Chapter 19 - Microbial Disease of the Skin and Wounds Flashcards

1
Q

*Folliculitis

pathogen

A

Staphylococcus

  • gram pos bacteria
  • facultative anaerobes
  • cocci typically arranged in clusters
  • tolerant of salt + desiccation
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2
Q

*Folliculitis

signs + symptoms

A
  • infection of the hair follicle
  • aka pimple
  • called a STY when it occurs at the eyelid base
  • spread of infection into surrounding tissues can produce furuncles
  • carbuncles occur when multiple furuncles grow together
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3
Q

*2 common types of Staphylococcus found on skin

A

1 Staphylococcus EPIDERMIS
2 Staphylococcus AUREUS

*-differ by beta-lactamase production + toxin production

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4
Q

which is more pathogenic? staph. epidermis or staph aureus?

A

Staphylococcus aureus is more pathogenic

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5
Q

*Staphylococcal Scalded Skin Syndrome [SSSS]

pathogen

A

some Staph.AUREUS strains

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6
Q
  • [SSSS]

* epidemiology + transmission

A
  • -disease occurs PRIMARILY IN INFANTS

- transmits by person-to-person spread of bacteria

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7
Q

[SSSS]

pathogenesis

A
  • no scarring bc dermis is unaffected

- death is rare but may occur due to secondary infections

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8
Q
  • [SSSS]

* diagnosis + treatment

A

*D-characteristic sloughing of skin

T-administer antimicrobial drugs

P-widespread presence of S. aureus makes prevention difficult

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9
Q

*Impetigo/Pyoderma + Erysipelas

pathogen

A
  • most caused by Staph. aureus

- some caused by Streptococcus pyogenes

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10
Q

*Impetigo/Pyoderma + Erysipelas

transmission + *epidemiology

A

-transmitted person-to-person contact or via fomites

  • -Impetigo [mostly children]
  • -Erysipelas [mostly elderly]
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11
Q

Impetigo/Pyoderma + Erysipelas

pathogenesis

A
  • most caused by S. AUREUS

- some caused by Streptococcus pyogenes

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12
Q

Impetigo/Pyoderma + Erysipelas

virulence factors

A

Strep.pyogenes + Staph.aureus have similar virulence factors:

  • -M protein
  • -hyaluronic acid
  • -pyogenic toxins
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13
Q

Necrotizing Fasciitis

pathogen

A

mostly caused by Strep. pyogenes

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14
Q

Necrotizing Fasciitis

*transmission

A
  • -Step. pyogenes enters thru breaks in skin

- person-to-person

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15
Q

*Necrotizing Fasciitis

virulence factors

A
  • -Exotoxin A + Streptolysin S are secreted

- various enzymes facilitate invasion of tissues (eating)

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16
Q

Necrotizing Fasciitis

diagnosis + treatment

A

D-early diagnosis is difficult bc symptoms are nonspecific

T-clindamycin + penicillin

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17
Q

*Acne

pathogen

A

commonly caused by Propionibacterium acnes

-grap pos, rod shaped diptheroids

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18
Q

Necrotizing Fasciitis

diagnosis + treatment

A

D-difficult to diagnose early bc symptoms are nonspecific

T-clindamycin + penicillin

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19
Q

*Pseudomonas Infection

pathogen

A

Pseudomonas aeruginosa

-found in soil, decaying matter, moist environments

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20
Q

*Pyocyanin

A
  • -discoloration seen w pseudomonas infection
  • -greenish pigment indicates massive infection
  • indicator for diagnosis
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21
Q

*Pseudomonas Infection

pathogenesis

A
  • infections can occur in BURN VICTIMS
  • -grows under surface of burn
  • p.aeruginosa kills cells, destroys tissue, + triggers shock
  • typically do not occur in healthy individualts
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22
Q
  • Pseudomonas Infection

* diagnosis + *treatment

A
  • D-pyocyanin discoloration

* T-difficult to treat due to multidrug resistance of P.aeruginosa

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23
Q

Cutaneous Anthrax

treatment + prevention

A

T- antimicrobial drugs

P-control of disease in animals

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24
Q

*Gas Gangrene

pathogen

A

several Clostridium species

-C.perfringens [bacterial endospore]

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25
Q

Gas Gangrene

epidemiology/pathogenesis

A
  • traumatic even must introduce endospores into dead tissue

- mortality rate exceeds 40%

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26
Q

*Gas Gangrene

virulence factors

A

C.perfringens secrete 11 toxins

forms endospores

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27
Q

Gas Gangrene

diagnosis + treatment + prevention

A

D-appearance:bubbling + blackening of infected skin

T-rapid treatment is crucial

  • surgical removal of dead tissue
  • administer ANTITOXIN + penicillin

P- proper cleaning of wounds

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28
Q

Poxvirus

pathogen

A

orthopoxvirus (variola virus)

-smallpox/variola

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29
Q

Poxvirus

signs + symptoms

A
  • disease progress thru series of stages

- PUS FILLED SKIN LESIONS

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30
Q

Poxvirus

epidemiology/pathogenesis

A

increase in monkeypox (rare) cases over the past decade

spread by inhalation

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31
Q

Herpes

pathogen

A

herpesviruses 1 + 2

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32
Q

Herpes

signs + symptoms

A
  • slow + spreading skin lesions

- recurrence of lesions is common

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33
Q

Herpes

epidemiology/transmission

A
  • spread bw mucous membranes of mouth + genitals

- herpes infections in adult are not life threatening

34
Q

Herpes

pathogenesis

A
  • painful lesions caused by inflammation + death cell

- causes fusions of cells to form SYNCYTIA

35
Q

*Herpes

diagnosis + *treatment

A

D- presence of characteristic lesions
-IMMUNOASSAY reveals presence of viral antigen

  • T-chemotherapeutic drugs help control the disease but do not cure it
  • ACYCLOVIR
36
Q

*Chickenpox+Shingles

pathogen

A

VARICELLA-ZOSTER VIRUS [VZV] causes both

37
Q

Chickenpox+Shingles

signs + symptoms

A

[chickenp]characterized by lesions on back + trunk that spreads across the body
[shingles]lesions localized to skin along w infected nerve

38
Q

Chickenpox+Shingles

epidemiology/population

A

[chknpx]mostly infants/young kids. more severe in adults

[shingles]risk increases w age

39
Q

Chickenpox+Shingles

pathogenesis

A
  • infected dermal cells cause rash characteristics of chickenpox
  • virus becomes latent in nerve ganglia
  • –reactivation causes shingles
40
Q

Chickenpox+Shingles

diagnosis + treatment

A

D-based on characteristic lesions

T-vaccines available against both
-treatment is for relief of symptoms

41
Q

Warts

pathogen

A

Papillomaviruses

42
Q

Warts

signs + symptoms

A

-benign epithelial growth on skin or mucous membranes

43
Q

Warts

transmission/pathogenesis

A
  • most are harmless

- transmitted via direct contact + fomites

44
Q

Warts

diagnosis + treatment

A

D-observation

T-various techniques although new warts can develop bc latent viruses

45
Q

*Rubella (german measles)

pathogen

A

rubella virus

46
Q

Rubella (german measles)

signs + symptoms

A

-children develop mild rash

47
Q

Rubella (german measles)

epidemiology/population

A

-mostly infants/young kids;

only humans

48
Q

Rubella (german measles)

transmission/pathogenesis

A

-spread via respiratory secretions

49
Q

congenital infection of rubella can result in…

A
  • teratogenic birth defects; or

- death of fetus

50
Q

*Rubella (german measles)

diagnosis + *treatment

A

D-rash or serological testing

*T-vaccines aimed for preventing rubella in pregnant women

51
Q

Measles [Rubeola]

pathogen

A

measles virus

52
Q

*Measles [Rubeola]

signs + symptoms

A

KOPLIK’S SPOTS

53
Q

Measles [Rubeola]

epidemiology + transmission

A
  • occurs mostly in infants/young kids; humans only
  • measles is highly contagious
  • spread via respiratory droplets
54
Q

Measles [Rubeola]

pathogenesis

A

-immune response to infected cells causes most symptoms

55
Q

Measles [Rubeola]

virulence factors

A

adhesion + fusion proteins help virus avoid immune recognition

56
Q

*Measles [Rubeola]

diagnosis + treatment + prevention

A

D-based on signs of measles

T-not available

  • P-MMR vaccine has measles immunization
  • very rare due to vaccination
57
Q

Mycoses Class by infection locations

A

1 SUPERFICIAL
2 SUBCUTANEOUS
3 SYSTEMIC

58
Q

Superficial Mycoses

signs + symptoms

A
  • RINGWORM, dermatophytes (fungal agent) growing in upper dead tissue layers of skin
  • -NOT a parasitic worm
  • white or black PIEDRA
  • Pityriasis versicolor
59
Q

Superficial Mycoses

pathogenesis + epidemiology

A
  • superficial fungi produce KERATINASE

- fungi transmitted via shared hair brushes/combs

60
Q

Superficial Mycoses

diagnosis + treatment

A

piedra: diagnosed by appears; treated by shaving hair
pityriasis: ID by green color under UV light; treated w topical or oral drugs

61
Q

Superficial Mycoses

diagnosis + treatment

A

piedra: diagnosed by appears; treated by shaving hair
pityriasis: ID by green color under UV light; treated w topical or oral drugs

62
Q

Normal Flora - YEAST

A

(fungi)

Malassezia

63
Q

Normal Flora - Bacteria

A

Staphylococcus, Micrococcus, Diptheroids

64
Q

Normal Flora

A
  • normally harmless
  • CANNOT be completely removed thru cleansing
  • may produce disease if they penetrate the epidermis or if the immune system is suppressed
65
Q

Sty

A

folliculitis at the eyelid base

66
Q

furuncles

A
  • boils

- occurs when the infection spreads into surrounding tissues

67
Q

carbuncles

A

when multiple furuncles grow together

68
Q

folliculitis and its variations

A

pimple=folliculitis>furuncles>carbuncles

69
Q

folliculitis is most commonly caused by…

A

staphylococcus

70
Q

folliculitis is most commonly caused by…

A

staphylococcus

71
Q

what causes the skin to slough off in SSSS?

A

the release of EXFOLIATIVE TOXINS by staph. aureus

72
Q

*Normal Flora - Yeast

A

(fungi)

Malassezia

73
Q

*folliculitis and its variations

A

pimple=folliculitis>furuncles>carbuncles

74
Q

*folliculitis is most commonly caused by…

A

staphylococcus

75
Q

*what causes the skin to slough off in SSSS?

A

the release of EXFOLIATIVE TOXINS by staph. aureus

76
Q

Impetigo/Pyoderma + Erysipelas

Diagnosis Treatment

A

D-impetigo has presence of vesicles
–erysipelas has swollen redness

T-penicillin + cleaning of infected areas

77
Q

*Acne

epidemiology

A

-normal flora on skin
-typically begins in adolescence,
can occur later in life

78
Q

*Acne

D + T

A

D-visual exam

T-antimicrobial drugs, drugs that exfoliate,

  • -ACCUTANE for severe acne
  • -blue light to kill bacteria
79
Q

Cutaneous Anthrax

pathogen

A

bacillus anthracis

80
Q

*Cutaneous Anthrax

epidemiology

A

-endospores get into skin via cut or scrape

81
Q

*Cutaneous Anthrax

diagnosis

A

ESCHAR - black painless ulcer

82
Q

Cutaneous Anthrax

prevention

A

control of disease in animals