Exam 3 (Clostridium & Bacillus) Flashcards
Clostridium bacteria Gram: O2 req: Endospores: Environment:
Gram: G+
O2 Req: obligate anaerobes
Endospores: yes (stains green)
Environment: soil and intestinal mucus
Virulence factor associated with Clostridium botulinum? How does it work?
Botulinum neurotoxin (blocks acetylcholine release) -AB-exotoxin
A pt has flaccid muscle paralysis that has taken weeks to months to neutralize with anti-toxin and has no evidence of tissue invasion by pathogen. What was the pt infected with?
Clostridium botulinum (or botulinum neurotoxin)
What is the main virulence factor of Clostridium tetani?
tetanospasmin
C. tetani
What is the mechanism of tetanospasmin?
the AB-exotoxin neurotoxin blocks GABA and glycine release which are both inhibitory controls for motor neurons. Uncontrolled muscle contraction. Opposite effect of botulinum toxin
Method to prevent tetanus in neonates?
passive immunization of IgG of pregnant women can prevent tetanus death by umbilical infection
What is the only Clostridial species with tissue invasion?
Clostridium perfringens
What are the three main virulence factors of C. perfringens?
- alpha toxin: lecithinase-phospholipase destroys membranes and causes alpha hemolysis
- theta toxin: cytolytic toxin causes beta hemolysis
- collagenase/hyaluronidase help tissue invasion from edges of dying tissues
What are two forms of gangrene? What pathogen can cause it?
- gas gangrene: anaerobic fermentation of amino acids
- uterine gangrene: puerperal fever
-clostridium perfringens
What is the only treatment for gangrene?
amputation
2 virulence factors of Clostridium difficile?
- Toxin A: enterotoxin inhibits intestinal tight junctions, fluid leak
- Toxin B: cytotoxin depolymerizes actin and epithelial cells round and leak
both cause diarrhea
How can clostridium difficile benefit from antibiotics?
-antibiotic-associated pseudomembranous colitis (PMC) caused by broad spectrum antibiotics that kill normal intestinal flora and allow resistant species to take over like toxin producing C. difficile
What are sources/causes of C. difficile infection?
- colonized intestines/genital tracts
- hospital environment
- prior antibiotics
Bacillus anthracis Gram: Shape: O2 req: Epidemiology:
Gram: G+
Shape: rods
O2 req: facultative anaerobe
Epidemiology: zoonotic infection “woolsorter’s disease”
What are the two virulence factors of Bacillus anthracis and what are their mechanisms?
- Edema factor: is an adenylate cyclase that incr cAMP and causes edema
- Lethal factor: metallo-protease that causes cell death with pulmonary edema
Are LF and EF of anthrax endo or exotoxins? Are they A or B portions?
A portions of exotoxins
Disease mechanism of inhalation anthrax?
- enters lungs, phagocytes take up (latency up to 2 months)
- to lymph nodes where spores germinate and cause pneumonial and meningitis type symptoms
- bloodstream: powerful toxins stim macrophage TNF-alpha and cause toxic shock death in 1-2 days
Symptoms of gastrointestinal anthrax?
- ulcers in mouth and esophagus (edema and sepsis)
- lethality of 100% if in lower intestines
Symptoms of skin anthrax? Lethality %?
- redness
- edema and vesicle rupture
- lethality of 20%
Epidemiology of bacillus anthracis?
- animal workers
- microbiological accidents
- bioterrorism
- contaminated meat