The Infectious Disease Cycle

When does the presence of a pathogen lead to disease? What will the infection outcome be?

  1. Virulence of the pathogen
  2. Opportunity to infect the host
  3. Persistence of the pathogen
  4. Immune status of the host
  5. Intervention strategies

Links in the infectious disease process and corresponding capabilities of a pathogen

Seven capabilities of a pathogen

  1. Maintain a reservoir
    1. Humans
      • Incubatory carriers: HIV+ status
      • Asymptomatic/Chronic carriers: Typhoid Mary
      • Convalescent carriers
    2. Animal Reservoirs (Zoonosis)
      • Cattle, pigs, poultry: Salmonella
      • Wild animals: Rabies
      • Rodents: Plague
      • Birds: West Nile
      • Bats: Ebola
      • Arthropods: Colorado Tick Fever
    3. Environmental
      • Soil: Clostridium tetani
      • Water: Vibrio cholerae
  2. Transmission to the host
    1. Portal of entry
      • Skin
      • Parenteral / Blood
      • Nose / Respiratory tract
      • Mouth / Digestive tract
      • Urogenital tract
      • Eye
      • Placenta
    2. Mode of transmission
      1. Respiratory droplets
        • Flu, cold, Pertussis
      2. Airborne
        • TB, Histoplasmosis
      3. Direct contact
        • STDs
        • Kissing
        • Touching
      4. Fecal-Oral route
      5. Parenteral transmission
        • Catheters, needles, vectors
      6. Fomites
        • Needles (AIDS, Hepatitis B)
        • Tissues (Flu, cold)
        • Utensils (typhoid fever)
        • Catheters (Staphylococcus, Enterococcus)
      7. Vectors
        • Insects (Malaria): mosquito, sandfly, flea, louse, housefly, kissing bug, tsetse fly
        • Other arthropods: tick, mite
      8. Transplants
        • Hepatitis (B,C), HIV, WNV
  3. Attachment to body surface
    1. Capsules
    2. Adhesins on pili/fimbriae
    3. Adhesins on cell surface
    4. Biofilms
  4. Invasion of the body
    1. Some pathogens are noninvasive (Streptococcus pneumoniae)
    2. Some invasive pathogens produce invasins
      • Phagocytosis by WBC: Coxiella, Mycobacterium, Listeria
      • Phagocytosis by intestinal M-cells: Salmonella, Shigella, Yersinia
      • Invasion of RBCs: Plasmodium
    3. Some invasive pathogens produce enzymes as virulence factors
      • Collagenase, hyaluronidase, elastase
      • DNAse, streptokinase
  5. Evading host defenses
    1. Intracellular life (e.g. Mycobacterium)
      • Inhibit fusion of phagolysosome
      • Resistance to lysosomal enzymes
      • Escaping phagosome
    2. Evading phagocytosis
      • Capsules: Neisseria meningiditis, Streptococcus pneumoniae, Bacillus anthracis
      • Surface proteins: S. pyogenes (M protein), N. gonorrhea
    3. Antigenic variation (N. gonorrhea, Trypanosoma brucei, Influenza virus)
    4. Special enzymes
      • IgA protease (N. gonorrhea)
      • C5a protease (S. pyogenes)
      • Coagulase (S. aureus)
    5. Serum resistance (N. gonorrhea)
    6. Cytolysins
      • streptolysin (S. pyogenes)
      • alpha toxin (C. perfringens)
  6. Growth within the host
    1. Tolerance of host environment: O2, salt, bile, temperature
    2. Obtaining nutrients
    3. Obtaining iron
      • Hemolysins release heme/iron
      • Siderophores - compete with transferrin
      • Ferritin receptors capture ferritin
  7. Exit strategy

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