By Deborah Jones
VANCOUVER, Canada, 1995
In the war between germs and antibiotics, this much is no longer in doubt: eventually, bacteria win every battle. The only question is: how long can the cavalry keep arriving with new drugs?
Forget plague in India. Forget, if you can, the so-called flesh-eating streptococcus that cost (federal Canadian) Opposition leader Lucien Bouchard his leg last year. For now, those bacteria do respond to drugs–if they’re treated early enough.
Worry, instead, about evolution. It’s not just a neat shape-shifting game played by amoebas, monkeys and humans. Bacteria evolve too. Routed two generations ago by the discovery of antibiotics, bacteria found ways to survive. Today, time-tested and inexpensive drugs like penicillin no longer kill the bugs that cause ear and throat infections, sexually transmitted diseases, even meningitis. These bacteria have evolved and are becoming immune to our miracle medicines faster than scientists thought possible. Meanwhile, our hospitals, with high levels of antibiotics and large populations of a bacteria, have become breeding grounds for resistant strains.
The result: doctors are forced to turn to newer, more expensive antibiotics, which is bad news for the already spiraling cost of health care. But there is much worse news: at least one bacterial infection already resists all available antibiotics.
This morning, at British Columbia’s Children’s Hospital, Dr. Paul Thiessen is examining kids with urinary tract infections. Some of these patients–who already suffer from the congenital birth defect spina bifida–have taken oral antibiotics without success, and Dr. Thiessen, head of the division of general pediatrics at the Vancouver hospital, is now prescribing intravenous alternatives.
Historically, medical researchers have invented new antibiotics to attack new forms of resistant bacteria – but “we’ve come to the end of that.”
We regularly run into strains of bacteria that are resistant,” says Dr. Thiessen, who works on the front lines of the war against disease. “But throughout history, medical science has invented a new antibiotic to attack that bacteria.”
Back in the war rooms of pure research, few microbiologists and biochemists are so upbeat. In Hamilton, Ont., Gerald Wright, an assistant professor of biochemistry at McMaster University, warns: “Only a handful of compounds stand between up and not having any control over bacterial infections.” In the past, says Wright, “people always figured that a new class of antibiotics would emerge. Now we’ve come to the end of that.”
While the scientists debate prognoses, I know this: my own healthy 7-year-old son, Gavin, has twice had infections in his ears and throat that required courses of more than two different antibiotics to clear up. When I was the 7-year-old, one antibiotic did the trick.
Bacteria prey mostly on the very young, the very old, and the very ill–those in robust health have stronger immune systems, leaving them better equipped for the fight against all germs. Our own bodies resist disease daily, and for millennia, our immune systems protected us from many diseases without help from artificial helpers such as antibiotics. Nowadays, who is willing to wait out the progress and gradual cure of illnesses such as strep throat or bacterial pneumonia, and risk discomfort, pain and perhaps even death in the process?
One or another common antibiotic will usually cure these infections, if only by wiping up enough bacteria so that our own embattled immune systems can mop up the stragglers–the drug-resistant mutants. The problem is that, increasingly, the mutants are in the majority. In these cases, doctors may have to try different types of antibiotics before hitting on the effective one. Canadian cases of drug-resistant bacteria causing common ear and throat infections and meningitis have already risen from two percent in the late 1980s to an average 14.5 percent in 1994. And in hospitals, up to one in 10 patients are infected by drug-resistant bacteria.
Bacterial diseases such as bubonic plague wiped out cities and waylaid civilizations. Then antibiotics changed human history.
Throughout history, bacterial infection has been one of our worst enemies. Viruses and other microbes did their share, but bacterial diseases such as bubonic plague wiped out cities and waylaid the development of entire civilizations.
That stopped when antibiotics arrived. As far back as 1500 B.C., healers used mold from animal dung to treat infections. In the 20th century, scientists found that some tiny creatures in the soil, such as the mold Penicillium notatum, make chemicals that poisons other microbes, including bacteria. It took years to harness these poisons for human use, and only in the 1930s and ’40s were drugs such as penicillin manufactured in amounts large enough to save lives.
How did the tide turn so quickly against antibiotics? That’s where evolution comes in. The survival instinct is built into nature, and bacteria have it in spades. One of the earliest and most ubiquitous life forms, the one-celled creatures have inhabited the Earth for millions of years precisely because they are so efficient at adapting their genetic makeup.
When we started to poison them with antibiotics, they fought back. Each colony of bacteria numbers thousands or millions of creatures; a few are mutants, able to resist a certain antibiotic by ingesting it, spitting it out or shielding themselves from it. So, even if a drug wipes out all of the susceptible bacteria in an infection, there are usually a few left. And since one bacterium can produce some 16,777,220 offspring within 24 hours, the few quickly become the many. Since those many are all resistant mutants, the antibiotic’s own firepower has cost it the battle.
Blame evolution, then, but spare some blame for human complacency. We have allowed our world to become awash in antibiotics and in so doing, we have helped bacteria in their selection of the fittest–the ones that resist our antibiotics. U.S. research indicates that seven out of 10 patients who seek medical help for a cold are given an antibiotic prescription–even though the common cold is caused by a virus, not bacteria. The useless drug likely won’t harm the individual patient, but every antibiotic prescription contributes to the worldwide problem: by killing only nonmutant bacteria, it encourages mutants to grow and spread. The problem worsens when the aptient fails to finsh the prescribed course, or passes antibiotics on to friends (practices that can harm you: when bacteria are hurt but not killed, they can attack with greater force).
Blame, too, the unique economics of drug research. In the early ’80s, says Wright, pharmaceutical companies turned their attention from making new antibiotics–each of which can cost $300 million to develop and test–to other, more profitable drugs that treat diseases such as arthritis and heart disease. Now, just as bacteria are becoming more resistant than ever before, there are fewer new antibiotics coming out of the pharmaceutical pipeline.
Meanwhile, about half of all antibiotics made worldwide are fed to farm animals, which then grow twice as fast–possibly because their bodies don’t have to use as much energy fighting infections. That helps meat producers but it also means mutant bacteria grow in greater numbers than normal.
The fight against bacteria has become a world war.
Nor does it help that the fight against bacteria has become a world war rather than a series of local ones. Drug-resistant bacteria find prime breeding ground in places where antibiotics are less regulated (in India, some antibiotics are sold by pharmacists without a doctor’s prescription) or inner cities where poor diet weakens immune systems. Because of air travel, “trends in other parts of the world will affect us,” says microbiologist Jo-Anne Dillon of the University of Ottawa, who tracks emerging resistant strains of gonorrhea for the World Health Organization. “We have to realize that we’re not in isolation in Canada.”
As if all this were not bad enough, scientists now know that different strains of bacteria can swap genetic information in packages called plasmids, allowing them to transfer the blueprint for antibiotic resistance without actually coming in contact with the drug. There-in lies the worst horror story of all.
They call it the Andromeda factor. “THEY” being the microbiologists; “it” being the bacterial threat now lying just over the horizon. The Andromeda Factor, named after The Andromeda Strain, the 1969 Michael Crichton book about a deadly bacteria to pass on survival secrets to its cousins.
On your lifelong compulsory tour of the world of bacteria, there’s one type you may well run up against in your lifetime, and one you absolutely don’t want to meet when your defences are down. The Andromeda horror scenario stars both. First, say hello (politely) to Staphylococcus aureus (affectionately known as Staph a.), the common and potentially lethal bacterium that causes blood poisoning by infecting a surgical wound. Already, some 40 percent of Staph a. in U.S. hospitals resist all but one antibiotic, vancomycin. (In Canada, the problem is better contained: less than one percent of patients in hospitals are infected with this resistant strain.)
Now, say a very distant hello to enterococcus, the monster bacterium–the one that already resists all available antibiotics including vancomycin. Lab experiments have proved that, because of the Andromeda Factor, enterococcus can swap plasmids with staphylococcus. The result is a staphylococcus that’s learned the trick of invulnerability. Enter, SuperStaph.
As you read this, Staph a. are swarming in huge numbers over your skin, and enterococci are breeding with abandon in your guts. The former can attack when the skin is broken; the latter when illness or drugs have weakened your immune system. But so far, SuperStaph is thought to live only in the lab. Julian Davies, head of the department of microbiology and immunology at the University of British Columbia and one of the world’s leading researchers in antibiotic resistance, says that if the Andromeda Factor makes the leap from horror story to real life, SuperStaph will likely show up first in hospitals. If that happens, he warns, hospitals would have to adopt stricter infection-control measures. And there would be no drugs to help people with weak immune systems combat bacterial infection.
Incurable diseases caused by resistant bacteria are still, thankfully, relatively uncommon. “It affects nowhere near the number of people who get knocked over by automobiles each year,” says Davies. But this much is certain: the problem will continue to worsen unless action is taken now. Most experts agree that brand-new antibiotics should be reserved for stubborn infections, to reduce the rate at which bacteria resist them. They also agree that older antibiotics to which bacteria have become resistant should be controlled, in the hope that the numbers of mutants will decline. Networks should be set up to monitor levels of resistance and provide information. And antibiotic use should be better regulated in all countries. Says Wright: “Antibiotics are part of our natural resources, and if we squander them they’re gone forever and useless to our children and grandchildren.”
Whether we can stop drug resistance before it spins out of control remains to be seen. But the sooner we put a stop to overuse of antibiotics, the better off we’ll all be.
Originally published in Chatelaine magazine, June 1995
Copyright © 1995 Deborah Jones