How antibiotics work and how bacteria respond is a complex topic.
Countless researchers devote their careers to studying just one aspect
of bacteria or plants or compounds. That's far beyond the scope of this
blog, and yet acquiring a very basic understanding of how they work,
what they can and cannot do, may help us use our limited supply of
industrially manufactured antibiotics and natural herbal antibiotics as
best as possible for our families. What follows is a gross
simplification of how bacteria and antibiotics work.
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