...but some are more equal than others. Or so patients seem to think.
Here's the bottom line. If you take nothing else away from this post: Antibiotics are not "strong" or "weak." They are targeted.
Patients ask me some questions about antibiotics that sound truly strange if you know anything at all about microbiology and antimicrobial agents. Granted, most patients don't have that background, and it would be unfair for me to expect them to know the difference between Gram-negative and Gram-positive bacteria or to know anything about activity spectra. Probably the most common question, in some form or another, is "is this a good one?"
The answer is not as simple as yes or no. Are the antibiotics on the market effective for treating bacterial infections? Yes. Will this antibiotic be effective against your bacterial infection? I don't know. And, chances are, neither does your doctor, at least, not for certain. Are the risks of taking this antibiotic going to outweigh the benefits? Probably, unless you're taking telithromycin for acute bacterial sinusitis (which is not an acceptable use of the drug).
That bit about telithromycin was a bit of pharmacy dark humor. If you didn't get the joke, forget I mentioned it and move on with your life.
The only way to know if a given antibiotic will be effective in treating a particular infection is to culture the microorganism causing the disease. This means taking a sample from the patient, growing the sample on a petri dish, and then trying to grow the sample in the presence of various antibiotics that are released by little discs inserted into the growth medium. The bacterial growth results are then compared to a table for each antibiotic to determine whether or not the antibiotic sufficiently inhibited bacterial proliferation to say that the antibiotic will be effective against an infection in a living person.
This process takes anywhere from three days to a week to get right. Most patients are not willing to wait that long, and the lab tests are both costly and time-intensive. Most doctor's offices are not equipped to do a lot of lab testing. As a result, most doctor's visits where patients complain of what sounds like an infection result in the patient being sent out the door with a prescription for some antibiotic that the doctor thinks will be appropriate.
You can't blame physicians for not taking the time to culture everything, though I imagine most infectious disease specialists would bite your head off for suggesting that it's acceptable to start throwing around prescriptions without doing a culture. My microbiology professor would have a heart attack if I showed him the script I transcribed from a phone conversation on Saturday; Tamiflu and an antibiotic. Tamiflu kills influenza A viruses, but not bacteria. Antibiotics kill bacteria, but not viruses. You could argue that the physician is just covering his bases and trying to help the patient.
You could also argue that this is a little bit like using a blunderbuss to kill a mosquito.
The point of culturing bacteria is that antibiotics are not like a set of progressively bigger guns. They're specific tools in a toolbox. Using the wrong antibiotic is like using a hammer instead of a screwdriver. The problem is not that the tool isn't "strong" enough, it's that it isn't specific enough. Even healthcare professionals throw around terminology that makes it sound like some antibiotics are explicitly more "powerful" than others, but what they're really talking about is antibiotics that are used as last resorts. There are certain antibiotics that are used after everything else has failed--not because they're better and the others are "weaker," but because bacteria are less likely to resist them.
Which brings me to my second point. Bacterial resistance.
Bacterial resistance is a matter of evolution, i.e., natural selection. Suppose that 99% of all bacteria exposed to genericillin die. The 1% of the population that survives does so because it has randomly developed a means to protect itself from genericillin; perhaps it breaks down genericillin by secreting enzymes before the drug can affect the bacteria. That 1% of the population goes about its life and continues to reproduce, so that 1% of the old population is now billions of bacteria. The population rebuilds itself rapidly (due to lack of competition for resources), so we expose the bacteria to genericillin again. But this time, it doesn't work, because these bacteria are immune to genericillin. They were never susceptible to genericillin. What we have done is selectively bred the organisms most fit to survive in a genericillin-laden environment and killed off all of their competition, permitting their population to explode.
You do not become "immune" to an antibiotic because antibiotics don't do anything to "you" (at least, not ideally). This is probably the biggest misunderstanding of antibiotic resistance that I encounter--patients who think that they have become "immune" to genericillin because they took too much of it.
This is a little like expecting to be immune to bullets because you've shot too many people.
Unfortunately, the situation is much worse than that. You aren't the only one who has to deal with the consequences of resistant bacteria. We all do. And we have no one to blame but ourselves. Every unnecessary antibiotic prescription, every antibiotic that someone stops taking halfway through their therapy or that they "save for later," every "borrowed" medication--all of these contribute to resistant bacteria. The resistant bacteria already exist, for the most part, results of genetic mutations. But we're selectively breeding them by killing off their competition. Curing syphilis today requires eight times the dose that was required in 1960.
I've said it before, and I'll say it again. I would rather see physicians overprescribe narcotics than antibiotics. Drug addiction and substance abuse are bad, from a public health perspective, but breeding "superbugs" is a great deal worse. Addicts are, as a rule, only hurting themselves; overuse of antibiotics hurts everyone.