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Microbiology: Pathogenesis, Virulence, and Infection Control

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  • Normal microbiota benefits

    Normal microbiota manufacture vitamins, compete with pathogens, and promote immune system maturation.
  • Dysbiosis

    Disruption of normal microbiota, often by antibiotics, which can compromise patient health.
  • Tropism

    Pathogen preference for a specific host and tissue; can change over time.
  • Pathogenicity vs Virulence

    Pathogenicity is the ability to cause disease; virulence is the degree of disease severity caused.
  • Virulence factors

    Mechanisms pathogens use to overcome defenses, damage host cells, or provoke harmful immune responses.
  • Infectious dose-50 (ID50)

    Number of microbes needed to infect 50% of exposed hosts; lower ID50 means higher infectivity.
  • Lethal dose-50 (LD50)

    Amount of toxin needed to kill 50% of affected hosts; lower LD50 means higher lethality.
  • Endotoxins

    Lipid A portion of LPS in Gram-negative bacteria; released when cells die; cause fever, inflammation, and shock.
  • Exotoxins

    Protein toxins secreted by Gram-positive and Gram-negative bacteria; target specific cells and cause diverse effects.
  • Types of exotoxins

    Type I: membrane-acting; Type II: membrane-damaging; Type III: intracellular (often AB toxins).
  • Capsules as virulence factors

    Capsules help pathogens evade immune system by blocking phagocytosis and complement binding.
  • Adhesins

    Virulence factors like fimbriae or pili that allow pathogens to attach specifically or nonspecifically to host cells.
  • Siderophores

    Molecules produced by bacteria to sequester iron from host proteins, promoting bacterial growth.
  • Portal of entry examples

    Respiratory tract, gastrointestinal tract, genitourinary tract, skin, conjunctiva, parenteral route, placenta.
  • Parenteral route

    Direct entry through punctures, bites, injections, or cuts, bypassing skin or mucous membranes.
  • Antigenic variation

    Pathogen changes surface molecules to evade immune detection and delay immune response.
  • Molecular mimicry

    Pathogen produces molecules resembling host molecules to avoid immune recognition.
  • Latency

    Pathogen persists quietly inside host causing persistent or recurrent disease, e.g., herpes viruses.
  • Biosafety levels (BSL)

    BSL-1: minimal risk; BSL-2: moderate hazards; BSL-3: serious airborne diseases; BSL-4: lethal exotic agents.
  • Standard precautions in healthcare

    Universal measures like hand hygiene, PPE, and safe injection to prevent transmission from all patients.
  • Transmission-based precautions

    Additional measures (contact, droplet, airborne) used when specific infections are suspected or confirmed.
  • Fomite

    Non-living object that can transmit pathogens, e.g., doorknobs, towels, medical equipment.
  • Superantigens

    Exotoxins that overstimulate the immune system, causing harmful excessive immune responses.
  • Coagulase function

    Enzyme that promotes clot formation, helping bacteria like Staphylococcus aureus evade immune defenses.
  • How pathogens obtain nutrients

    Pathogens invade tissues, produce enzymes like lipases and proteases, and use siderophores to scavenge nutrients.
  • Immune evasion strategies

    Include antigenic variation, molecular mimicry, antigenic masking, interference with phagocytosis, and immune suppression.
  • Portal of exit

    Routes pathogens use to leave the host, e.g., respiratory secretions, feces, urine, blood, genital secretions.
  • Difference between true and opportunistic pathogens

    True pathogens cause disease in healthy hosts; opportunistic pathogens cause disease when defenses are weakened.
  • Role of kinases in pathogenesis

    Enzymes that alter host cell signaling to aid invasion, survival, or immune interference.
  • Why endotoxin release can be deadly

    Endotoxin causes fever, inflammation, hypotension, and can lead to septic shock and organ failure.