BIO 150 – Exam 3: Principles of Disease, Immunity, and Immune Disorders

Principles of Disease & Epidemiology

Key Definitions

• Pathology: Study of disease.

• Etiology: Cause of a disease.

• Pathogenesis: Development of disease.

• Infection: Invasion or colonization of the body by pathogens.

• Disease: Abnormal state in which the body is not performing normal functions.

• Epidemiology: Study of where and when diseases occur and how they spread in populations.

• Morbidity rate: Number of people affected relative to total population in a given time period.

• Mortality rate: Number of deaths from a disease relative to the population in a given time.

Symbiotic Relationships

Type	Who Benefits?	Example
Commensalism	One organism benefits; other is unaffected	Staphylococcus epidermidis on skin
Mutualism	Both organisms benefit	E. coli in large intestine
Parasitism	One benefits at the expense of the other	Influenza viruses on host cells

Koch's Postulates

• The same pathogen must be present in every case of the disease.

• The pathogen must be isolated from the diseased host and grown in pure culture.

• The pathogen from the pure culture must cause the disease when inoculated into a healthy, susceptible lab animal.

• The pathogen must be isolated from the inoculated animal and shown to be the original organism.

Key point: Koch's postulates establish the etiology of infectious disease, which is essential for treatment and prevention.

Communicable vs. Noncommunicable Diseases

• Communicable disease: Can be spread from one host to another (directly or indirectly).

• Contagious disease: Communicable disease that is easily spread (e.g., influenza).

• Noncommunicable disease: Not spread from host to host; caused by opportunistic pathogens or environmental sources (e.g., tetanus from soil).

Frequency of Disease Occurrence

Term	Definition	Example
Sporadic	Occurs occasionally in isolated cases	Tetanus in the US
Endemic	Constantly present in a population/region	Common cold
Epidemic	Sudden increase above expected level in a region	Influenza outbreak
Pandemic	Worldwide epidemic	COVID-19, influenza 1918

Incidence vs. Prevalence

• Incidence: Number of new cases in a given time period.

• Prevalence: All cases (old + new) at a specific point in time.

Severity/Duration of Disease

Type	Definition	Example
Acute	Develops rapidly; short duration	Flu
Chronic	Develops slowly; long duration	TB, Lyme disease
Subacute	Between acute and chronic	—
Latent	Causative agent remains inactive for a time before becoming active	Shingles/chickenpox

Predisposing Factors

• Gender

• Inherited traits (e.g., sickle cell gene)

• Climate and weather

• Lack of vaccination

• Fatigue

• Age

• Lifestyle and nutrition

• Chemotherapy

Stages of Disease

Stage	Description
Incubation period	Time between infection and first symptoms; pathogen multiplying but no signs/symptoms yet
Prodromal period	Mild, early signs/symptoms begin; highly contagious
Period of illness	Most severe signs and symptoms; peak pathogen numbers
Period of decline	Signs/symptoms subside; still vulnerable to secondary infections
Period of convalescence	Body returns to pre-disease state; recovery

Reservoirs and Transmission

• Human reservoirs: Carriers may have inapparent infections or latent diseases.

• Animal reservoirs (zoonoses): Diseases transmitted from animals to humans (e.g., rabies, Lyme disease, West Nile).

• Nonliving reservoirs: Soil and water.

Vectors

Type	Description	Example
Mechanical	Arthropod carries pathogen on its feet/body (no reproduction in vector)	Housefly carrying Salmonella
Biological	Pathogen reproduces inside the arthropod; transmitted via bite or feces	Mosquito transmitting malaria

Modes of Transmission

Type	Description	Example
Direct contact	Close association between infected and susceptible host	Kissing, sexual contact
Congenital (vertical)	Mother to fetus/newborn	HIV, rubella, syphilis
Indirect contact	Spread via fomite (nonliving object)	Doorknob, shared needles
Droplet	Airborne droplets <1 meter	Sneezing, coughing
Vehicle – Airborne	Dust or droplet nuclei >1 meter	TB, measles
Vehicle – Waterborne	Contaminated water	Cholera, Giardia
Vehicle – Foodborne	Contaminated food	Salmonella, E. coli O157

Healthcare-Associated Infections (HAIs)

• Also called nosocomial infections – acquired while receiving treatment in a healthcare facility.

• Require three factors: microorganisms in the healthcare environment, compromised host, and chain of transmission.

Epidemiology

• CDC collects and analyzes US epidemiological information; publishes the Morbidity and Mortality Weekly Report (MMWR).

• Emerging infectious diseases: new, increasing in incidence, or showing potential to increase – most are zoonotic, viral, and vector-borne.

Microbial Mechanisms of Pathogenicity

Key Terms

• Pathogenicity: Ability of a microbe to cause disease.

• Virulence: Degree of pathogenicity; how severe or damaging.

• Virulence factors: Structures or products that allow a pathogen to cause infection.

• ID50: Infectious dose for 50% of the test population.

• LD50: Lethal dose that kills 50% of the test population.

• Adhesin (ligand): Surface molecule on pathogen that binds to host cell receptor.

Portals of Entry

• Mucous membranes: Respiratory, GI, genitourinary tracts, conjunctiva (most common entry).

• Skin: Requires a break or wound; few pathogens penetrate intact skin.

• Parenteral route: Deposited directly into tissues via puncture, bite, surgery, or injection.

• During pregnancy/birth: Mother to fetus (e.g., HIV, rubella).

Note: The greatest number of pathogens enter through the respiratory system.

Microbial Adherence Mechanisms

• Adhesion requires a lock-and-key match: adhesin (ligand) on pathogen binds to receptor on host cell surface.

• Structures used for adhesion include fimbriae (pili), capsules, and viral spikes.

Capsules & Cell Wall Components

• Capsules: Prevent phagocytosis (e.g., Streptococcus pneumoniae).

• M protein: (Streptococcus pyogenes) resists phagocytosis.

• Mycolic acid: (Mycobacterium tuberculosis) resists digestion inside phagocytes.

• Gram-negative outer membrane: Protects from lysozyme and complement.

Exoenzymes and Their Effects

Enzyme	What It Does	Pathogen
Hyaluronidase	Breaks down hyaluronic acid; allows pathogen to spread	Streptococcus, Staphylococcus, Clostridium
Collagenase	Breaks down collagen in connective tissue	Clostridium perfringens
Coagulase	Converts fibrinogen to fibrin; bacteria hide in clot	Staphylococcus aureus
Streptokinase	Dissolves fibrin clots; allows bacteria to spread	Streptococcus
IgA protease	Destroys IgA antibodies on mucous membranes	Neisseria, H. influenzae

Mechanisms to Avoid Phagocytosis

• Capsule formation

• Antigenic variation (e.g., Neisseria gonorrhoeae, Influenza)

• Intracellular survival (e.g., Mycobacterium tuberculosis, Listeria, Legionella)

• Invasins: induce host cell membrane ruffling (e.g., Salmonella)

Direct Damage by Pathogens

• Disrupt host cell function

• Use host cell nutrients

• Produce toxic waste products

• Multiply inside host cells causing lysis

• Siderophores: steal iron from host proteins

Exotoxins vs. Endotoxins

Property	Exotoxins	Endotoxins
Bacterial source	Gram+ and Gram-	Gram- only
Chemical nature	Proteins (A-B structure)	Lipopolysaccharide (LPS) – lipid A
Relation to organism	Secreted by living cells	Part of outer membrane; released on cell death
Heat stability	Unstable (destroyed at 60–80°C)	Stable (withstands autoclaving at 121°C)
Toxicity	High (toxic in minute amounts)	Low (requires high doses)
Fever-producing	Usually no	Yes
Toxoid formation	Yes (can be inactivated for vaccines)	No
Immune response	Stimulates antitoxin antibodies	Poor stimulation of antitoxins
Representative diseases	Tetanus, botulism, diphtheria, gas gangrene	Typhoid fever, UTIs, meningococcal meningitis

Types of Exotoxins

Type	Mechanism	Example
A-B toxins	B (binding) subunit attaches to host; A (active) subunit disrupts function	Cholera, diphtheria, botulinum toxins
Membrane-disrupting	Form pores in cell membrane causing lysis	Streptolysin, leukocidins
Superantigens	Overstimulate T cells → massive cytokine release	Toxic shock syndrome toxin (TSST-1), staph enterotoxins

Cytopathic Effects (CPE) of Viruses

• Halts normal cell metabolism

• Inclusion bodies (e.g., Negri bodies in rabies)

• Syncytium formation (e.g., HIV, measles)

• Induces chromosomal and antigenic changes

• Loss of contact inhibition (may lead to cancer)

Innate Immunity: Nonspecific Defenses

Innate vs. Adaptive Immunity

Type	Also Called	Key Features
Innate	Non-specific	Born with it; same response to all pathogens; 1st & 2nd line of defense
Adaptive	Specific / Acquired	Developed after exposure; unique response per microbe; 3rd line; uses B & T cells

PAMPs and PRRs

• PAMPs: Pathogen-Associated Molecular Patterns (e.g., peptidoglycan, LPS, dsRNA)

• PRRs: Pattern Recognition Receptors on phagocytes, dendritic cells, endothelial cells

• TLRs: Toll-Like Receptors, a type of PRR that triggers immune activation

First Line of Defense – Physical & Chemical Barriers

• Physical barriers: Skin (keratinized), hair follicles, mucous membranes, cilia, normal microbiota

• Chemical barriers: Sebum, lactic acid, lysozyme (tears, saliva), stomach acid, digestive enzymes, acidic vaginal pH, antimicrobial chemicals in semen

Second Line of Defense – Internal Defenses

• Phagocytic cells: Survey tissues, ingest and destroy microbes

• Steps of phagocytosis:

  1. Chemotaxis

  2. Adherence

  3. Ingestion

  4. Phagolysosome formation

  5. Digestion

  6. Discharge

• Natural Killer (NK) cells: Kill virus-infected and cancer cells by releasing perforin and granzymes

Inflammatory Response

• Non-specific local response to tissue damage or pathogen entry

• Cardinal signs: Rubor (redness), Calor (heat), Tumor (swelling), Dolor (pain), Loss of function

• Steps: Injury/Immediate → Vascular Reactions → Edema/Pus Formation → Resolution/Scar Formation

Fever

• Systemic response triggered by pyrogens (e.g., LPS)

• Benefits: Inhibits microbe multiplication, decreases iron availability, increases metabolism and phagocytosis

Complement System

• Over 30 proteins in plasma; activated in a cascade

• Outcomes: Cell lysis (MAC), opsonization, inflammation

Other Antimicrobial Substances

Substance	Mechanism
Interferons (IFNs)	Induce antiviral proteins in neighboring cells; enhance phagocytosis
Iron-binding proteins	Decrease iron availability to microbes
Antimicrobial peptides	Lyse bacterial cell membranes

Adaptive Immunity: Specific Defenses

Types of T Cells & Their Roles

T Cell Type	Surface Marker	MHC Required	Role
Helper T (TH)	CD4	MHC II	Activate cytotoxic T cells and B cells; secrete cytokines
Cytotoxic T (TC/CTL)	CD8	MHC I	Kill virus-infected and cancer cells
Regulatory T (Treg)	CD4	MHC II	Suppress immune response; prevent autoimmunity
Memory T cells	CD4 or CD8	—	Rapid response upon re-exposure

MHC I vs. MHC II

Feature	MHC I	MHC II
Found on	All nucleated cells	APCs only (macrophages, dendritic cells, B cells)
Presents to	Cytotoxic T cells (CD8+)	Helper T cells (CD4+)
Source of antigen	Intracellular	Extracellular

Cell-Mediated Immunity (CMI)

• Carried out by cytotoxic T cells (TC cells)

• Targets: virus-infected cells, cancer cells, transplanted cells

• Mechanism: TC cell binds via CD8 + MHC I + antigen, releases perforin and granzymes → apoptosis

Antibody-Mediated (Humoral) Immunity

• Carried out by B cells → plasma cells secrete antibodies

• Most B cell activation requires Helper T2 (TH2) cells

• B cells have MHC II on their surface

• Memory B cells enable rapid secondary response

Antibody (Immunoglobulin) Structure

• Y-shaped protein; 2 heavy + 2 light chains

• FAb regions: variable, antigen-binding

• Fc region: constant, binds immune cells, triggers complement

Classes of Immunoglobulins

Class	Structure	Key Features
IgM	Pentamer	First produced; complement activator; agglutination
IgG	Monomer	Most abundant; crosses placenta; opsonization
IgA	Dimer	Secretions (tears, saliva, milk); mucosal defense
IgE	Monomer	Allergic reactions; histamine release
IgD	Monomer	On naive B cells; antigen receptor

Primary vs. Secondary Immune Response

Feature	Primary	Secondary
Trigger	First exposure	Re-exposure
Speed	Slow (days–weeks)	Fast (hours–days)
Magnitude	Low antibody titer	High antibody titer
Antibody class	IgM first, then IgG	Mostly IgG
Cells involved	Naive B + TH cells	Memory B cells
Duration	Short-lived	Long-lasting

Mechanisms of Antibody Action

• Opsonization: Antibodies coat microbe, enhancing phagocytosis

• Agglutination: Cross-link antigens into clumps

• Neutralization: Block surface receptors on viruses/toxins

• Antitoxin: Neutralizes bacterial exotoxins

• Complement activation: Antibody-antigen complex triggers complement cascade

Types of Adaptive Immunity

Type	How Acquired	Memory?	Example
Natural Active	Infection; body makes antibodies	Yes	Flu infection
Natural Passive	Mother to fetus/infant	No	IgG via placenta; IgA via milk
Artificial Active	Vaccination	Yes	MMR vaccine
Artificial Passive	Injection of preformed antibodies	No	Rabies immune globulin

Active vs. Passive Immunity

Feature	Active	Passive
Antigen exposure	Yes	No
Immune memory	Yes	No
Onset	Days to weeks	Immediate
Duration	Long-lasting	Short-lived

Vaccines

• Antigen or antigen mixture used to induce artificial active immunity

• Provokes primary response; memory cells formed

• Herd immunity: immunity in most of the population limits spread

Applications of Immunology

Biochemical Tests

• Based on enzyme-mediated metabolic reactions

• Physiological reactions reveal enzyme systems; visualized by color change

Serology

• In vitro diagnostic testing of serum

• Detects, identifies, and quantifies antibodies or antigens

• Principle: unknown antibody detected using known antigen, or vice versa

Agglutination and Precipitation

Test	Antigen Type	Description	Example
Agglutination	Whole cells	Antibody-mediated clumping	Blood typing
Precipitation	Soluble molecules	Antigen-antibody complexes in solution	RPR test

Western Blot

• Proteins separated by gel electrophoresis, detected by antibodies

• Used for HIV verification

Neutralization Reactions

• Viral hemagglutination: viruses agglutinate RBCs

• Hemagglutination inhibition: patient serum neutralizes virus, preventing agglutination

Molecular/Genotypic Methods

• PCR: Amplifies DNA/RNA; highly sensitive

• Hybridization: Probes bind specific sequences for identification

Vaccine Types

Type	Description
Inactivated	Killed microorganisms; not infectious
Attenuated (Live)	Living, non-virulent strains
Toxoid	Chemically modified exotoxin
Recombinant DNA	Gene cloned and expressed in another microbe

• Adjuvants: Chemical additives to improve vaccine effectiveness (e.g., alums, monophosphoryl lipid A)

Immune Disorders

Hypersensitivity / Immunopathology

• Immunopathology: Study of disease states from overreactivity (allergy, autoimmunity) or underreactivity (immunodeficiency)

The Four Types of Hypersensitivity

Type	Name	Onset	Ig Involved	Mechanism	Examples
I	Anaphylactic / Immediate	<30 min	IgE	IgE binds mast cells → degranulation	Hay fever, asthma, anaphylaxis
II	Cytotoxic	5–12 hrs	IgG, IgM	Ab binds cell surface → complement → lysis	Transfusion reactions, Rh incompatibility
III	Immune Complex	3–8 hrs	IgG, IgM, IgA	Immune complexes lodge in tissues → complement → tissue damage	Serum sickness, SLE, RA
IV	Delayed / Cell-Mediated	24–48 hrs	None (T cells)	CTLs and macrophages cause tissue damage	Contact dermatitis, TB test, graft rejection

Type I – Anaphylactic (IgE-Mediated Immediate)

• Sensitization: Allergen exposure → IgE produced → binds mast cells

• Provocation: Allergen re-exposure → mast cell degranulation → histamine, leukotrienes, prostaglandins released

• Effects: Vasodilation, smooth muscle contraction, increased mucus, skin manifestations

• Atopic diseases: Hay fever, asthma, eczema, food/drug allergies

• Systemic anaphylaxis: Rapid, life-threatening; triggers include bee venom, antibiotics

• Treatment: Avoidance, steroids, monoclonal antibodies, cromolyn, antihistamines, desensitization

Type II – Cytotoxic (IgG & IgM)

• Antibodies bind cell surface antigens → complement activation → cell lysis

Blood Type	Antigens on RBC	Antibodies in Serum
A	A	Anti-B
B	B	Anti-A
AB	A and B	Neither
O	None	Anti-A and Anti-B

• Transfusion reactions: Wrong blood type → hemolysis, shock, kidney failure

• Hemolytic disease of the newborn: Rh- mother, Rh+ fetus; prevented by RhoGAM

Type III – Immune Complex

• Antibody + excess soluble antigen → large complexes lodge in tissues → complement activation → tissue damage

• Examples: Serum sickness, Arthus reaction, SLE, rheumatoid arthritis

Type IV – Delayed/Cell-Mediated (T Cells)

• T cells respond to antigens on self or transplanted tissues

• Symptoms arise 24–48 hours after exposure

• Examples: Contact dermatitis, TB skin test, graft rejection, some chronic diseases

Autoimmunity

• Immune system attacks self-antigens (autoantibodies or T cells)

• Systemic (multiple organs) or organ-specific

Disease	Target	Hypers. Type	Characteristics
Systemic lupus erythematosus (SLE)	Systemic	III	Antibodies against RBCs, WBCs, platelets, DNA
Rheumatoid arthritis	Joints	II, III, IV	Vasculitis, antibodies against other antibodies
Graves' disease	Thyroid	III	Antibodies against TSH receptors
Myasthenia gravis	Muscle	III	Antibodies against acetylcholine receptors
Type I diabetes	Pancreas	IV	T cells attack insulin-producing cells
Multiple sclerosis	Myelin	II, IV	T cells and antibodies destroy neurons

Immunodeficiency Diseases

Primary (Congenital)

Condition	What's Deficient	Result
DiGeorge syndrome	T cells (thymus absent/underdeveloped)	Recurrent fungal, protozoan, viral infections
ADA deficiency	T cell development blocked	Recurrent infections
X-linked SCID	T and B cells	Severe combined immunodeficiency
Congenital agammaglobulinemia	B cells/antibodies absent	Recurrent bacterial infections
Hypogammaglobulinemia	Low immunoglobulin/B cells	Recurrent bacterial infections

Secondary (Acquired)

• Caused by infection, metabolic disease, chemotherapy, radiation

• AIDS: HIV infects T helper cells, monocytes, macrophages, APCs; depletion of T helper cells impairs immune responses, leading to cancers and opportunistic infections

Additional info: This guide covers core concepts from BIO 150 Exam 3, including disease principles, epidemiology, mechanisms of pathogenicity, innate and adaptive immunity, immunological applications, and immune disorders. It is suitable for exam preparation and review in a college-level microbiology course.