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22 Cards in this Set

  • Front
  • Back
Spore Forming Rods
Bacillus and Clostridium
 Release of potent exotoxins causes disease
Bacillus anthracis
Causative agent of anthrax
 UNIQUE protein capsule, antiphagocytic
 Aerobic growth conditions
 Spores are very stable, resistant to heat, drying, UV and
disinfectants; spores germinate and toxins are made
 Humans exposed to spores usually through contact with animals or
soil
 Used in bio-terrorism and warfare
Bacillus anthracis exotoxin
Encoded on pXO1 plasmid
 Plasmid contains virulence factors which are transcribed optimally
@ 37 C, increased CO2 and serum proteins
 ?? Where are these conditions found ??
 Exotoxin composed of 3 separate proteins:
 Edema factor (EF)
 Protective antigen (PA)
 Lethal factor (LF)
 Separately proteins are not toxic, but combined are lethal
 pXO2 plasmid encodes capsule genes
 **BOTH plasmids required for virulence**
Prevention and Treatment of Bacillus antracis
 RAPID treatment is essential
 Antibiotics: penicillin, doxycyclin, ciprofloxacin or levofloxacin
 Vaccine against PA protein is available

Remember: capsule protects AND is made of protein
 cutaneous and respiratory routes for spores
 animal hides and/or soil
Bacillus cereus
Causes food poisoning when spores enter food product
 Motile, non-encapsulated, resistant to penicillin
 ENTEROTOXIN is responsible for illness
 2 types of enterotoxin
(i) Heat labile: nausea, abdominal pain, diarrhea. Lasts 12-24hrs
(ii) Heat stable: SEVERE nausea and vomiting, short incubation
 Antibiotic treatment useless….preformed toxins
Clostridium
 Anaerobic > differentiates this bacteria from other
spore-forming bacilli
 Botulism, tetanus, gas gangrene and pseudomembranous
colitis
 POWERFUL EXOTOXINS RAPID DIAGNOSIS
Clostridium botulinum
Rapidly fatal food poisoning from lethal neurotoxin
 Neurotoxin blocks Ach release in autonomic system; flaccid
muscle paralysis:
Afebrile, bilateral cranial nerve palsies, double vision,
trouble swallowing, muscle weakness
Respiratory paralysis DEATH
Treatment: antitoxin and respiratory assistance
 Smoked fish, improperly canned vegetables
Proper cooking destroys spores
Action of Botulinum Neurotoxin
Botulism toxin inhibits the release of acetylcholine, not allowing the muscle to contract.
Infant Botulism
Honey contamination with spores
Spores germinate and bacteria colonizes
intestine
Neurotoxin release
2-3 days of constipation
Trouble swallowing, muscle weakness
Clinical Manifestations of Clostridium botulinum
1. entry
2. absorption
3. spread of toxin
4. disease (flaccid paralysis)
Clostridium tetani
Tetanus
 Rusty nail contaminated with spores punctures
skin; wound provides anaerobic environment
 Exotoxin: tetanospasmin
Sustained contraction of skeletal muscles
Severe muscle spasms (lock jaw); high
mortality at this stage
 Booster (inactivated toxoid) given every 10 years
Clinical Manifestations of Clostridium tetani
1. entry
2. spread of toxin
3. no exit
4. disease (rigid paralysis, jaw locked, cardiac failure, respiratory failure)
Clostridium perfringens
Gas gangrene
 Seen in soldiers wounded in battle
2 classes of clostridium perfringens infection
i) Wound infection/cellulitis
-necrotic skin exposed to bacteria, damage to local
tissues; skin feels moist, spongy, with ‘crackly’ pockets
(ii) Clostridial myonecrosis
-bacteria inoculated from trauma into muscles; exotoxin
secretion destroys adjacent muscles; as muscles degrade get
black fluid excreeted from skin
-FATAL unless treated with oxygen, antibiotics
(penicillin) and removal of damaged tissue
Clostridium difficile
Causes antibiotic-associated
pseudomembranous colitis
 Seen more commonly in hospitals than tetanus,
anthrax or botulism
 Overuse of broad-spectrum antibiotics destroys
normal intestinal flora
 Infects colon and releases exotoxins
Toxin A: diarrhea
Toxin B: cytotoxic to colon cells
Clostridium difficile symptoms and treatment
Symptoms: severe diarrhea, abdominal cramping, fever
 Possible cause of diarrhea in patients on antibiotics
 Treatment
discontinue antibiotic treatment
Administer metronidazole or vancomycin
Clinical manifestations of Clostridium
difficile
1. entry
2. spread
3. disease
Non-Spore Forming Rods
2 medically important bacilli
Listeria monocytogenes and
Corynebacterium diptheriae
Listeria monocytogenes
Causative agent of listeriosis; immunocompromised are at
high risk
 Found in foods such as soft cheeses, unpasteurized milk, cold
cuts, pâté
 PSYCHROPHILE survives in refrigerator
 Variety of symptoms:
General malaise, diarrhea, meningitis, septicaemia,
still-birth/abortions
 Facultative intracellular aerobe
 Crosses 3 protective barriers (blood-brain, GI and fetoplacental)
 Treatment: ampicillin or trimethoprim-sulfamethoxazole
Clinical Manifestations of Listeria
monocytogenes
1. entry
2. invasion
3. spread
4. disease (meningitis, endocarditis)
5. exit
Corynebacterium diptheriae
Causative agent of diptheria
Colonization of pharynx and release of exotoxins into
bloodstream
 Exotoxin damages heart and neural cells
 Treatment (3 steps):
(i) Antitoxin
(ii) Penicillin or erythromycin
(iii) DPT vaccine
 Can be lysogenized by a bacteriophage (virus that infects
bacteria)
Clinical manifestations of C. diptheriae
1. entry
2. spread
3. disease
4. exit