🧫 BIG PICTURE: MICROBIOLOGY

Microbiology = study of microscopic life + infectious agents

Major Groups
• Bacteria – prokaryotic, single-celled
• Archaea – prokaryotic, no peptidoglycan (so many antibiotics don’t work), extremophiles (live
in extreme environments like heat/salt)
• Fungi – eukaryotic (yeasts, molds)
• Protozoa – eukaryotic, often parasitic
• Algae – eukaryotic, photosynthetic
• Viruses – not cells, no metabolism or ribosomes, must use host machinery to replicate
• Helminths – parasitic worms

Prokaryotes vs Eukaryotes (CORE)

Prokaryotes
• No nucleus or organelles
• Circular DNA
• Binary fission (NOT mitosis → simple split, no spindle fibers or phases)
• Faster division (~20 min in optimal conditions like E. coli)
Eukaryotes
• Nucleus + organelles
• Linear chromosomes
• Mitosis/meiosis

Key Microbial Groups

Bacteria
• Roles: decomposition, normal microbiota, disease
• Most are beneficial
• Can use host tissue as nutrient source (steal iron, glucose, amino acids → contributes to
virulence)
Fungi
• Cell wall = chitin
• Membrane = ergosterol (drug target, NOT in bacteria)
• Yeasts (single-cell) vs molds (hyphae)
• Dimorphic = mold (environment) → yeast (body)
Protozoa
• Trophozoite (active, feeding, causes disease) vs cyst (infectious, resistant survival form)
Viruses
• Not living
• Must infect host
• Can be latent (remain inactive in host cells)
Helminths
• Multicellular parasites
• Identified by eggs

History (VERY TESTABLE)

• Hooke → cells
• Leeuwenhoek → first microbes
• Redi → disproved spontaneous generation (maggots come from flies, not meat)
• Pasteur → biogenesis (“life comes from life”), fermentation
• Koch → germ theory (specific microbes cause disease)
• Jenner → vaccine
• Fleming → penicillin

Koch’s Postulates (Know Steps)

1. Present in diseased
2. Isolate
3. Cause disease
4. Re-isolate
Limitations:
• Asymptomatic carriers (can have pathogen but not be sick)
• Some pathogens cannot be cultured in lab

Prokaryotic Cell Structure (HIGH-YIELD)

DNA
• Chromosome = essential genes
• Plasmids = antibiotic resistance, virulence
Appendages
• Pili / fimbriae → attachment to surfaces/host (important for infection)
• Sex pilus → DNA transfer between bacteria (conjugation → spreads resistance)
• Flagella → movement (present in both prokaryotes & eukaryotes, but structurally different)

Bacterial Envelope (VERY IMPORTANT)

Glycocalyx
• Capsule → prevents phagocytosis (immune evasion)
• Slime layer → biofilms (helps bacteria stick and survive on surfaces)
Cell Wall (Peptidoglycan)
• NAG + NAM
• Prevents osmotic lysis (cell bursting due to water entering)
• Target of penicillin (inhibits transpeptidation → weak wall → cell bursts)
Outer Membrane (Gram - ONLY)
• Contains LPS
• Lipid A = endotoxin → triggers fever, inflammation, septic shock

Gram Stain (HIGH-YIELD)

Gram +
• Thick peptidoglycan
• Purple
Gram -
• Thin wall + outer membrane
• LPS present
• Pink

Transport + Survival
• Diffusion, osmosis, active transport
• Hypotonic → water enters cell → may burst
• Hypertonic → water leaves cell → shrinks (used in food preservation like salt)

Endospores
• Bacillus, Clostridium
• Heat + chemical resistant
• Survival structure (NOT reproduction)

Eukaryotic Cells (Important)

Organelles:
• Nucleus → DNA
• ER → protein/lipid synthesis (start of secretion pathway)
• Golgi → modifies and packages proteins
• Mitochondria → ATP
• Lysosome → digestion

Fungi (HIGH-YIELD)
• Chitin cell wall
• Ergosterol membrane (drug target)
• Yeasts, molds, dimorphic

Protozoa (IMPORTANT)
• Cyst = infectious, resistant
• Trophozoite = active
Motility:
• Flagella
• Pseudopods
• Cilia

Helminths
• Flatworms, roundworms
• Identified by eggs

🧫 MICROBIAL GROWTH
Binary Fission
1→2→4→8
• NOT mitosis

Growth Curve (VERY TESTABLE)

1. Lag – adaptation, enzyme production (NOT dividing yet)
2. Log – rapid growth (MOST antibiotic sensitive)
3. Stationary – nutrients low, waste accumulates
4. Death – cells die from toxins + lack of nutrients

Measuring Growth
• Plate count → most accurate (counts live cells)
• Turbidity → fast, indirect estimate (cloudiness, NOT exact count)

Environmental Factors
Temperature
• Psychrophiles (cold)
• Mesophiles (37°C pathogens like humans)
• Thermophiles (heat)
Example:
• Listeria = psychrotroph (can grow in refrigerator temps)
pH
• Bacteria: neutral
• Fungi: acidic
Oxygen (VERY IMPORTANT)
• Obligate aerobes
• Obligate anaerobes
• Facultative anaerobes
• Microaerophiles
⚠️Oxygen is toxic due to ROS (reactive oxygen species)
→ damages DNA, proteins, membranes
→ catalase + SOD protect cells

Nutrition
• CHONPS
• Trace elements
• Vitamins (fastidious organisms need complex media, NOT minimal)
• Heterotrophic bacteria require preformed organic nutrients

⚡ METABOLISM (HIGH-YIELD)
Metabolism
• Catabolism → breaks down molecules, produces ATP
• Anabolism → builds molecules, requires ATP

ATP
• Ribonucleotide (NOT deoxyribonucleotide)
• Ribose + adenine + 3 phosphate groups

Enzymes
• Lower activation energy (make reactions easier, NOT harder)
• Specific to substrate

Redox Reactions
• Oxidation (loss of electrons) + reduction (gain of electrons) occur together

Energy Production
Glycolysis
• Cytoplasm
• No oxygen required
• 2 ATP + NADH
Krebs Cycle
• Mitochondrial matrix (eukaryotes)
• Produces CO₂ + electron carriers
ETC
• Inner mitochondrial membrane
• Requires oxygen (final electron acceptor)
• ~34 ATP
👉 Aerobic respiration produces more ATP than anaerobic

Fermentation
• No oxygen
• Regenerates NAD⁺ (keeps glycolysis running)
• 2 ATP only
Products:
• Lactic acid
• Ethanol + CO₂
⚠️Lactic acid lowers pH → inhibits microbial growth

Other Pathways
• Anaerobic respiration → uses nitrate instead of oxygen
• Pentose phosphate pathway → produces NADPH (protects from oxidative stress) + ribose (for
DNA/RNA)
• Galactose → glucose conversion = isomerization

Antibiotics (Natural Concept)

• Many antibiotics are naturally produced by microbes to compete with other organisms

⚡ MICROBIOLOGY GENERAL
Direct vs Indirect Counting
• Direct = actual cell count (plate count, microscopy)
• Indirect = estimate (turbidity, metabolic activity)

Growth Limits in Culture

• Nutrients
• Space
• Waste buildup

Oxygen Toxicity
• Oxygen forms ROS
• Damages DNA, proteins, membranes

Mannoproteins
• Found in fungi (NOT bacteria)

Cell Secretion (Eukaryotes)

• ER → Golgi → vesicles → secretion (proteins made, modified, then released)
STUDY GUIDE 2:
I. MICROBIAL GENETICS (CORE IDEAS)
Genetics Basics
• DNA = genetic material
• Genes → proteins → traits (phenotype)
• DNA change → protein change → possible phenotype change
👉 Proteins determine structure/function → that’s why mutations affect traits

Genome / DNA
• Genome = chromosome + plasmids
• DNA:
o Double helix, antiparallel
👉 Antiparallel = one strand 5’→3’, other 3’→5’
o A–T, G–C
👉 Hydrogen bonding: A–T (2 bonds), G–C (3 bonds → stronger)
o Polymerase adds only to 3’ end
o ⚠️Nucleotides ALWAYS added to 3’ OH (never 5’)
👉 This is why ALL synthesis (DNA & RNA) is 5’ → 3’

Chromosome vs Plasmid
Chromosome
• Essential genes
• Bacteria: circular
Plasmid
• Non-essential, circular
• Carry:
o Antibiotic resistance
o Virulence genes
• Easily transferred → major source of resistance spread
👉 Transferred mainly by conjugation → rapid spread between bacteria

Genotype vs Phenotype
• Genotype = genetic makeup
• Phenotype = observable trait
⚠️Key: phenotype can change with environment, genotype does not
👉 Example: same bacteria, different temp → different protein expression

II. DNA REPLICATION (VERY HIGH-YIELD)

Key Rules
• Semiconservative
👉 Each new DNA = 1 old strand + 1 new strand
• Requires ATP
• Occurs 5’ → 3’ only
• ⚠️Always adds to 3’ end

Main Enzymes
• Helicase → unwinds DNA
👉 Breaks hydrogen bonds between bases
• DNA polymerase → adds nucleotides
👉 Also proofreads (3’→5’ exonuclease activity)
• Ligase → connects fragments
👉 Seals gaps between Okazaki fragments

Strands
• Leading → continuous
• Lagging → discontinuous (Okazaki fragments)
👉 Lagging happens because DNA must still go 5’→3’

IV. TRANSCRIPTION (DNA → mRNA)

• Enzyme: RNA polymerase
👉 Does NOT need a primer (unlike DNA polymerase)
• Base pairing:
o A–U, G–C

Prokaryotes
• Cytoplasm
• No nucleus
• Transcription + translation occur together
👉 Ribosomes can start translating before transcription finishes
• Polycistronic mRNA
👉 One mRNA codes for multiple proteins (operons)

Sigma Factor (VERY TESTABLE)

• Helps RNA polymerase find promoter
• Required for initiation (NOT termination)
👉 Recognizes -10 and -35 promoter regions

V. TRANSLATION (mRNA → PROTEIN)

Key Facts
• Ribosome: 70S (prokaryotes)
👉 30S + 50S subunits (important drug targets)
• Start codon: AUG (methionine)

Ribosome Sites
• A = incoming tRNA
• P = growing chain
• E = exit
👉 Order matters: A → P → E

Codon vs Anticodon
• Codon → mRNA
• Anticodon → tRNA

• Peptidyl transferase → forms peptide bonds and transfers growing chain

👉 Actually part of ribosome (rRNA = ribozyme)

VI. PROKARYOTE vs EUKARYOTE DNA

Prokaryotes
• No introns
• Faster expression
• Polycistronic
Eukaryotes
• Introns + exons
• RNA processing required
👉 Splicing removes introns before translation
⚠️Key difference: Prokaryotes = NO introns

VII. MUTATIONS
• Change in DNA
Types:
• Spontaneous
• Induced
• Transposons (“jumping genes”)
⚠️Not always harmful → can give antibiotic resistance
👉 Mutations can change drug target → resistance

VIII. HORIZONTAL GENE TRANSFER

• Transformation → naked DNA
• Conjugation → plasmid via pilus (MOST IMPORTANT)
👉 Requires cell-to-cell contact
• Transduction → bacteriophage
👉 Virus transfers bacterial DNA

IX. ANTIBIOTICS (KNOW BY TARGET)

Translation (important clarification)
30S inhibitors
• Tetracyclines → block tRNA binding
👉 Stops amino acids from entering ribosome
• Aminoglycosides → misread mRNA
👉 Leads to wrong proteins → cell death (e.g., gentamicin)

50S inhibitors
• Macrolides → block exit tunnel
👉 Prevents growing protein from leaving ribosome (e.g., azithromycin)
• Chloramphenicol → block peptide bond
👉 Inhibits peptidyl transferase
• Clindamycin → same (also 50S)
• Linezolid → blocks initiation

X. ANTIBIOTIC RESISTANCE
• ⚠️Resistance is drug-specific
👉 Example: DNA gyrase mutation → affects quinolones ONLY

IMMUNOLOGY

XI. IMMUNITY OVERVIEW

Innate Immunity
• Fast
• Non-specific
• No memory
• Recognizes PAMPs via PRRs
👉 Detects general patterns (not specific pathogens)
• Interferons
👉 Released by virus-infected cells → warn nearby cells + inhibit viral replication

XIII. INNATE INTERNAL DEFENSES

• Neutrophils → first responders
👉 Most abundant WBC, short lifespan, rapid response
• Macrophages → phagocytosis + APC
👉 Present antigen on MHC II to T cells
• Dendritic cells → activate T cells
👉 Most important antigen-presenting cells
• NK cells → kill infected cells (no MHC needed)
👉 Detect “missing self” (low MHC I)

XIV. COMPLEMENT SYSTEM

• MAC → lysis
👉 Forms pores in membrane → cell bursts

XVII. ANTIBODIES
Functions
• Neutralization
👉 Block toxin/virus binding
• Opsonization
👉 Tags pathogen for phagocytosis
• Complement activation
• ⚠️Not limited to neutralization
👉 They do multiple roles (not just one)

XVIII. MHC (VERY IMPORTANT)

• MHC I → CD8
👉 All nucleated cells present intracellular antigens
• MHC II → CD4
👉 Only APCs present extracellular antigens
• Antigens presented on MHC, NOT on T cell receptors
👉 TCR recognizes antigen-MHC complex

XIX. T CELLS
CD4 (Helper)
• Activate immune response
👉 Activate BOTH B cells and CD8 cells
CD8 (Cytotoxic)
• Kill infected cells
• Use perforin + granzymes
👉 Perforin = holes, granzymes = apoptosis
• Destroy the entire infected host cell

XX. CLONAL SELECTION

• Only specific lymphocytes activated
• → effector + memory cells

XXI. PRIMARY vs SECONDARY RESPONSE

Feature | Primary | Secondary
Speed | Slow | Fast
Antibody | IgM | IgG
Strength | Low | High
• Secondary response is stronger and faster
👉 Due to memory B + T cells

XXII. IMMUNITY TYPES

Humoral
• B cells
• Antibodies
• Extracellular Cell-mediated
• T cells
• Intracellular
• Long-term immunity requires BOTH memory B and T cells
👉 Not just antibodies

XXIII. ACTIVE vs PASSIVE

Active
• Infection/vaccine
• Memory
• Vaccines = ACTIVE immunity
Passive
• Preformed antibodies
• Immediate
• No memory
👉 Stimulate immune system to make memory cells

XXIV. IMMUNE DISORDERS

• Allergy → IgE + histamine
• Autoimmune → self-attack
• Immunodeficiency → weak system
• Loss of CD4 affects entire immune system
👉 Because CD4 coordinates immune response

XXV. HIV
• Infects CD4 T cells
• Weakens immune system
👉 Destroys immune coordination → opportunistic infections

XXVI. PATHOGEN EVASION

• Capsules (avoid phagocytosis)
• Antigenic variation
• Latency
• Intracellular hiding
👉 Prevent opsonization and engulfment

FINAL STUDY NOTES

🦠 I. ANTIMICROBIAL RESISTANCE (AMR)
🔑 Core Concept
 Resistance develops via:
o Natural selection
o Genetic mutations
o Horizontal gene transfer (HGT)
➡️Antibiotics kill susceptible bacteria → resistant survive → spread

⚙️Key Resistance Mechanisms

1. Enzymatic destruction
o Beta-lactamases (VERY IMPORTANT)
o Examples:
 Klebsiella pneumoniae → produces carbapenemases (KPC)
 NDM-1 = plasmid-mediated carbapenem resistance
2. Efflux pumps
o Pump drugs out of cell
3. Target modification
o Alters ribosomes/enzymes
4. Reduced permeability
o Gram-negative bacteria → fewer porins
5. Biofilms
o Protective barrier → hard to treat

🧬 Important Organisms
 Stenotrophomonas → Gram-negative, highly resistant
 Klebsiella pneumoniae → carbapenem resistance
🌍 Impact
 Increased mortality
 Limited treatment options
 Threatens:
o Surgery
o Cancer therapy
o Transplants

II. FOODBORNE ILLNESS

🦠 Common Pathogens
 Salmonella → commonly poultry (VERY TESTABLE)
 Norovirus
 Campylobacter

🤒 Symptoms
 Diarrhea
 Vomiting
 Fever
 Abdominal pain

✅ Prevention
 Clean → Separate → Cook → Chill

🦠 III. BACTERIAL PATHOGENESIS

🔄 Stages
1. Exposure
2. Colonization
3. Immune evasion
4. Infection

🧬 Virulence Factors
 Capsule → prevents phagocytosis
 Antigenic variation
 Intracellular survival

🧫 IV. BACTERIOPHAGES
🔑 Key Points
 Infect bacteria only
 Obligate intracellular
⚠️VERY IMPORTANT
 Genome = DNA OR RNA (never both)
 Highly specific (NOT broad spectrum)

🔄 Life Cycles
 Lytic → destroys host
 Lysogenic → integrates into genome

💡 Application
 Phage therapy = alternative to antibiotics
 Used in agriculture + medicine

🍄 V. FUNGAL DISEASES (FINAL EXPANDED MASTER SECTION)

🔑 Key Concept
• Fungal infections are often opportunistic
→ Occur mainly in immunocompromised patients (HIV, chemo, transplant, antibiotics)

⚙️Fungal Pathogenesis (VERY HIGH-YIELD 🔥)

👉 How fungi actually cause disease
Fungi must be able to:
1. Adhere to host cells
• Stick to tissues (skin, mucosa)
• Important first step for infection
2. Invade host tissues
• Penetrate deeper layers → spread infection
3. Compete for nutrients
• Use host nutrients (glucose, iron, amino acids)
4. Resist innate immunity
• Survive phagocytosis
• Avoid complement system
5. Evade adaptive immunity
• Avoid antibodies and T-cell responses
⚠️Key:
• If fungi can’t do these → no disease
• These = virulence factors

🧍 Normal Fungal Microbiota

• Many fungi are normal flora
Common sites:
• Skin → Malassezia
• Oral cavity → Candida
• GI tract → Candida, Saccharomyces
• Vagina → Candida
• Respiratory tract → Aspergillus
👉 Become pathogenic when:
• Immune system weakens
• Microbiome disrupted (ex: antibiotics)

🦠 Major Fungal Pathogens

1. Yeasts
• Candida albicans
• Normal flora
• Causes:
o Thrush (oral)
o Vaginitis
o Skin & nail infections
o Systemic infections (candidemia)
⚠️Overgrowth after:
• Antibiotics
• Immunosuppression

• Cryptococcus neoformans
• Found in soil + bird droppings
• Causes:
o Meningitis (brain infection)
o Pneumonia
⚠️Major in AIDS patients

2. Molds
• Aspergillus fumigatus
• Inhaled spores
• Causes:
o Lung infections
o Allergic reactions

• Mucor (Mucorales)
• Causes:
o Mucormycosis (invasive, deadly)
⚠️Invades blood vessels → tissue death
3. Dimorphic Fungi ⭐ (EXAM FAVORITE)
👉 Mold (environment) → Yeast (body)
• Histoplasma capsulatum
• Soil (bird/bat droppings)
• Lung infection → can spread

• Coccidioides immitis
• Desert soil (VERY relevant in California)
• Causes Valley fever

• Blastomyces dermatitidis
• Soil/wood
• Lung + skin disease

4. Other Important Pathogens

• Pneumocystis jirovecii
• Causes pneumonia in immunocompromised

• Trichophyton rubrum
• Causes:
o Ringworm
o Athlete’s foot

🧠 Sites of Infection
• Brain → Cryptococcus
• Lungs → Aspergillus, Histoplasma, Coccidioides
• Skin → Trichophyton
• Mouth → Candida
• Vagina → Candida
• Blood → systemic infection

⚠️Outcomes of Infection
• Localized → skin/nails
• Pulmonary → lungs
• Systemic → bloodstream spread
• Opportunistic → only in weak immunity

🦠 CDC-STYLE CLINICAL PATTERNS (ADDED)

🔹 Superficial Infections
Ringworm (Tinea)
• Cause: Trichophyton
• Symptoms:
o Ring-shaped rash
o Itching
• Transmission:
o Person → person
o Animal → human
👉 Same fungi cause:
• Athlete’s foot
• Jock itch
• Nail infections

Vaginal Yeast Infection

• Cause: Candida albicans
• Symptoms:
o Itching
o Discharge
o Irritation

Environmental Lung Infections

👉 Caused by inhaling spores
• Blastomycosis → Blastomyces
• Histoplasmosis → Histoplasma
• Valley fever → Coccidioides
⚠️Key:
• Many exposed → no symptoms
• Some → severe disease

🐾 Zoonotic Fungal Infections

Sporotrichosis
• Cause: Sporothrix
• Transmission:
o Cuts (rose thorns 🌹)
⚠️Emerging:
• Sporothrix brasiliensis
• Spread via cats → humans
• More severe

🏠 Mold Infections
• Aspergillus → aspergillosis
• Mucor → mucormycosis
⚠️Found everywhere but dangerous in:
• Immunocompromised

🏥 Healthcare-Associated Infections
• Candidemia (Candida in blood)
• Candida auris (drug-resistant)
• Aspergillus outbreaks
• Mucormycosis
⚠️Risk factors:
• Catheters
• Ventilators
• Surgery

🧬 HIV/AIDS-Associated Fungal Infections

👉 Occur when CD4 < 200
• Oral thrush (Candida)
• Pneumocystis pneumonia
• Cryptococcal meningitis
• Histoplasmosis

💊 Antifungal Drugs (FULL + FIXED)

1. Polyenes
• Amphotericin B, Nystatin
Mechanism:
• Bind ergosterol → membrane damage
Side effects:
• Nephrotoxicity (VERY HIGH-YIELD)

2. Azoles
• Fluconazole, itraconazole, voriconazole, etc.
Mechanism:
• Inhibit ergosterol synthesis
Side effects:
• Liver toxicity

3. Echinocandins
• Caspofungin, micafungin
Mechanism:
• Inhibit glucan (cell wall synthesis)

4. Nucleoside Analogs
• Flucytosine
Mechanism:
• Inhibit DNA/RNA synthesis
Side effects:
• Bone marrow suppression

5. Allylamines
• Terbinafine
Mechanism:
• Block ergosterol production

⚠️Key:
• Antibiotics DO NOT work on fungi
• Can worsen fungal infections

🚨 Antifungal Resistance
• Fungi evolve to survive drugs
• Leads to:
o Harder treatment
o Limited options

💊 VII. ANTIVIRAL DRUGS (FULLY EXPANDED)

🔑 Key Concept
• Target viral replication steps (since viruses use host cells)
• Do NOT work like antibiotics
________________________________________
🫁 Influenza (Flu)
Drugs:
• Oseltamivir (Tamiflu) – oral
• Zanamivir (Relenza) – inhaled
• Peramivir – IV
• Baloxavir marboxil – single-dose oral
• Amantadine / Rimantadine (older; Influenza A only)
📌 Mechanisms:
• Neuraminidase inhibitors → block viral release
• Amantadine → blocks uncoating
________________________________________
🦠 COVID-19 (SARS-CoV-2)
Drugs:
• Paxlovid (nirmatrelvir/ritonavir) – oral
• Remdesivir – IV
• Molnupiravir – oral
📌 Mechanism:
• Inhibit viral replication enzymes (RNA polymerase/protease)
________________________________________
🧬 Herpes Viruses (HSV, VZV)
Drugs:
• Acyclovir
• Valacyclovir
• Famciclovir
📌 Mechanism:
• Nucleoside analogs → block viral DNA replication
________________________________________
🧪 Hepatitis Viruses
Hepatitis C (HCV)
• Sofosbuvir
• Ribavirin
Hepatitis B (HBV)
• Tenofovir
• Entecavir
📌 Mechanism:
• Inhibit viral polymerases / reverse transcriptase
________________________________________
🧬 HIV/AIDS (Antiretrovirals)
Drug Classes:
• Integrase inhibitors
o Dolutegravir
• NRTIs
o Abacavir, Lamivudine, Tenofovir
• NNRTIs
o Rilpivirine
• Protease inhibitors
📌 Mechanisms:
• Reverse transcriptase inhibitors → block RNA → DNA conversion
• Integrase inhibitors → block DNA integration
• Protease inhibitors → block viral maturation (NOT release)
• Entry inhibitors → block viral entry
________________________________________
🧫 Cytomegalovirus (CMV)
Drugs:
• Ganciclovir / Valganciclovir
• Cidofovir / Foscarnet
📌 Mechanism:
• Inhibit viral DNA synthesis

💉 VIII. VACCINES (EXPANDED + FULLY INTEGRATED)

🔑 Key Concept
• Vaccines stimulate the immune system to recognize pathogens before infection occurs
• Leads to adaptive immunity + memory cell formation → faster, stronger secondary
response

🧪 Types of Vaccines (Mechanisms)

1. 🧬 Live-Attenuated Vaccines
• Contain weakened (attenuated) live virus
• Mimic natural infection → strong, long-lasting immunity
• Usually one or few doses needed
Examples:
• MMR vaccine
• Varicella vaccine
⚠️Key:
• Small risk in immunocompromised patients
• Can replicate slightly → better immune activation

2. 🧫 Inactivated (Killed) Vaccines

• Contain dead virus (cannot replicate)
• Safer than live vaccines
Examples:
• Inactivated Polio Vaccine (IPV)
• Hepatitis A vaccine
⚠️Key:
• Weaker immune response → boosters required

3. 🧩 Subunit / Recombinant Vaccines

• Contain only specific antigens (pieces of virus)
• No whole pathogen
Examples:
• HPV vaccine
• Hepatitis B vaccine
⚠️Key:
• Very safe
• More targeted immune response
• Often require adjuvants (boost immune response)

4. 🧬 mRNA Vaccines
• Deliver mRNA instructions → host cells produce viral protein
• Immune system recognizes protein as foreign
Examples:
• COVID-19 mRNA vaccines
⚠️Key:
• No live virus involved
• Rapid development
• Strong immune response

Vaccines by Viral Disease (HIGH-YIELD)

🫁 Influenza (Flu)
• Trivalent: 2 Influenza A + 1 Influenza B
• Tetravalent (modern): 2 A + 2 B
📌 Updated yearly due to:
• Antigenic drift (mutation)

🧬 MMR
• Protects against:
o Measles
o Mumps
o Rubella

🦠 COVID-19
• mRNA + viral vector vaccines
• Target: Spike protein of SARS-CoV-2

🧪 Hepatitis
• Hep A → acute infection
• Hep B → chronic infection
📌 Vaccination prevents:
• Liver damage
• Transmission

🧬 HPV
• Prevents:
o Cervical cancer
o Other cancers
o Genital warts

🧫 Varicella-Zoster Virus
• Chickenpox (primary infection)
• Shingles (reactivation later in life)
⚠️Key:
• NOT the same as smallpox (Variola virus)

🧠 Polio (IPV)
• Inactivated vaccine
• Prevents paralysis

👶 Rotavirus
• Oral vaccine
• Prevents:
o Severe diarrhea
o Dehydration in infants

🐕 Rabies
• Post-exposure prophylaxis (PEP)
• Given after exposure
⚠️Key:
• Used commonly in healthcare