Introduction to Microorganisms

Every other biological discipline is organised around relatedness — botany studies plants, zoology animals. Microbiology is organised around what you cannot see.

The consequence is that its members share almost nothing biologically. Bacteria are prokaryotes; fungi are eukaryotes, more closely related to you than to bacteria; viruses are not cells at all; prions are not even alive by most definitions. They are grouped because of a single historical fact — they all required Leeuwenhoek's microscope before anyone knew they existed.

That is why the first thing this course does is classify. Without the three-way division in the next three sections, the subject has no structure at all.

Look at what a prokaryote lacks and what it uniquely has, because that gap is where antibiotics live.

Peptidoglycan is present in bacteria and in nothing human. So a drug that blocks peptidoglycan synthesis — penicillin — destroys the bacterium and leaves your cells untouched. That is selective toxicity, and it is the whole basis of chemotherapy.

The bacterial ribosome is likewise different from yours (70S versus 80S), which is why a second whole class of antibiotics targets protein synthesis.

Keep this in mind through Unit 2: every structural feature you learn is a potential drug target, and the ones humans share are the ones nobody can safely attack.

Every cellular organism on earth — bacterium, fungus, you — contains both DNA and RNA. DNA stores the information and RNA carries it, which is the central dogma from your Intro to Medicine course.

A virus carries one or the other, never both. That single fact is the cleanest dividing line in all of microbiology, and it follows from what a virus is: not an organism that runs its own metabolism, but a package of instructions that borrows somebody else's machinery.

It also explains obligate intracellular parasite — with no ribosomes and no metabolism, a virus has no choice. It must be inside a cell or it is inert.

Read the prion definition again and notice what is missing: there is no nucleic acid at all. No DNA, no RNA — just a protein.

Everything else in microbiology reproduces by copying a nucleic-acid template. A prion instead converts: a misfolded protein touches a normally-folded one and makes it adopt the same wrong shape, which then converts the next. The information is carried in the fold, not in a sequence.

That is why prion diseases behave so unusually — they cannot be killed by anything that targets nucleic acid, they survive standard sterilisation, and there is nothing to sequence. It is also why the discovery was resisted for years: it appeared to violate the central dogma.

Compare this table with §2 and the clinical problem becomes obvious.

A bacterium differs from your cells in almost every respect — peptidoglycan wall, 70S ribosomes, no nucleus — which gives a drug designer plenty of targets. A fungus is a eukaryote, like you: nucleus, mitochondria, 80S ribosomes, ER and Golgi. Nearly everything you could attack, you share.

That is why antifungals are fewer and more toxic than antibacterials, and why they concentrate on the few genuine differences — chiefly ergosterol in the fungal membrane where you have cholesterol, and the fungal cell wall, which you do not have at all.

Selective toxicity is easy against a distant relative and hard against a close one. That single principle predicts the whole shape of anti-infective therapy.