Microbiology Essentials: Disease Mechanisms and Host Defenses

Posted on Jul 2, 2025 in Microbiology

Chapter 14: Microbial Interactions and Disease Patterns

Differentiating Key Microbiological Terms

  • Etiology/Pathogenesis: Etiology is the study of the cause of a disease, while pathogenesis describes the manner in which a disease develops.
  • Infection/Disease: Infection refers to the colonization of the body by microorganisms, whereas disease is any change in the state of health.

Understanding Symbiotic Relationships

  • Symbiosis: The living together of unlike organisms.
  • Commensalism: One organism benefits, while the other is unaffected.
  • Mutualism: Both organisms benefit.
  • Parasitism: One organism benefits, and the other is harmed.

Classifying Disease Duration

  • Acute Disease: Characterized by rapid onset malaise, with symptoms lasting approximately 5 days.
  • Chronic Disease: Involves persistent symptoms, such as coughing and breathing difficulty, lasting for months.
  • Subacute Disease: A patient has no symptoms and is a known carrier.

Symptoms vs. Signs of Disease

  • Symptoms: Subjective changes in the body that a patient feels and cannot be objectively measured by a physician.
  • Signs: Objective changes that a physician can observe and measure.

Local vs. Systemic Infections

Local infections can become systemic infections when pathogens enter blood or lymph vessels and are subsequently spread throughout the body.

Stages of Disease Progression

  1. Incubation Period
  2. Prodromal Period
  3. Period of Illness
  4. Period of Decline
  5. Period of Convalescence

Factors in Disease Emergence (MC Review)

The emergence of new infectious diseases is influenced by various factors, except for an inherent ‘need’ of bacteria to cause disease.

Case Study: Ornithologists and Infection Risk

Ornithologists studying barn owls are most likely to acquire infection by contaminating their hands while handling owls and their nests.

Misconceptions in Disease Association

The pairing of “anthrax” with “nonliving” is not correctly matched, as anthrax is caused by a living bacterium.

Chapter 15: Microbial Pathogenicity and Virulence

Pathogenicity vs. Virulence

  • Pathogenicity: The ability of a microorganism to produce disease.
  • Virulence: The degree of pathogenicity.

Role of Capsules and Cell Walls in Pathogenicity

Capsules and certain cell wall components contribute to pathogenicity by allowing encapsulated bacteria to resist phagocytosis and continue growing within the host.

Key Virulence Factors and Their Mechanisms

  • Hemolysins: Lyse red blood cells and may supply nutrition for bacterial growth.
  • Leukocidins: Destroy neutrophils and macrophages that are active in phagocytosis.
  • Coagulase: Causes fibrinogen in the blood to clot, which may protect the bacterium from phagocytosis.
  • Bacterial Kinases: Break down fibrin clots, allowing bacteria to spread through tissues.
  • Hyaluronidase: Hydrolyzes hyaluronic acid, which binds cells together, thereby allowing bacteria to spread through tissues.
  • Siderophores: Acquire iron from host iron-transport proteins, essential for bacterial growth.
  • IgA Proteases: Destroy IgA antibodies, a key component of mucosal immunity.

Impact of Drugs on Microbial Pathogenicity

  • Targeting Iron in Host Blood: Inhibits bacterial growth by limiting essential iron.
  • Targeting N. gonorrhoeae Fimbriae: Would prevent the adherence of Neisseria gonorrhoeae to host cells.
  • Targeting S. pyogenes M Protein: Would prevent Streptococcus pyogenes from attaching to host cells and make it susceptible to phagocytosis.

Exotoxins vs. Endotoxins: A Comparison

  • Exotoxins:
    • Source: Primarily Gram-positive bacteria.
    • Composition: Proteins.
    • Toxigenicity: High.
    • Mechanism: Destroy specific cell parts or functions.
    • Example: Botulinum toxin.
  • Endotoxins:
    • Source: Gram-negative bacteria (part of the outer membrane).
    • Composition: Lipid A component of LPS.
    • Toxigenicity: Generally lower.
    • Effects: Systemic, causing fever, weakness, aches, and shock.
    • Example: Toxins causing Salmonellosis.

Pathogenicity Factors in Fungi, Protozoa, Helminths

  • Fungi: Virulence factors in fungi include capsules, metabolic products, toxins, and allergic responses. Some fungi produce toxins that cause disease when ingested.
  • Protozoa and Helminths: These parasites elicit symptoms by destroying host tissues or producing metabolic waste products.

Microbial Evasion of Host Immunity

  • Viruses: Avoid host immune responses by growing inside host cells.
  • Protozoa: Evade immunity through mutations that change their surface antigens.

Identifying Specific Pathogens

The Opa gene is used to identify the endotoxin-producing bacterium Neisseria gonorrhoeae, which grows in high CO2 conditions.

Impact of Plasmids on Virulence

The removal of plasmids reduces virulence in Streptococcus mutans.

Common Portals of Entry for Pathogens

Blood is not typically considered a primary portal of entry for pathogens, but rather a route for systemic spread once entry has occurred.

Preventing Pathogen Adherence

Vaccination against fimbriae would prevent adherence, thereby preventing subsequent stages of infection.

Interpreting ID50 Values

Given an ID50 of 500 for Campylobacter and 100 for Cryptosporidium, the statement that “Campylobacter is more virulent” is false. A lower ID50 indicates higher virulence.

Capsules and Virulence

An encapsulated bacterium can be virulent because its capsule resists phagocytosis.

Blocking Microbial Attachment

A drug that binds to mannose on human cells would prevent the attachment of pathogenic E. coli.

Vaccine Efficacy and Portals of Entry

If a vaccine was administered via a portal of entry that is not natural for the pathogen (e.g., skin for smallpox), it would likely not cause widespread disease.

Diverse Mechanisms of Immune Evasion

The frequent mutation of surface protein genes in Neisseria gonorrhoeae represents a distinct mechanism for avoiding host defenses compared to other strategies.

Characteristics of Successful Pathogens

A successful pathogen typically does not kill its host before it has been transmitted to a new host.

Chapter 16: Innate Immunity and Host Defenses

Physical and Chemical Barriers to Microbial Entry

  • Urinary System: Outward flow of fluid, presence of lysozyme, and acidic environment.
  • Genital System: Outward flow of fluids/secretions, and an acidic environment in females.

Understanding Inflammation

Inflammation: The body’s localized response to tissue damage, characterized by symptoms of redness, immobility (loss of function), swelling, and heat.

The Role of Interferons in Immunity

  • Interferons (IFNs): Defensive proteins produced by host cells.
  • IFN-alpha and IFN-beta: Induce uninfected cells to produce antiviral proteins, inhibiting viral replication.
  • IFN-gamma: Produced by lymphocytes, it activates phagocytes to enhance their ability to kill bacteria.

Complement System and Endotoxic Shock

The complement system can contribute to endotoxic shock when endotoxin binds C3b via the alternative pathway. This activates C5-C9, leading to cell lysis. Additionally, free cell wall fragments can bind more C3b, resulting in further C5-C9 mediated damage to host cell membranes.

Oxidative Bursts in Host Defense

Oxidative Bursts: Phagocytic cells produce toxic oxygen products (e.g., superoxide, hydrogen peroxide) during an oxidative burst, which are highly effective at killing pathogens.

Hemolysis in Transfusion Reactions

Hemolysis of red blood cells occurs during a transfusion reaction when a recipient’s antibodies combine with donor antigens, activating the complement system and causing red blood cell lysis.

Microbial Evasion of the Complement System

Microbes evade the complement system by various mechanisms, including:

  • Inhibiting the formation of C3b.
  • Preventing the formation of the Membrane Attack Complex (MAC).
  • Hydrolyzing C5a.

Key Components of Innate Immunity

  • Toll-like Receptors (TLRs): Part of innate immunity, they recognize pathogen-associated molecular patterns (PAMPs) and facilitate the adherence of phagocytes to pathogens.
  • Transferrins: Innate immune proteins that bind iron, limiting its availability for microbial growth.
  • Antimicrobial Peptides (AMPs): Innate immune molecules that directly kill or inhibit the growth of bacteria and other microbes.

Phagocytic Agranulocytes

Agranulocytes, specifically monocytes, are not actively phagocytic until they differentiate into macrophages and wander out of the bloodstream into tissues.