Even if you don’t believe in it, evolution can kill you.

Natural selection constantly acts on natural variation to produce organisms with new traits. When the organism is a bacterium, and the new trait is the ability to withstand antibiotics, we have a big problem.

Every second of every day, millions of natural genetic experiments are being conducted across the globe. Most do not yield new traits, or new traits are harmful to the host.

But if there’s only a one-in-a-billion chance of producing a useful new characteristic, and we’re dealing with organisms that number in the trillions, it’s a virtual certainty that we’ll see “improbable” new traits emerge.

During the 20th Century, antibiotic drugs led to widespread optimism that the scourge of infectious disease was about to become a thing of the past. Faith in technology assumed that newer antibiotics would be developed to counter emerging resistance to older drugs.

In the 21st Century, the bugs are winning. We naively thought that wholly synthetic antibiotics, with no counterparts in nature, would frustrate germs’ resistance mechanisms. Repurposing existing cellular operations, bacteria tweak and augment their defenses to create functionally new abilities.

Their chemical counterwarfare might degrade an antibiotic molecule until it’s ineffective, or toughen cell structures that the antibiotic attacks. Nature is endlessly innovative.

When we swallow or inject an antibiotic, it circulates throughout the body in order to reach targeted germs, exposing “innocent bystanders” too. An antibiotic kills off vulnerable germs and creates “vacant” spaces where they had resided. The hardiest, the “resistant” ones, continue to grow and spread into those spaces. If they’re disease germs — pathogens — they can sicken us right away, or just linger in the body to flare up into an untreatable infection later.

In a healthy human host, a few surviving germs might be mopped up by the body’s own immune system. If the host is immune-compromised by age or disease, or the new germ population especially virulent, tough germs spread to become the dominant species, no longer responsive to the initial antibiotic.

The more we overuse antibiotics, the less they work when we really need them.

Call it collateral damage. Loss of beneficial germs can compromise our health in many ways. We’re just starting to discover how our bodies’ “own” germs enhance and improve health.

Antibiotics are routinely added to some animal feed just to encourage faster growth, a chance “side effect.” Crowded pens and feedlots foster epidemics that are treated by giving antibiotics to the entire flock or herd. Multiple germ populations evolve toward resistant forms. Some of them remain with the carcass despite processing. Then we eat them.

Moreover, myriads of potentially harmful bacterial species are exposed to the excreted and discarded antibiotics that we flush into sewers. That’s where a broader ecological transformation occurs. The world is rapidly becoming populated by germs we can’t fight.

Antibiotic use revs up germ evolution in hospitals. Although serious drug-resistant germs have been spreading out into the community environment itself, inpatient facilities are hotspots. Each patient harbors unique germs, often including pathogens that made them sick in the first place. Then various antibiotics, alone or in combination, work their magic. Sometimes it’s black magic. Hospitals are dangerous places. They’re full of sick people.

After one antibiotic fails, subsequent drugs might trigger the same chain of events that inactivated the original. It can happen very rapidly. We respond with a newer drug, and then yet another, each with the potential for its own serious side-effects, such as kidney damage or hearing loss. Lucky victims just get the trots.

Increasingly, emerging strains are immune to all or most antibiotics; these are termed “multiple drug-resistant” (MDR) germs. Adding to our problem is germs’ ability to transfer chunks of genetic material directly from one bug to another, sharing and spreading the ability to resist one or more drugs. When one germ spits out “R-factors,” other germs soak them up into their own genetic machinery. Instead of evolving over multiple generations, the resistance trait spreads across a mixed population of germs all at once.

Antibiotics are not big profit-generators for manufacturers. Entrepreneurs prefer drugs that control rather than cure. A simple blood pressure medicine can sustain a life-long paying customer, whereas there’s relatively little fiscal incentive to develop a new single-episode one-and-done antibiotic. There are some promising approaches under study, like using phage viruses to attack bacterial infections, but don’t hold your breath.

Doctors must deal with individual cases, weighing society’s liabilities against the wellbeing of the individual patient. Sometimes we figure blasting away with antibiotics “just in case” is “erring on the side of caution.” But if using an antibiotic is in fact ineffective as a treatment, and if the drug risks adverse individual as well as group side-effects, that’s not “staying on the safe side.”

This winter, the big three — middle ear infections, sinusitis, bronchitis — will trigger widespread inappropriate antibiotic use. Most of these episodes are caused by viruses, which antibiotics won’t help.

Don’t “request” an antibiotic; your provider already knows they’re available. If an antibiotic is proposed, ask which germ is the target, and whether you could benefit from a trial of other measures first.

Before you shell out big bucks on an easy, convenient, useless Z-pak, remember: for every new gorillacillin, there’s a Godzillabacter that’s nastier.

Jon Hauxwell, MD, is a retired family physician who grew up in Stockton

and lives outside Hays.