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Author: Amelia Virostko

1. Introduction

  1. Require complex media for growth and/or take longer time to culture under standard conditions
  2. Stool samples generally cultured on MacConkey agar
  3. Legionella pneumophila, Mycobacterium tuberculosis, Bacillus fragilis, Bordetella pertussis, Heliobacter pylori

2. B. pertussis

  1. Gram-negative coccibacillus that causes whooping cough
  2. Non-motile strict aerobe
  3. Use Bordet-Gengou media containing potato starch, blood, and glycerol or Charcoal- cephalixin blood agar (CCBA) to grow
  4. Epidemiology: obligate human pathogen
  5. Encounter and transmission: inhalation of aspirations
    1. Highly infective during first 2-4 weeks of infection therefore isolate patients
  6. Stages of infection/damage
    1. Incubation period
      1. highly infectious
      2. lasts 1-2 weeks
    2. Catharral phase
      1. low-grade fever, rhinorrhea, and progressively worsening cough
      2. accumulate mucus as cilia killed by bacteria
      3. lasts 1-2 weeks
      4. highly contagious
    3. Paroxysmal phase
      1. severe coughing episodes followed by a rapid inhalation of air that produces a whooping sound
      2. lasts 6-12 weeks
      3. non-infectious
      4. hemorrhage from internal cough
      5. secondary infection, especially in infants
    4. Convalescence phase
      1. lasts 2-6 weeks
      2. not contagious
      3. do not treat with antibiotics at this time
  7. Entry/Spread/Multiplication
    1. Strong tropism for ciliated cells in the bronchial tubes
    2. Multiply extracellularly and inhibit mucociliary clearance
  8. Damage
    1. Damage or kill host cells and tissue of the trachea
  9. Virulence Factors
    1. Filamentous hemagglutinin (FHA): agglutinates RBC, forms filaments, and attaches to ciliated cells
    2. Pertactin: attaches to protein receptors
    3. Hemolysin: cytotoxin
    4. Pertussis toxin: A-B toxin that constitutively activates Gi
    5. Adenylate cyclase toxin: impairs host cell ability to phagocytose bacteria, inhibits chemotaxis and the superoxide burst of neutrophils
    6. Tracheal cytotoxin: cell wall fragment that kills ciliated cells
    7. Type III secretion system: translocates additional toxins to cause cell
  10. Treatment
    1. Naturally penicillin-resistant
    2. Treat infected individuals and close contacts with erythromycin
    3. Acellular vaccine given at 2, 4, 6, and 18 months of age and at 5 years of age
  11. Outcome
    1. Often no long-term complications

3. H. pylori

  1. Gram-negative, spiral-shaped helical rod
  2. Causes gastric and duodenal ulcers
  3. Epidemiology/Encounter/Transmission
    1. Infects 50% of individuals but is often clinically silent
    2. Mode of transmission unclear
  4. Entry/Multiplication/Persistence
    1. Extracellular replication
    2. Produces urease to raises pH to tolerate gastric environment
    3. Immune response insufficient to clear bacteria immediately
  5. Damage
    1. Superficial gastritis: occurs shortly after infection and can persist for long periods
    2. Chronic gastritis
    3. Gastric or duodenal ulcers
    4. Can cause gastric adenocarcinoma and MALT lymphoma
  6. Virulence Factors
    1. Cag: pathogenicity island that encodes Type IV secretion system
    2. Urease
    3. Flagella
    4. VacA: vaculoating toxin
    5. LPS: less potent than in most Gram-negative bacteria
      1. Lewis antigen: evasion of immune response
  7. Treatment
    1. Antimicrobials and proton-pump inhibitorsåç