Imagine a bacterium as a house. There are different ways to get into the house and destroy the inhabitants. Direct access (doors--front, back, garage, balcony, doggie), ventilation (windows, heating, air conditioning, dryer vent, chimney, cracks), water (plumbing, leaking, flooding). The agents of death can be bullets, falling trees, hurricanes and tornadoes, air-, insect-, or human-borne disease, carbon monoxide, radiation, fire. There are all kinds of options here.
Just as there are different ways to enter a house and kill the residents, there are different ways that substances enter bacteria and kill them. Bacteria differ in what they are susceptible to. That's why antibiotics, natural or synthetic, have to be selected for the specific condition they are treating.
When bacteria encounter an antibiotic, they begin to respond. Most die pretty quickly, but due to genetic diversity, some hang on a bit longer. They learn what the threat is. They generate possible responses. Those bacteria in the meantime make more bacteria, with their specific genetic advantages, and some of their descendants are even better adapted to the antibiotic, and the cycle continues. Because they are reproducing quickly, as fast as twenty minutes per generation, they can adapt. Individual bacteria may die, but if the chosen antibiotic doesn't wipe out all the bacteria quickly, the species as a whole survives. They become resistant. Those resistant bacteria rebound with a vengeance and seek to share the knowledge they acquired in the recent battle with other bacteria far and wide.
Some of the earliest antibiotics worked by disrupting the cell wall, either by breaking down the wall or by preventing the bacteria from repairing the wall. They specifically work on the peptidoglycan layer of the cell wall and are thus effective on Gram-positive bacteria. Penicillin family (penicillin, ampicillin, amoxicillin) and cephalosporin (cephalexin) antibiotics act in this manner.
Another way antibiotics operate is by disrupting the cytoplasmic membrane (which is distinct from the cell wall mentioned above). Polypeptides like polymyxin B and bacitracin work this way. These antibiotics work like a harsh detergent roughing up the cytoplasmic membrane of Gram-negative bacteria. The membrane isn't destroyed, but is so shaken by the experience that it lets the antibiotics through to do their work. Eventually, the bacteria respond by altering the amount of antibiotic that penetrates through the membrane, so that little to nothing gets through. The bacteria do this by changing the locks, so to say. They modify the size of the door or increase security.
Other antibiotics interfere with the bacterial DNA replication process or inhibit DNA enzymes. Bacteria don't actually live all that long. If they can't make babies, the little community they have sought to colonize in or on you dies out. Quinolone family antibiotics (-ofloxacins like ciprofloxacin, levofloxacin, and moxifloxacin) work this way.
Some antibiotics slow or prevent bacterial RNA protein synthesis. This includes several classes of antibiotics--lincosamides (clindamycin), macrolides (azithromycin, clarithromycin, erythromycin), and tetracyclines (doxycycline, minocycline, tetracycline). The antibiotics bind to the RNA. No protein can be made. No growth. No offspring. To combat this threat, the bacteria make internal adjustments such that the target of the antibiotics, the RNA, isn't affected. They drank the Kool-Aid, but it didn't matter because Poison Control was already on the scene.
Carbapenem antibiotics (end in -penem) greatly inhibit some bacterial enzymes to prevent cell wall synthesis. They're often used when all else fails. Kind of like Indiana Jones in the Raiders of the Lost Ark using his whip to escape his foes in the marketplace. He fights on and the bad guys keep coming. He finally whips out his pistol and dispatches the last assassin without a second thought. The bacteria are learning to make their own compounds to disable these broad-spectrum antibiotics of last resort. Which means the antibiotics of last resort are losing this battle.
Inhibiting folate synthesis, a process essential to nucleic acid synthesis, is another way antibiotics work. These antibiotics don't kill the bacteria; they just don't let the bacteria reproduce. This includes the sulfonamides like silver sulfadiazine and trimethoprim-sulfamethoxazole.
By producing toxic free radicals, metronidazole is in a class by itself. It works against anaerobic bacteria.
Over the millennia, bacteria have evolved different mechanisms to protect themselves. One of these mechanisms involves efflux pumps. They're basically sump pumps, varying in sophistication from the entry-level ones that act on only a single substance to the highly complex that remove all kinds of foreign matter.
Sometimes bacteria take a "if you can't beat them, join them" approach, like when they decide to live in cleaning solutions. They can even adapt themselves to digest antibiotics as if they were food. This extreme adaptability and all the other adaptations bacteria make don't bode well for us. Unfortunately for us, the bacteria don't stop there.
Once they learn how to adapt, they have massive bacteria networking parties and share all they know with each other so that they can kill us more efficiently.
It's a wonder any of us are still alive.
As you ponder about how antibiotics and bacteria work, think of industrial antibiotics as snipers. If the conditions are perfect, the sniper hits the mark, and the mark dies. But if any one thing goes wrong, the sniper misses. Now think of herbal antibiotics as paper inflicting cuts everywhere. Death by a thousand paper cuts. But it's really not just paper cuts. Herbs work everywhere, each making their own little contributions. Herbs have numerous natural chemical compounds. Industrial pharmaceuticals have concentrated one of those compounds to act like a sniper with a massive, long-range bullet. Herbs keep all their active constituents, acting more like a shotgun to inflict death. And when herbs are combined, there are even more shotgun pellets, so to say, to do the job. The sniper's bullet kills immediately if it hits the target, while death by a thousand paper cuts takes longer. But fortunately, the target can't evade or defeat the paper cuts.
That's how herbs work. It's not an exciting topic, I know, but it's important to have at least a rudimentary understanding.
Links to related posts:
How Herbal Antibiotics Work
Acquiring Antibiotics
For further reading:
Armageddon Medicine, p 208.
Herbal Antibiotics, pp 14-17.
https://www.cdc.gov/drugresistance/about.html
https://www.cdc.gov/drugresistance/threat-report-2013/pdf/ar-threats-2013-508.pdf
https://en.wikipedia.org/wiki/List_of_antibiotics
03.16.2020
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