A teaspoon of garden soil holds more bacterial cells than there are people on Earth. The bread you ate this week was raised by a fungus. The yogurt, the cheese, the pickle and the soy sauce were made by microbes, and so was the insulin in many a pharmacy fridge. And a cut that goes red, a cold that goes round a classroom, a hospital infection that no antibiotic touches: also microbes.
Microbiology is the study of all of these: bacteria, archaea, viruses, fungi and a few other tiny things. It is where biology gets quantitative fast, because microbes multiply in minutes. This piece covers concepts only (what the groups are, how populations grow, how drugs and vaccines work in principle), not how to grow anything. It is not medical advice; if you are unwell, or worried about an infection, see a health professional.
Antonie van Leeuwenhoek looked at pond water through hand-ground lenses in the 1670s and saw "animalcules". Two centuries later Pasteur and Koch tied particular microbes to particular diseases. For a long time everything without a nucleus was called a bacterium. In 1977 Carl Woese and George Fox used ribosomal RNA to show that a group of odd microbes from swamps, hot springs and salt lakes were not bacteria at all. The living world has three domains: Bacteria, Archaea (single cells that look like bacteria but are in some of their molecular machinery nearer to us), and Eukarya (cells with a nucleus: animals, plants, fungi and protists).
Fungi are eukaryotes, closer to animals than to plants: yeasts, moulds and mushrooms, with cell walls of chitin that digest food outside the body. Viruses are a different kind of thing: a strand of DNA or RNA in a protein coat that cannot copy itself without a host cell's machinery. Whether to call them alive is a definition argument, not a measurement; what is clear is that they are enormously abundant, and the most numerous kind, the bacteriophages that infect bacteria, are estimated at around 1031 particles on Earth.
A quick, non-clinical way to sort bacteria is the Gram stain, invented by Hans Christian Gram in 1884: a thick wall of peptidoglycan keeps the purple dye (Gram-positive), a thin one lets it wash out (Gram-negative, which also have an outer membrane). It matters later, because it shapes which drugs reach which cells.
Typical diameters (they vary a lot): hair 70 µm, skin cell 30 µm, yeast 8 µm, E. coli about 2 µm long, a typical virus 0.1 µm (100 nm). Circles are drawn at true relative size; anything under one pixel is shown as a dot.
Set the field to 1 mm (1,000 µm) and a human hair is a 7% sliver of the view while a bacterium would need 500 side-by-side to cross it. Set it to a hair's width and you can fit 35 E. coli end to end. A typical virus is about twenty times smaller than the bacterium it can infect, which is why ordinary light microscopes cannot see one.
A bacterium grows, then divides in two. If conditions are good, each cell of a fast species such as Escherichia coli can divide about every 20 minutes. That is three doublings an hour, and 230 after ten hours: one cell becomes more than a billion (1.07 billion). Left unchecked for two days, the mass would exceed the Earth's. Nature never allows that, because food runs out, waste builds up and the culture stops.
A culture's life in a closed container has four phases. A lag phase while cells adjust and make the right enzymes; an exponential phase, a straight line on a log plot; a stationary phase, as food runs out; and a death phase. Biologists therefore plot on a log scale: constant doubling then looks like a straight line, and the slope is the growth rate. What Ecology (35/48) says about logistic growth holds here too, since a flask is a population with a ceiling.
Model, not an experiment: start at 1,000 cells/mL, capacity 109 cells/mL (illustrative), N = 1 / (1/Nexp + 1/K) with Nexp = N0·2(t − lag)/td. Not a protocol.
With a 30-minute doubling time and a one-hour lag, the model reaches half of its capacity at about 11 hours and is flat soon after. Slow the doubling to 3 hours and in 24 hours it has grown only about 200-fold, nowhere near the ceiling. A small change in doubling time is a huge change in numbers: that is why food left warm goes off so much faster than food left cold.
Your gut, skin and mouth are inhabited by communities of microbes, most of them harmless and many of them useful. The old claim that microbes outnumber your own cells ten to one has been revised: a 2016 estimate by Ron Sender, Shai Fuchs and Ron Milo puts it at roughly one to one, about 38 trillion bacteria and 30 trillion human cells in a typical adult, with large uncertainty. The genes are a different story: the microbial genes in a gut outnumber human genes by something like a hundred to one.
What is well supported: gut microbes help break down fibre and make some vitamins and short-chain fatty acids; they train the immune system, especially early in life; and a stable community resists invaders. The clearest medical use is also the most dramatic: for repeated Clostridioides difficile infections, which can follow antibiotics, restoring a healthy community has worked well enough that microbiome-based treatments have been approved by regulators in recent years. What is less well supported are the sweeping claims: that your microbiome "causes" obesity, mood or autism in people, that a probiotic yogurt will "rebalance" a healthy gut, or that a single stool test can score your health. Many links come from mouse studies or correlations in small human samples, and cause and effect are hard to separate. A community's diversity is the idea that holds up best, and ecologists already have a number for it.
Invented abundances for illustration, not data from any real gut. Shannon H uses natural logs; evenness J = H / ln(richness); Simpson index = 1 − Σp².
Four species at 40, 30, 20 and 10% give H = 1.28; four equal species give the maximum, ln 4 = 1.39; a community that is 97% one species is about 0.17. The same number can be raised by adding species or by evening them out. Antibiotics tend to reduce diversity in the gut, which usually recovers, though not always fully; and the question of which diversity matters for health is open.
An antibiotic is a poison chosen to hit something bacteria have and we do not. Penicillin, found by Alexander Fleming in 1928 and made into a medicine in the 1940s by Howard Florey, Ernst Chain and colleagues, blocks the building of the bacterial cell wall, a structure human cells lack. Other classes target the bacterial ribosome (which differs from ours), the enzymes that copy bacterial DNA, or the pathway for making folate. They do nothing against viruses, which have none of these targets.
Resistance is natural selection in plain view. In 1943 Salvador Luria and Max Delbrück showed that bacterial resistance mutations arise at random before the drug is added, not in response to it. Among a billion cells there are a few that happen to survive; the drug removes their competitors; they take over. Bacteria can also swap resistance genes between species on small DNA circles called plasmids. A 2022 analysis in The Lancet estimated that in 2019 resistant bacterial infections were directly responsible for about 1.27 million deaths worldwide and associated with 4.95 million.
Expected values for 109 cells that regrow to the same size between rounds, with no cost of resistance. Illustrative: a real infection also has the immune system, drug levels that vary, and chance. Not guidance on treatment.
With one resistant cell in ten million (10−7) among a billion, 100 cells are resistant at the start. A drug that kills 99.9% of the susceptible cells leaves their share at 10−4 after round one, about 0.09 after round two and 99% after round three. A stronger kill (more nines) hastens the takeover of the survivors, since competitors are removed. That is why microbiologists talk about slowing resistance and not stopping it: stewardship means using drugs only where they will work, and matching the drug to the target, and why you take a prescription as your clinician directs.
A virus is at heart a copy instruction. It enters a cell, hijacks its machinery, and the cell makes thousands of new particles. For public health the key number is the basic reproduction number R0: how many people one case infects in a fully susceptible population. If it is above 1, an outbreak grows; below 1, it fades. R0 is not a fixed constant of a virus: it depends on contacts, climate and behaviour. Measles is commonly quoted at 12 to 18, among the highest known; seasonal influenza is far lower, nearer 1 to 2.
A vaccine, in concept, shows the immune system a harmless version or piece of a pathogen (a weakened or inactivated virus, a purified protein, or the instructions to make one) so that memory cells are ready when the real one arrives. Edward Jenner's 1796 experiment with cowpox began it; smallpox was declared eradicated in 1980, and rinderpest, a cattle virus, in 2011. If each case infects R0 people but a fraction of contacts are protected, the effective number falls:
R₀ values are illustrative and vary by place and time. Simple well-mixed model: no waning immunity, no clustering of the unvaccinated, which in real life lowers protection. Describes how the idea works; not advice about any vaccine.
At R0 = 3 and a vaccine that is 90% effective, you need 74% coverage (0.667 ÷ 0.9). At 15 you need 1 − 1/15 = 93.3% immune, so about 104% coverage with a 90% vaccine: not reachable, which is why a measles-like virus returns when coverage slips even a few points, and why immunity from earlier infection or a second dose counts. Real populations are lumpy: unvaccinated people cluster in families and schools, so the average can hide pockets that sustain outbreaks.
Most microbes do chemistry we depend on. Yeasts ferment sugars to carbon dioxide and alcohol: the bubbles in bread, the base of beer and wine. The East Asian mould Aspergillus oryzae (koji) makes soy sauce, miso and sake; lactic acid bacteria sour yogurt, kimchi, sauerkraut and Ethiopia's injera batter; bacteria raise cassava gari in West Africa. In soil, Rhizobium bacteria in the roots of beans, peas and clover turn nitrogen from the air into a form plants can use, and fungi called mycorrhizae trade nutrients with roots (the popular "wood wide web" story of trees talking through them has been criticised in a 2023 review as going beyond the evidence). Sewage plants are managed microbial communities.
Industry uses them as factories. In 1978 a team at Genentech and City of Hope made human insulin in engineered E. coli, and human insulin made that way reached patients in 1982. The heat-stable DNA-copying enzyme in PCR, Taq polymerase, comes from Thermus aquaticus, a microbe from a Yellowstone hot spring. Fungi cause trouble too: a chytrid fungus has driven declines in hundreds of amphibian species worldwide, which links the subject back to ecology.
Ideal gas at 25 °C and 1 atm (24.46 L per mole). Yeast fermentation C₆H₁₂O₆ → 2 C₂H₅OH + 2 CO₂ (glucose 180.16 g/mol). Real dough also dissolves some CO₂, and flour supplies sugar from its starch. A back-of-envelope, not a recipe.
To double a 500 mL lump of dough, you need 500 mL of new gas, which is 0.0204 mole of CO2 and so 0.0102 mole of glucose, about 1.8 g of sugar, if the dough holds every bubble. If the dough holds only 60% of the gas, the figure is 3.1 g. A few grams of sugar will raise a loaf; flour starch, broken down by enzymes, supplies it. Fermentation is a few lines of chemistry run by millions of cells.
Microbes are small, abundant and fast. They divide exponentially until something stops them, they swap genes, they are the first chemists of the planet, and they evolve in front of us. That one picture explains why infections grow, why drugs lose power, why vaccines have thresholds, and why bread rises.
Try this: this week, find three foods in your kitchen that microbes made (bread, yogurt, cheese, vinegar, soy sauce, pickles). Ask which kind: yeast, bacterium or mould, and what it did to the food. (Observation only; do not taste anything that looks or smells off.)
Sources. Domains (Woese and Fox, 1977), the Gram stain (1884), growth phases, antibiotic targets, plasmids, R0 and the vaccination threshold are standard textbook microbiology (Madigan; Willey). The Luria–Delbrück experiment (1943), and the microbial cell counts of Sender, Fuchs and Milo (2016), were checked against encyclopaedia summaries. The antimicrobial-resistance burden is Murray et al., The Lancet (2022). Smallpox eradication (WHO, 1980), rinderpest (2011), recombinant insulin (1978, 1982) and Taq polymerase are standard history, given in outline. Not medical advice. All interactive numbers were computed in node.