B6.088 Gangrene Flashcards
(110 cards)
1
Q
gram + organisms on this test
A
staph strep pyogenes clostridium actinomyces Propionibacterium
2
Q
gram - organisms on this test
A
bacteroides
fusobacterium
prevotella
porphyromonas
3
Q
how are strep species serotyped
A
surface carbohydrate antigens
4
Q
B hemolytic strep
A
Group A: s.pyogenes
Group B: s.agalactiae
5
Q
resp tract infections associated with GAS
A
strep throat
pharyngitis
6
Q
skin infections associated with GAS
A
impetigo
erysipelas/ cellulitis (dermis)
necrotizing faciitis (subQ tissue)
7
Q
systemic infections associated with GAS
A
bacteremia
rheumatic fever
acute glomerulonephritis
streptococcal TSS
8
Q
impetigo (strep)
A
usually occurs in young kids (2-5)
honey colored crusty lesions
“crusty, weeping”
9
Q
erysipelas
A
raised, bright red plaques with sharply defined borders
coalescing bullae
10
Q
time frame of TSS and necrotizing fasciitis
A
within less than 24 hours of infection
11
Q
time frame of acute glomerulonephritis after GAS infection
A
2-3 weeks after initial infection
12
Q
adhesins on GAS
A
M protein: >160 serotypes
protein F: binds fibronectin
lipoteichoic acid
13
Q
capsule of GAS
A
hyaluronic acid
prevents immune system attack
14
Q
streptolysin O
A
pore forming toxin
lyses target cells
15
Q
hyaluronidase
A
spreads through tissues and breaks down hyaluronic acid
sometimes mutated/inactivated
16
Q
streptococcus pyrogenic exotoxins (Spe)
A
superantigen
can cause scarlet fever and TSS
17
Q
streptokinases
A
activate plasminogen to dissolve clots
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
19
Q
function of clindamycin in GAS infection
A
suppresses toxin production
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
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
22
Q
infections associated with staph
A
80% of skin and soft tissue infections ortho infections endocarditis nosocomial blood infections septic shock
23
Q
ESKAPE organisms
A
have antibiotic resistance enterococcus staph aureus klebsiella actinobacter pseudomonas enterobacter
24
Q
how do you acquire MRSA from MSSA
A
within 2 yrs of methicillin use
associated with increased mortality
25
VISA
vancomycin intermediate: thickened cell wall
26
VRSA
vancomycin resistant
| resistance plasmid from enterococci
27
adherence factors of staph aureus
protein A - binds the Fc region of Abs
fibronectin binding proteins
collagen binding proteins
28
virulence factors of staph aureus that aren't adherence factors
```
4 cytolysins
leukocidins
phenol-soluble modulins
12 enterotoxins (superantigens)
secreted enzymes: proteases, nucleases, hyaluronidase, coagulase
```
29
skin infections associated with staph aureus
95% of all staph infections are skin infections
| cellulitis, impetigo, folliculitis, abscess
30
cellulitis
warm, red, swollen soft tissue that is tender to the tough
31
impetigo (staph)
classically, erythematous papules and pustules with yellow "honey" crusting
typically on face
large bullae suggest staph
32
furuncle / abscess
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 >>> GAS
33
cause of scalded skin syndrome
diffuse exfoliation
exfoliative dermatitis caused by toxin producing strains: exfoliative toxins ETA and ETB
toxins absorbed by bloodstream
34
symptoms of SSS
localized tender erythema, systemic spread, fever, blisters
usually involves children < 5
mortality and scarring are rare
35
cause of TSS
superantigen carried by 20% of staph aureus isolates
36
symptoms of TSS
sudden fever followed by headache, sore throat, diffuse red rash, skin desquamation
shock within 48 h
37
epidemiology of TSS
6,000 cases/ year in US
5% fatality w ttx
65% fatality w/o ttx
38
TSST-1 toxin
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
39
C3b defense against staph
activated by staph cell wall fragments
| opsonizes bacteria and enhances phagocytosis
40
neutrophil defense against staph
engulf the bacteria
| intracellular killing by O2 radicals
41
predispositions to staph infections?
C3 hypercatabolism
neutropenia
reduced production of H2O2 and O2
lazy leukocyte
42
topical ttx of staph aureus
bacitracin
| muprirocin
43
ttx of MSSA
1st gen cephs, amoxicillin- clavulanate, nafcillin/ oxacillin
44
ttx of MRSA
```
clindamycin
Bactrim
doxycycline
linezolid
vancomycin (only IV)
daptomycin (only IV)
```
45
VISA/VRSA ttx
resistant to methicillin as well
| linezolid, daptomycin, quinupristin / dalfopristin
46
lab diagnosis of staph aureus
catalase +
coagulase +
beta hemolytic
mannitol fermentation
47
aerotolerance of anaerobes
most are aerotolerant
tolerate brief exposure to variable levels of O2
-some have SOD and catalase
-some have a very active NADH oxidoreductase
48
why can anaerobes not grow in presence of high O2
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
endogenous anaerobes (normal flora)
```
opportunists
gram neg:
bacteroides
fusobacterium
prevotella
prophyromonas
gram pos:
actinomyces
Propionibacterium
mobiluncus
lactobacillus
```
50
exogenous anaerobes
clostridium (G+)
| spore forming
51
areas of body with high conc of anaerobic flora
gingival crevice
colon
1000:1
anaerobes: aerobes
52
additional sites where anaerobes can thrive
hypoxic tissues (wounds, diabetics)
dental plaque
tonsillar crypts
microenvironments where aerobes or facultative anaerobes deplete O2
53
predisposing conditions to anaerobic infections
```
breeches in mucocutaneous barrier
displacement of normal flora
compromised vascular supply
trauma with tissue destruction
antecedent infection
```
54
clues to an anaerobic infection
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
virulence factors of anaerobes
anti-phagocytic capsule
tissue destructive enzymes
beta-lactamase production (can protect themselves and other species in mixed infections)
SOD production (aerotolerant anaerobes)
56
function of SOD production in anaerobes
protect bacteria from toxic O2 radicals as they move out of usual niche
57
identification challenges associated with anaerobes
air in sample
identification takes several days or longer
often derived from normal flora sample
58
where is bacteroides fragilis found
colon and female GU tract
59
what allows b. fragilis to be the most common anaerobe isolated from human infection
highly tolerant to O2 (produces SOD)
polysaccharide capsule
modified LPS has little/no endotoxin activity
60
how does one get infected w b.fragilis
often released from colon after trauma
- intra abdominal abscesses
- peritonitis
- bacteremia
- skin and soft tissue infections
61
how is b. fragilis identified/ diagnosed?
```
bile resistant (grows in 20% bile)
catalase +
indole -
```
62
antibiotic resistance of b. fragilis
conjugative plasmids, transposons encoding high level of antibiotic resistance
- penicillin resistant
- kanamycin +/ vancomyin + blood agar plates (KV BAP)
63
2nd most common anaerobic bacteria causing infections
prevotella
| porphyromonas
64
prevotella and porphyromonas normal locations
```
normal flora of:
oropharynx
nose
GIT
GUT
```
65
characteristics of prevotella
```
saccharolytic
sensitive to penicillin
kanamycin resistant (grow on KV BAP)
```
66
characteristics of porphyromonas
asacchrolytic
no growth on KV BAP
sensitive to penicillin
67
clinical manifestations of fusobacterium
pleuropulmonary abscess
intra-abdominal abscess
systemic infection
68
lab diagnosis of fusobacterium
```
slender, spindle shaped Gram - with tapered ends
Kanamycin sensitive (no growth on KV BAP)
```
69
treatment of gram neg anaerobes
metronidazole
carbapenem
B lactam + B lactamase inhibitor
70
why are gram neg anaerobes so difficult to control
endogenous origin
normal flora
polymicrobial infections
71
description of Propionibacterium (p. acnes)
```
gram + bacilli
anaerobic
non spore forming
catalase +
indole +
diphtheroid (cube shaped)
```
72
infections with p.acnes
human acne
| opportunistic infections
73
normal flora of p.acnes
oral
nasopharynx
skin
GIT
74
DOC for p.acnes
benzoyl peroxide
| erythromycin
75
description of actinomyces
gram + bacilli
anaerobic
catalase -
indole -
76
infections with actinomyces
actinomycosis abscesses
- cervicofacial or "lumpy jaw" (50%)
- thoracic, abdominal, pelvic, CNS
77
distinguishing features of actinomyces infections
abscesses with sulfur granules
| molar tooth colonies
78
treatment of actinomyces
surgical treatment + penicillin
79
etiology of bacterial vaginosis
displacement of normal flora (typically lactobacilli)
| polymicrobial: gardnerella, mobiluncus
80
distinguishing features of mobiluncus
fishy odor of discharge + KOH
"clue cells" : coccobacilli adhering to epithelial cells
pH > 4.5
81
treatment of mobiluncus
metronidazole or clindamycin
82
features of lactobacilli
gram + bacillus
| facultative to strict anaerobe
83
normal flora of lactobacilli
oral
GI
GU
84
infections associated with lactobacilli
transient bacteremia after gyn procedure or birth
endocarditis
septicemia in immunocompromised
85
DOC for lactobacilli
vanc resistance
| penicillin + aminoglycoside
86
4 types of clostridium
```
clostridium botulinum (botulism)
c. diff (pseudomembranous colitis)
clostridium perfringens (gas gangrene)
clostridium tetani (tetanus)
```
87
features of all clostridium
```
spore forming
gram + bacilli
anaerobes
saprophytic (love dead organic matter)
opportunists
all produce highly degradative enzymes and/or extremely potent exotoxins
```
88
4 types of botulism
1. classical / food bore
2. infant
3. wound
4. undetermined
89
food borne / classical botulism
ingestion of improperly canned food
| germinated spores in food (preformed toxin)
90
infant botulism
ingestions of spores from soil, dust, honey
| in vivo production of toxin
91
wound botulism
contamination of traumatic wound with spores
| in vivo production of toxin
92
lethal dose of botox
1-2 mg
93
structure of A-B exotoxins of botulism
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
effect of A-B exotoxins
blocks fusion of vesicles and release of ACh
| inhibit nerve pulses
95
botulism incubation
18-26 hours
96
systemic symptoms of botulism
weakness, dizziness, dry mouth, nausea, vomiting
97
neuro features of botulism
```
blurred vision
inability to swallow
difficulty in speech
descending weakness (flaccid paralysis)
respiratory paralysis
```
98
diagnosis of botulism
clinical symptoms only
99
ttx of botulism
```
antiserum
-history of questionable food ingestion
-toxin-receptor binding blocks Ab binding
antibiotics:
-only in case of infection
prevention:
-proper food handling
```
100
description of c. perfringens
```
large gram + bacilli
occasional spores
non motile
encapsulated
double zone of B hemolysis
lecithinase activity (egg yolk)
```
101
a toxin of c. perfringens
lecithinase (phospholipase C)
- lyses a variety of cells
- cellulitis w gas formation
- fasciitis (suppurative myositis)
- myonecrosis (gas gangrene)
102
process of gas gangrene formation
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
treatment of c. perfringens fasciitis or myonecrosis
prompt and extensive debridement
penicillin + clindamycin
hyperbaric chamber
no effective antitoxin
104
description of clostridium tetani
ubiquitous
peritrichous flagella
terminal round spore (drum stick)
culture: swarming on blood agar, faint hemolysis
105
c. tetani toxins
bacterium is not invasive, but secretes toxins that spread
- tetanolysin
- tetanospasmin (neurotoxin)
106
function of tetanospasmin
A-B toxin
| blocks release of inhibitory neurotransmitter GABA
107
pathogenesis of c. tetani
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
clinical symptoms of c.tetani
```
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
diagnosis of c.tetani
based on clinical symptoms
| can grow in wound of immunized individuals
110
treatment of c.tetani
humoral immunity through antitoxin antibodies
no cell mediated immunity
immunization with tetanus toxoid
