3.20 Flashcards by sophie rosen

Clostridium characteristics (4)

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

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

malachite green

endospores stain green

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Clostridium

Virulence Factor:

spore formation is essential for all Clostridial

pathogenicities who infect by stable endospores

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

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

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Botulism,

a severe form of food poisoning (often home canning)

► paralysis

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wound botulism is also possible from

“infant botulism”

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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Clostridium botulinum

Virulence Factors:

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

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Clostridium botulinum
No tissue invasion
-acts through —

toxins

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While spores are heat-stable,

botulinum toxin is heat—

labile

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Anti-toxin neutralization

takes

weeks to months!

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

C.tetani

Bacterial growth remains localized but tetanus toxin spreads

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Ø tetanospasmin

(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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Clostridium tetani
No tissue invasion
-acts through —

toxins

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Tetanus toxin prevents

muscle relaxation

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tetanus = “—”

Tetanus effects can be (2)

lockjaw

general or localized

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

neonatal

only Clostridial species

WITH tissue invasion

Clostridium perfringens

VF (3)

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

Clostridium perfringens
diseases
gangrene (2)

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

Clostridium perfringens

vaccine

No vaccination is possible

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

Clostridium difficile
No tissue invasion
-acts through —

toxins

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

Clostridium difficile

VF (2)

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

Result from both: diarrhea

C.botulinum
TX (1)
EPIDEMIOLOGY (2)

botulinum antitoxin

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

C.tetani TX (2) EPIDEMIOLOGY (2)

toxoid vaccination anti-tetanus serum (passive immunity) environment (soil, water, sewage) + gastointestinal tract (humans, animals)

C.perfringens TX (1) EPIDEMIOLOGY (2)

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

C.difficile | EPIDEMIOLOGY (3)

colonized intestines, genital tract hospital environment prior antibiotics

B. anthracis | characteristics (2)

* zoonotic infection “woolsorter’s disease” | * Gram+ rods, facultative anaerobe

Virulence factors: Anthrax toxins (2)

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

A = EF =

adenylate cyclase ► cAMP ► edema (like cholera toxin)

A = LF =

metallo-protease ► MAP kinase ► death cell death with pulmonary edema

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

``` 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) ```

Gastrointestinal anthrax: | 2

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

Skin anthrax: symptoms (3) lethality

redness edema vesicle (bottom) rupture. 20%

Bacillus anthracis | EPIDEMIOLOGY (4)

``` animal workers microbiological accidents bioterrorism contaminated meat ```