Microbiology & Pathology · study companion
Bugs & Cells
Seven units, one story: the microbes that make us sick, how our cells and tissues respond, and what happens when the response goes wrong. Every diagram is something you can touch. Tap a part, press play, drag a slider.
Unit 1 · Pathogenic bacteria
Anatomy of a bacterium
Bacteria are prokaryotes: no nucleus, no mitochondria, and a cell wall we don't have. Those differences are exactly what antibiotics aim at. Tap any part.
Why "70S" matters: our ribosomes are 80S. That size difference is why drugs like tetracyclines, aminoglycosides (30S subunit), macrolides and clindamycin (50S subunit) can jam bacterial protein synthesis while mostly sparing ours.
Unit 1 · Pathogenic bacteria
The Gram stain, step by step
One 5-minute stain splits most bacteria into two camps. The secret is the cell wall: thick peptidoglycan holds purple dye, thin peptidoglycan plus an outer membrane lets it wash out.
Zoomed into the cell envelope. Cytoplasm is at the bottom, the outside world at the top.
- Mycobacterium (TB)
- Waxy mycolic acid wall repels the dye. Use the acid-fast (Ziehl–Neelsen) stain: they show up red.
- Mycoplasma
- No cell wall at all, so nothing to stain. Also why penicillin can't touch it.
- Treponema (syphilis)
- Too thin to see. Use darkfield microscopy.
- Chlamydia, Rickettsia
- Live inside our cells.
Unit 1 · Pathogenic bacteria
Shapes & arrangements
Shape plus Gram color is the first clue a lab gives a doctor. "Gram-positive cocci in clusters" already says Staphylococcus before any culture grows.
Word roots that help: coccus = berry, bacillus = little rod, staphyle = bunch of grapes, streptos = twisted chain, diplo- = pair, vibrio = to vibrate (comma-shaped, darts around).
Unit 1 · Pathogenic bacteria
The bacterial growth curve
Drop bacteria into fresh broth and count them every hour. You always get the same four phases. Press play, or drag the time slider.
The dish counts cells on a normal scale; the graph uses a log scale. That's why the dish looks empty for hours, then fills almost at once.
E. coli can divide by binary fission every ~20 minutes in the lab. In 10 hours that's 30 doublings: 230 ≈ 1 billion cells from one.
Drugs that block cell-wall building (penicillins) work best in the log phase, when cells are actively dividing. Spore-formers like Bacillus and Clostridium make spores when nutrients run out in the stationary phase.
Unit 1 · Pathogenic bacteria
Oxygen needs
Grow bacteria in a tube of thioglycolate broth: oxygen is high at the top (the pink band is the indicator) and absent at the bottom. Where the bacteria settle tells you how they handle oxygen. Tap a tube.
Why oxygen can kill: using O2 makes toxic by-products (superoxide, hydrogen peroxide). Superoxide dismutase and catalase neutralize them. Obligate anaerobes lack these enzymes, so air poisons them.
Unit 1 · Pathogenic bacteria
How bacteria cause disease
A pathogen has to do four things: stick, get in, survive our defenses, and do damage. The tools it uses for each are called virulence factors.
Exotoxin vs endotoxin
| Exotoxin | Endotoxin | |
|---|---|---|
| What it is | Protein, actively secreted | Lipid A part of LPS, built into the outer membrane |
| Made by | Gram-positive and Gram-negative | Gram-negative only |
| Released | While the bacterium is alive | Mostly when the bacterium dies and breaks apart (lysis) |
| Potency | Extremely toxic in tiny amounts (botulinum is the deadliest known) | Less toxic per gram |
| Heat | Most destroyed by heat | Heat-stable |
| Vaccine | Can be made into a toxoid (tetanus, diphtheria) | No toxoid |
| Effect | Specific: each toxin hits one target | General: macrophages release TNF, IL-1, IL-6 → fever, low blood pressure, septic shock, DIC |
Toxin field guide
| Toxin | Bacterium | What it does | Result |
|---|
Unit 1 · Pathogenic bacteria
Rogues' gallery
The pathogens that come up again and again. Each card links the bug to its signature weapon and to the cell damage you'll meet in Unit 2.
Unit 2 · Cellular adaptation & injury
The big picture
A cell under stress has three possible fates: it adapts, it gets injured and recovers, or it is injured past repair and dies. Tap each stage.
Example running through every stage: a heart muscle cell.
What injures cells
Unit 2 · Cellular adaptation & injury
Adaptation lab
Adaptations are reversible changes in a cell's size, number or type that let it survive a new demand. Switch modes and watch the tissue change.
When is an adaptation harmful? The same change can be healthy or a step toward disease.
Name that adaptation
Read the scenario, decide, then reveal.
Unit 2 · Cellular adaptation & injury
Good adaptation, bad adaptation
Cells step up when the body needs more from them. Milk glands multiply when a mother breastfeeds. The same change becomes harmful when the signal driving it is abnormal and never switches off. Pick a tissue and press play: both lanes start the same and part ways at the fork.
Ask two questions
- 1 · Is the signal normal?
- Prolactin during nursing, exercise, pregnancy hormones: normal demands. Unopposed estrogen, high blood pressure, cigarette smoke: abnormal ones.
- 2 · Does it switch off?
- A physiologic adaptation reverses when the need ends; extra cells are even removed by . A stimulus that never stops keeps the tissue adapted, and over years adapted tissue can become disordered (dysplasia), turn cancerous, or simply wear out.
Unit 2 · Cellular adaptation & injury
Cell injury: past the point of no return
Drag the slider to raise the severity or length of an injury such as low oxygen. Early changes reverse if oxygen returns. Past the red line, the cell is committed to death.
Low oxygen → mitochondria make less ATP → the Na⁺/K⁺ pump slows → sodium and water flood in. The cell switches to anaerobic glycolysis, lactic acid builds up, and the falling pH clumps the chromatin.
Once membranes break, cell proteins leak into the blood. That's how labs detect dead cells: troponin for heart muscle, ALT/AST for liver cells, CK for skeletal muscle.
Unit 2 · Cellular adaptation & injury
Necrosis vs apoptosis
Necrosis is a messy explosion that injures the neighborhood. Apoptosis is a tidy, programmed implosion that nobody notices. Play both at once.
| Feature | Necrosis | Apoptosis |
|---|---|---|
| Cell size | Enlarged (swelling) | Reduced (shrinkage) |
| Nucleus | Pyknosis → karyorrhexis → karyolysis | Fragments into nucleosome-sized pieces |
| Plasma membrane | Disrupted | Intact; flips phosphatidylserine outward as an "eat me" signal |
| Cell contents | Digested by enzymes, leak out | Packaged into apoptotic bodies |
| Inflammation | Frequent | None |
| How many cells | Usually groups of cells | Usually single cells |
| Physiologic or pathologic | Always pathologic | Often physiologic (embryo shaping, removing old cells); can be pathologic (DNA damage, viral infection) |
| Machinery | ATP runs out; enzymes and Ca²⁺ run wild | Caspases. Intrinsic route: mitochondria release cytochrome c (BCL-2 family controls it). Extrinsic route: death receptors (Fas, TNF receptor) |
Unit 2 · Cellular adaptation & injury
Patterns of necrosis
Dead tissue doesn't all look the same. The pattern tells you the cause, and pathologists name it by what they see. Sketches below are simplified microscope views.
Afterward: dead tissue that isn't cleared often calcifies (dystrophic calcification).
Bridge · Units 1 + 2
Where bacteria meet cells
The two units are one story. Each row follows a bacterium from its weapon to the pattern of cell damage a pathologist would see.
Review
Flashcards & mnemonics
Tap the card (or press space) to flip it. Arrow keys move between cards.
Mnemonics
Review
Quiz
Every answer comes with the reason. Pick a unit or mix both.
Unit 1 · Pathogenic bacteria
Where bacteria normally live
Trillions of bacteria live on and in you without causing harm. Disease often starts when a normal resident reaches the wrong place or overgrows, or when a true pathogen arrives from outside. Tap a body site. Green dots are normally sterile.
Words you need
Unit 1 · Pathogenic bacteria
Chain of infection & course of disease
For an infection to spread, six links have to hold. Infection control is the art of breaking any one of them. Tap a link, then break it.
Isolation precautions
| Precaution | Spread by | Examples | What you wear / do |
|---|---|---|---|
| Standard | Everything, every patient | All care | Hand hygiene before and after contact; gloves for body fluids; safe sharps |
| Contact | Touch, fomites | MRSA, VRE, C. difficile, ESBL/CRE, scabies | Gown + gloves; dedicated equipment. For C. diff: soap and water (alcohol gel does not kill spores) and bleach cleaning |
| Droplet | Large droplets (>5 µm) within about 1–2 m | N. meningitidis, pertussis, influenza, mumps, group A strep pneumonia | Surgical mask within 2 m; patient masked for transport |
| Airborne | Droplet nuclei (<5 µm) that stay suspended | Tuberculosis, measles, varicella | N95 respirator; negative-pressure room with door closed |
Stages of an infectious disease
Unit 1 · Pathogenic bacteria
How the body fights back
Most bacteria that land on you never cause disease, because barriers keep them out and phagocytes eat the ones that get in. Here is a neutrophil doing its job, and the tricks bacteria use at each step.
Three lines of defense
From endotoxin to septic shock
Tap any box. Gram-positive bacteria trigger the same cascade through lipoteichoic acid and superantigens.
Unit 1 · Pathogenic bacteria
Antibiotics & resistance
Every antibiotic exploits a difference between bacterial cells and ours. Tap a target on the cell to see which drugs hit it, then watch how bacteria share the genes that defeat them.
| Class | Target | Kills or stops? | Examples | Remember |
|---|
How resistance genes move between bacteria
Five ways to defeat a drug
Unit 1 · Pathogenic bacteria
Identifying the bug in the lab
The lab works like a decision tree: Gram stain and shape first, then a handful of quick bench tests. Walk the tree yourself. Each branch is a real test.
Media & bench tests
| Medium or test | What it does | Remember |
|---|
Killing bacteria outside the body
Sterilization kills everything, spores included. Disinfection kills most pathogens on objects. Antisepsis is disinfection on living skin. -cidal kills; -static only stops growth.
| Method | How | Kills spores? | Used for |
|---|
Unit 2 · Cellular adaptation & injury
Why cells break: the mechanisms
Whatever the cause, injury runs through a handful of final pathways. ATP depletion is the one to know cold: follow it from a blocked artery to a swollen cell. Tap any box.
The other pathways
Free radicals
- Lipid peroxidation
- Radicals attack the double bonds in membrane fats and start a chain reaction. Membranes leak.
- Protein damage
- Oxidized side chains and cross-links. Enzymes stop working; misfolded proteins pile up.
- DNA breaks
- Single-strand breaks and base damage. Drives aging and cancer.
Unit 2 · Cellular adaptation & injury
A heart attack, hour by hour
A coronary artery blocks at time zero. Scrub forward from minutes to months and watch the muscle die, get cleaned up and turn to scar. The microscope lags behind the biochemistry by hours; the blood tests sit in between.
Schematic curves. Troponin is the test used today: sensitive, specific to heart muscle, and stays up for a week. CK-MB falls within 2–3 days, so it can catch a second infarct.
Infarcts elsewhere
Unit 2 · Cellular adaptation & injury
Apoptosis: the pathways
Two routes switch on the caspases, the enzymes that take a cell apart from the inside. One starts at a receptor on the surface, the other inside the mitochondria. Tap any step.
When cells are meant to die
Normal housekeeping
- Embryo
- Webbing between fingers removed; extra neurons pruned.
- Hormone withdrawal
- Endometrium each cycle; the lactating breast after weaning; prostate after castration.
- Turnover
- Gut lining cells, neutrophils after a few days, lymphocytes once an infection is cleared.
- Quality control
- Self-reactive T and B cells are deleted; cells with unrepairable DNA damage are removed.
When the damage is too much
- DNA damage
- Radiation, chemotherapy, hypoxia. p53 stops the cycle; if repair fails it orders apoptosis.
- Misfolded proteins
- ER stress. Alzheimer, Parkinson, Huntington.
- Infection
- Cytotoxic T cells kill virus-infected cells (viral hepatitis). HIV depletes CD4 cells.
- Obstructed ducts
- Pancreas, parotid, kidney: atrophy by apoptosis.
Other ways a cell can die
Unit 2 · Cellular adaptation & injury
Things that pile up inside cells
A stressed cell can fill with a normal substance it can't clear fast enough, an abnormal product it can't break down, or a pigment. Most of these are reversible; several are the first clue to a disease.
Pathologic calcification
Calcium lands on damaged tissue
Blood calcium is normal. Calcium deposits in dead or dying tissue: old necrosis (caseous, fat), atherosclerotic plaques, damaged or aging heart valves (aortic stenosis), dead parasites, and the laminated psammoma bodies of some tumors.
Calcium lands on normal tissue
Blood calcium is high: hyperparathyroidism, bone destruction (myeloma, metastases, Paget disease), vitamin D excess (sarcoidosis), kidney failure. Deposits form in healthy tissue that loses acid: lungs, kidneys (nephrocalcinosis), stomach lining, blood vessels.
Unit 2 · Cellular adaptation & injury
How cells age
A normal body cell can only divide so many times. Every division trims the protective caps on its chromosomes until it stops for good. Drag the divisions slider; then see what stem cells and cancer cells do differently.
The hallmarks of aging
Unit 3 · Inflammation & repair
Acute inflammation, live
A splinter carries bacteria under the skin. Within minutes the nearest small vessels change, and within hours neutrophils are crawling out of the blood toward the invaders. Play it, or step through.
The five cardinal signs
Unit 3 · Inflammation & repair
Mediators, and where the drugs act
Every sign of inflammation is caused by a chemical. The arachidonic acid cascade is the one you must know because aspirin, ibuprofen, steroids and montelukast each cut it at a different point. Tap a node; then switch on a drug and watch what it blocks.
The rest of the cast
Unit 3 · Inflammation & repair
Outcomes, chronic inflammation & granulomas
Acute inflammation ends one of four ways. When the cause won't go away, the neutrophils hand over to macrophages and lymphocytes, and sometimes the body walls the problem off in a granuloma. Watch one assemble.
Building a granuloma
Kinds of exudate & systemic effects
Unit 3 · Inflammation & repair
Wound healing
A clean sutured cut and a gaping wound heal by the same steps, but the gaping wound needs far more granulation tissue, contracts, and leaves a bigger scar. Scrub the timeline from the first clot to a mature scar.
Tensile strength: 10% at one week (sutures out), ~70–80% by 3 months. Never 100%.
What can go wrong
Unit 4 · Immunity
How an immune response is organized
Innate defenses buy time; the adaptive response learns the enemy and remembers it. The hand-off happens when a dendritic cell shows a piece of the invader to a T cell. Play the storyboard.
Cast of cells
Unit 4 · Immunity
Antibodies & immune memory
One Y-shaped molecule, five flavors, and a response that gets faster and stronger the second time. Tap parts of the antibody; then expose the body to the same antigen twice.
Primary vs secondary response
Unit 4 · Immunity
Hypersensitivity, types I to IV
The same machinery that protects you can hurt you. Four patterns, remembered as ACID: Allergic, Cytotoxic, Immune complex, Delayed. Each has its own animation.
| Type | Mediator | Timing | Mechanism | Examples |
|---|
Unit 4 · Immunity
When immunity fails or misfires
Too little (immunodeficiency), the wrong target (autoimmunity), or the wrong recipient (transplant rejection). HIV is the model of acquired deficiency: watch CD4 cells fall over a decade and the infections that arrive at each level.
Primary immunodeficiencies
Autoimmunity
| Disease | Target | Mechanism | Clue |
|---|
Transplant rejection
Unit 4 · Immunity
Vaccines & herd immunity
A vaccine is a rehearsal: the immune system meets a harmless version of the enemy and builds memory. Herd immunity is what happens when enough people have rehearsed. Run the outbreak simulator and change the vaccination rate.
Kinds of vaccine
Unit 5 · Hemodynamics
Fluid balance & edema
Fluid leaves capillaries at the arterial end and returns at the venous end, with lymphatics mopping up the rest. Tip the balance and tissue swells. Move the two pressures, or pick a disease.
| Transudate | Exudate | |
|---|---|---|
| Cause | Pressure imbalance (heart failure, low albumin) | Inflammation: leaky vessels |
| Protein | Low (<3 g/dL), specific gravity <1.012 | High, specific gravity >1.020 |
| Cells | Few | Many (neutrophils, debris) |
| Looks | Clear, straw-colored | Cloudy, fibrinous or purulent |
Hyperemia vs congestion
More blood flowing in
Arterioles dilate: exercise, inflammation, blushing. Tissue is red and warm with oxygenated blood.
Blood can't get out
Venous outflow is blocked: heart failure, a clot. Tissue is blue-red (cyanotic), swollen, and eventually hypoxic. Chronic congestion: nutmeg liver (right heart failure), heart-failure cells in the lung (hemosiderin-laden macrophages, left heart failure).
Unit 5 · Hemodynamics
Hemostasis & thrombosis
Normal hemostasis plugs a hole and then stops. Thrombosis is the same machinery firing inside an intact vessel. Play the normal sequence, then see which anticoagulant blocks which step.
Virchow's triad
What happens to a thrombus
Drugs that stop clots
| Drug | Blocks | Used for | Watch for |
|---|
Unit 5 · Hemodynamics
Embolism: a clot on the move
A piece of a deep-vein thrombus breaks loose. Follow it through the heart to the lungs, then see where arterial emboli and the odd ones (fat, air, amniotic fluid) end up.
Unit 5 · Hemodynamics
Shock
Shock is the circulation failing to deliver oxygen to tissues. The pump, the pipes or the volume can fail. Pick a type to see the circuit change, then drag severity through the three stages and watch the vital signs.
| Type | Problem | Preload | Cardiac output | Vascular resistance | Skin | Examples |
|---|
Unit 6 · Neoplasia
Benign or malignant?
Both are clones of cells growing when they shouldn't. The difference is behavior: a benign tumor pushes, a malignant one invades and spreads. Watch two tumors grow side by side, then build a tumor name.
| Feature | Benign | Malignant |
|---|---|---|
| Differentiation | Well differentiated: looks like the tissue it came from | Ranges from well differentiated to anaplastic (no resemblance) |
| Nuclei | Normal | Pleomorphic, large, dark (hyperchromatic), big nucleoli, high nucleus-to-cytoplasm ratio, abnormal mitoses |
| Growth rate | Slow; may stop | Variable, often fast; outgrows blood supply → central necrosis |
| Local growth | Expands; often encapsulated; pushes neighbors aside | Infiltrates and destroys; no capsule; irregular border |
| Metastasis | Never | Frequently (the single most reliable sign of malignancy) |
Name that tumor
Unit 6 · Neoplasia
How a cancer starts
Cancer is a disease of accumulated mutations: gas pedals stuck on (oncogenes) and brakes cut (tumor suppressors). Watch a normal colon crypt become a cancer one mutation at a time, then explore the hallmarks every cancer must acquire.
Two hits
The hallmarks of cancer
Carcinogens
Unit 6 · Neoplasia
Invasion & metastasis
To spread, a cancer cell has to let go of its neighbors, chew through the basement membrane, get into a vessel, survive the trip, get out, and grow somewhere new. Most fail. Play the cascade.
Routes & destinations
Unit 6 · Neoplasia
Grading, staging & the clinic
Grade is how abnormal the cells look; stage is how far the tumor has spread. Stage predicts survival far better. Build a TNM stage, then browse markers and paraneoplastic syndromes.
Tumor markers
| Marker | Cancer | Remember |
|---|
Paraneoplastic syndromes & systemic effects
Numbers that matter
Approximate US figures: new cases vs deaths per year, in thousands. Lung is third in cases but first in deaths.
- Screening that works
- Pap smear / HPV test (cervix), mammography (breast), colonoscopy or stool tests (colon), low-dose CT in heavy smokers (lung). PSA is debated: it finds many cancers that would never have caused harm.
- Diagnosis
- Biopsy is the gold standard: excision, core needle, fine-needle aspiration (cytology), frozen section during surgery. Then immunohistochemistry (which tissue?), flow cytometry (blood cancers), molecular tests (HER2, EGFR, BRAF) that choose the drug.
- Risk factors you can change
- Tobacco (≈ 1 in 3 cancer deaths), obesity and inactivity, alcohol, UV exposure, HPV and HBV (vaccinate), processed meat. Age is the one you can't.
Unit 7 · Viruses, fungi & parasites
Viruses: how they hijack a cell
A virus is a genome in a protein coat with no metabolism of its own. It has to break in, take over the machinery, copy itself and get out. Pick a virus type and play its life cycle; the differences are what antivirals exploit.
Drift vs shift: why flu comes back every year
The viruses to know
Unit 7 · Viruses, fungi & parasites
Fungi
Fungi are eukaryotes like us, which is why antifungals are harder to make than antibiotics: the drugs aim at the two things we don't have, a chitin wall and ergosterol. Flip the thermostat and watch a dimorphic fungus change shape.
Antifungal targets
The fungi to know
Unit 7 · Viruses, fungi & parasites
Parasites & prions
Protozoa are single cells; helminths are worms; ectoparasites live on the skin. Malaria kills more people than any other parasite, so start with its life cycle. Prions aren't alive at all.
The parasites to know
Prions
A misfolded protein that converts its neighbors
Normal prion protein (PrPC, α-helix rich) sits on neurons. The disease form (PrPSc, β-sheet rich) is insoluble, resists proteases, and forces normal copies to refold like itself. Neurons die, the brain turns spongy (vacuoles), with no inflammation and no immune response.
- Diseases
- Creutzfeldt–Jakob disease (sporadic, rapid dementia with myoclonus, death within a year), variant CJD (from BSE, "mad cow"), kuru (cannibalism), fatal familial insomnia, Gerstmann–Sträussler.