Clostridium-Bacillus Flashcards

(47 cards)

1
Q
Clostridium 
shape 
gram 
spores? 
O2
A

Gram+
rods
endospore forming
obligate anaerobic (spores are O2 resistant)

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2
Q

where Clostridium species can be found

A

soil or intestines

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3
Q

endospore staining

A

use of malachite green to stain for spores/ test sterility

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4
Q

Main Clostridium virulence factor

A

spore formation

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5
Q

Clostridium spore formation

usefulness of spores?

A

spore formation is essential for all Clostridial pathogenicities who infect by stable endospores

§ spores are very resistant against destruction or
sterilization such as multiple hours of boiling
§ spores are not subject to antibiotics

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6
Q

Clostridium botulinum causes?

A

Botulism, a severe form of food poisoning (often home canning) ► paralysis

wound botulism is also possible from soil or fecal contamination

“infant botulism” in 3-20 week infants without full intestinal flora causes muscle weakness but rarely severe and generally resolves as intestinal flora develops

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7
Q

Virulence Factors: of Clostridium botulinum

A

botulinum neurotoxin

spore formation

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8
Q
botulinum neurotoxin 
type of toxin?
causes what?
invasive? 
neutralization?
A

AB exotoxin
blocks Acetylcholine release
► flaccid muscles including respiratory paralysis ► death
No tissue invasion -acts through toxins

Anti-toxin neutralization takes weeks to months!

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9
Q

Clostridium botulinum spores and toxins with heat

A

spores heat stable but toxin heat labile

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10
Q

Clostridium tetani found at? how does it cause disease?

A

Dirty, puncture wounds (knife, bullet, tattoo) are typical opportunities for anaerobic growth of C.tetani

Bacterial growth remains localized but tetanus toxin spreads (no tissue invasion, works through toxin)

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11
Q

virulence factor of c tentani

A

tetanospasmin

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12
Q
tetanospasmin 
type of toxin?
blocks what/causes? 
localized effect? 
anti-toxin?
A

(tetanus AB-exotoxin neurotoxin, plasmid-encoded)

blocks GABA (gamma-aminobutyric acid) and glycine release ► loss of inhibitory input to motor neuron excitation ► uncontrolled muscle contraction “spastic paralysis” (prevents relaxation)

Toxin effect may be localized and one-sided (on opposite side of infection);

anti-toxin usually too late

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13
Q

tetanus toxin general or local effect

A

can be either

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14
Q

tetanus prevention

neonatal?

A

DTaP vax
Passive immunization (IgG) of pregnant women can prevent
neonatal tetanus death by umbilical infection

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15
Q

Clostridium perfringens invasion?

A

only Clostridial species WITH tissue invasion

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16
Q

Clostridium perfringens virulence factors

A

α-toxin
θ-toxin
collagenase
hyaluronidase

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17
Q

α-toxin of Clostridium perfringens

A

membrane destruction

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18
Q

θ-toxin Clostridium perfringens

A

cytolytic toxin

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19
Q

collagenase, hyaluronidase of Clostridium perfringens

A

e facilitate tissue invasion from the edges of necrotizing tissues

20
Q

Clostridium perfringens diseases
limiting?
size?
mortaility

A

self-limiting but some are massive:
anaerobic fermentation (of amino acids) ► gas­ (H2, CO2) ► gas gangrene
puerperal (“childbed”) fever: uterine gangrene
40-100 mortality

21
Q

Clostridium perfringens vax/ treatment?

A

no vax possible

Ab against the a toxin: if it fails must amputate

22
Q

Clostridium difficile invasion?

A

no, acts thru toxins

23
Q

Clostridium difficile associated with what conditon

A

Antibiotic-associated pseudomembranous colitis (PMC) results from broad-spectrum antibiotics that kill much of the other normal intestinal bacterial flora, giving resistant species like toxin-producing Clostridium difficile a chance to take over.

Also observed after antimicrobial chemo-therapy

24
Q

virulence factors of Clostridium difficile

A

toxin a: enterotoxin
toxin b: cytotoxin
adehsin

25
Clostridium difficile toxin a effects
inhibits intestinal tight-junctions ► fluid leak
26
Clostridium difficile toxin b effects
rounding of epithelial cells ► fluid leak
27
effects of both toxin a and b of Clostridium difficile
diarrhea
28
C.botulinum treatment
botulinum antitoxin
29
C.botulinum epidemiology
environment (soil, water, sewage) | + gastointestinal tract (humans, animals)
30
C.tetani treamtment
toxoid vaccination clean wound anti-tetanus serum (passive immunity)
31
C.tetani epidemiology
``` environment (soil, water, sewage) gastointestinal tract (humans, animals) ```
32
C.perfringens treatment
surgery intervention, | amputation
33
C.perfringens epidemiology
environment (soil, water, sewage) + gastointestinal tract (humans, animals)
34
C.difficile epidemiolgy
colonized intestines, genital tract hospital environment prior antibiotics
35
``` bacillus gram shape spores? o2 ```
gram + rods spore forming strict aerobes or facultative anerobes
36
B. anthracis from animals or humans? shape and gram? o2 use
• zoonotic infection “woolsorter’s disease” from animals • Gram+ rods, facultative anaerobe
37
B. anthracis virulence factors
spore formation capsule edema toxin lethal toxin
38
Anthrax toxins
edema toxin and lethal factor, both are AB exotxins with B being common and A being the variable portion
39
edema factor
acts as an adenylate cyclase to cause increased cAMP for increased fluid production
40
lethal factor
metallo protease to destroy MAP kinase and kill cell
41
edema/ lethal factor cell entry
A/ B seperate due to decreased pH in endosome
42
poly-glutamic acid capsule of anthrax
inhibition of phagocytosis
43
when does anthrax cause disease
Disease is created when spores germinate and produce toxins
44
inhalation anthrax
``` Inhalation anthrax: 1. entry lungs, uptake by lung phagocytes; -- latency of 2 months or more may occur 2. to lymph nodes [spore germination-phagocytes die]; -- pneumonial and meningitis type symptoms are seen 3. bloodstream -> powerful toxins (macrophage TNF-α: toxic shock death in 1-2 days) ```
45
GI anthrax
• ulcers in mouth, esophagus -> edema + sepsis • Lethality if in lower intestines: 100%
46
skin anthrax presentation | lethality?
• redness (inflammatory cytokines) edema (EdTx) with vascular and vesicle rupture. • Lethality: 20%
47
Bacillus anthracis epidemiology
animal workers microbiological accidents bioterrorism contaminated meat