3.20 Flashcards
Clostridium characteristics (4)
Gram+ rods endospore forming obligate anaerobic (spores are O2 resistant) environment (soil) + intestinal mucus
Endospore staining
(also: used for aerobic
endospore formers like
Gram+ Bacillus) (2)
malachite green
endospores stain green
Clostridium
Virulence Factor:
spore formation is essential for all Clostridial
pathogenicities who infect by stable endospores
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
Botulism,
a severe form of food poisoning (often home canning)
► paralysis
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
Clostridium botulinum
Virulence Factors:
Ø botulinum neurotoxin (AB-exotoxin) blocks Acetylcholine release
► flaccid muscles including respiratory paralysis ► death
Clostridium botulinum
No tissue invasion
-acts through —
toxins
While spores are heat-stable,
botulinum toxin is heat—
labile
Anti-toxin neutralization
takes
weeks to months!
Dirty, puncture wounds (knife, bullet, tattoo) are typical opportunities for anaerobic growth of
C.tetani
Bacterial growth remains localized but tetanus toxin spreads
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
Clostridium tetani
No tissue invasion
-acts through —
toxins
Tetanus toxin prevents
muscle relaxation
tetanus = “—”
Tetanus effects can be (2)
lockjaw
general or localized
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
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
