Antibiotics for Bacterial Infections: Classes and How They Work

Antibiotics are one of the most important medical breakthroughs of the last century. They don’t cure colds or the flu - those are viral. But when you have a bacterial infection like strep throat, a bad urinary tract infection, or a skin abscess, antibiotics can mean the difference between a few days of feeling awful and something much worse. Around 73 billion doses of antibiotics are used worldwide every year. That’s a lot. And yet, many people still don’t understand how they actually work.

What Antibiotics Actually Do

Antibiotics don’t just kill bacteria. Some stop them from multiplying. That’s called bacteriostatic. Others punch holes in the bacterial cell wall until it bursts - that’s bactericidal. Either way, your immune system finishes the job. The key is that antibiotics target things only bacteria have. Human cells don’t have the same structures, so the drugs usually leave us alone.

The first antibiotic, penicillin, was discovered in 1928 by Alexander Fleming. It wasn’t until the 1940s that scientists figured out how to make enough of it to save lives - especially soldiers during World War II. Today, we have over 100 different types. But not all work the same way. They’re grouped by how they attack bacteria.

Class 1: Cell Wall Builders - Beta-Lactams and Glycopeptides

Think of a bacterial cell like a brick house. The walls are made of peptidoglycan - a tough mesh that keeps the cell from bursting under pressure. Beta-lactam antibiotics - including penicillins and cephalosporins - trick the bacteria into thinking they’re building blocks for the wall. But instead of helping, they jam the machinery.

These drugs bind to proteins called penicillin-binding proteins (PBPs). Those proteins normally stitch the wall together. When blocked, the wall stays weak. Water rushes in, and the cell explodes. It’s like cutting the support beams of a house while it’s being built.

Cephalosporins come in four generations. First-gen, like cefalexin, are good against common skin and throat bugs. Second-gen, like cefuroxime, add some coverage against gut bacteria. Third-gen, like ceftriaxone, can handle tougher Gram-negative bugs like E. coli and even Pseudomonas. Fourth-gen, like cefepime, cover almost everything - but they’re saved for serious hospital infections because overuse leads to resistance.

Vancomycin, a glycopeptide, works the same way but is used only when other antibiotics fail. It’s often the last line against MRSA - a superbug resistant to most penicillins.

Class 2: Protein Factory Saboteurs - Macrolides, Tetracyclines, Aminoglycosides, Oxazolidinones

Bacteria need proteins to survive. They build them using tiny machines called ribosomes. Antibiotics in this group sneak in and break those machines.

Macrolides like azithromycin bind to the 50S part of the ribosome. They stop the ribosome from moving along the genetic code, so no new proteins get made. That’s why they’re often used for pneumonia, bronchitis, and some STIs. They’re also good for people allergic to penicillin.

Tetracyclines, like doxycycline, attach to the 30S ribosomal subunit. They block the tRNA from docking, so the building blocks can’t be added. Doxycycline is also used for Lyme disease, acne, and even some tick-borne illnesses. But it makes your skin super sensitive to sunlight. And kids under 8? No way. It stains developing teeth permanently.

Aminoglycosides - like gentamicin - are powerful but risky. They bind to the 30S ribosome and make the bacteria read their DNA wrong. That creates broken proteins, which kill the cell. But they’re toxic to kidneys and ears. They’re usually given in hospitals for severe infections like sepsis. And here’s a key detail: they need oxygen to get inside bacteria. So they don’t work on anaerobes - the kind that live in deep wounds or the gut.

Linezolid, an oxazolidinone, is special. It’s the first fully synthetic antibiotic in this group. It stops protein production before it even starts - by blocking the ribosome from assembling. It’s used for resistant skin infections and pneumonia caused by MRSA. But it’s expensive and can cause nerve damage or low blood counts if used too long.

Class 3: DNA Destroyers - Fluoroquinolones

Fluoroquinolones - like ciprofloxacin and levofloxacin - go straight for the bacteria’s genetic code. They target two enzymes: DNA gyrase and topoisomerase IV. These enzymes untangle DNA so it can be copied. Block them, and the bacteria can’t replicate. No replication = no infection spread.

These drugs are broad-spectrum. They work on Gram-positive and Gram-negative bacteria. That’s why they’re often prescribed for urinary tract infections, sinus infections, and even anthrax. But they’ve got serious downsides. The FDA added black box warnings in 2022: tendon rupture, nerve damage, and even long-term disability in rare cases. They’re no longer first-line for simple infections. Doctors now reserve them for when nothing else works.

Class 4: Folate Blockers and DNA Breakers - Sulfonamides and Nitroimidazoles

Sulfonamides, like sulfamethoxazole, don’t attack the cell wall or ribosomes. They steal the building blocks bacteria need to make folic acid - a vitamin essential for DNA and protein production. Humans get folic acid from food, but bacteria have to make it themselves. So this starves them.

But resistance is high. That’s why sulfamethoxazole is almost always paired with trimethoprim (as co-trimoxazole). Together, they block two steps in the same pathway. It’s still used for urinary infections and Pneumocystis pneumonia - especially in people with weakened immune systems.

Metronidazole is a different beast. It’s activated inside anaerobic bacteria and parasites. Once activated, it shreds their DNA. That’s why it’s the go-to for C. difficile infections, bacterial vaginosis, and certain stomach ulcers caused by H. pylori. But if you drink alcohol while taking it, you’ll get sick - vomiting, flushing, rapid heartbeat. That’s because it blocks the breakdown of alcohol in your liver. About 60-70% of people feel this reaction.

Why Some Antibiotics Stop Working

Antibiotic resistance isn’t science fiction. It’s happening now. In 72 countries, more than half of E. coli infections don’t respond to fluoroquinolones. In hospitals, up to 50% of MRSA strains are resistant to vancomycin in some areas.

Resistance happens because bacteria evolve. If you take an antibiotic when you don’t need it - say, for a viral cold - you kill off the weak bacteria but leave the strong ones. Those survivors multiply. Soon, the whole population is resistant.

Some bacteria produce enzymes like beta-lactamase that chop up penicillin. Others change their cell wall so the drug can’t bind. Some pump the antibiotic out before it can do damage. And some even swap resistance genes with other bacteria like trading cards.

The WHO calls this a global health crisis. In 2021, antibiotic resistance contributed to nearly 1.3 million deaths worldwide. That’s more than malaria or HIV.

What Doctors Do Differently Now

Back in the 90s, doctors often prescribed broad-spectrum antibiotics “just in case.” Now, guidelines are stricter. The CDC says 30% of outpatient antibiotic prescriptions are unnecessary. That’s millions of doses wasted - and resistance fueled.

Today, many doctors use tests like procalcitonin to tell if an infection is bacterial or viral. If levels are low, it’s likely viral. No antibiotics needed. That cuts unnecessary use by 23%.

Also, doctors are switching to narrow-spectrum antibiotics whenever possible. In Europe, 85% of strep throat cases are treated with penicillin - simple, cheap, and targeted. In the U.S., that number is only 45%. Broader drugs like azithromycin are overused, even though they don’t work better.

New Hope on the Horizon

There are new antibiotics, but they’re rare. Only 16 new drugs in development target the WHO’s priority pathogens. Most pharmaceutical companies don’t invest heavily - antibiotics don’t make as much money as cancer drugs.

One promising drug is cefiderocol. It’s a cephalosporin that tricks bacteria into sucking it in like iron. Once inside, it kills even the toughest Gram-negative bugs. It’s used for infections that no other antibiotic can touch.

Phage therapy - using viruses that eat bacteria - is also being tested. Early trials in the UK and Europe show promise for hard-to-treat ear infections and wounds. It’s not mainstream yet, but it might be the future.

And then there’s the UK’s “Netflix model.” Instead of paying per pill, the government pays a flat fee for access to new antibiotics. That means companies can make money without pushing overuse. It’s a radical idea - and it might save lives.

What You Should Know

Don’t ask for antibiotics for a cold. Don’t skip doses. Don’t save leftover pills for next time. Don’t share them. Antibiotics are not painkillers. They’re precision tools.

If you’re prescribed one, take it exactly as directed. Even if you feel better after two days, finish the course. That’s how you stop resistant bugs from surviving.

And if you’re ever unsure - ask your doctor: Is this infection bacterial? Is this antibiotic really necessary? There’s no shame in asking. It’s your health.