Microbiology · Exam 1 · Class of 2028

Microbiology Exam 1 Cram Sheet

Lectures 1–2 — Review of General Microbiology, and Antibiotics and Resistance.

L1 · Types of Pathogens L1 · Bacterial Structures L1 · Gram Stain L1 · Growth & Death Curves L1 · Viruses & Phages L2 · Terms & Drug Selection L2 · Therapeutic Index & Clearance L2 · Drug Lines & Their Organisms L2 · Mechanisms of Action L2 · Resistance & Problems

How to use this: this is a condensed, night-before-the-exam reference, not a replacement for the full study guide — it assumes you've already learned the material and just need the highest-yield facts at a glance. If a term feels unfamiliar, go back to the full guide for the explanation.

L1 · Types of Pathogens

Term	What you need to know
Prokaryotic vs eukaryotic	PRO: no nuclear membrane, few organelles, circular naked DNA, peptidoglycan wall, 70S ribosomes. EU: nuclear membrane, many organelles, linear DNA + histones, carbohydrate wall, 80S ribosomes.
The five types	Bacteria (prokaryotic) · fungi, protozoa, helminths (eukaryotic) · viruses (noncellular infectious agents).
Chlamydias vs Rickettsias	Both tiny obligate intracellular. Rickettsias ARE arthropod-transmitted (fleas, ticks, lice); Chlamydias are NOT.
Mycoplasmas	Tiny, pleomorphic, LACK A CELL WALL. M. pneumoniae.
Fungi	Yeasts unicellular (Candida albicans) · molds multicellular and filamentous (Penicillium notatum).
Protozoa	Trophozoite = motile feeding; cyst = dormant resistant. Apicomplexa essentially nonmotile — Plasmodium.
Helminths	Flatworms: no body cavity, blind-pouch gut. Roundworms: complete gut, cuticle, spines and hooks.
Prion vs viroid	PRION = misfolded protein, NO nucleic acid. VIROID = short RNA, NO protein coat, plants only.

L1 · Bacterial Structures

Term	What you need to know
Flagellum / pilus / fimbriae	Motility · plasmid-coded, CONJUGATION · adhesion to membranes.
Glycocalyx	Biofilms · prevents desiccation · prevents phagocytosis (pathogenicity factor).
Plasmids	Small circular dsDNA, NOT essential. May encode antibiotic resistance, metal tolerance, enzymes, toxins.
Endospores	Survival mechanism. BACILLUS and CLOSTRIDIUM.

L1 · Gram Stain

Term	What you need to know
Peptidoglycan	NAG + NAM alternating, crosslinked by a short peptide bridge. TRANSPEPTIDASES = target of beta lactams.
Steps	Crystal violet → iodine → DECOLORIZE acetone alcohol ~10s (MOST CRITICAL) → safranin.
Gram positive	Thick peptidoglycan + teichoic acids. RETAINS crystal violet → purple. PHYSICALLY strong.
Gram negative	Outer membrane (LPS) + periplasm + thin peptidoglycan. LOSES it → red. CHEMICALLY strong.
Lipopolysaccharide	LIPID A (endotoxin) · core polysaccharide · O-POLYSACCHARIDE (classification).

L1 · Growth & Death Curves

Term	What you need to know
Growth	Increase in NUMBER, not size, by binary fission → exponential.
Four phases	Lag (adjustment) → exponential (MOST VULNERABLE, e.g. penicillin) → stationary (growth = death) → death (exponential, in own wastes).
Death curve	Rate of death under a control method is CONSTANT. Decimal reduction time = time to kill 90%.

L1 · Viruses & Phages

Term	What you need to know
6 phage steps	Adsorption → penetration → replication → assembly → maturation → release.
Lytic vs lysogenic	LYTIC: host destroyed, generalized transduction. LYSOGENIC: prophage, may gain a toxin gene, immune to reinfection, specialized transduction.
Animal vs phage	Entire virion ENGULFED · UNCOATING required · release by BUDDING.

L2 · Terms & Drug Selection

Term	What you need to know
Antibiotic (precisely)	A substance PRODUCED BY A MICROBE that in small amounts inhibits another microbe. Antimicrobial drug = interferes with microbial growth in a host. Chemotherapy = use of drugs to treat disease.
MBC vs MIC	MBC = minimum level killing 99.9% of test organisms (bactericidal). MIC = minimum level inhibiting growth (bacteriostatic).
What makes a good agent	Selective toxicity · favorable pharmacokinetics · appropriate spectrum · few side effects · low toxicity · low hypersensitivity · good therapeutic index · LITTLE resistance development.
Eukaryotic pathogens	Harder — cell structure and physiology resemble the host, so great possibility of toxic side effects. Fewer drugs available.
Choosing the agent	Kirby Bauer disk diffusion (zone corrected for concentration, molecular weight, diffusion). E test = MIC read directly in µg/ml where the zone meets the strip.

L2 · Therapeutic Index & Clearance

Term	What you need to know
Therapeutic window	Range of plasma concentrations spanning minimum concentration for efficacy and for toxicity.
Therapeutic index	TI = max tolerated dose ÷ MIC = TD50 ÷ ED50. HIGHER = wider safety margin = safer drug.
Drug clearance	Renal + hepatic + all other tissues. Drives dosing: do NOT let concentration fall below MIC, and remember onset is not instant.

L2 · Drug Lines & Their Organisms

Term	What you need to know
Fungi produce	Penicillin ← Penicillium chrysogenum · cephalosporins ← Cephalosporium acremonium · griseofulvin ← Penicillium griseofulvum.
Gram-positive rods produce	Bacitracin ← Bacillus subtilis · polymyxin ← Paenibacillus polymyxa.
Actinomycetes produce (most)	Chloramphenicol ← S. venezuelae · streptomycin ← S. griseus · neomycin ← S. fradiae · tetracycline ← S. aurofaciens · amphotericin B ← S. nodosus · nystatin ← S. noursei.
THE TWO EXCEPTIONS	Gentamycin ← MICROMONOSPORA purpurea. Erythromycin ← SACCHAROPOLYSPORA erythraea. Both non-Streptomyces — high yield.
Other	Vancomycin ← Amycolatopsis orientalis · rifamycin ← Amycolatopsis rifamycinica. Quinolones and sulfonamides are ARTIFICIAL (sulfa from coal tar dyes, Domagk 1935).

L2 · Mechanisms of Action

Term	What you need to know
5 targets	Cell wall · protein synthesis · nucleic acid · plasma membrane · essential metabolites.
Cell wall	Penicillins (PBPs, transpeptidase, autolysins) · cephalosporins (1st Gram+ → 4th oral) · bacitracin (bactoprenol; TOPICAL only) · vancomycin (binds NAG/NAM; last line vs resistant S. aureus) · isoniazid (mycolic synthesis) vs ethambutol (its incorporation).
Protein synthesis	Chloramphenicol 50S peptide bond · aminoglycosides 30S codon misreading · tetracyclines tRNA attachment · streptogramins TWO components on 50S · erythromycin 50S translocation.
Nucleic acid	Rifamycin — RNA polymerase (TB). Quinolones — DNA GYRASE (UTI, hospital-acquired).
Membrane / metabolites	Polymyxin B — attaches lipid components of outer + inner membrane (topical). Sulfonamides — mimic PABA, block folate.
Antifungals	POLYENES bind ergosterol → pores. AZOLES block ergosterol SYNTHESIS. ECHINOCANDINS block beta-glucan (CELL WALL, not membrane). Griseofulvin — microtubules. Tolnaftate — squalene epoxidase.
Antivirals	Remdesivir — nucleotide analog, terminates RNA transcription · protease inhibitors · integrase inhibitors · CCR5 block (attachment) · neuraminidase (escape) · amantadine (uncoating) · interferon (alpha in hepatitis; PEG = finite duration BUT greater adverse effects).

L2 · Resistance & Problems

Term	What you need to know
Resistance defined	Avoiding an antibiotic's effects by DESTROYING it, TRANSPORTING it out, or CHANGING to block it.
Why it occurs	Genetic variation means some are already less susceptible; the antibiotic SELECTS them. The drug does not create resistance.
Genetic mechanisms	Random mutation · plasmid swapping (conjugation) · transposons · transduction · transformation · binary fission shares all.
Biochemical mechanisms	No access: decreased permeability (beta-lactams, quinolones), decreased transport (aminoglycosides), increased efflux (tetracyclines, quinolones). Inactivation: beta-lactamases. Target modification: gyrase. Bypass: vanA, vanB, TMP.
Biofilms + ESKAPE	Barrier sequesters drug · organisms metabolically LESS active · proximity ENHANCES gene transfer. ESKAPE = E. faecium, S. aureus, K. pneumoniae, A. baumannii, P. aeruginosa, Enterobacter.
4 problems with therapy	SUPERINFECTION · DIRECT TOXICITY · HYPERSENSITIVITY · RESISTANCE.
Direct toxicity (high yield)	Aminoglycosides = renal + AUDITORY · chloramphenicol = aplastic anemia · ciprofloxacin = seizures · doxycycline = esophageal ulcers · tetracycline = tooth discoloration (binds calcium during development) · amphotericin B = renal + hepatic · sulfamethoxazole = hyperkalemia · chloroquine = dysrhythmias.
Hypersensitivity	Mostly BETA LACTAMS (penicillin, cephalosporins) and quinolones. Immediate or delayed; hives → anaphylaxis.
Drug combinations	Indifference (no interaction) · SYNERGISM (greater than either) · ANTAGONISM (less than either).

L3 · Flora & the Two Definitions

Term	What you need to know
INFECTION vs DISEASE	INFECTION = microbes PENETRATE HOST DEFENSES, ENTER TISSUES AND MULTIPLY. DISEASE = ANY DEVIATION FROM HEALTH, microbial or not. Disease is the BROADER term.
RESIDENT FLORA	Bacteria, fungi, protozoa, viruses AND ARTHROPODS. Most areas in contact with the outside environment carry them.
HIGHEST NUMBERS	LARGE INTESTINE — mainly STRICT or FACULTATIVE ANAEROBES. Bacteria are 10–30% OF FECAL VOLUME.
Skin flora	STAPHYLOCOCCI, CORYNEBACTERIUM, PROPIONIBACTERIUM, YEASTS, MYCOBACTERIUM SMEGMATIS.
Oral flora	AEROBIC STREPTOCOCCI are the most common oral residents.
Respiratory flora	STAPH. AUREUS, NEISSERIA MENINGITIDIS. The LOWER RESPIRATORY TRACT IS ESSENTIALLY STERILE.
STERILE SITES	Heart and blood vessels · kidneys and bladder · brain and spinal column · middle and inner ear · interior of the eyes · BLOOD AND CSF (cerebrospinal fluid) · urine in the kidneys and bladder · AMNIOTIC FLUID.
The numbers	~30 TRILLION human cells vs ~38 TRILLION non-human. ~50% of the human genome is NON-HUMAN genetic material.

L3 · Pathogens, Dose & Adhesion

Term	What you need to know
TRUE (FRANK) PATHOGEN	Causes disease in HEALTHY people with NORMAL defenses. INFLUENZA, RABIES, PLAGUE BACTERIUM, MALARIAL PROTOZOAN.
OPPORTUNISTIC PATHOGEN	Causes disease when defenses are COMPROMISED, or when it grows somewhere UNNATURAL to it. SOMETIMES IT IS THE PATIENT'S OWN FLORA.
WEAKENS HOST DEFENSES	AGE (elderly, young children, premature infants) · genetic/acquired immunological defects · IMMUNOSUPPRESSING DRUGS AND ORGAN TRANSPLANTS · STRESS · chronic conditions (liver disease, diabetes) · INFLAMMATION · primary infections. Write them as COMORBIDITIES.
PORTALS OF ENTRY	SKIN · GASTROINTESTINAL · RESPIRATORY · UROGENITAL · CONJUNCTIVA · PREGNANCY AND BIRTH. EXOGENOUS (outside) or ENDOGENOUS (within).
INFECTIOUS DOSE (ID50)	MINIMUM microbes needed to infect 50% of a population. SMALL ID50 = GREATER VIRULENCE.
The ID50 range	MEASLES 1 PARTICLE · TB 10 bacteria · smallpox 10–100 · plague 100–500 · SARS-CoV-1 ~280 · influenza A ~790 · gonorrhea 1,000 · CHOLERA 100,000,000.
ADHESION MECHANISMS	FIMBRIAE (attachment pili) · FLAGELLA · ADHESIVE SLIMES/CAPSULES (dextran slime, glycocalyx) · SUCTION DISKS of protozoans · VIRAL SPIKE or CAPSID PROTEINS · HOOKS AND BARBS of helminths and insect larvae.

L3 · ★ ENDOTOXIN vs EXOTOXIN

Term	What you need to know
ENDOTOXIN — what	LIPID A OF THE LIPOPOLYSACCHARIDE.
ENDOTOXIN — who	GRAM-NEGATIVE ONLY. It is part of their outer membrane.
ENDOTOXIN — released how	FROM LYSED OR DAMAGED bacteria — i.e. when the organism DIES.
EXOTOXIN — what	PROTEINS.
EXOTOXIN — who	Certain GRAM-POSITIVE AND GRAM-NEGATIVE bacteria.
EXOTOXIN — released how	SECRETED BY LIVING bacteria.
The one-liner	ENDO = STRUCTURAL LIPID FROM A DEAD GRAM-NEGATIVE. EXO = PROTEIN SECRETED BY A LIVING ORGANISM, EITHER GRAM.
EXOENZYMES	Attack host defenses to allow DEEPER INVASION: MUCINASE, HYALURONIDASE, COAGULASE, BACTERIAL KINASES.
TOXIGENICITY	Capacity to produce toxins, grouped by TISSUE TARGETED: NEUROTOXINS, ENTEROTOXINS, HEMOTOXINS, NEPHROTOXINS.
ANTIPHAGOCYTIC FACTORS	LEUKOCIDINS destroy leukocytes (-cidin = to kill). CAPSULES avoid phagocytosis or resist digestion inside the phagocyte.

L3 · Patterns & Manifestations

Term	What you need to know
LOCALIZED	Confined to a specific tissue. BOILS, WARTS.
SYSTEMIC	Spreads to SEVERAL SITES via the bloodstream. MEASLES, CHICKEN POX, ANTHRAX, RABIES.
FOCAL	An agent BREAKS LOOSE from a local site and spreads.
MIXED	SEVERAL MICROBES growing SIMULTANEOUSLY at one site.
PRIMARY / SECONDARY	PRIMARY = the initial infection. SECONDARY = a DIFFERENT microbe complicating it, e.g. bacterial lung infection on top of a viral URI.
SUPERINFECTION	A secondary infection from DISRUPTION OF THE NATURAL MICROFLORA. Classic: ANTIBIOTICS FOR STREP THROAT → VAGINAL YEAST INFECTION. IF THE STEM MENTIONS ANTIBIOTICS, IT IS A SUPERINFECTION.
SIGN	OBJECTIVE evidence noted by an OBSERVER; often more precise and MAY BE MEASURED. Example: INFLAMED PHARYNX.
SYMPTOM	SUBJECTIVE evidence SENSED AND DESCRIBED BY THE PATIENT. Example: SORE THROAT.
SEQUELAE	LONG-TERM OR PERMANENT damage: PARALYSIS from polio · BLINDNESS from gonococcal conjunctivitis · STERILITY from syphilis · DEAFNESS from meningitis · ARTHRITIS from Lyme disease.
PORTAL OF EXIT	How pathogens DEPART the host — and therefore how they reach the next one.

L3 · Reservoirs & Transmission

Term	What you need to know
RESERVOIR	The PRIMARY HABITAT from which a pathogen ORIGINATES. Living or nonliving.
Living reservoirs	Someone with an OBVIOUS ACTIVE INFECTION is likely contagious. ASYMPTOMATIC CARRIERS may be HUMANS OR ANIMALS.
PASSIVE CARRIERS	MEDICAL OR DENTAL PERSONNEL — carrying it without being infected.
VECTORS	A LIVE ANIMAL that transmits disease: MOSQUITOES, FLEAS, TICKS; also FLIES, FRUIT FLIES, COCKROACHES.
NONLIVING RESERVOIRS	SOIL AND WATER.
ZOONOSIS	Animal infections spread to humans and vice versa. Can be BACTERIAL, VIRAL, FUNGAL OR PROTOZOAN. CANNOT BE ELIMINATED WITHOUT ERADICATING THE ANIMAL RESERVOIR.
DIRECT transmission	HORIZONTAL (kissing, sexual) · VERTICAL (MOTHER TO CHILD, transplacental or vaginal birth) · DROPLET (saliva, vomit, feces, blood) · BIOLOGICAL VECTORS.
INDIRECT transmission	VEHICLES and FOMITES (inanimate objects), and AIRBORNE DROPLET NUCLEI.

L3 · ★ NOSOCOMIAL INFECTIONS

Term	What you need to know
DEFINITION	HAI = HOSPITAL-ACQUIRED INFECTION. ACQUIRED OR DEVELOPING DURING A HOSPITAL STAY. May PROLONG THE STAY OR END IN DEATH.
MOST COMMON SITES	URINARY TRACT · RESPIRATORY TRACT · SURGICAL INCISIONS.
MOST COMMON ORGANISMS	Gram-negative: E. COLI, PSEUDOMONAS, KLEBSIELLA. Gram-positive: STAPHYLOCOCCI, STREPTOCOCCI. Fungi: YEASTS. The wider list goes by ESKAPE.
MITIGATION — the answer	UNIVERSAL PRECAUTIONS for sample collection and patient care, based on the assumption that ALL PATIENT SPECIMENS ARE POSSIBLY INFECTIOUS. You do not decide which to be careful with.
The fomite link	An INANIMATE OBJECT carries the organism between patients — which is why the same few organisms keep reappearing.

L3 · Epidemiology & Koch

Term	What you need to know
EPIDEMIOLOGY	Study of the FREQUENCY AND DISTRIBUTION of disease in human populations.
REPORTABLE / NOTIFIABLE	Must be reported to PUBLIC HEALTH AUTHORITIES. In the US the CDC publishes the MORBIDITY AND MORTALITY WEEKLY REPORT.
PREVALENCE	TOTAL EXISTING cases against the entire population, usually A PERCENTAGE.
INCIDENCE	NEW cases OVER A TIME PERIOD, against the general healthy population.
MORTALITY RATE	DEATHS due to a disease, PER 100,000.
MORBIDITY RATE	CASES — people afflicted — PER 100,000.
THE 100-YEAR TREND	DEATH RATE DROPPED while MORBIDITY REMAINED RELATIVELY HIGH. People stopped DYING of these; they did not stop GETTING them.
ENDEMIC	STEADY frequency over a long period in a particular LOCATION, often because the RESERVOIR IS PRESENT.
SPORADIC	OCCASIONAL cases at IRREGULAR intervals.
EPIDEMIC	Prevalence INCREASING BEYOND WHAT IS EXPECTED for that population.
PANDEMIC	A GLOBAL epidemic.
KOCH'S POSTULATES (1880s)	1. FIND the microbe in EVERY CASE. 2. ISOLATE and CULTIVATE IT ARTIFICIALLY. 3. INOCULATE a susceptible healthy subject. 4. RE-ISOLATE from the new subject.
WHERE KOCH FAILS	Organisms that CANNOT BE CULTIVATED ARTIFICIALLY — M. LEPRAE and LEGIONELLA PNEUMOPHILA. VIRUSES AND PRIONS break all the old rules.
MOLECULAR KOCH (Falkow, 1988)	1. The PROPERTY should ASSOCIATE WITH PATHOGENIC STRAINS. 2. INACTIVATING the gene should cause MEASURABLE LOSS OF VIRULENCE. 3. REVERTING it should RESTORE pathogenicity. The shift is FROM THE ORGANISM TO THE GENE.

L4 · The Chain of Infection

Term	What you need to know
THE SIX LINKS, IN ORDER	1. INFECTIOUS AGENT → 2. RESERVOIR → 3. PORTAL OF EXIT → 4. MODE OF TRANSMISSION → 5. PORTAL OF ENTRY → 6. SUSCEPTIBLE HOST. Break ANY link and transmission stops.
LIVING reservoirs	HUMANS, ANIMALS — and the deck marks PLANTS and FUNGI with a question mark.
NON-LIVING reservoirs	SOIL, WATER, AIR, FOOD and FOMITES.
ACTIVE carrier	IS INFECTED, may or may not show symptoms. TYPHOID MARY (Mary Mallon) carried SALMONELLA TYPHI asymptomatically.
PASSIVE carrier	IS NOT INFECTED but still transmits — the healthcare or food worker with poor hand hygiene. THE DISTINCTION IS WHETHER THEY ARE INFECTED.

L4 · Zoonoses & Vectors

Term	What you need to know
ZOONOSIS	An ANIMAL infection that spreads to humans AND THE REVERSE. Can be BACTERIAL, VIRAL, FUNGAL or PROTOZOAN — all four.
WHY THEY CANNOT BE ERADICATED	You would have to eradicate the ANIMAL RESERVOIR too — harder with MULTIPLE reservoirs, and worse if the pathogen lies dormant as a FUNGAL SPORE or PROTOZOAN CYST.
HUMANS IN PLAGUE / ANTHRAX	The ACCIDENTAL HOST.
RABIES	Reservoir MAMMALS · BITE/SALIVA · human-to-human RARE (organ transplantation).
INFLUENZA	Reservoir BIRDS and PIGS · respiratory droplet and contact · human-to-human YES.
EBOLA / MARBURG / NIPAH	Reservoir FRUIT BATS (Ebola also small primates) · BODY FLUIDS · human-to-human YES.
COMMONEST ZOONOSIS	RABIES in the UNITED STATES; MALARIA WORLDWIDE. From the recording, not a slide.
VECTOR vs RESERVOIR	VECTOR = a LIVING thing that TRANSMITS (mosquitoes, fleas, ticks, flies, cockroaches). RESERVOIR HARBORS it. Malaria: birds may be the reservoir, MOSQUITOES the vector.

L4 · Modes of Transmission

Term	What you need to know
DIRECT — VERTICAL	MOTHER TO CHILD.
DIRECT — HORIZONTAL	Usually MUCOUS MEMBRANE contact — sexual contact, kissing. Droplets: coughing, sneezing, saliva, blood, sweat, tears.
INDIRECT contact	Onto an INANIMATE SURFACE first — that is FOMITE transmission.
VEHICLE — FOOD	GI ILLNESS is the commonest result.
VEHICLE — WATER	Drinking water, plus POOLS, SPAS and WATER PARKS.
VEHICLE — SOIL	Contaminates produce, HANDS and FINGERNAILS; pinworms in children.
VEHICLE — AIR	Usually an INDOOR phenomenon. Ventilation, filtration and CROWDING matter.

L4 · Fomites & Nosocomial Infection

Term	What you need to know
FOMITE	A NON-LIVING SURFACE OR OBJECT that may transmit pathogens.
HAI consequences	LONGER STAYS, long-term disability, PREVENTABLE DEATHS, expense, risk to safety AND quality of care.
HIGHEST-RISK groups	IMMUNOCOMPROMISED, pediatric, geriatric, HIV, OPEN WOUNDS or BURNS, surgical patients.
CATHETERS	Indwelling devices are the problem because STAPH. AUREUS and STAPH. EPIDERMIDIS form BIOFILMS.
Clinical fomites	Scalpels, syringes, CATHETERS, bed rails, gurneys, PHONES, remotes, KEYBOARDS, floors, mops, pillows, bedding, CURTAINS, STETHOSCOPES, NECKTIES, stuffed animals, greeting cards, FLOWERS.
NOT JUST HOSPITALS	A public restroom, HOTEL ROOM, cruise ship cabin or AEROPLANE TRAY TABLE is a fomite-filled room too.

L4 · The Studies

Term	What you need to know
BIRTHDAY CAKE (Dawson 2017)	Blowing out candles → 15× MORE bacteria on the frosting vs the no-blow control. THEY NEVER IDENTIFIED THE ORGANISMS. Said nothing about fungi or VIRUSES in saliva.
THE CANDLE TEST	Try blowing out a candle WHILE WEARING a face covering — the droplet-size demonstration.
KEYBOARDS (Ide 2019)	75 studies reviewed. Keyboards, mice/pads, tablets. Grew COLIFORMS (E. coli) and MRSA.
VIRAL FOMITES (Boone & Gerba 2007)	1.7M deaths/yr diarrheal, 1.5M respiratory. VIRUSES CAUSE ~60% OF HUMAN INFECTIONS and CANNOT be cured with antibiotics. CROWDED INDOOR SPACES consistently INCREASE morbidity and mortality.
PATIENT ITEMS (Kanamori 2017)	Soap/sanitizer dispensers, humidifiers, nebulizers, pressure transducers, STETHOSCOPES, suction, THERMOMETERS, ULTRASOUND PROBE AND GEL, BP monitors, IV pumps, telemetry wires.
CFU	COLONY-FORMING UNIT — used because you cannot know if a colony began from ONE cell or a THOUSAND. Reported per GRAM or per mL.

L4 · Disinfection & History

Term	What you need to know
FIVE BEST PRACTICES, in order	1. STANDARDIZE cleaning policy · 2. Select EPA-REGISTERED disinfectants · 3. Educate ALL staff INCLUDING environmental services · 4. MONITOR compliance with feedback · 5. NO-TOUCH decontamination technology.
SEMMELWEIS, 1840s	Handwashing with CHLORINE solution, by obstetricians.
LISTER, 1860s	Handwashing and wound treatment with CARBOLIC ACID.
CHEMICAL AGENTS	Bleach, quaternary ammonium salts, phenolics — work ONLY at the CORRECT CONCENTRATION and for ADEQUATE CONTACT TIME. They are toxic.
OZONE / H2O2 / STEAM	THE ROOM MUST BE VACANT to reduce harm to humans. Time-consuming; can damage surfaces and devices.
COATINGS	From MARINE ANTI-FOULING paint (copper, arsenic, mercury, tin since the 1960s). ANTI-FOULING PREVENTS ATTACHMENT; ANTIMICROBIAL KILLS. Must be NONTOXIC, cost effective, available, STABLE and DURABLE.

L4 · Fomites & Resistance

Term	What you need to know
WHAT DRIVES MDR	EXTENSIVE ANTIBIOTIC USE. MDR, XDR and TDR strains — MRSA and CRKP — are especially problematic in hospitals.
BIOFILM	A POLYMICROBIAL NETWORK resistant to CLEANING, HEAT and ANTIMICROBIAL DRUGS. Staphylococcus and Pseudomonas form them.
THE CORE ARGUMENT	A fomite carrying a persistent pathogen CANNOT BE TOLD APART FROM A CLEAN SURFACE.
ANTISEPTIC STUDY (Lompo 2023)	Burkina Faso and Benin. LIQUID SOAP most contaminated — 51 of 69 samples. Risks: inconsistent preparation, RECYCLED soft-drink bottles, broken pumps, TOPPING UP.
>10,000 CFU/mL organisms	KLEBSIELLA PNEUMONIAE, PSEUDOMONAS AERUGINOSA, ACINETOBACTER — all GRAM-NEGATIVE. From MATERNITY, NEONATOLOGY, SURGERY and INTERNAL MEDICINE.
CONJUGATION	Donor and recipient NEED NOT be the same genus or species. Once a cell gains a resistance plasmid, ALL its offspring have it.
TRANSFORMATION	COMPETENT cells take up DNA fragments FROM THE ENVIRONMENT. A lesser factor.
TRANSDUCTION	Requires a BACTERIOPHAGE acting as the vector.

L5 · ★ HE READ OUT THE EXAM LIST

Term	What you need to know
How this list exists	The last three minutes of the lecture are a revision plan. These are his words, in his order.
1. THE THREE LINES	“Know those three lines — first, second, third — and KNOW WHAT BELONGS IN EACH. First line: know which are PHYSICAL, which are CHEMICAL, which are MICROBIOLOGICAL.”
2. RECOGNITION	“What do we call the receptors that the white blood cells have?” → PATTERN RECOGNITION RECEPTORS (PRRs), detecting PAMPs and DAMPs.
3. MACROPHAGE vs NEUTROPHIL	“Know the difference between a macrophage and a neutrophil, our two major phagocytes. But HOW are they different?”
4. THE DIFFERENTIAL	“What do we USE it for? And what can it TELL us?”
5. INFLAMMATION	“Know the major characteristics AND HOW DO THEY COME ABOUT? How is it that we have the redness, the heat, the pain?”
6. FEVER	“What CAUSES fever? Why is fever GOOD? Why is fever BAD?”
7. INTERFERON	“WHEN do we produce interferon? What kind of invading organism?” → VIRUS. And: “remember that IT DOES NOT KILL A VIRUS, but it prevents the viral spread.”
8. COMPLEMENT	“Three pathways, ALL GETTING TO C3. Which is first? THE ALTERNATIVE. Then the LECTIN. Then the CLASSICAL — and the classical is the one associated with the THIRD line of defense.”
★ THE ORDER MATTERS	“Organisms have to hit these barriers IN ORDER — physical and chemical first, then the white blood cell processes, and ONLY AFTER that can they start an adaptive response.” A sequence, not a menu.
✗ NOT asked to memorize (1)	The TYPES OF MUCINS — only that different surfaces get different ones.
✗ NOT asked to memorize (2)	The CHART OF TOXINS defensins can unfold.
✗ NOT asked to memorize (3)	The proteins protecting human cells from the MEMBRANE ATTACK COMPLEX — “you don’t need to fuss about that one.”
✗ NOT asked to memorize (4)	The MAC ASSEMBLY CHART — just know it forms a PORE.
✗ NOT asked to memorize (5)	The REFERENCE RANGES for the differential. The PROPORTIONS matter; the numbers do not.

L5 · The Three Lines of Defense

Term	What you need to know
FIRST LINE	PHYSICAL, CHEMICAL, MICROBIOLOGICAL and GENETIC barriers AT THE PORTAL OF ENTRY. NONSPECIFIC.
SECOND LINE	Protective CELLS, physiological processes, antimicrobial substances. NONSPECIFIC.
THIRD LINE	ACQUIRED on exposure to ANTIGENS — antibodies or defensive cell lines, and IMMUNOLOGICAL MEMORY. SPECIFIC.
THE ONE-LINE VERSION	TWO of the three lines are NONSPECIFIC. Only the THIRD is specific.
THE ORGANIZING IDEA	Innate immunity covers a huge range WITHOUT a receptor per organism — it recognizes PATTERNS SHARED ACROSS PATHOGEN FAMILIES.

L5 · First Line — Barriers

Term	What you need to know
EPIDERMIS	STRATIFIED SQUAMOUS. RAPID DESQUAMATION sheds transient flora. KERATIN works because MOST PATHOGENS LACK KERATINASE.
KERATINOCYTES	Make ANTIMICROBIAL PEPTIDES, packed into LAMELLAR BODIES, secreted into a WATERPROOF LIPID LAYER.
MUCOUS MEMBRANES	MUCH GREATER AREA than skin. THIN, PERMEABLE, NOT KERATINIZED — the price of gas exchange and absorption.
MUCUS / MUCINS	Glycoproteins, proteoglycans, peptides, enzymes. MUCINS = the GIGANTIC GLYCOPROTEINS. Made by the GUT GOBLET CELL.
LACRIMAL APPARATUS	Washes the eye AND carries LYSOZYME — physical and chemical at once.
URINE	Mechanical flush + HIGH OSMOLALITY + inhibitory pH.
LYSOZYME acts on	PEPTIDOGLYCAN.
SEMEN	SPERMINE, LYSOZYME, LACTOFERRIN, PHOSPHOLIPASE.
VAGINAL SECRETIONS	LACTIC ACID, BETA DEFENSIN, HYDROGEN PEROXIDE. (Easy to swap with the semen list — don’t.)
NORMAL FLORA — BOTH barriers	COMPETES for space and nutrients (PHYSICAL) and makes ANTIMICROBIAL SUBSTANCES (CHEMICAL). Colonization begins AFTER BIRTH.
SKIN FLORA	STAPH EPIDERMIDIS, other COAGULASE-NEGATIVE staphs, CORYNEFORM bacteria.
★ ATOPIC DERMATITIS	DYSBIOSIS with LESS antimicrobial peptide. Colonizing with COAGULASE-NEGATIVE STAPHS DIMINISHED STAPH AUREUS.
GUT COMMENSALS — 3 extras	DIGEST what we cannot · PROVIDE VITAMINS · help develop GALT.

L5 · Plasma Proteins & Defensins

Term	What you need to know
COAGULATION	Clot LIMITS PATHOGEN MOBILITY, reduces blood/fluid loss.
KININ	Produces BRADYKININ — dilates vessels, relaxes smooth muscle.
PROTEASE INHIBITORS	Block MICROBIAL proteases. ONE TENTH of all serum proteins. Example: ALPHA-2 MACROGLOBULIN.
DEFENSINS — size & mechanism	30–40 AMINO ACIDS, AMPHIPATHIC — they DAMAGE MEMBRANES.
DEFENSINS — range	BACTERIA, FUNGI, and ENVELOPED VIRUSES (an envelope IS a membrane).
DEFENSINS — ANTICHAPERONES	The ONLY innate components that NEUTRALIZE A BROAD RANGE OF TOXINS BY UNFOLDING THEM.
★ THE GENETIC DEFENSE	GENE COPY NUMBER varies: 2–14 alpha, 2–12 beta. COPY NUMBER DETERMINES HOW MUCH PROTEIN.
ALPHA DEFENSIN LOCATIONS	4 of 6 in NEUTROPHIL GRANULES; the other 2 from intestinal PANETH CELLS.
PENTRAXINS	Bind pathogens and TARGET THEM FOR PHAGOCYTOSIS. SHORT = HEPATOCYTES (serum amyloid P, C-REACTIVE PROTEIN). LONG = myeloid/endothelial/epithelial.
ACUTE-PHASE — the signal	Bacteria → MACROPHAGES make IL-6 → LIVER raises defensive proteins and LOWERS ALBUMIN.
★ CRP and SERUM AMYLOID A	Rise OVER 100-FOLD. That is why CRP is used for infection, inflammation and TISSUE DAMAGE. CRP is a PENTRAXIN OPSONIN.

L5 · Recognition — PAMPs & DAMPs

Term	What you need to know
THREE things to sort	HEALTHY SELF · NON-SELF · ALTERED SELF (virus-infected or cancerous).
PRR	PATTERN RECOGNITION RECEPTOR.
PAMP	PATHOGEN ASSOCIATED MOLECULAR PATTERN — marks NON-SELF.
DAMP	DAMAGE ASSOCIATED MOLECULAR PATTERN — marks ALTERED SELF.
WHY PATTERNS	Each receptor sees a pattern shared by a pathogen FAMILY — that is how a limited set covers a wide range.
MACROPHAGES are best at	BACTERIAL and FUNGAL CARBOHYDRATES, via LECTIN RECEPTORS.
NK CELLS are best at	CHANGED CELL SURFACE PROTEINS on virus-infected cells.
★ TOLL-LIKE — location decides	ON THE SURFACE → INFLAMMATORY CYTOKINES. IN ENDOSOMES → INTERFERON.
RIG (retinoic acid inducible gene)	Detects VIRAL RNA → interferon.
CYCLIC GMP CYCLASE	Detects VIRAL DNA → interferon.
SCAVENGER RECEPTORS	Eliminate microbes — or, with NO infection, CELLULAR DEBRIS and APOPTOTIC CELLS.

L5 · Inflammation & Fever

Term	What you need to know
FIVE CARDINAL SIGNS	RUBOR (redness) · CALOR (heat) · TUMOR (swelling) · DOLOR (pain) · FUNCTIO LAESA (loss of function).
INFLAMMASOME	Macrophage senses infection → protein structure converts PRO IL-1β → FUNCTIONAL IL-1β in LARGE QUANTITIES.
★ HOW IL-1β GETS OUT	PORES form in the macrophage membrane — and the cell DIES by PYROPTOSIS.
INFLAMMASOME MUTATIONS	Cause AUTOINFLAMMATORY DISEASES.
TNF-α	DILATES vessels → heat, swelling, redness, pain.
IL-6	Increases TEMPERATURE.
CHEMOKINES	CXCL8, CCL2, IL-12 — attract other white cells.
EXTRAVASATION — step 1 ROLLING	L-SELECTIN (leukocyte) → CD34 vascular addressin (endothelium).
EXTRAVASATION — step 2 FIRM	LFA-1 integrin → ICAM-1 immunoglobulin-like molecule.
EXTRAVASATION — step 3	DIAPEDESIS — squeezing between endothelial cells, guided by chemokines.
FEVER — the three pyrogens	IL-1β, IL-6, TNF-α.
★ FEVER — THE 5 BENEFITS	(1) DECREASES viral and bacterial replication — in BACTERIA by STARVING THEM OF IRON. (2) MORE NEUTROPHILS. (3) MORE T CELL PROLIFERATION. (4) BETTER IMMUNE SIGNALING. (5) ENHANCES TISSUE RESISTANCE TO TNF-α DAMAGE.
★ TNF-α LOCAL vs SYSTEMIC	LOCAL: clots blood in venules → PREVENTS SPREAD TO THE BLOOD. SYSTEMIC: all tissues at once → SHOCK, ORGAN FAILURE, DEATH.

L5 · Complement

Term	What you need to know
THE BASICS	30+ PROTEINS, ubiquitous in blood and lymph, circulating as inactive ZYMOGENS, activated by CLEAVAGE in a cascade.
WHAT MAKES IT WORK	A unique HIGH-ENERGY THIOESTER BOND.
★ THE THIOESTER BOND	C3 cleaved → C3a + C3b, exposing the bond on C3b. Attacked by WATER → soluble, useless. Reacts with a HYDROXYL or AMINO group on a pathogen → COMPLEMENT FIXATION.
C3a does	RECRUITS PHAGOCYTES.
ORDER OF ACTIVATION	ALTERNATIVE (1st, quickest) → LECTIN (2nd) → CLASSICAL (last). DISCOVERED in a different order: classical, alternative, lectin.
ALL THREE CONVERGE ON	CLEAVING C3 — by far the most important molecule in the cascade.
★ CLASSICAL is BOTH	Triggered by C-REACTIVE PROTEIN (innate) OR ANTIBODY (adaptive).
PROPERDIN (factor P)	INCREASES activation — binds C3 convertase on microbial surfaces.
FACTOR H + FACTOR I	REDUCE activation — H makes C3b cleavable by I → iC3b, which cannot form a convertase.
MEMBRANE regulators	DECAY ACCELERATING FACTOR (DAF) and MEMBRANE COFACTOR PROTEIN (MCP) disrupt C3bBb on HUMAN cells.
OPSONIN	A protein bound to a pathogen that FACILITATES PHAGOCYTOSIS. C3b is the opsonin.
CR1	Binds C3b → phagocytosis; ALSO protects human cells by disrupting C3 convertase.
C5a	RECRUITS NEUTROPHILS + MOST POTENT ANAPHYLATOXIN.
C5b	INITIATES THE MEMBRANE ATTACK COMPLEX.
MAC protection	S PROTEIN, CLUSTERIN, FACTOR J block C5b/C6/C7. CD59 (PROTECTIN) and HRF block C9.
★ THE EVASION — and its exception	STREP PYOGENES and STAPH AUREUS coat in SIALIC ACID, which FACTOR H binds → their C3b is inactivated. ANTIBODY MASKS THE SIALIC ACID — so they resist complement ONLY WHEN NO SPECIFIC ANTIBODY IS PRESENT.
C3a and C5a in extremis	ANAPHYLACTIC SHOCK.

L5 · Interferon

Term	What you need to know
★ THE ONE THING	INTERFERON DOES NOT KILL VIRUSES. It STOPS SPREAD TO SURROUNDING TISSUE.
ALPHA	From LYMPHOCYTES and MACROPHAGES. ACTIVATES NK CELLS.
BETA	From FIBROBLASTS and EPITHELIAL CELLS. Assists B and T CELL MATURATION + inflammatory response.
GAMMA	From T CELLS. INHIBITS CANCER CELLS, STIMULATES B CELLS, ACTIVATES MACROPHAGES.
HOW IT PROTECTS	Binds cell surfaces → INDUCES ANTIVIRAL PROTEINS. Also INHIBITS CANCER GENES and SUPPRESSES TUMORS.
PLASMACYTOID DENDRITIC CELLS	Professional interferon producers — within 6 HOURS, 60% of transcription is type 1 interferon.

L5 · Leukocytes & the Differential

Term	What you need to know
★ NEUTROPHILS	55–90% · LOBED nuclei, LAVENDER granules · PHAGOCYTES.
★ EOSINOPHILS	1–3% · ORANGE granules, BILOBED · destroy EUKARYOTIC pathogens · MINOR phagocyte.
★ BASOPHILS	0.5% · CONSTRICTED nuclei, DARK BLUE granules · release POTENT CHEMICAL MEDIATORS.
★ MONOCYTES/MACROPHAGES	3–7% · LARGEST WBC, KIDNEY-SHAPED nucleus · phagocytic, HOUSEKEEPING, ANTIGEN PRESENTATION, cytokines.
★ LYMPHOCYTES	20–35% · B (adaptive humoral) · T (adaptive cell-mediated) · NON-B NON-T incl. NK = INNATE.
MAST CELLS	Related to basophils but NONMOTILE and CONNECTIVE-TISSUE BOUND. Common progenitor UNSURE.
MACROPHAGE origin	FINAL DIFFERENTIATION OF A MONOCYTE, in tissue.
DIFFERENTIAL COUNT — what it does	Totals EACH TYPE and asks whether they are in NORMAL PROPORTION — proportion, not just total.
DIFFERENTIAL — 6 USES	INFECTION TYPES · INFLAMMATION · ALLERGIES · IMMUNE DISORDERS · LEUKEMIA · MYELODYSPLASTIC SYNDROME.
MACROPHAGE vs NEUTROPHIL	MACROPHAGE: LONG-LIVED, tissue-resident, WORKS FIRST and RAISES THE ALARM. NEUTROPHIL: SHORT-LIVED dedicated killer, circulates, WAITS FOR THE ALARM.
RESPIRATORY BURST	NADPH OXIDASE → SUPEROXIDE → picks up H ions and RAISES pH so digestive granules can work.
LIMITING THE DAMAGE	CATALASE degrades H2O2 → H2O + O2.
WHY NEUTROPHILS DIE	They CANNOT REPLENISH GRANULE CONTENTS.
PUS	DEAD ORGANISMS + DEAD NEUTROPHILS + DEAD TISSUE.
NETOSIS	Neutrophil BURSTS — DNA and defensive proteins form a NEUTROPHIL EXTRACELLULAR TRAP (NET).
DENDRITIC CELLS	Patrol tissue, take antigen to the NEAREST LYMPH NODE. An IMMATURE one FAILS TO MAKE A GOOD CONNECTION for activation.

L5 · NK Cells & Coordination

Term	What you need to know
NK CELLS kill	Cells infected by VIRUSES, BACTERIA or PROTOZOAN PARASITES — INTRACELLULAR infection.
CD56 DIM vs BRIGHT	DIM = KILLING virally infected cells. BRIGHT = CYTOKINE SECRETION to maintain inflammation.
UTERINE NK (uNK)	CD56 BRIGHT — work with FETAL TROPHOBLASTS to enlarge the SPIRAL ARTERIES. PREECLAMPSIA postulated to involve abnormal KIR activity, MORE INHIBITORY than activating.
NK CYTOTOXICITY rises	20–100 FOLD on exposure to type 1 interferons.
WHICH STIMULUS, WHICH FUNCTION	IFN-α/β → favors CYTOTOXICITY. IL-12 → favors CYTOKINE PRODUCTION.
★ THE ONE REQUIREMENT	NK receptors MUST INHIBIT KILLING OF HEALTHY SELF-CELLS. Killing happens when ACTIVATING > INHIBITORY.
HOW NK KILLS	Releases CYTOTOXIC GRANULES → APOPTOSIS. Target shrinks, chromatin condenses. MACROPHAGE cleans up.
NK ↔ MACROPHAGE	Macrophages RECRUIT and ACTIVATE NK; NK return IFN-γ which enhances macrophage phagocytosis.
IF NK CANNOT COPE	They stimulate DENDRITIC CELLS → secondary lymphoid tissue → ADAPTIVE response. Control passes to T CELLS.
ILC1 / ILC2 / ILC3	ILC1 = INTRACELLULAR (hold till NK arrive). ILC2 = MUCOSAL, LARGE EXTRACELLULAR PARASITES (worms). ILC3 = EXTRACELLULAR BACTERIA and FUNGI.
LTi CELLS	LYMPHOID TISSUE INDUCER — facilitate development of SECONDARY LYMPHOID TISSUE.
PRIMARY lymphoid organs	THYMUS → T cells. BONE MARROW → B cells.
SECONDARY lymphoid	SPLEEN, LYMPH NODES, SALT (skin), MALT (mucosal), GALT (gut — PEYER’S PATCHES and APPENDIX), BALT (bronchial).
LYMPHATICS reach everywhere EXCEPT	CNS, BONE, PLACENTA, THYMUS.
INDUCED INNATE RESPONSE	4 HOURS – 4 DAYS. STILL NONSPECIFIC. Macrophages, neutrophils, dendritic cells.
★ THE CLOSING CONTRAST	NO INNATE → infections UNCONTROLLED, and adaptive CANNOT BE DEPLOYED. NO ADAPTIVE → CONTROLLED at first but NEVER CLEARED. Innate is the PREREQUISITE, not the backup.

L6 · The Four Kinds of Acquired Immunity

Term	What you need to know
THE TWO AXES	ACTIVE (you make it) vs PASSIVE (you receive it) × NATURAL vs ARTIFICIAL. Four boxes — place the scenario.
NATURAL ACTIVE	Recovery from infection, INCLUDING subclinical or asymptomatic.
NATURAL PASSIVE	MATERNAL ANTIBODY — placenta, then milk. 99% is acquired IN UTERO.
ARTIFICIAL ACTIVE	VACCINATION. Degree and duration vary by disease.
ARTIFICIAL PASSIVE	IMMUNOTHERAPY — pooled serum (gamma globulin) or donor antibody. Hepatitis A, rabies, tetanus.
SPECIES IMMUNITY	A special type of INNATE immunity — illnesses we cannot get BECAUSE we are human.
ANTIBODY TITRES	What tells you whether a vaccine on your record is still effective, or whether you need a booster.

L6 · Leukocytes & MHC

Term	What you need to know
★ THE MNEMONIC	“NEVER LET MONKEYS EAT BANANAS” — Neutrophils, Lymphocytes, Monocytes, Eosinophils, Basophils. HIGHEST to LOWEST.
The figures (from L5)	Neutrophils 55–90% · Lymphocytes 20–35% · Monocytes 3–7% · Eosinophils 1–3% · Basophils 0.5%.
MHC = ?	MAJOR HISTOCOMPATIBILITY COMPLEX, also called HUMAN LEUKOCYTE ANTIGEN (HLA).
★ WHERE MHC IS NOT	On ALL cells EXCEPT RED BLOOD CELLS.
★ WHICH CHROMOSOME	CHROMOSOME 6, in a multi-gene complex of classes I, II, III.
MHC does two jobs	RECOGNITION OF SELF, and REJECTION OF FOREIGN TISSUE.
★ CLASS I	Displays self molecules. Read by CYTOTOXIC (Tc) T CELLS.
★ CLASS II	The IMMUNE REGULATORY receptors. On MACROPHAGES, APCs and B CELLS. REQUIRED for an APC to activate a T HELPER (CD4) cell.
Why transplants work at all	Each MHC profile is unique but can be CLOSE ENOUGH to another’s.

L6 · Clonal Selection

Term	What you need to know
How many genes	MORE THAN 500 are used to build lymphocyte receptors.
★ SELF-REACTIVE CLONES	ELIMINATED before the fetus is harmed. A defect here = inherited autoimmune disorder such as SCID.
How big is the naive pool	10¹⁴ to 10¹⁸ variations — UP TO A QUINTILLION.
★ THE POINT TO HOLD	SPECIFICITY EXISTS BEFORE THE ANTIGEN DOES. It is pre-programmed. Antigen SELECTS a clone; it does NOT instruct one. Getting this backwards is the classic error.

L6 · The Two Receptors

Term	What you need to know
B-CELL RECEPTOR	= IMMUNOGLOBULIN. FOUR chains: 2 identical HEAVY + 2 identical LIGHT. Y-shaped. Variable + constant regions. SECRETED as antibody.
T-CELL RECEPTOR	TWO parallel chains. Small — “one fork” of the Y. NEVER SECRETED. Recognizes antigen ONLY with MHC.
Young vs mature B cell	YOUNG carries a small IgM; MATURE carries IgD.
Variable region genes	LOCKED IN for the life of the cell AND its progeny, including memory cells.
B-cell maturation	BONE MARROW STROMAL CELLS → migrate to lymph nodes, spleen, GALT.
T-cell maturation	The THYMUS and its hormones — which is why the thymus unites the immune and endocrine systems.
★ CD MARKERS	CD = CLUSTER OF DIFFERENTIATION. CD4 = T HELPER. CD8 = T CYTOTOXIC.

L6 · Antigens

Term	What you need to know
EPITOPE	= ANTIGENIC DETERMINANT. The small molecular group actually recognized. One antigen may carry MANY.
★ SIZE DECIDES	Most antigenic: foreign cells and molecules OVER 100,000 MW, usually large proteins.
★ HAPTEN	UNDER 1,000 MW — NOT antigenic unless attached to a LARGER CARRIER. Drugs, metals, industrial chemicals. This is how occupational LATEX allergy arises.
AUTOANTIGEN	Self tissue for which TOLERANCE IS INADEQUATE → some autoimmune disorders.
ALLOANTIGEN	A marker of one individual antigenic to ANOTHER OF THE SAME SPECIES → the BLOOD GROUPS and the MHC profile. Incompatibility → transfusion reaction or graft-versus-host disease.
HETEROPHILIC	From an UNRELATED SPECIES with similar determinants. Mammalian heart muscle × group A strep cell wall.
★ SUPERANTIGEN	A potent T-CELL STIMULATOR → CYTOKINE STORM. Staph toxins: toxic shock syndrome toxin, enterotoxin.
ALLERGEN	Any antigen provoking allergy = TYPE I HYPERSENSITIVITY. Classified by PORTAL OF ENTRY: inhaled · ingested · injected · contact.

L6 · Presentation & the Interleukins

Term	What you need to know
The three-way collaboration	An APC + a T HELPER CELL + an antigen-specific B or T CELL.
What the APC does	ALTERS the antigen and attaches it to its CLASS II MHC receptor.
★ INTERLEUKIN 1	From the APC. Activates the T helper cell. ALSO an ENDOGENOUS PYROGEN → fever and inflammation.
★ INTERLEUKIN 2	From the ACTIVATED T HELPER. Activates B cells and other T cells. Its DYSREGULATION → LUPUS and RHEUMATOID ARTHRITIS.
Swapping these two	Is the easy mistake. IL-1 comes FROM the APC; IL-2 comes FROM the helper.
B-cell expansion gives	PLASMA CELLS (secrete antibody) + MEMORY CELLS.
★ MEMORY CELLS	They PAUSE PARTWAY THROUGH MITOSIS — which is why the secondary response is so fast.
The naming	B-cell responses = ANTIBODY-MEDIATED (AMI) or HUMORAL-MEDIATED (HMI). T-cell responses = CELL-MEDIATED (CMI).

L6 · ★ THE FIVE IMMUNOGLOBULINS

Term	What you need to know
Structure	Y-shaped, FOUR chains. Fab = antigen-binding (two of them). Fc = crystallizable, binds immune cells AND allows the SWIVEL.
★ IgG	MONOMER. MOST PREVALENT. The ONLY one crossing the PLACENTA. LONG-TERM IMMUNITY. Huge titre in SECONDARY responses.
★ IgA	MONOMER or DIMER. SECOND most prevalent. MUCOSAL — saliva, tears, colostrum, mucus. Local immunity: enteric, respiratory, genitourinary.
★ IgM	PENTAMER — by far the LARGEST, so TOO BIG for the placenta. FIRST RESPONDER of the primary response. Important COMPLEMENT FIXER. Binds B cells.
★ IgD	MONOMER. HIGH titre in NEWBORNS, very LOW in adults/children. Binds B cells — trigger for activation AND regulation.
★ IgE	MONOMER. LEAST common in serum and SHORTEST-LIVED. ALLERGENS and PARASITIC WORMS. Binds MAST CELLS and BASOPHILS → asthma, anaphylaxis, via histamine.
Which two bind B cells?	IgM and IgD.
THE FOUR ANTIBODY ACTIONS	AGGLUTINATION · OPSONIZATION · COMPLEMENT FIXATION · NEUTRALIZATION.
OPSONIZATION	Coating so phagocytes can engulf. Matters most for SLIPPERY envelopes, WAXY capsules, SLIME layers. Greek: something cooked with food — a coating.
NEUTRALIZATION	Blocking the virus’s ATTACHMENT SPIKE PROTEINS so it cannot enter — and making it easier to phagocytose.
★ AGGLUTINATION	CROSS-LINKING adjacent cells. IgM is best — its pentamer has TEN binding sites.
COMPLEMENT FIXATION	Antibody binds, complement proteins bind the remaining sites and use PERFORINS to lyse the envelope.

L6 · Primary vs Secondary, and T Cells

Term	What you need to know
PRIMARY response	IgM and IgG, with a GRADUAL rise in titre. Plus MEMORY B CELLS.
★ SECONDARY response	RAPID and STRONGER, because of MEMORY CELLS. A much higher titre of IgG, then gradual IgM.
Also called	The ANAMNESTIC RESPONSE.
Titre unit	BAU — binding antibody units.
Does titre reach zero?	In a healthy person with robust responses, NO.
T cells need	Activation by SOME TYPE OF MHC MOLECULE. All T cells produce CYTOKINES.
★ THE FOUR T CELLS	TH (CD4) conducts · TC (CD8) lyses virally infected, cancer and foreign cells · TD delayed hypersensitivity (allergy HOURS to DAYS later) · TS suppressor, limits other T and B cells.
Sensitized T cells become	LONG-LASTING MEMORY T CELLS.

L6 · Applications

Term	What you need to know
PASSIVE immunization lasts	TWO TO THREE MONTHS.
HORSE SERUM	Early antitoxins for tetanus and diphtheria. STILL used for diphtheria, botulism, spider/snake bites. Risks: SERUM SICKNESS, ANAPHYLAXIS.
POOLED GAMMA GLOBULIN	Hepatitis A, hepatitis B, HIV, measles, generally immunodeficient patients.
★ -mab	MONOCLONAL ANTIBODY (a protein).
★ -omab	MOUSE.
★ -ximab	CHIMERIC.
★ -zumab	HUMANIZED.
★ -umab	ENTIRELY HUMAN.
Two examples	ADALIMUMAB (Humira) — RA, psoriatic arthritis, Crohn, plaque psoriasis. PEMBROLIZUMAB (Keytruda) — melanoma, lung cancer.
VACCINATION is	Deliberate exposure to material that is ANTIGENIC BUT NOT PATHOGENIC.
The history	LADY MONTAGU brought it to England · JENNER gave the first effective human vaccination (COWPOX → SMALLPOX) · PASTEUR later did RABIES.
★ AN EFFECTIVE VACCINE	Low toxicity · protects on exposure · stimulates BOTH AMI AND CMI · produces MEMORY B and T cells · generally NOT many doses · cheap, easy, long shelf-life.
STERILIZING vaccine	The best option — the target is rendered NON-FUNCTIONING and UNABLE TO MUTATE.
Vaccine contents	Killed whole cells / inactivated virus · LIVE ATTENUATED · acellular or subunit antigens · TOXOIDS · genetically engineered.
★ MARROW DONATION	Requires a close CLASS I MHC match plus DNA testing. Harvested from STERNUM, FEMUR or ILIAC CREST. Peripheral stem cells by APHERESIS after a mobilizing drug. The RECIPIENT gets drug and radiation therapy first, TO REDUCE REJECTION RISK.