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MM Test 3 > B6.088 Gangrene > Flashcards

B6.088 Gangrene Flashcards

1
Q

gram + organisms on this test

A 
staph
strep pyogenes
clostridium
actinomyces
Propionibacterium
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2
Q

gram - organisms on this test

A

bacteroides
fusobacterium
prevotella
porphyromonas

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3
Q

how are strep species serotyped

A

surface carbohydrate antigens

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4
Q

B hemolytic strep

A

Group A: s.pyogenes

Group B: s.agalactiae

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5
Q

resp tract infections associated with GAS

A

strep throat

pharyngitis

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6
Q

skin infections associated with GAS

A

impetigo
erysipelas/ cellulitis (dermis)
necrotizing faciitis (subQ tissue)

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7
Q

systemic infections associated with GAS

A

bacteremia
rheumatic fever
acute glomerulonephritis
streptococcal TSS

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8
Q

impetigo (strep)

A

usually occurs in young kids (2-5)
honey colored crusty lesions
“crusty, weeping”

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9
Q

erysipelas

A

raised, bright red plaques with sharply defined borders

coalescing bullae

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10
Q

time frame of TSS and necrotizing fasciitis

A

within less than 24 hours of infection

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11
Q

time frame of acute glomerulonephritis after GAS infection

A

2-3 weeks after initial infection

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12
Q

adhesins on GAS

A

M protein: >160 serotypes
protein F: binds fibronectin
lipoteichoic acid

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13
Q

capsule of GAS

A

hyaluronic acid

prevents immune system attack

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14
Q

streptolysin O

A

pore forming toxin

lyses target cells

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15
Q

hyaluronidase

A

spreads through tissues and breaks down hyaluronic acid

sometimes mutated/inactivated

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16
Q

streptococcus pyrogenic exotoxins (Spe)

A

superantigen

can cause scarlet fever and TSS

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17
Q

streptokinases

A

activate plasminogen to dissolve clots

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18
Q

drugs of choice for GAS infections

A

all isolates susceptible to penicillin (no beta lactamase)
strep throat: amoxicillin
cellulitis: penicillin, ceftriaxone
TSS: penicillin + clindamycin

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19
Q

function of clindamycin in GAS infection

A

suppresses toxin production

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20
Q

why might you see recurrent disease from GAS

A

re-infection from an asymptomatic family member

colonization with different bacteria that produce beta-lactamase

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21
Q

describe the staph species

A 
gram + cocci
clusters
non motile, non spore forming
facultative anaerobes
catalase +
oxidase -
major component of normal skin and nares flora
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22
Q

infections associated with staph

A 
80% of skin and soft tissue infections
ortho infections
endocarditis
nosocomial blood infections
septic shock
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23
Q

ESKAPE organisms

A 
have antibiotic resistance
enterococcus
staph aureus
klebsiella
actinobacter
pseudomonas
enterobacter
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24
Q

how do you acquire MRSA from MSSA

A

within 2 yrs of methicillin use

associated with increased mortality

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25
Q

VISA

A

vancomycin intermediate: thickened cell wall

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26
Q

VRSA

A

vancomycin resistant

resistance plasmid from enterococci

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27
Q

adherence factors of staph aureus

A

protein A - binds the Fc region of Abs
fibronectin binding proteins
collagen binding proteins

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28
Q

virulence factors of staph aureus that aren’t adherence factors

A 
4 cytolysins
leukocidins
phenol-soluble modulins
12 enterotoxins (superantigens)
secreted enzymes: proteases, nucleases, hyaluronidase, coagulase
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29
Q

skin infections associated with staph aureus

A

95% of all staph infections are skin infections

cellulitis, impetigo, folliculitis, abscess

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30
Q

cellulitis

A

warm, red, swollen soft tissue that is tender to the tough

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31
Q

impetigo (staph)

A

classically, erythematous papules and pustules with yellow “honey” crusting
typically on face
large bullae suggest staph

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32
Q

furuncle / abscess

A

associated with a hair follicle
infection occurring in deep tissues at base of hair follicle resulting in collection of pus
tender to palpation
may or may not spontaneously drain purulent material
staph aureus&raquo_space;> GAS

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33
Q

cause of scalded skin syndrome

A

diffuse exfoliation
exfoliative dermatitis caused by toxin producing strains: exfoliative toxins ETA and ETB
toxins absorbed by bloodstream

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34
Q

symptoms of SSS

A

localized tender erythema, systemic spread, fever, blisters
usually involves children < 5
mortality and scarring are rare

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35
Q

cause of TSS

A

superantigen carried by 20% of staph aureus isolates

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36
Q

symptoms of TSS

A

sudden fever followed by headache, sore throat, diffuse red rash, skin desquamation
shock within 48 h

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37
Q

epidemiology of TSS

A

6,000 cases/ year in US
5% fatality w ttx
65% fatality w/o ttx

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38
Q

TSST-1 toxin

A

released into blood
binds TCR and MHC2 simultaneously
nonspecifically activated 10-20% of T cells
cytokine storm (IFNy, IL-2)
capillary leakage > hypotension > shock > death

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39
Q

C3b defense against staph

A

activated by staph cell wall fragments

opsonizes bacteria and enhances phagocytosis

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40
Q

neutrophil defense against staph

A

engulf the bacteria

intracellular killing by O2 radicals

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41
Q

predispositions to staph infections?

A

C3 hypercatabolism
neutropenia
reduced production of H2O2 and O2
lazy leukocyte

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42
Q

topical ttx of staph aureus

A

bacitracin

muprirocin

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43
Q

ttx of MSSA

A

1st gen cephs, amoxicillin- clavulanate, nafcillin/ oxacillin

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44
Q

ttx of MRSA

A 
clindamycin
Bactrim
doxycycline
linezolid
vancomycin (only IV)
daptomycin (only IV)
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45
Q

VISA/VRSA ttx

A

resistant to methicillin as well

linezolid, daptomycin, quinupristin / dalfopristin

46
Q

lab diagnosis of staph aureus

A

catalase +
coagulase +
beta hemolytic
mannitol fermentation

47
Q

aerotolerance of anaerobes

A

most are aerotolerant
tolerate brief exposure to variable levels of O2
-some have SOD and catalase
-some have a very active NADH oxidoreductase

48
Q

why can anaerobes not grow in presence of high O2

A

high redox potential of tissues due to dissolved O2
oxidation of sulfide to disulfide > inactive bacterial enzymes
all e- used to reduce O2 > blocks biosynthesis

49
Q

endogenous anaerobes (normal flora)

A 
opportunists
gram neg:
bacteroides
fusobacterium
prevotella
prophyromonas
gram pos:
actinomyces
Propionibacterium
mobiluncus
lactobacillus
50
Q

exogenous anaerobes

A

clostridium (G+)

spore forming

51
Q

areas of body with high conc of anaerobic flora

A

gingival crevice
colon
1000:1
anaerobes: aerobes

52
Q

additional sites where anaerobes can thrive

A

hypoxic tissues (wounds, diabetics)
dental plaque
tonsillar crypts
microenvironments where aerobes or facultative anaerobes deplete O2

53
Q

predisposing conditions to anaerobic infections

A 
breeches in mucocutaneous barrier
displacement of normal flora
compromised vascular supply
trauma with tissue destruction
antecedent infection
54
Q

clues to an anaerobic infection

A

foul odor
lesion near mucosal surface
infections with tissue necrosis and abscess formation
presence of underlying disease: tissue necrosis, impaired blood supple
previous abx therapy
infection following a bite wound
“sulfur granules” exudating

55
Q

virulence factors of anaerobes

A

anti-phagocytic capsule
tissue destructive enzymes
beta-lactamase production (can protect themselves and other species in mixed infections)
SOD production (aerotolerant anaerobes)

56
Q

function of SOD production in anaerobes

A

protect bacteria from toxic O2 radicals as they move out of usual niche

57
Q

identification challenges associated with anaerobes

A

air in sample
identification takes several days or longer
often derived from normal flora sample

58
Q

where is bacteroides fragilis found

A

colon and female GU tract

59
Q

what allows b. fragilis to be the most common anaerobe isolated from human infection

A

highly tolerant to O2 (produces SOD)
polysaccharide capsule
modified LPS has little/no endotoxin activity

60
Q

how does one get infected w b.fragilis

A

often released from colon after trauma

  • intra abdominal abscesses
  • peritonitis
  • bacteremia
  • skin and soft tissue infections
61
Q

how is b. fragilis identified/ diagnosed?

A 
bile resistant (grows in 20% bile)
catalase +
indole -
62
Q

antibiotic resistance of b. fragilis

A

conjugative plasmids, transposons encoding high level of antibiotic resistance

  • penicillin resistant
  • kanamycin +/ vancomyin + blood agar plates (KV BAP)
63
Q

2nd most common anaerobic bacteria causing infections

A

prevotella

porphyromonas

64
Q

prevotella and porphyromonas normal locations

A 
normal flora of:
oropharynx
nose
GIT
GUT
65
Q

characteristics of prevotella

A 
saccharolytic
sensitive to penicillin
kanamycin resistant (grow on KV BAP)
66
Q

characteristics of porphyromonas

A

asacchrolytic
no growth on KV BAP
sensitive to penicillin

67
Q

clinical manifestations of fusobacterium

A

pleuropulmonary abscess
intra-abdominal abscess
systemic infection

68
Q

lab diagnosis of fusobacterium

A 
slender, spindle shaped Gram - with tapered ends
Kanamycin sensitive (no growth on KV BAP)
69
Q

treatment of gram neg anaerobes

A

metronidazole
carbapenem
B lactam + B lactamase inhibitor

70
Q

why are gram neg anaerobes so difficult to control

A

endogenous origin
normal flora
polymicrobial infections

71
Q

description of Propionibacterium (p. acnes)

A 
gram + bacilli
anaerobic
non spore forming
catalase +
indole +
diphtheroid (cube shaped)
72
Q

infections with p.acnes

A

human acne

opportunistic infections

73
Q

normal flora of p.acnes

A

oral
nasopharynx
skin
GIT

74
Q

DOC for p.acnes

A

benzoyl peroxide

erythromycin

75
Q

description of actinomyces

A

gram + bacilli
anaerobic
catalase -
indole -

76
Q

infections with actinomyces

A

actinomycosis abscesses

  • cervicofacial or “lumpy jaw” (50%)
  • thoracic, abdominal, pelvic, CNS
77
Q

distinguishing features of actinomyces infections

A

abscesses with sulfur granules

molar tooth colonies

78
Q

treatment of actinomyces

A

surgical treatment + penicillin

79
Q

etiology of bacterial vaginosis

A

displacement of normal flora (typically lactobacilli)

polymicrobial: gardnerella, mobiluncus

80
Q

distinguishing features of mobiluncus

A

fishy odor of discharge + KOH
“clue cells” : coccobacilli adhering to epithelial cells
pH > 4.5

81
Q

treatment of mobiluncus

A

metronidazole or clindamycin

82
Q

features of lactobacilli

A

gram + bacillus

facultative to strict anaerobe

83
Q

normal flora of lactobacilli

A

oral
GI
GU

84
Q

infections associated with lactobacilli

A

transient bacteremia after gyn procedure or birth
endocarditis
septicemia in immunocompromised

85
Q

DOC for lactobacilli

A

vanc resistance

penicillin + aminoglycoside

86
Q

4 types of clostridium

A 
clostridium botulinum (botulism)
c. diff (pseudomembranous colitis)
clostridium perfringens (gas gangrene)
clostridium tetani (tetanus)
87
Q

features of all clostridium

A 
spore forming
gram + bacilli
anaerobes
saprophytic (love dead organic matter)
opportunists
all produce highly degradative enzymes and/or extremely potent exotoxins
88
Q

4 types of botulism

A
  1. classical / food bore
  2. infant
  3. wound
  4. undetermined
89
Q

food borne / classical botulism

A

ingestion of improperly canned food

germinated spores in food (preformed toxin)

90
Q

infant botulism

A

ingestions of spores from soil, dust, honey

in vivo production of toxin

91
Q

wound botulism

A

contamination of traumatic wound with spores

in vivo production of toxin

92
Q

lethal dose of botox

A

1-2 mg

93
Q

structure of A-B exotoxins of botulism

A

released during growth and autolysis of bacteria

  • heavy chain (B): targeting to axon terminal
  • light chain (A): protease that cleaves SNAP-25 protein (required for ACh vesicle fusion w axon)
94
Q

effect of A-B exotoxins

A

blocks fusion of vesicles and release of ACh

inhibit nerve pulses

95
Q

botulism incubation

A

18-26 hours

96
Q

systemic symptoms of botulism

A

weakness, dizziness, dry mouth, nausea, vomiting

97
Q

neuro features of botulism

A 
blurred vision
inability to swallow
difficulty in speech
descending weakness (flaccid paralysis)
respiratory paralysis
98
Q

diagnosis of botulism

A

clinical symptoms only

99
Q

ttx of botulism

A 
antiserum
-history of questionable food ingestion
-toxin-receptor binding blocks Ab binding
antibiotics:
-only in case of infection
prevention:
-proper food handling
100
Q

description of c. perfringens

A 
large gram + bacilli
occasional spores
non motile
encapsulated
double zone of B hemolysis
lecithinase activity (egg yolk)
101
Q

a toxin of c. perfringens

A

lecithinase (phospholipase C)

  • lyses a variety of cells
  • cellulitis w gas formation
  • fasciitis (suppurative myositis)
  • myonecrosis (gas gangrene)
102
Q

process of gas gangrene formation

A
  1. spores germinate > vegetative cells
  2. growth, fermentation of carbs > gas formation
  3. distention of tissue > interference with blood supply
  4. bacteria produce necrotizing toxin & hyaluronidase > spread
  5. tissue necrosis extends > increased bacterial growth
  6. hemolytic anemia > severe toxemia > death
103
Q

treatment of c. perfringens fasciitis or myonecrosis

A

prompt and extensive debridement
penicillin + clindamycin
hyperbaric chamber
no effective antitoxin

104
Q

description of clostridium tetani

A

ubiquitous
peritrichous flagella
terminal round spore (drum stick)
culture: swarming on blood agar, faint hemolysis

105
Q

c. tetani toxins

A

bacterium is not invasive, but secretes toxins that spread

  • tetanolysin
  • tetanospasmin (neurotoxin)
106
Q

function of tetanospasmin

A

A-B toxin

blocks release of inhibitory neurotransmitter GABA

107
Q

pathogenesis of c. tetani

A
  1. contamination of dead tissue with spores
  2. germination into vegetative cells
  3. secretion of tetanospasmin
  4. transport of toxin to CNS via retrograde axonal transport or via blood
  5. binding of toxin to gangliosides in spinal cord or brainstem
  6. toxin mediated neuro disorders
108
Q

clinical symptoms of c.tetani

A 
4-5 day incubation
no fever, but profuse sweating
pain around wound, neck, jaw
convulsive tonic contraction (at site of injury, jaw muscles)
interference w respiration
death
109
Q

diagnosis of c.tetani

A

based on clinical symptoms

can grow in wound of immunized individuals

110
Q

treatment of c.tetani

A

humoral immunity through antitoxin antibodies
no cell mediated immunity
immunization with tetanus toxoid

MM Test 3 (31 decks)

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