How Antibiotics Work: Core Concepts in Antimicrobial Pharmacology

What antibiotics are (and what they are not)

Antibiotics are medicines designed to treat infections caused by bacteria. They work by interfering with bacterial structures or processes that are essential for bacterial survival or growth.

It helps to separate “antimicrobials” into categories:

• Antibacterial drugs (antibiotics): target bacteria (e.g., pneumonia caused by Streptococcus pneumoniae).
• Antiviral drugs: target viruses (e.g., influenza, HIV). Antibiotics do not treat viral infections like colds or most sore throats.
• Antifungal drugs: target fungi (e.g., yeast infections, invasive candidiasis).
• Antiparasitic drugs: target parasites (e.g., malaria, giardiasis).

In everyday language, people often say “antibiotics” to mean “any infection medicine,” but in pharmacology, antibiotics specifically mean antibacterial therapy.

Selective toxicity: why bacteria can be targeted without harming human cells

The central idea behind antibiotic therapy is selective toxicity: an antibiotic should harm the bacterium more than it harms the human host.

This is possible because bacteria and human cells are different in several key ways. Antibiotics exploit these differences by targeting features that are:

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• Present in bacteria but absent in humans (best case for safety).
• Similar but sufficiently different so the drug binds better to the bacterial version than the human version.

Common bacterial targets (conceptual map)

• Cell wall synthesis: Many bacteria have a rigid cell wall made of peptidoglycan; human cells do not. Drugs that block cell wall building can weaken bacteria until they rupture.
• Protein synthesis (ribosomes): Bacterial ribosomes are structurally different from human ribosomes. Some antibiotics bind bacterial ribosomes and disrupt protein production.
• DNA/RNA processes: Some antibiotics interfere with bacterial DNA replication or transcription enzymes that differ from human enzymes.
• Metabolic pathways: Bacteria may rely on certain nutrient-making steps (e.g., folate synthesis) that humans do not perform in the same way.

Selective toxicity is not absolute. Side effects happen because:

• Some targets are not perfectly unique (partial overlap).
• Antibiotics can disturb helpful bacteria in the body (the microbiome), leading to issues like diarrhea or yeast overgrowth.
• Patient-specific factors (kidney/liver function, allergies) change how safely a drug can be used.

Key terms you will see throughout the course

Pathogen

A pathogen is a microbe capable of causing disease. In this course, the word often refers to bacteria, but the concept applies broadly (viruses, fungi, parasites).

Practical example: Escherichia coli can be a pathogen in a urinary tract infection, even though related strains may live harmlessly in the gut.

Infection vs colonization

Colonization means bacteria are present on or in the body but are not causing tissue damage or symptoms. Infection means bacteria are invading or triggering inflammation and causing signs/symptoms (and often abnormal labs or imaging).

Practical example: A urine culture may grow bacteria in someone without urinary symptoms (colonization). Treating colonization “just because bacteria are found” can expose the patient to side effects and promote resistance without benefit.

Bactericidal vs bacteriostatic

These terms describe what an antibiotic tends to do to bacteria under typical conditions:

• Bactericidal: kills bacteria.
• Bacteriostatic: stops bacteria from multiplying, allowing the immune system to clear them.

In practice, the distinction is useful but not absolute. The same drug may behave differently depending on the organism, drug concentration at the infection site, and patient factors.

Practical framing: If a drug is bacteriostatic, think “puts the bacteria on pause.” If bactericidal, think “actively reduces the bacterial count.” Clinicians may prefer bactericidal therapy in certain high-stakes infections (e.g., endocarditis, meningitis) where rapid bacterial reduction is important.

Minimum inhibitory concentration (MIC) — conceptual only

The minimum inhibitory concentration (MIC) is the lowest concentration of an antibiotic that prevents visible bacterial growth in a standardized lab test.

How to think about MIC without numbers:

• A lower MIC generally means the bacteria are inhibited by a smaller amount of drug (more “susceptible”).
• A higher MIC means you need more drug to inhibit growth (less “susceptible” or potentially resistant).

MIC is not the whole story because the relevant question is whether the antibiotic can reach effective levels at the site of infection safely.

Time-dependent vs concentration-dependent killing (intuitive)

Antibiotics differ in what best predicts their effectiveness:

• Time-dependent killing: works best when drug levels stay above the bacteria-inhibiting threshold for a large portion of the dosing interval. Intuition: “Keep the pressure on consistently.”
• Concentration-dependent killing: works best when the peak concentration is high relative to what the bacteria can tolerate. Intuition: “Hit hard with a high peak.”

Practical implication (no equations): Time-dependent drugs often benefit from more frequent dosing or prolonged infusion strategies, while concentration-dependent drugs often benefit from dosing strategies that achieve higher peaks (within safety limits).

How clinicians choose an antibiotic: a structured walkthrough

Choosing an antibiotic is a matching problem: match the likely bacteria and the infection site with a drug that can reach that site, is safe for the patient, and is likely to work given local resistance.

Step 1: Identify the suspected site of infection

The site matters because it changes both the likely organisms and whether the drug can reach effective concentrations.

• Lung (pneumonia): need good penetration into respiratory tissues/secretions.
• Urinary tract: many drugs concentrate well in urine; others do not.
• Skin/soft tissue: consider tissue penetration and whether abscess drainage is needed.
• Central nervous system: requires drugs that can cross into cerebrospinal fluid, especially during inflammation.
• Bone/joint: prolonged therapy and good bone penetration are often needed.

Practical mini-check: Ask, “Can this drug realistically get to the infection?” A great lab result is not helpful if the drug cannot reach the target tissue.

Step 2: List the most likely organisms for that site and scenario

Clinicians start with an educated guess (empiric therapy) based on:

• Community vs hospital setting: hospital-acquired infections often involve more resistant organisms.
• Patient-specific exposures: recent antibiotics, recent hospitalization, indwelling devices, wounds, aspiration risk.
• Clinical syndrome: for example, a purulent skin infection suggests different likely bacteria than non-purulent cellulitis.

Practical mini-check: Write down 2–5 “top suspects” rather than trying to cover every bacterium on earth. Overly broad coverage increases harm and resistance pressure.

Step 3: Consider patient factors that affect safety and dosing

• Allergies: what happened, how severe, and how long ago (a vague “allergy” label can unnecessarily limit options).
• Kidney function: many antibiotics require dose adjustment to avoid toxicity.
• Liver function: some drugs require caution or adjustment.
• Age and pregnancy status: safety profiles differ across populations.
• Immune status: immunocompromised patients may need broader initial coverage or bactericidal options depending on the scenario.
• Drug interactions: consider common interacting medications (e.g., anticoagulants, antiarrhythmics).
• Route feasibility: can the patient take oral therapy reliably, or is IV needed initially?

Practical mini-check: Before finalizing, ask, “Is this drug safe for this person at an effective dose?”

Step 4: Use local resistance patterns (the antibiogram) and recent cultures

Resistance varies by region, hospital, and even unit. A local antibiogram summarizes how often local bacterial isolates are susceptible to different antibiotics.

• If local resistance to a drug is high for the suspected organism, choose an alternative.
• If the patient has prior culture results (e.g., previous urine cultures), those can be highly predictive of what will work now.

Practical mini-check: Prefer the narrowest effective option that local data supports.

Step 5: Start empiric therapy when needed, then “de-escalate” with data

When infection is likely and delaying treatment is risky, clinicians start empiric antibiotics based on steps 1–4. Then they refine once new information arrives:

• Culture and susceptibility results: switch to the most targeted effective antibiotic.
• Clinical response: improving fever, symptoms, labs.
• Source control: drainage of abscess, removal of infected device, relief of obstruction.

Practical step-by-step example (workflow):

1. Define syndrome: “Dysuria and frequency” suggests lower UTI.
2. Assess severity: stable outpatient vs systemic illness.
3. Pick likely organisms: often enteric Gram-negative bacteria.
4. Check patient factors: kidney function, pregnancy, allergies.
5. Consult local resistance: choose an agent likely to work locally.
6. Send cultures when appropriate: especially if complicated infection or prior resistance.
7. Reassess in 48–72 hours: narrow therapy or stop if infection is unlikely.

Step 6: Match dosing strategy to killing behavior (time vs concentration)

After choosing the drug, clinicians choose a dosing approach that fits how the drug works:

• Time-dependent: prioritize maintaining adequate levels through the day (e.g., scheduled dosing, sometimes extended infusion in severe cases).
• Concentration-dependent: prioritize achieving a strong peak while monitoring for toxicity.

This step connects pharmacology to bedside practice: the “right drug” can fail if delivered in a way that does not reliably achieve effective exposure at the infection site.