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microbiology > Clostridium-Bacillus > Flashcards

Clostridium-Bacillus Flashcards

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
Q

Clostridium difficile toxin a effects

A

inhibits intestinal tight-junctions ► fluid leak

26
Q

Clostridium difficile toxin b effects

A

rounding of epithelial cells ► fluid leak

27
Q

effects of both toxin a and b of Clostridium difficile

A

diarrhea

28
Q

C.botulinum treatment

A

botulinum antitoxin

29
Q

C.botulinum epidemiology

A

environment (soil, water, sewage)

+ gastointestinal tract (humans, animals)

30
Q

C.tetani treamtment

A

toxoid vaccination
clean wound
anti-tetanus serum (passive immunity)

31
Q

C.tetani epidemiology

A 
environment (soil, water, sewage)
gastointestinal tract (humans, animals)
32
Q

C.perfringens treatment

A

surgery intervention,

amputation

33
Q

C.perfringens epidemiology

A

environment (soil,
water, sewage)
+ gastointestinal tract
(humans, animals)

34
Q

C.difficile epidemiolgy

A

colonized intestines, genital tract
hospital environment
prior antibiotics

35
Q 
bacillus 
gram
shape 
spores? 
o2
A

gram +
rods
spore forming
strict aerobes or facultative anerobes

36
Q

B. anthracis
from animals or humans?
shape and gram?
o2 use

A

• zoonotic infection “woolsorter’s disease” from animals
• Gram+ rods,
facultative anaerobe

37
Q

B. anthracis virulence factors

A

spore formation
capsule
edema toxin
lethal toxin

38
Q

Anthrax toxins

A

edema toxin and lethal factor, both are AB exotxins with B being common and A being the variable portion

39
Q

edema factor

A

acts as an adenylate cyclase to cause increased cAMP for increased fluid production

40
Q

lethal factor

A

metallo protease to destroy MAP kinase and kill cell

41
Q

edema/ lethal factor cell entry

A

A/ B seperate due to decreased pH in endosome

42
Q

poly-glutamic acid capsule of anthrax

A

inhibition of phagocytosis

43
Q

when does anthrax cause disease

A

Disease is created when spores germinate and produce toxins

44
Q

inhalation anthrax

A 
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
Q

GI anthrax

A

• ulcers in mouth, esophagus
-> edema + sepsis
• Lethality if in lower
intestines: 100%

46
Q

skin anthrax presentation

lethality?

A

• redness (inflammatory cytokines)
edema (EdTx) with vascular and vesicle rupture.
• Lethality: 20%

47
Q

Bacillus anthracis epidemiology

A

animal workers
microbiological accidents
bioterrorism
contaminated meat

microbiology (42 decks)

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