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Microbiology > 3.20 > Flashcards

3.20 Flashcards

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1
Q

Clostridium characteristics (4)

A 
Gram+ rods
endospore forming
obligate anaerobic (spores are O2 resistant)
environment (soil) + intestinal mucus
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2
Q

Endospore staining
(also: used for aerobic
endospore formers like
Gram+ Bacillus) (2)

A

malachite green

endospores stain green

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3
Q

Clostridium

Virulence Factor:

A

spore formation is essential for all Clostridial

pathogenicities who infect by stable endospores

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4
Q

spore formation is essential for all Clostridial
pathogenicities who infect by stable endospores
(2)

A

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

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5
Q

Botulism,

A

a severe form of food poisoning (often home canning)

► paralysis

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6
Q

wound botulism is also possible from

“infant botulism”

A

soil or fecal contamination

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

Clostridium botulinum

Virulence Factors:

A

Ø botulinum neurotoxin (AB-exotoxin) blocks Acetylcholine release
► flaccid muscles including respiratory paralysis ► death

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8
Q

Clostridium botulinum
No tissue invasion
-acts through —

A

toxins

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9
Q

While spores are heat-stable,

botulinum toxin is heat—

A

labile

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10
Q

Anti-toxin neutralization

takes

A

weeks to months!

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11
Q

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

A

C.tetani

Bacterial growth remains localized but tetanus toxin spreads

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12
Q

Ø tetanospasmin

A

(tetanus AB-exotoxin neurotoxin, plasmid-encoded) blocks GABA (gammaaminobutyric acid) and glycine release ► loss of inhibitory input to motor neuron excitation ►
uncontrolled muscle contraction “spastic paralysis”
Toxin effect may be localized and one-sided (on opposite side of infection); anti-toxin usually
too late

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13
Q

Clostridium tetani
No tissue invasion
-acts through —

A

toxins

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14
Q

Tetanus toxin prevents

A

muscle relaxation

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15
Q

tetanus = “—”

Tetanus effects can be (2)

A

lockjaw

general or localized

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16
Q

Passive immunization (IgG) of pregnant women can prevent
— tetanus death by umbilical infection (250,000/yr
worldwide)

A

neonatal

17
Q

only Clostridial species

WITH tissue invasion

A

Clostridium perfringens

18
Q

Clostridium perfringens

VF (3)

A
  • α-toxin: membrane destruction
  • θ-toxin: cytolytic toxin
  • collagenase, hyaluronidase facilitate tissue invasion from the edges of necrotizing tissues
19
Q

Clostridium perfringens
diseases
gangrene (2)

A

• anaerobic fermentation (of amino acids)
► gas­ (H2, CO2) ► gas gangrene
• puerperal (“childbed”) fever: uterine gangrene

20
Q

Clostridium perfringens

vaccine

A

No vaccination is possible

Antibody against α-toxin fails to stop gas gangrene: amputate

21
Q

Clostridium difficile
No tissue invasion
-acts through —

A

toxins

22
Q

Antibiotic-associated pseudomembranous colitis

(PMC) results from

A

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

23
Q

Clostridium difficile

VF (2)

A

Ø toxin A (enterotoxin):
inhibits intestinal tight-junctions ► fluid leak
Ø toxin B (cytotoxin):
► rounding of epithelial cells ► fluid leak

Result from both: diarrhea

24
Q

C.botulinum
TX (1)
EPIDEMIOLOGY (2)

A

botulinum antitoxin

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

25
Q

C.tetani
TX (2)
EPIDEMIOLOGY (2)

A

toxoid vaccination
anti-tetanus serum
(passive immunity)

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

26
Q

C.perfringens
TX (1)
EPIDEMIOLOGY (2)

A

surgery intervention,
amputation

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

27
Q

C.difficile

EPIDEMIOLOGY (3)

A

colonized intestines, genital tract
hospital environment
prior antibiotics

28
Q

B. anthracis

characteristics (2)

A
  • zoonotic infection “woolsorter’s disease”

* Gram+ rods, facultative anaerobe

29
Q

Virulence factors: Anthrax toxins (2)

A

anthrax; edema factor (EF), lethal factor (LF)

30
Q

A = EF =

A

adenylate cyclase ► cAMP­ ► edema (like cholera toxin)

31
Q

A = LF =

A

metallo-protease ► MAP kinase ► death

cell death with
pulmonary edema

32
Q

Disease is created when spores
germinate and produce toxins.
Inhalation anthrax:
(3)

A 
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)
33
Q

Gastrointestinal anthrax:

2

A

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

34
Q

Skin anthrax:
symptoms (3)
lethality

A

redness
edema
vesicle (bottom) rupture.

20%

35
Q

Bacillus anthracis

EPIDEMIOLOGY (4)

A 
animal workers
microbiological
accidents
bioterrorism
contaminated meat

Microbiology (42 decks)

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