The Lab / Core medicine / Lesson 19
A bacterium is a single cell with a few parts your own cells lack or build differently: a woven wall, its own protein factories, a coiled loop of instructions and a home-made vitamin. Take one apart, piece by piece, then watch six families of antibiotics each break a different piece.
Educational, not for clinical use
Build the idea
A bacterium (plural bacteria) is a living thing made of a single cell, far smaller than one of your own cells. Most bacteria are harmless, but some cause infections: they get into the body and multiply where they should not.
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Like your cells, a bacterium is wrapped in a thin, oily skin, its cell membrane. It keeps the watery inside in, and lets food in and waste out through small gates.
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Outside the membrane, most bacteria have a tough cell wall of peptidoglycan: sugar chains tied by short bridges, like a woven net. Water keeps pushing in; the wall stops the cell swelling until it bursts. The new bar tracks wall strength. Your cells have none.
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New wall bricks keep arriving, each with a two-part tip. Proteins, chains of small building blocks, do the cell’s work. Enzymes are proteins that each speed up one job; wall-building enzymes grab the tip and tie the brick in with a fresh bridge.
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A purple stain sorts bacteria in two. Gram-positive bacteria have a thick wall on the outside and stay purple. Gram-negative bacteria have a thin wall hidden under an extra outer membrane, a second oily skin that keeps many large drug molecules out.
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Inside floats the bacterium’s DNA, the long molecule that carries its instructions for building every part. Your DNA sits in a walled-off centre, the nucleus; in most bacteria it is one loop, coiled up tightly and loose in the cell.
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Before it divides, the bacterium copies its DNA. The loop is so tightly coiled that copying would knot it. Untangling enzymes cut the DNA, pass a strand through the gap and seal it again, over and over, so copying can run.
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Ribosomes are the cell’s protein factories. Each has a small part that reads a copied instruction and a large part that links building blocks into a protein chain. Bacterial ribosomes are shaped differently from yours, so a drug can grip theirs alone.
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New DNA needs fresh DNA letters, and making them needs folate, a vitamin. You get folate from food. Many bacteria cannot take it in, so they build their own on an assembly line, with one enzyme for each step.
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With its wall, proteins and copied DNA ready, the bacterium pinches in two. Each half grows and splits again, so their numbers double and double. This growth is what lets an infection spread, and it needs every part you have met.
Build the idea
An antibiotic is a medicine that harms bacteria by hitting a part your cells lack or build differently. Some kill bacteria; others stop their growth while your white blood cells, the body’s defence cells (Lesson 18), clear them. Key measures: growth, and bacteria alive.
What changes it
Beta-lactams, such as penicillins and cephalosporins, jam the wall-building enzymes. New bridges stop forming while the bacterium keeps growing, so its wall weakens, water pushes in and the cell bursts. They kill bacteria that are growing.
What changes it
Glycopeptides such as vancomycin grab the two-part tip of each new brick, so wall-building enzymes cannot tie it in. The wall weakens and gram-positive bacteria die. The molecule is too big to pass an outer membrane, so gram-negative bacteria escape.
What changes it
Aminoglycosides, such as gentamicin, grip the ribosome’s small part so it misreads the instructions. Faulty proteins pile up and punch holes in the membrane, and the bacterium dies. They are aimed mostly at gram-negative bacteria.
What changes it
Macrolides, such as azithromycin, block the ribosome’s large part, where the chain leaves. Tetracyclines, such as doxycycline, block the small part, so building blocks cannot dock. Protein making stalls and growth stops, but most bacteria stay alive for white blood cells to clear.
What changes it
Fluoroquinolones, such as ciprofloxacin, jam the untangling enzymes just after they cut the DNA. The cuts are never sealed, so copying halts and the broken DNA kills the bacterium.
What changes it
Sulfonamides block an early step on the folate line; trimethoprim blocks a later one. Without folate there are no new DNA letters, so copying and growth stop. Two blocks on one line work better than either alone. Your cells use food folate instead.
Start with Next, or use the arrow keys. Pictures are illustrative, not measurements. How long a drug stays in the blood is Lesson 17.
Loading reference values…
Normal teaching baseline.
The blue line on each bar, and the large number beside it, show where an illustrative teaching model sits: not a patient measurement and not a sourced value. The shaded bands are the reference ranges quoted under each row. The picture and every bar come from the same model. Selecting a condition applies it to the model, and the dashed line shows the model without it. Separately, an arrow labelled “Cited” appears only where the quoted source gives that row’s direction; where it does not, no arrow is shown and the marker is the teaching model alone. The source describes cell counts, so it can give a direction for the total count but not for the shares.
The six antibiotic families are animated in the Lesson and in Explore freely, and the antibiotic control above lowers the model’s bacteria. They are not listed as states, with arrows, because the reference used on this tab gives no direction for any antibiotic family on these values, and every state here must quote its source.
An illustrative teaching model of one kind of bacterium multiplying in the body, with white blood cells clearing a few. Pick the kind of wall, add drugs (they combine) and see how the parts, the growth and the bacteria over time change. Dashed marks are the untreated bacterium, this lesson’s normal; solid marks are your settings.
Each drug blocks one piece of the machinery by a fixed illustrative share. Beta-lactams and vancomycin stop new wall bridges; aminoglycosides make the ribosome misread, so proteins come out faulty; macrolides and tetracyclines stall the ribosome; fluoroquinolones leave the DNA cut; sulfonamides with trimethoprim cut off folate, so fewer DNA letters are made. Growth needs working proteins and copied DNA. A weak wall does not stop growth by itself; it makes growing bacteria burst.
Killing comes from three routes: a weak wall in a growing cell, faulty proteins, and cut DNA. Because wall drugs need growth to kill, a growth-stopping drug given with them blunts their killing in this model, a well-known teaching point. A drug that only stops growth leaves the bacteria alive; white blood cells then clear them slowly. Vancomycin does not reach the wall of a gram-negative bacterium at all in this model, because it is too big to pass the intact outer membrane, so on its own it leaves that bacterium and its growth curve unchanged; aminoglycosides reach gram-positive bacteria less well; the beta-lactam-cutting enzyme stands for a common kind of resistance.
Over time, the bacteria grow toward a ceiling, a few are cleared by white blood cells, and drugs start partway along. Left out: how drugs are absorbed, spread and cleared (Lesson 17), every other kind of resistance, the many differences between bacterial species, side effects, and every real-world difference between people. Nothing here is a prediction for a real infection, and nothing here is a treatment plan.