Infection and Disease

Pathogens and Disease

Pathogens are microorganisms capable of causing disease. The interaction between pathogens and the host determines the outcome of infection.

• True Pathogens: Microorganisms that can cause disease in healthy individuals.

• Opportunistic Pathogens: Normally harmless microbes that cause disease when the host's immunity is weakened or when they enter unusual body sites.

• Normal Biota (Flora): Microorganisms that normally inhabit the body without causing disease; they can sometimes cause endogenous infections.

• Endogenous Infection: Infection caused by a person's own normal microbiota.

• Infectious Dose (ID): The minimum number of microbes required to establish an infection.

Example: Staphylococcus aureus can be a harmless skin commensal but may cause infection if introduced into a wound.

Communicability and Disease Transmission

Diseases can be classified based on their ability to spread between hosts.

• Communicable: Diseases that can be transmitted from one host to another.

• Contagious: Highly communicable diseases that spread easily (e.g., measles).

• Non-Communicable: Diseases that cannot be transmitted between individuals (e.g., tetanus).

Nosocomial (Hospital-Acquired) Infections

Nosocomial infections are acquired in healthcare settings, often due to weakened immunity or exposure to pathogens.

• Common sites: urinary tract, wounds, surgical sites.

• Prevention strategies include:

  • Handwashing

  • Sterile techniques

  • Proper use of personal protective equipment (PPE)

  • Disinfection and sanitation procedures

Virulence Factors

Virulence factors are microbial components that enhance the ability to cause disease.

• Fimbriae: Allow bacteria to attach to host cells.

• Capsules: Protect bacteria from phagocytosis.

• Coagulase: Causes blood to clot around bacteria, aiding immune evasion.

• Leukocidins: Toxins that destroy white blood cells.

Disease Frequency Terms

Symptoms vs. Signs

• Symptoms: Subjective experiences felt by the patient (e.g., pain, nausea, fatigue).

• Signs: Objective observations that can be measured (e.g., rash, fever, swelling).

• Sequelae: Long-term consequences that remain after a disease has resolved.

Reservoirs and Transmission

• Reservoir: The natural habitat where a pathogen normally lives (e.g., humans, animals, soil).

• Direct Transmission: Person-to-person contact.

• Indirect Transmission: Spread via contaminated objects (fomites), food, water, or air.

• Vertical Transmission: Mother-to-child transmission (e.g., during childbirth or breastfeeding).

• Vector: Living organism (often an insect) that transmits disease (e.g., mosquitoes for malaria).

• Endogenous Transfer: Movement of microbes from one body site to another within the same individual.

Symbiotic Relationships

• Mutualism: Both organisms benefit.

• Commensalism: One benefits; the other is unaffected.

• Parasitism: One benefits while the host is harmed.

Normal Microbiota and Microbial Antagonism

• Colonization begins during and shortly after birth.

• Microbial Antagonism: Normal microbiota prevent pathogen growth by competing for nutrients and space.

Endotoxins

• Produced by Gram-negative bacteria.

• Consist of lipopolysaccharide (LPS) from the outer membrane.

• Released when bacterial cells die or break apart.

• Can cause fever, inflammation, and septic shock.

Innate (Non-Specific) Immunity

First Line of Defense

The first line of defense includes physical and chemical barriers that prevent pathogen entry.

• Physical Barriers: Skin, mucous membranes, cilia, tears, saliva.

• Chemical Barriers: Lysozyme, stomach acid, sebum, antimicrobial peptides.

Inflammation

Inflammation is a localized response to tissue injury or infection, characterized by four classic signs:

Inflammation Process:

1. Initial tissue injury

2. Blood vessel dilation

3. Increased permeability

4. Edema and pus formation

5. Healing and repair

• Edema: Fluid accumulation in tissues causes swelling.

• Chemotaxis: Movement of immune cells toward chemicals released at infection sites.

• Diapedesis: White blood cells squeeze through blood vessel walls into tissues.

Fever

• Caused by pyrogens released by pathogens or immune cells, which reset the hypothalamic temperature set point.

• Benefits:

  • Inhibits microbial growth

  • Increases immune activity

Phagocytosis Steps

1. Chemotaxis: Phagocyte moves toward infection.

2. Engulfment: Pathogen is surrounded and enclosed.

3. Phagolysosome Formation: Lysosome fuses with phagosome.

4. Destruction: Digestive enzymes destroy the pathogen.

Key Cells of Innate Immunity

• Neutrophils: First responders; highly phagocytic.

• Macrophages: Large phagocytes that engulf pathogens and present antigens.

• Leukocytes: General term for white blood cells.

Proteins and Molecules in Innate Immunity

• Interferons: Proteins that interfere with viral replication.

• Complement System: Group of proteins that enhance inflammation, attract phagocytes, and destroy pathogens.

• Antimicrobial Peptides: Proteins that damage microbial membranes.

• Cytokines: Chemical messengers that coordinate immune responses.

• PAMPs: Pathogen-Associated Molecular Patterns recognized by innate immune cells.

Induced vs. Non-Specific Defenses

• Non-Specific: Always present (e.g., skin, mucous membranes).

• Induced: Activated after infection occurs (e.g., inflammation, fever, interferons).

Adaptive (Specific) Immunity

B Cells vs. T Cells

• B Cells (Humoral Immunity): Produce antibodies against extracellular pathogens.

• T Cells (Cell-Mediated Immunity): Attack infected or abnormal cells directly.

MHC Markers

• MHC I: Found on all nucleated cells; presents antigens to cytotoxic T cells.

• MHC II: Found on antigen-presenting cells; presents antigens to helper T cells.

Antigen-Presenting Cells (APCs)

• Include macrophages, dendritic cells, and B cells.

• Display antigens on MHC II molecules to activate helper T cells.

Antibodies (Immunoglobulins)

Key Antibody Reactions

• Neutralization: Antibodies block toxins or viruses.

• Opsonization: Antibodies coat pathogens to enhance phagocytosis.

• Agglutination: Antibodies clump pathogens together.

• Complement Fixation: Antibodies activate the complement system.

Primary vs. Secondary Immune Response

• Primary Response: First exposure; slow response; IgM appears first.

• Secondary Response: Faster and stronger due to memory cells; IgG dominates.

Cells and Their Functions

Immunity and Vaccines

Types of Immunity

Vaccines

• Attenuated (Live): Weakened pathogen; strong, long-lasting immunity; not recommended for immunocompromised patients.

• Inactivated (Killed): Killed pathogen; safer for immunocompromised individuals; often requires boosters.

Therapeutic Concepts

• Clonal Deletion: Removal of self-reactive lymphocytes to prevent autoimmune disease.

• Prophylaxis: Preventive treatment before disease develops.

• Selective Toxicity: Ability to harm pathogens without harming host cells.

Written Response Focus

• Why must self-reactive lymphocytes be removed? To prevent autoimmune diseases in which the immune system attacks the body's own tissues.

• Safest vaccine for immunocompromised people? Inactivated vaccines, because they cannot replicate and cause infection.

• Difference between attenuated and inactivated vaccines?

  • Attenuated: live but weakened organisms.

  • Inactivated: killed organisms that cannot reproduce.

• Which antibody appears first and which appears later?

  • First: IgM

  • Later/long-term: IgG

High-Yield Exam Questions

1. What is the difference between true and opportunistic pathogens?

2. What virulence factor helps bacteria resist phagocytosis?

3. What are the four signs of inflammation?

4. What is chemotaxis?

5. Which cells are the first responders during infection?

6. What is the function of complement proteins?

7. Which antibody appears first during infection?

8. Which antibody crosses the placenta?

9. What is the role of helper T cells?

10. Why are attenuated vaccines generally avoided in immunocompromised individuals?

Additional info: Academic context and definitions have been expanded for clarity and completeness. Tables have been reconstructed for comparison and classification purposes.