How antibiotics work: five targets, five classes
Antibiotics attack structures that bacteria have and the host animal does not. This article covers the five main targets — cell wall, protein synthesis, nucleic acids, the folate pathway and the cell membrane — with the antibiotic classes that hit each one.
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This content is for education and information only. It is not a diagnosis, treatment or dosage recommendation and does not replace examination by a veterinarian. For treatment decisions, consult your veterinarian and the product’s approved label.
For an antibiotic to be useful it has to damage the bacterium without damaging the host. This is called selective toxicity, and it is possible because bacteria have structures that animal cells either lack entirely or build differently.
Almost every antibiotic in use attacks one of five targets. Knowing which group a drug belongs to makes it much easier to understand why it works against some bacteria and not others, and how resistance arises.
1. Cell wall synthesis
Most bacteria carry a rigid wall of peptidoglycan outside the cell membrane. That wall holds the cell together against high internal pressure. Animal cells have no equivalent — which makes it an ideal target.
Beta-lactams (penicillins, cephalosporins, amoxicillin and relatives) block the enzymes that cross-link the peptidoglycan strands. A growing bacterium cannot repair its wall and bursts under its own internal pressure. Beta-lactams are therefore usually bactericidal, and they only work on bacteria that are actively dividing.
The classic resistance mechanism against this group is the beta-lactamase enzyme: the bacterium produces an enzyme that breaks the antibiotic’s ring structure open.
2. Protein synthesis
Bacteria build proteins on a 70S ribosome; animal cells use an 80S ribosome. That structural difference underpins the largest group of antibiotics.
The subgroups are defined by which ribosomal subunit they bind:
- Tetracyclines (doxycycline, oxytetracycline, chlortetracycline) bind the 30S subunit and block the incoming amino acid.
- Aminoglycosides (neomycin, gentamicin) bind the 30S subunit and cause the genetic code to be misread.
- Macrolides (tylosin, erythromycin, tilmicosin), lincosamides (lincomycin), amphenicols (florfenicol) and pleuromutilins (tiamulin) bind the 50S subunit and stall the growing protein chain.
Most of this group is bacteriostatic: it stops bacteria multiplying rather than killing them, leaving the clearing-up to the immune system. That is one reason the response can be weaker in an immunosuppressed animal.
3. Nucleic acid synthesis
Bacterial DNA has to be unwound and rewound during division. The enzymes that do this are DNA gyrase and topoisomerase IV.
Quinolones and fluoroquinolones (enrofloxacin, danofloxacin, marbofloxacin, flumequine) block those enzymes. DNA cannot be replicated and the bacterium dies, so this group is bactericidal.
Fluoroquinolones are listed as critically important antimicrobials in many countries, which means their use is expected to be deliberately restricted.
4. The folate pathway
Most bacteria must synthesise their own folate to build DNA precursors; animals take folate in ready-made from the diet. That difference gives another selective target.
Sulfonamides block one step of the pathway and trimethoprim blocks the next. This is why the two are so often formulated together: cutting the same chain in two places gives a stronger result than either alone and slows the emergence of resistance. The principle is called synergy.
5. The cell membrane
The last group attacks the bacterial outer membrane directly. Polymyxins (colistin) bind the lipopolysaccharide of the gram-negative outer membrane and disrupt its permeability, so the cell contents leak out.
Because colistin is a last-line option in human medicine, its use in animals is specifically restricted in many countries.
Summary
| Target | Example classes | Effect |
|---|---|---|
| Cell wall | Penicillins, cephalosporins | Bactericidal |
| Protein synthesis (30S) | Tetracyclines, aminoglycosides | Mostly bacteriostatic |
| Protein synthesis (50S) | Macrolides, lincosamides, amphenicols, pleuromutilins | Mostly bacteriostatic |
| Nucleic acid | Fluoroquinolones | Bactericidal |
| Folate pathway | Sulfonamides + trimethoprim | Bactericidal in combination |
| Cell membrane | Polymyxins | Bactericidal |
Why one antibiotic does not work on every bacterium
For an antibiotic to work it has to reach its target and the target has to be there. Gram-negative bacteria have an extra outer membrane that keeps many molecules out. Mycoplasmas have no cell wall at all — which is precisely why beta-lactams, whose target is the cell wall, have no effect on them.
Which antibiotic is appropriate in a given case depends on the organism, the animal species, how the drug distributes in the body, and what is authorised in your country. That decision belongs to the veterinarian who examines the animal.
For how resistance develops and what slows it down, see What is antimicrobial resistance (AMR)?
References
- Giguère S. et al. — Antimicrobial Therapy in Veterinary Medicine, Wiley-Blackwell
- WOAH — Terrestrial Animal Health Code, Chapter 6.10: Responsible and prudent use of antimicrobial agents
Educational only — not a diagnosis, treatment or dosage recommendation.