type 2 (monomicrobial) necrotizing skin infection?

A

can occur in patients with known risk factors
- eg. group A strep (GAS) or s.aureus

76
Q

what are clues to know if it is necrotizing fasciitis?

A
  • rapidly progressive (cm in an hr)
  • pain disproportionate to apparent tissue damage
  • prominent systemic signs/symptoms
  • anesthesia of effected care
77
Q

how is Dx made in necrotizing fasciitis?

A

made surgically
- tissue biopsies important for Dx

78
Q

amputation of limb with necrotizing fasciitis may be necessary. T or F

A

T

79
Q

concomitant signs of infection:

A

systemic toxicity: fever, tachycardia, hypotension
- elevated WBC count, pain

80
Q

what does necrotizing fasciitis look like?

A

dusky purplish skin discolouration develops near the site of injury
- simultaneous presence of hemorrhagic bullae

81
Q

what is the Tx for type 1 (polymicrobial) necrotizing skin infection?

A

broad spectrum antibiotic coverage of both aerobes an anaerobes (piperacillin, tazobactam)

82
Q

what is the Tx for type 2 (monomicrobial) necrotizing skin infection?

A

GAS (IV high dose penicillin or ampicillin)
- IVIg should be considered especially in cases of streptococcal toxic shock syndrome
- clindamycin to decrease toxin production

83
Q

what does clindamycin do?

A

is a protein synthesis inhibitor; reduces toxin production

84
Q

what are the strains of GAS that cause necrotizing fasciitis?

A
  • exotoxin A (super antigen)
  • M proteins, streptolysin S
  • streptokinase, hyaluronidase, deoxyribonucleases
85
Q

super antigens produce a non specific an uncontrolled immune response, resulting in wide range tissue damage. Which inflammatory cells are involved?

A

causes over production of cytokines that over stimulate macrophages
macrophages release massive amounts of O2 free radicals, causing rapid tissue damage

86
Q

what does IVIg do?

A

neutralize/reduce effects of endotoxin an modulate the inflammatory response

87
Q

streptococcus pyogenes releases what?

A

endotoxins that are super antigens

88
Q

what is the causative pathogen in varicella (chickenpox)?

A

human herpes virus 3 (varicella zoster)

89
Q

what is the incubation period for varicella?

A

2-3 weeks

90
Q

what are the symptoms of varicella (chickenpox)

A

pleomorphic rash (1-2 days) preceded by fever, malaise, headache and abdominal pain

91
Q

where does varicella (chickenpox) most commonly occur?

A

trunk (abundant), face, arms, legs
- may affect mouth, pharynx and vagina

92
Q

what are the 5 steps of the varicella rash (shingles)?

A
  1. macule
  2. papule
  3. vesicles
  4. pustules
  5. scab/crust within 4-7 days of rash onset
93
Q

what ages should Varivax vaccine be given?

A

1st dose: 12-15 months of age
2nd dose: 18 months of age

94
Q

what population of people should recieve the shingrix vaccine?

A

50 an up
- 2 dose series

95
Q

what is the Tx for herpes zoster (shingles)?

A

oral antiviral agents (acyclovir)

96
Q

what is the patho of the reactivation of the herpes virus varicella-zoster?

A

reactivated virus moves along the peripheral nerves into the cutaneous sensory nerves of the skin. viral DNA becomes dormant in the dorsal root ganglion

97
Q

why does the reactivation of the herpes virus varicella zoster occur?

A

usually associated with altered immune responses

98
Q

how is HSV-2 primarily transmitted?

A

sexual contact

99
Q

how is HSV-1 most commonly transmitted?

A

via oral routes

100
Q

infections of HSV usually occurs between which ages?

A

15-29

101
Q

how does the HSV rash appear?

A

painful short lived vesicles that occur near the margins of the lips
- reoccurrence triggered by emotional upset, stress, hormonal fluctuations, sunlight and disease

102
Q

what signs symptoms are associated with HSV?

A

flu like symptoms, malaise, fever, muscle pain

103
Q

what do antiviral drugs do?

A

shorten healing time and protect cells

104
Q

topical treatments apply directly to the lesion (docosanol an acyclovir). T or F

A

T

105
Q

what does valacyclovir do?

A

can help reduce frequency of eruptions and shorten healing time

106
Q

what is dermatomycoses (ringworm)?

A

fungal infection transmitted via direct contact (ppl an animals) fomites

107
Q

how is dermatomycoses (ringworm) Dx?

A

by skin scrapings and processed in the lab using potassium hydroxide (KOH)

108
Q

what does KOH do?

A

dissolves epithelial tissue, allowing a clear view of the fungal hyphae

109
Q

what is the Tx for dermatomycoses (ringworm)?

A

topical anti fungal meds

110
Q

how does dermatomycoses (ringworm) appear?

A

lesions start small, then expand outward; open at centre with a raised an scaley boarder (erythematous an scaling patches that are round an oval)

MICRO (4 decks)

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