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47 Cards in this Set

  • Front
  • Back
Gram-Positive Rods: Species
1. Bacillus spp. 2. Clostridium spp. 3. Corynebacterium diptheria 4. Listeria monocytogenes
Bacillus Species
1. B. anthracis 2. B. cereus
Bacillus anthracis: Identification
1. Nonmotile (as opposed to other Bacillus spp.) 2. Forms Medusa's head colonies on blood agar
Bacillus anthracis: Virulence Factors
1. Capsule 2. Anthrax toxin 3. Spores
Bacillus anthracis: Virulence Factors-Capsule
1. Glutamic acid polymer 2. Prevents phagocytosis and lysis (from antibody + complement)
Bacillus anthracis: Virulence Factors-Anthrax Toxin
1. A-B toxin; Protective Factor + Edema OR Lethal Factor 2. Caused localized edema and cell death 3. Highly toxic
Bacillus anthracis: Disease
1. Cutaneous anthrax 2. Pulmonary anthrax 3. Gastrointestinal anthrax
Bacillus anthracis: Disease-Cutaneous Anthrax
1. Initial itching papule at inoculation site 2. Forms ulcer that can lead to necrosis (eschar) with massive edema, septicemia, and possible death 3. Inoculation of spores or bacteria from soil or animal products into a superficial wound or abrasion
Bacillus anthracis: Disease-Pulmonary Anthrax
1. Inhalation of spores from contaminated items (e.g. wool, fur, and hides) 2. Virus-like respiratory illness with high mortality rate due to respiratory failure
Bacillus anthracis: Disease-Gastrointestinal Anthrax (Transmission)
1. Ingestion of bacteria in contaminated meat 2. GI symptoms 3. Rare
Bacillus anthracis: Epidemiology
1. Occupational disease of individuals who handle wool, furs, and hides 2. Cutaneous disease most common 3. GI disease rare in humans, but seen in developing countries
Bacillus cereus: Epidemiology-Habitat
1. Soil (ubiquitous) 2. Foods: A) Grains B) Vegetables C) Dairy
Bacillus cereus: Pathogenesis
1. Spores survive initial cooking, but germinate into toxin-producing vegetative cells in the absence of prompt refrigeration 2. Reheating inactivates heat-labile toxin (preventing immediate diarrhea), but spares heat-stable toxin (emetic form) and vegetative cells (future diarrheal form)
Bacillus cereus: Disease
Food poisoning: 1. Emetic form 2. Diarrheal form
Bacillus cereus: Disease-Food Poisoning (Emetic Form Transmission)
Ingestion of preformed heat-stable enterotoxin in reheated foods (e.g. rice and beans)
Bacillus cereus: Disease-Food Poisoning (Emetic Form Clinical Manifestation)
1. Rapid onset: 1-5 hours (similar to S. aureus) 2. Symptoms: A) Nausea B) Vomiting C) Abdominal cramps
Bacillus cereus: Disease-Food Poisoning (Diarrheal Form Transmission)
Ingestion of multiplying bacteria, which produce heat-labile enterotoxin in GI, from contaminated meat, vegetables, or sauces
Bacillus cereus: Disease-Food Poisoning (Diarrheal Form Clinical Manifestation)
1. Slow onset: 10-15 hours (similar to Clostridium perfringens) 2. Symptoms: A) Diarrhea B) Severe cramps
Bacillus cereus: Prevention
Refrigeration of foods after cooking
Clostridium Species
1. C. perfringens 2. C. tetani 3. C. botulinum 4. C. difficile
Clostridium perfringens:
Soft tissue infections, gas gangrene, food poisoning, necrotizing enteritis, septicemia
Clostridium tetani: Epidemiology-Habitat
1. Soil, water, sewage 2. Normal flora of many animals
- Rare in US due to vaccine
Clostridium tetani: Identification
1. Small rods with tennis racquet shape due to presence of terminal spore 2. Strict anaerobe (very sensitive to oxygen)
- Toxin would not be detected (its bound to motor neurons and internalized by cells)
Clostridium tetani: Virulence Factors
1. Tetanospasmin 2. Spore
Clostridium tetani: Virulence Factors-Tetanospasmin
1. A-B type 2. Neurotoxin 3. Blocks release of inhibitory neurotransmitters (e.g. GABA, glycine) 4. Results in spastic paralysis due to unregulated excitation
1. A-B type 2. Neurotoxin 3. Blocks release of inhibitory neurotransmitters (e.g. GABA, glycine) 4. Results in spastic paralysis due to unregulated excitation
Clostridium tetani: Disease
Tetanus; severe, unopposed muscle contraction. Most evident in the jaw - lockjaw.
Clostridium tetani: Prevention
1. Vaccination with tetanus toxoid as part of DPT or DT vaccine 2. Formaldehyde-inactivated 3. Boosters: every 10 years and after probable exposure
Clostridium botulinum: Identification
Detection of botulinum toxin in patient specimens or food via immunoassay. Anaerobic
Clostridium botulinum: Virulence Factors
1. Botulinum toxin 2. Spore
Clostridium botulinum: Virulence Factors-Botulinum toxin
1. A-B type 2. Neurotoxin 3. Blocks release of ACh at cholinergic synapses, leading to flaccid paralysis
1. A-B type 2. Neurotoxin 3. Blocks release of ACh at cholinergic synapses, leading to flaccid paralysis 4. Recovery period prolonged because nerve endings must regenerate
Clostridium botulinum: Disease
1. Food botulism 2. Infant botulism
Clostridium botulinum: Disease-Adult Botulism
1. Food-borne; ingestion of preformed toxins (e.g. canned goods) 2. Symptoms (variable onset): A) Weakness B) Dizziness C) Blurred vision D) Fixed/dilated pupils E) Dry mouth F) Flaccid paralysis G) Death via respiratory paralysis
Clostridium botulinum: Disease-Infant Botulism
1. Contaminated honey 2. C. botulinum colonizes GI and produces toxin in vivo 3. Infants
Symptoms: A) Initially nonspecific (failure to thrive, constipation) B) Progress to: i. flaccid paralysis (floppy baby syndrome) ii. respiratory arrest (1% to 2% of patients)
Clostridium difficile: Epidemiology-Habitat
Part of normal GI flora in some individuals
Clostridium difficile: Identification
1. Detection of toxin in stool samples via immunoassay 2. Ability to kill cultured cells (i.e. cytotoxicity test)
Clostridium difficile: Virulence Factors
1. Antibiotic resistance 2. Enterotoxin (Toxin A) 3. Cytotoxin (toxin B) 4. Adhesion factor 5. Sporulation
Clostridium difficile: Virulence Factors-Enterotoxin or Toxin A
Promotes fluid secretion and intestinal hemorrhage (similar to cholera toxin)
Clostridium difficile: Virulence Factors-Cytotoxin or Toxin B
Damages mucosal membranes by depolymerizing cellular cytoskeleton
Clostridium difficile: Disease
Pseudomembranous colitis
Clostridium difficile: Disease-Pseudomembranous Colitis
1. Profuse, foul-smelling, liquid (sometimes bloody) diarrhea 2. Leukocytes in stool 3. Fever 4. Abdominal pain
Clostridium difficile: Transmission
1. Endogenous (normal flora) 2. Exogenous via spores (e.g. nosocomially on hands/fomites)
C. diphtheriae: Epidemiology and Identification
1. Uncommon in the US due to vaccine 2. Small, pleomorphic irregular-staining gram-positive rods that contain metachromatic granules 3. Tellurite medium
C. diphtheriae: Pathogenesis
1. Diptheria toxin (encoded by a bacteriophage). 2. A-B toxin. A subunit is an ADP-ribosyltransferase that inactivates elongation factor EF-2 -> which inhibits protein synthesis
C. diphtheriae: Clinical symptoms
1. Exudative pharyngitis (dysphagia, fever, malaise) 2. Thick pseudomembrane
L. monocytogenes: Characteristics
1. Short gram-positive rod that exhibits tumbling motility at room temp and is easily grown on agar, even at cold temperatures. 2. Ubiquitous in nature - animals, soil and asymptomatic colonizers of the human GI.
L. monocytogenes: Pathogenesis
1. Ingestion and subsequent transmucosal uptake of GI cells. 2. Evades phagocytosis by invading cells
L. monocytogenes: Clinical symptoms
1. Early onset disease (granulomatosis infantisptica); due to transplacental transmission. Marked by miscarriage or birth complications by sepsis, multiorgan abcesses and granulomas
2. Late onset disease; transmitted during childbirth. Results in meningitis or meningoencephalitis.
3. Adult listeriosis (pregnant, elderly or immunocompromised) can present bacteremia, sepsis or meningitis.