Clostridium-Bacillus Flashcards
Clostridium shape gram spores? O2
Gram+
rods
endospore forming
obligate anaerobic (spores are O2 resistant)
where Clostridium species can be found
soil or intestines
endospore staining
use of malachite green to stain for spores/ test sterility
Main Clostridium virulence factor
spore formation
Clostridium spore formation
usefulness of spores?
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
Clostridium botulinum causes?
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
Virulence Factors: of Clostridium botulinum
botulinum neurotoxin
spore formation
botulinum neurotoxin type of toxin? causes what? invasive? neutralization?
AB exotoxin
blocks Acetylcholine release
► flaccid muscles including respiratory paralysis ► death
No tissue invasion -acts through toxins
Anti-toxin neutralization takes weeks to months!
Clostridium botulinum spores and toxins with heat
spores heat stable but toxin heat labile
Clostridium tetani found at? how does it cause disease?
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)
virulence factor of c tentani
tetanospasmin
tetanospasmin type of toxin? blocks what/causes? localized effect? anti-toxin?
(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
tetanus toxin general or local effect
can be either
tetanus prevention
neonatal?
DTaP vax
Passive immunization (IgG) of pregnant women can prevent
neonatal tetanus death by umbilical infection
Clostridium perfringens invasion?
only Clostridial species WITH tissue invasion
Clostridium perfringens virulence factors
α-toxin
θ-toxin
collagenase
hyaluronidase
α-toxin of Clostridium perfringens
membrane destruction
θ-toxin Clostridium perfringens
cytolytic toxin
collagenase, hyaluronidase of Clostridium perfringens
e facilitate tissue invasion from the edges of necrotizing tissues
Clostridium perfringens diseases
limiting?
size?
mortaility
self-limiting but some are massive:
anaerobic fermentation (of amino acids) ► gas (H2, CO2) ► gas gangrene
puerperal (“childbed”) fever: uterine gangrene
40-100 mortality
Clostridium perfringens vax/ treatment?
no vax possible
Ab against the a toxin: if it fails must amputate
Clostridium difficile invasion?
no, acts thru toxins
Clostridium difficile associated with what conditon
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
virulence factors of Clostridium difficile
toxin a: enterotoxin
toxin b: cytotoxin
adehsin
Clostridium difficile toxin a effects
inhibits intestinal tight-junctions ► fluid leak
Clostridium difficile toxin b effects
rounding of epithelial cells ► fluid leak
effects of both toxin a and b of Clostridium difficile
diarrhea
C.botulinum treatment
botulinum antitoxin
C.botulinum epidemiology
environment (soil, water, sewage)
+ gastointestinal tract (humans, animals)
C.tetani treamtment
toxoid vaccination
clean wound
anti-tetanus serum (passive immunity)
C.tetani epidemiology
environment (soil, water, sewage) gastointestinal tract (humans, animals)
C.perfringens treatment
surgery intervention,
amputation
C.perfringens epidemiology
environment (soil,
water, sewage)
+ gastointestinal tract
(humans, animals)
C.difficile epidemiolgy
colonized intestines, genital tract
hospital environment
prior antibiotics
bacillus gram shape spores? o2
gram +
rods
spore forming
strict aerobes or facultative anerobes
B. anthracis
from animals or humans?
shape and gram?
o2 use
• zoonotic infection “woolsorter’s disease” from animals
• Gram+ rods,
facultative anaerobe
B. anthracis virulence factors
spore formation
capsule
edema toxin
lethal toxin
Anthrax toxins
edema toxin and lethal factor, both are AB exotxins with B being common and A being the variable portion
edema factor
acts as an adenylate cyclase to cause increased cAMP for increased fluid production
lethal factor
metallo protease to destroy MAP kinase and kill cell
edema/ lethal factor cell entry
A/ B seperate due to decreased pH in endosome
poly-glutamic acid capsule of anthrax
inhibition of phagocytosis
when does anthrax cause disease
Disease is created when spores germinate and produce toxins
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)
GI anthrax
• ulcers in mouth, esophagus
-> edema + sepsis
• Lethality if in lower
intestines: 100%
skin anthrax presentation
lethality?
• redness (inflammatory cytokines)
edema (EdTx) with vascular and vesicle rupture.
• Lethality: 20%
Bacillus anthracis epidemiology
animal workers
microbiological accidents
bioterrorism
contaminated meat
