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Microbiology > 19 > Flashcards

19 Flashcards

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1
Q

Normal Flora - YEAST

A

(fungi)

Malassezia

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2
Q

Normal Flora - Bacteria

A

Staphylococcus, Micrococcus, Diptheroids

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3
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
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4
Q

Wounds

A
  • trauma to any tissue of the body
  • allows microbes to infect the deeper tissues

ex) cuts, scrapes, surgery, burns, bites

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5
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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6
Q

Sty

A

folliculitis at the eyelid base

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7
Q

furuncles

A
  • boils

- occurs when the infection spreads into surrounding tissues

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8
Q

carbuncles

A

when multiple furuncles grow together

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9
Q

folliculitis and its variations

A

pimple=folliculitis>furuncles>carbuncles

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10
Q

folliculitis is most commonly caused by…

A

staphylococcus

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11
Q

Staphylococcus

A
  • gram pos bacteria
  • facultative anaerobes
  • cocci typically arranged in clusters
  • tolerant of salt + desiccation
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12
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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13
Q

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

A

Staphylococcus aureus is more pathogenic

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14
Q

staph. epidermis vs staph aureus

Virulence Factors

A

COAGULASE [+ aureus][-epiderm]

B-Lactamase [90% of aureus][-epiderm]

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15
Q

Folliculitis - diagnosis

A

-isolation of gram-pos bacteria in grapelike clusters from PUS

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16
Q

Folliculitis - treatment

A 
1 DICLOXACILLIN (semi synth penicillin) (drug of choice)
2 VANCOMYCIN used to treat resistant strains
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17
Q

Folliculitis - prevention

A
  • hand antisepsis

- proper procedures in hospitals to minimize MRSA infections

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18
Q

Staphylococcal Scalded Skin Syndrome
[SSSS]

pathogen + virulence factors

A
  • some Staph. AUREUS strains

- 1 or 2 different EXFOLIATIVE TOXINS cause SSSS

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19
Q

Staphylococcal Scalded Skin Syndrome
[SSSS]

pathogenesis

A
  • no scarring bc dermis is unaffected

- death is rare but may occur due to secondary inifections

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20
Q

Staphylococcal Scalded Skin Syndrome
[SSSS]

epidemiology

A
  • disease occurs PRIMARILY IN INFANTS

- transmitter by person-to-person spread of bacteria

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21
Q

Staphylococcal Scalded Skin Syndrome
[SSSS]

diagnosis

A

characteristic sloughing of skin

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22
Q

Staphylococcal Scalded Skin Syndrome
[SSSS]

treatment

A
  • administer antimicrobial drugs

- widespread presence of S. aureus makes prevention difficult

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23
Q

what causes the skin to slough off in SSSS?

A

the release of EXFOLIATIVE TOXINS by staph. aureus

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24
Q

Impetigo [Pyoderma] + Erysipelas

pathogens + virulence factors

A
  • most caused by S. AUREUS

- some caused by Streptococcus pyogenes

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25
Q

Streptococcus pyogenes

A
  • gram pos coccus in chains
  • similar virulence factors to staph. aureus:
  • -M protein
  • -hyaluronic acid
  • -pyrogenic toxins
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26
Q

Impetigo [Pyoderma] + Erysipelas

pathogenesis

A

bacteria invade where skin is compromised

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27
Q

Impetigo [Pyoderma] + Erysipelas

epidemiology

A
  • Impetigo [mostly childten]
  • Erysipelas [mostly elderly]

-transmitted person-to-person contact or via formites

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28
Q

Impetigo [Pyoderma] + Erysipelas

diagnosis

A

-presence of vesicles is diagnosis for Impetigo

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29
Q

Impetigo [Pyoderma] + Erysipelas

treatment

A

penicillin + careful cleaning of infected areas

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30
Q

Impetigo [Pyoderma] + Erysipelas

prevention

A

proper hygiene + cleanliness

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31
Q

Necrotizing Fasciitis
[flesh eating bacteria]

pathogen + virulence factors

A
  • most caused by Strep. pyogenes
  • Exotoxin A + Streptolysin S are secreted
  • various enzymes facilitate invasion of tissues
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32
Q

Necrotizing Fasciitis (flesh eating bacteria)

pathogenesis

A

Step. pyogenes enters thru breaks in skin

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33
Q

Necrotizing Fasciitis (flesh eating bacteria)

epidemiology

A

person-to-person

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34
Q

Necrotizing Fasciitis (flesh eating bacteria)

diagnosis

A

-difficult to diagnose early bc symptoms are nonspecific

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35
Q

Necrotizing Fasciitis (flesh eating bacteria)

treatment

A

1 clindamycin

2 Penicillin

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36
Q

Acne

pathogen + virulence factors

A

commonly caused by Propionibacterium acnes

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37
Q

Acne

epidemiology

A
  • propionibacteria are normal bacteria

- typically begins in adolescence but may occur later

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38
Q

Acne

diagnosis

A

visual examination of skin

39
Q

Acne

treatment

A
  • antimicrobial drugs
  • drugs that exfoliate dead skin cells
  • ACCUTANE
  • BLUE-LIGHT WAVELENGTH to destroy bacteria
40
Q

Propionibacterium acnes

A
  • gram pos
  • ROD SHAPED diphtheroid
  • normal flora
41
Q

Pseudomonas

pathogen + virulence factors

A

Pseudomonas aeruginosa

-virulence factors: adhesins, toxins, + polysaccharide capsule

42
Q

Pseudomonas

pathogenesis

A
  • can occur in burn victims
  • bacteria kills cells, destroys tissue, + triggers shock
  • PYOCYANIN discoloration indicates massive infections
43
Q

pyocyanin discoloration

A

greenish pigment seen in pseudomonas that indicates massive infection

44
Q

Pseudomonas

epidemiology

A
  • P. aeruginosa is not normal microbiota

- can cause infections throughout the body once inside

45
Q

Pseudomonas aeruginosa

A
  • found in soil, decaying matter, + moist environments
  • not normal flora
  • multidrug resistance
46
Q

Pseudomonas

diagnosis

A
  • difficult diagnosis

- pyocyanin discoloration

47
Q

Pseudomonas

treatment

A

-difficult to treat due to multidrug resistance

48
Q

Pseudomonas

prevention

A

-p. aeruginosa is widespread but infection usually doesn’t occur in healthy individuals

49
Q

Cutaneous Anthrax

A
  • caused by Bacillus anthracis
  • occurs when anthrax spores get into the skin (cut + scrape)
  • characterized by ESCHAR
  • bioterrorism tool (spores in mail)
50
Q

ESCHAR

A

black, painless, ulcer

51
Q

Gas Gangrene

signs + symptoms

A
  • blackening of infected skin + muscle

- presence of gas bubbles

52
Q

Gas Gangrene

pathogens + virulence factors

A

caused by several CLOSTRIDIUM species
-C. perfringens
-

53
Q

Gas Gangrene

pathogenesis + epidimiology

A
  • traumatic even must introduce endospores into dead tissue

- mortality rate exceeds 40%

54
Q

Gas Gangrene

diagnosis

A

appearance

55
Q

Gas Gangrene

treatment + prevention

A

rapid treatment is crucial

  • surgical removal of dead tissue
  • administer ANTITOXIN + penicillin
  • prevents w proper cleaning of wounds
56
Q

Clostridium perfringens

A

endospore-forming bacteria

-vegetative cells secrete 11 toxins

57
Q

Poxviruses

A
  • smallpox aka VARIOLA
    rare: orf, cowpox, monkeypox
  • first human disease eradicated globally
58
Q

Poxviruses

signs + symptoms

A

-diseases progress through a series of stages

59
Q

Poxviruses

pathogens + virulence factors

A

caused by ORTHOPOVIRUS aka VARIOLA virus

60
Q

Poxviruses

pathogenesis

A

inhalation of virus

61
Q

Poxviruses

epidemiology

A

-increase in monkeypox cases over the past decade

62
Q

Poxviruses

diagnosis, treatment + prevention

A
  • treatment is immediate vaccination
  • vaccines discontinued in 80’s since eradicated
  • bioterrorism scare
63
Q

Herpes

signs + symptoms

A
  • slow + spreading skin lesions

- recurrence of lesions is common

64
Q

Herpes

pathogens + virulence factors

A
  • caused by human herpesviruses 1 + 2

- virulence factors: various proteins produced

65
Q

Herpes

pathogenesis

A
  • painful lesions caused by inflammation + death cell

- causes fusions of cells to form SYNCYTIA

66
Q

Herpes

epidemiology

A
  • spread bw mucous membranes of mouth + genitals

- herpes infections in adult are not life threatening

67
Q

Herpes

diagnosis

A
  • presence of characteristic lesions

- IMMUNOASSAY reveals presence of viral antigen

68
Q

Herpes

treatment + prevention

A

chemotherapeutic drugs help control the disease but do not cure it
-ACYCLOVIR

69
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

70
Q

Chickenpox + Shingles

pathogen

A

VARIVELLA-ZOSTER VIRUS [VZV] causes both

71
Q

Chickenpox + Shingles

pathogenesis

A
  • infected dermal cells cause rash characteristics of chickenpox
  • virus becomes latent in nerve ganglia
  • –reactivation causes shingles
72
Q

Chickenpox + Shingles

epidemiology

A

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

[shingles]risk increases w age

73
Q

Chickenpox + Shingles

diagnosis

A

based on characteristic lesions

74
Q

Chickenpox + Shingles

treatment + prevention

A
  • vaccines available against both

- treatment is for relief of symptoms

75
Q

Warts

A
  • benign epithelial growth on skin or mucous membranes
  • Papillomaviruses cause warts
  • most are harmless
  • transmitted via direct contact + formites
76
Q

Papillomavirus

A
  • may cause warts

- some are ONCOGENIC due to ability to integrate into host cell DNA

77
Q

Rubella (german measles)

A
  • mostly infants/young kids; only humans
  • children develop mild rash
  • cased by rubella virus
  • spread via respiratory secretions
  • diagnosis: rash or serological testing
78
Q

congenital infection of rubella can result in…

A
  • teratogenic birth defects; or

- death of fetus

79
Q

rubella vaccine is aimed for…

A

preventing rubella in pregnant women

80
Q

Measles [Rubeola]

signs + symptoms

A

KOPLIK’S SPOTS

81
Q

Measles [Rubeola]

pathogen + virulence factors

A
  • caused by measles virus

- adhesion + fusion proteins help virus avoid immune recognition

82
Q

Measles [Rubeola]

pathogenesis

A

-immune response to infected cells causes most symptoms

83
Q

Measles [Rubeola]

epidemiology

A
  • occurs mostly in infants/young kids; humans only
  • measles is highly contagious
  • spread via respiratory droplets
84
Q

Measles [Rubeola]

diagnosis

A

based on signs of measles

85
Q

Measles [Rubeola]

treatment + prevention

A
  • no treatments
  • MMR vaccine has measles immunization
  • very rare due to vaccination
86
Q

Mycoses

A
  • caused by fungi
  • most are OPPORTUNISTIC pathogens
  • mycoses is classified by infection locations
87
Q

Mycoses Class by infection locations

A

1 SUPERFICIAL
2 SUBCUTANEOUS
3 SYSTEMIC

88
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
89
Q

Piedra

A

irregular nodules on hair shaft

-white piedra is dandruff

90
Q

Pityriasis versicolor

A

hypo or hyperpigmented patches of scaly skin

91
Q

Superficial Mycoses

pathogens

A

Piedraia hortae[cause black piedra]
Trichosporon beigelii[cause white piedra]
Malassezia furfur[cause pityriasis]

92
Q

Superficial Mycoses

pathogenesis + epidemiology

A
  • superficial fungi produce KERATINASE

- fungi transmitted via shared hair brushes/combs

93
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

Microbiology (26 decks)

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