Microbiology Finals Study Guide: Viruses, Immunity, Immune Disorders, and Antimicrobial Drugs

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Chapter 6 – Viruses, Viral Life Cycles, and Acellular Agents

Core Concepts of Viruses

Viruses are unique infectious agents that lack cellular structure and metabolic machinery, making them obligate intracellular parasites. They must infect host cells to replicate.

Structure: Viruses consist of a nucleic acid genome (DNA or RNA) encased in a protein coat called a capsid, which is made of subunits called capsomeres. Some viruses possess an additional envelope—a lipid membrane derived from the host, embedded with viral spike proteins.
Naked vs. Enveloped Viruses: Naked viruses lack an envelope, while enveloped viruses have one. This distinction affects their environmental stability and mechanisms of cell entry and exit.

Viral Entry Mechanisms

The method by which viruses enter host cells depends on their structural features.

Enveloped Viruses: Enter cells via membrane fusion (fusion of viral envelope with host membrane) or endocytosis.
Naked Viruses: Cannot use fusion (no envelope); rely on endocytosis or direct genome injection (as seen in bacteriophages).
Key Point: Fusion requires a lipid envelope; naked viruses lack this, so cannot fuse with the host cell membrane.

Viral Life Cycles

Viruses replicate through distinct cycles, affecting host cell fate.

Lytic Cycle: Virus replicates, assembles, and lyses the host cell, releasing new virions. Results in acute cell destruction.
Lysogenic Cycle: Viral genome integrates into the host genome, replicating passively. The cell is not immediately destroyed; the virus can later switch to the lytic cycle.
Terminology: In bacteria, the integrated viral genome is a prophage; in eukaryotes, it is a provirus (e.g., HIV).

Viral Evolution and Immunity

Viruses evolve rapidly, affecting host immunity and epidemiology.

Antigenic Drift: Gradual point mutations in viral surface antigens (e.g., influenza HA/NA), causing seasonal variation. Immunity is partially retained.
Antigenic Shift: Abrupt reassortment of genome segments between co-infecting viruses, producing a new virus with novel properties. Can expand host range dramatically.
Comparison: Antigenic shift can change host range in a single step; drift only causes gradual changes.

Acellular Agents: Prions

Prions are infectious proteins, distinct from viruses and other pathogens.

Definition: Prions are misfolded proteins that induce normal proteins to misfold, propagating disease.
Diseases: Cause transmissible spongiform encephalopathies (e.g., Creutzfeldt-Jakob disease, mad cow disease/BSE, scrapie).
Properties: Extremely resistant to heat, radiation, and standard disinfection.

Chapter 11 – Innate Immunity & the Cellular Defenders

First-Line (Barrier) Defenses

Innate immunity provides immediate, non-specific protection against pathogens.

Stomach Acid: Acts as a chemical barrier; raising stomach pH (e.g., with antacids or PPIs) increases infection risk.
Lysozyme: Enzyme in tears, saliva, and mucus that hydrolyzes bacterial peptidoglycan, especially effective against Gram-positive bacteria.

The Lymphatic System

The lymphatic system is central to immune surveillance and response.

Leukocytes: White blood cells (WBCs) are key immune cells.
Lymph Nodes: Act as filtering stations where immune cells sample lymph for antigens.

Classification of WBCs by Nucleus and Staining

WBCs are classified based on nucleus morphology and staining properties, aiding identification and correlating with function.

Eosin: Acidic, pink dye stains eosinophils.
Baso: Basic, blue dye stains basophils.
Neutro: Neutral dye stains neutrophils (lilac color).
Reason: Nucleus shape and granule staining allow rapid identification and relate to cell function.

Granulocytes

Granulocytes are WBCs with visible cytoplasmic granules, each with specialized roles.

Cell	Key Role	Notes
Neutrophils	First responders; release antimicrobial peptides and enzymes	Most numerous; elevated in acute bacterial infection; multilobed nucleus
Eosinophils	Defense against parasites; drive allergic inflammation	Elevated in parasitic infections and allergies
Basophils	Release histamine; stimulate inflammation	Small, lobed nucleus; few granules; smooth membrane
Mast cells	Tissue-resident; release histamine	Larger, round nucleus; many granules; membrane projections

Mast Cell vs. Basophil: Mast cells are larger, have a round nucleus and many granules; basophils are smaller, have a lobed nucleus and fewer granules.

Agranulocytes

Agranulocytes lack visible granules and bridge innate and adaptive immunity.

Examples: Monocytes/macrophages, dendritic cells, lymphocytes.
Function: Macrophages and dendritic cells act as antigen-presenting cells (APCs).

Nutritional Immunity – Iron

The host limits pathogen access to iron, a vital nutrient, as a defense mechanism.

Iron Sequestration: Host proteins bind iron to starve pathogens.
Bacterial Countermeasures: Siderophores (high-affinity iron-scavenging molecules) and specialized receptors steal iron from host sources.

Chapter 12 – Adaptive Immunity

Antigens and Epitopes

Adaptive immunity targets specific molecules called antigens, with recognition focused on epitopes.

Antigen: Any molecule that triggers an immune response.
Epitope: The specific region of an antigen bound by a receptor or antibody; one antigen can have multiple epitopes.

Stages of the Adaptive Immune Response

The adaptive response proceeds through four stages:

Antigen Presentation: Antigen is displayed to lymphocytes.
Lymphocyte Activation: Matching lymphocyte is activated.
Lymphocyte Proliferation and Differentiation: Clonal expansion into effector and memory cells.
Antigen Elimination and Memory: Pathogen is cleared; memory cells persist.

Branches: Humoral immunity (B cells, antibody-mediated) and cellular immunity (T cells, cell-mediated).

Antigen-Presenting Cells (APCs)

APCs process antigens and present them on MHC molecules to T cells.

Examples: Dendritic cells, macrophages, B cells.

T Cells

T cells are central to cellular immunity, with distinct functions.

Cytotoxic T cell (Tc, CD8+): Kills infected or abnormal cells directly.
Helper T cell (Th, CD4+): Coordinates immune response, activates B cells and other immune cells via cytokines.
Memory Tip: CD8 = Cytotoxic ("8 = ate/kill the cell"); CD4 = Helper.

B Cells and Receptors

B cells recognize antigens directly, while T cells require antigen presentation.

BCR (B-cell receptor): Binds free, soluble antigen.
TCR (T-cell receptor): Binds epitopes presented by other cells (via MHC).
Comparison: BCR = free antigen; TCR = presented antigen.

B Cell Activation Pathways

T-dependent antigens: Require helper T-cell (CD4+) assistance; produce high-affinity antibodies, class switching, and memory (protein antigens).
T-independent antigens: Activate B cells without T-cell help (repetitive polysaccharide antigens); produce weaker response, little/no memory, mostly IgM.

Chapter 13 – Immune Disorders: Deficiency, Cancer, Autoimmunity, Hypersensitivity

Immunodeficiencies

Immunodeficiencies are conditions where immune function is impaired.

Primary (congenital): Genetic or developmental defects.
Secondary (acquired): Caused by aging, chronic disease, or external factors.
Examples:
- HIV: Infects and depletes CD4+ helper T cells, leading to AIDS.
- Epstein-Barr Virus (EBV): Infects B cells; associated with mononucleosis and certain cancers.
- Immune amnesia: (e.g., after measles) Virus wipes out immune memory cells, increasing susceptibility.

Immunity and Cancer

Immune Surveillance: The immune system detects and destroys tumor cells.
Immunotherapy: Can be prophylactic (prevent cancer, e.g., HPV vaccine) or therapeutic (treat existing cancer).

Autoimmune Disease Mechanisms

Autoimmunity arises from loss of self-tolerance, with several mechanisms:

Molecular mimicry: Microbial antigens resemble self-antigens, causing cross-reactivity.
Bystander activation: Inflammation activates nearby self-reactive cells.
Tissue damage + antigen release: Hidden self-antigens become exposed.
Epitope spreading: Response broadens to additional self-epitopes over time.
Persistent infection: Chronic stimulation drives autoimmunity.

Microbiome and Hypersensitivities

Hygiene Hypothesis: Reduced early-life microbial exposure increases allergies/hypersensitivities due to under-trained immune system.

Hypersensitivities – Gell and Coombs Classification

Hypersensitivity reactions are classified into four types based on mechanism and clinical features.

Type	Name	Mechanism	Examples
I	Immediate / Allergic	IgE-mediated; triggers mast cell/basophil histamine release	Allergies, atopic asthma, atopic dermatitis, anaphylaxis
II	Cytotoxic / Cytolytic	IgG/IgM antibodies bind cell-surface antigens → cell destruction	Hemolytic transfusion reactions, hemolytic disease of the newborn
III	Immune Complex	Antibody–antigen complexes deposit in tissues (noncytotoxic reactions)	Serum sickness, lupus-type reactions
IV	Delayed	T-cell mediated (not antibody); delayed onset (24–72 hr)	Contact dermatitis (poison ivy), TB skin test, transplant rejection

Memory Tip: "ACID" — Allergic (IgE), Cytotoxic (antiBody), Immune complex, Delayed (T-cell).
Note: Type II can be split into cytotoxic/cytolytic vs. noncytotoxic reactions.

Chapter 15 – Antimicrobial Drugs & Resistance

Naming Convention

-ase: Suffix denotes an enzyme (e.g., β-lactamase destroys β-lactam drugs).

Major Antibiotic Classes

Antibiotics are grouped by their mechanism of action and target.

Class	Target / Mechanism	Notes
β-lactams (penicillins, cephalosporins)	Inhibit cell wall (peptidoglycan) synthesis	Defeated by β-lactamases (enzymes that cleave β-lactam ring)
Glycopeptides (e.g., vancomycin)	Inhibit cell wall synthesis (bind cell wall precursors)	Used against resistant Gram-positives
Quinolones (fluoroquinolones)	Inhibit DNA gyrase/topoisomerase → block DNA replication
Antifolate sulfa drugs (sulfonamides)	Inhibit folic acid synthesis (block DHPS in folate pathway)	Selective: humans get folate from diet; bacteria must synthesize it

Key Pairing: β-lactams attack cell wall; β-lactamases confer resistance by destroying the drug.

Measuring Antimicrobial Activity

Zone of Inhibition: Clear area around an antibiotic disk on a bacterial lawn; larger zone = more effective drug.
Kirby-Bauer Disk-Diffusion Test: Used to determine susceptibility, intermediate, or resistance to a drug.

Antimicrobial Resistance Mechanisms

Bacteria develop resistance through various strategies.

Enzymatic destruction: e.g., β-lactamases.
Efflux pumps: Expel the drug from the cell.
Target modification: Alter drug binding sites.
Reduced permeability/altered porins: Limit drug entry.
Spread: Resistance spreads via mutation and horizontal gene transfer (plasmids, conjugation, transformation, transduction).
Selective Pressure: Overuse/misuse of antibiotics accelerates resistance development.