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Med Micro Test 3 > Skin Infections > Flashcards

Skin Infections Flashcards

1
Q

Steps of skin infections

A
  1. exposure to pathogens
  2. Adherence to skin or mucosa
  3. invasion thru epithelium
  4. Colonization and growth
  5. Toxicity effects or invasiveness
  6. Tissue damage
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2
Q

Factors that could contribute to wound becoming infected..

A
  1. dose of bacteria
  2. virulence of the organism
  3. Vascular integrity
  4. Immune system strength
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3
Q

Bacteria on skin that prevent pathogen attachment and outcompete

A

Staphylococcus epidermis

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4
Q

Skin disease resistance mechanisms (5)

A
  1. dry layer regenerating with keratinocytes
  2. cell secrete antimicrobial peptides and lysozyme
  3. lactic acid and fatty acids produced by sebaceous glands
  4. Lots of salt
  5. Sweat glands cool off the body
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5
Q

Keritinocytes (skin cells)

A

sentinels detecting pathogens and damage associated molecular patterns

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6
Q

What parts of the skin can become infected?

A

epidermis, dermis, and hypodermis

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7
Q

Folliculitis

A

Hair follicle infection

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8
Q

Abscess

A

localized collection of pus created by host defense to prevent spreading

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9
Q

Cellulitis

A

involves all layers of skin, leads to fever, and occassionally causes bacteremia

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10
Q

Gangrene

A

advanced cellulitis with significant tissue necrosis & death

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11
Q

Osteomyelitis

A

bone infection often due to contamination of open fractures

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12
Q

Most common skin condition

A

Acne vulgaris

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13
Q

How is acne caused?

A

follicles trap sebum and dead epithelial cells which clogs pore. Lipases digest the surplus of trapped oil, which leads to inflammation.

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14
Q

How do we treat acne?

A

Doxycline which is a ribosome inhibitor

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15
Q

Impetigo

A

superficial bacerial infection common in children causing the skin to flake off

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16
Q

Bacteria that cause impetigo

A

streptococcus pyogenes

Staph aureus

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17
Q

How can we distinguish between staph bacteria types?

A

Coagulase

Staph aureus is coagulase positive

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18
Q

How can we distinguish between staph and strept?

A

Staph is catalase positive and strept is catalase negativeq

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19
Q

What type of hemolysis is streptococcus pyogenes?

A

beta, group A

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20
Q

How is strept pyogenes spread?

A

fomites (normally on skin or respiratory)

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21
Q

How does strept pyogenes penetrate into deeper layers?

A

proteases like hyalurondiase and exotoxin B

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22
Q

How do we treat streptococcus pyogenes

A

penicillin

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23
Q

Necrotizing fasciitis

A

flesh eating infection

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24
Q

What causes necrotizing fasciitis?

A

many microbes
Group A streptococcus
Clostridium perferinges (gas gangrene)

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25
Q

Bacteremia

A

widespread desquamation of skin, shock, multiorgan failure, and death caused by exotoxins

26
Q

Where is Staph aureus found?

A

in your nose

27
Q

How is staph aureus transmitted?

A

through air droplets and on skin

28
Q

How do hospitals prevent staph aureus infection before surgery?

A

chlorhexidine

29
Q

What people are more at risk for a staph aureus infection?

A

Chediak-Higashi disease (defect in lysosomal enzyme)

30
Q

Staph aureus causes infection by…

A
  1. Protein A
  2. Coagulase
  3. Hemolsisn and leukocidins
  4. Salt tolerance and toxins
31
Q

Protein A

A

prevents antibodies from tagging the protein

32
Q

Coagulase

A

forms fibrin coat around the organism

33
Q

Hemolysins and leukocidins

A

destroy RBCs and WBCs

34
Q

Staphylococcal scaled skin syndrome

A

Exfoliatin disrupts desmoglein 1, the epidermis then splits away

35
Q

How is staph scaled skin syndrome treated?

A

Mupirocin (inhibits tRNA synthesis)

Systemic antibiotics

36
Q

1st mechanism of resistance to staph aureus

A

Expression of beta lactamases (cuts the beta lacatam ring so the drug doesn’t work as well)

37
Q

2nd mechanism of resistance to staph aureus

A

change in the structure of penicillin binding proteins

38
Q

Drug that treats bacteria that changed their PBP

A

vancomycin

39
Q

Vancomycin characteristics

A

Gram positive

bactericidal

40
Q

How does vanco work?

A

Peptidoglycan synthesis is prevented (transglycosylase is inhibited)

41
Q

Dermatophytoses

A

caused by fungi (ringworm, tinea, jock itch, athletes foot)

42
Q

Types of bacteria that cause dermatophytoses (3)

A
  1. trichophyton
  2. microsporum
  3. epidermophyton
43
Q

How are fungal skin infections transferred?

A

human to human, fomites, or zoophilic

44
Q

Why do fungal infections rarely invade?

A

they grow best at 25 C and are unable to survive at 37 C

45
Q

fungal infection associated with rose thorns

A

Sporothrix schenckii

46
Q

Tinea capitis

A

scalp

47
Q

Tinea barabe

A

beard

48
Q

Tinea axillaris

A

armpit

49
Q

Tinea corporis

A

body

50
Q

tinea cruris

A

groin

51
Q

tinea pedis

A

feet

52
Q

tinea unguium

A

nail

53
Q

How are fungal infections diagnosed?

A

collect skin, nail, or hair
dissolve in 10% KOH
Stain with calcofluor white or grow on sabaroud media

54
Q

What causes most tinea pedis (athletes foot) infections?

A

Trichophyton rubrum

55
Q

How do we treat fungal infections?

A 
topical itraconazole (AZOLE)
1 month oral for nail infections
56
Q

How does azole work?

A

blcocks the production of membrane protein ergosterol and causes the accumulation of lanosterol
fungistatic

57
Q

How does hook worm enter the skin?

A
  1. Contact with soil
  2. Enters break in the skin (larva)
  3. Goes into the small intestine and becomes an adult
  4. Eggs are released in feces
58
Q

What drug do we use to treat worm infections?

A

Albendazole

59
Q

How does albendazole work?

A

inhibits microtubules that affect glucose transport

60
Q

Symptoms of worm infection

A

itching & localized rash
Weight loss
Anemia and protein deficiency
cognitive and physical developmental delays

61
Q

How do you diagnose hookworm infections?

A

eggs in stool

Med Micro Test 3 (4 decks)

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