Missing Microbes: How the Overuse of Antibiotics Is Fueling Our Modern Plagues (28 page)

The situation reminds me of
Where’s Waldo?
, a children’s book illustrating scores of people busily at work or at play with one character, Waldo, hiding in the crowd. The child’s task is to find Waldo. If Waldo was a rare microbe and disappeared, we might not notice at all unless we looked for him specifically. When you take a broad-spectrum antibiotic, which is the kind most commonly prescribed, it may be the case that rare microbes occasionally get wiped out entirely. The critical point is that once the population hits zero, there is no bouncing back. As far as your body is concerned, that species is now extinct.

Why might it matter? By all rights, those puny species should be inconsequential. But microbes employ a powerful stratagem for their survival. Any small population of, say, a few hundred cells can explode into 10 billion or more cells by next week. The trigger for their massive bloom could be some component of a food you’ve eaten for the first time that only they have the enzymes to digest. Favored by a new, exclusive food supply, the rare microbe goes into overdrive and multiplies by 1 million percent. This blossoming could be good for you, too, because some of the energy captured in that new food by these microbes might end up in your bloodstream. But when food is in short supply, which was generally the case for most humans until quite recently, and people need to eat unfamiliar plants or animals, it would be useful to have a repertoire of enzymes to help us metabolize a wide variety of food chemicals. The genes of our flexible partners, our resident microbes, provide those enzymes.

Now consider what the consequences might be if one of your rare microbes went extinct. Imagine that it is ancient and has been dwelling in
Homo sapiens
for 200,000 years. One possibility is that it doesn’t matter. Perhaps that microbe was a marginal player, so good riddance. Another possibility is that it is a “contingency” organism. You carry it and others in your baggage, not for everyday use but because it is like that set of hiking boots with crampons: useful when you need to walk across a glacier but dead weight the rest of the time. Or maybe it is that wedding dress from Grandma, beautiful but used only every other generation. Loss of such contingency species might not have much consequence except when you’re suddenly faced with glaciers or weddings.

Another possibility is that you need contingency species only at certain times in your life, like that cane you keep in the attic for when you get old. In a way, the loss of contingency microbes represents the loss of biodiversity. Let’s say that every cornfield in Iowa had the same high-producing strain of corn. For a while, all would be well; crop yields would be high. But if a pathogen emerged—a corn blight—that targeted that high-producing strain, then all of Iowa’s cornfields would be susceptible to disease. In weeks, we could go from bountiful fields to acre after acre of diseased plants, and famine would not be far behind. Even small declines in biodiversity can make a community much more susceptible to an introduced pathogen. And as shown by the pine beetle and
C. diff,
it is the way of nature that pathogens are always present, with more just over the horizon.

An epidemic arising in one locale puts the whole world at risk. We have seen this with the spread of influenza. When a new strain was recognized in Mexico in 2009, people in California and Texas fell ill days later, and others in New York City a few days after that. A few weeks later, this particular flu had spread across the United States and the rest of the world. We were relatively lucky that it was not a highly lethal strain, considering the hundreds of millions of people it infected. Its lack of potency notwithstanding, thousands of people all over the world still died. Even when a strain is not that virulent, when billions of people are infected the number of deaths add up. And if the strain is worse, as it was in 1918–19, then deaths are in the millions. We also were fortunate with the SARS epidemic in 2002, which was caused by a virus newly introduced to humans by animals, probably bats. Luckily its spread from person to person was not very efficient. It was devastating in a few places, but it died out from its own inability to transmit efficiently among humans. We dodged that bullet.

Our increased vulnerability to pathogens because of the “smaller” world in which we live is occurring just when our ancient microbial defenses are degrading. Such a conjunction provides fuel for raging conflagrations, either relatively local, like
Salmonella
or
E. coli
outbreaks, or potentially more global. The consequences of such a scenario are scarcely imaginable, but we have precedents to inform us. In the fourteenth century, the Black Death decimated Europe. We don’t fully understand its cause, but changes in rodent populations were part of it. Another major factor was overcrowded, filthy medieval towns and cities, which were like tinder for the rat-borne plague. It lasted four years, and when it was over about one-third of the population of Europe had died, some 25 million people.

Another more recent plague, AIDS, has affected more than 100 million people worldwide since it came to us from chimpanzees. As terrible as HIV is, the disease does not pass easily from person to person like an influenza virus, so in one way—its speed of transmission—it is less frightening than a fast-spreading pestilence.

I am less interested in history books than in what might happen next. Plagues are inevitable wherever people congregate. This means that with a global population of 7 billion that is rising by 80 million a year—about the population of Germany—the questions are what will cause the next big plague, who will be affected, and when will it happen. Public-health measures will try mightily to minimize the costs, but it’s possible we will be overwhelmed. The Great Influenza of 1918–19 killed tens of millions in an era without commercial airplanes and other forms of rapid mass travel to spread it. With a huge world population that is essentially contiguous, and with so many of us with weakened defenses because of our compromised internal ecosystems, we are vulnerable as never before.

I see many parallels between our changing climate and our changing resident microbes. The modern epidemics—asthma and allergic reactions, obesity, and metabolic disorders—are not only diseases but also external signs of internal change. We may see the problem when a child with an altered microbial ecosystem and diminished immune status encounters a mild pathogen that can easily damage the child’s pancreas and lead to juvenile diabetes. Or the problem can show up when another child encounters a peanut or gluten, which are relatively recent additions to the human diet. Changes in their resident microbes and immune maturation similarly conspire to put them at risk, in this case for severe allergies to nuts or gluten. Like the worsening hurricane seasons we are seeing, these outcomes are bad enough, but they also are indicators of our larger imbalances, the loss of our reserves.

It’s likely that a potentially deadly mutated microbe is now living in some animal somewhere in the world. It may have gained a new gene that helps it spread. Maybe it will crash into one of our domesticated animal species living in densely packed barns not far from where we live. Perhaps it will jump to an intermediary host, or maybe that new host will be us. In any case, the gathering storm is already here.

Fortunately we humans are on high ground when it comes to such storms; our diverse microbes with their 20 million genes help us resist disease. They are the guerrilla warriors defending the home domain as long as we protect them. However, recent studies suggest that some otherwise normal individuals have lost 15–40 percent of their microbial diversity and the genes that accompany it.

This is the greatest danger before us: pathogens causing an epidemic against which we are helpless. Ecological theory tells us that the people whose resident bacteria have been disrupted the most will be the most vulnerable. All things being equal, the asthmatic, the obese, and those with the modern epidemic diseases will be the ones at highest risk to succumb. Human history and prehistory are pockmarked by prior plagues, and the world was more disconnected then. Genetic studies suggest that we come from a tiny founding population; our ancestors may have been survivors of some earlier cataclysm that was possibly related to climate change. But as contentious as the climate-change debate is these days, global warming may not be our biggest worry.

Unless we change our ways, we are facing an “antibiotic winter,” a much greater peril, a worldwide plague that we cannot stop. Population biology is against us; we are no longer protected by isolation. We now live in one hugely connected village, and there are billions of us. And today many millions of us live with degraded defenses. When the plague comes, it could be fast and intense. Without high ground, like a river that overflows its natural banks, there is no sanctuary. All of this risk has been magnified by what in retrospect we will see as our reckless and profligate ways of abusing antibiotics. As concerned as I am about health problems such as diabetes or obesity, the most important reason why I am sounding an alarm is my fear of a catastrophic “antibiotic winter.”

We talk about a pre-antibiotic era and an antibiotic era; if we’re not careful, we’ll soon be in a post-antibiotic era. This now is a major focus of the CDC, and I share its concern. But I am thinking about a different concept, not only the failure of antibiotics because of resistance but also the increased susceptibility of millions because of a degraded ecosystem. The two go hand in hand, but in a smaller interconnected world the second is a deluge waiting to happen and growing each day.

16.

SOLUTIONS

Last summer a relative called to ask me about a spreading rash on her leg. She e-mailed a picture: an ugly raised red blotch about two inches in diameter with a little dark spot in the center and a rim that looked like it had been marked by a highlighter. It resembled a bull’s-eye. Because it was summer and she had been staying in Connecticut, two words came instantly to mind:
Lyme disease
.

I recommended that she start antibiotics immediately. She took her medication every day until the rash was gone and for several days more, even after she felt better, to complete the full course.

As hoped, the drug cured her infection, making both of us happy that we have effective antibiotics. I want to keep it that way. I’m not against antibiotics any more than I’m against ice cream—both great at serving their purpose—but sometimes there can be too much of a good thing. Overprescription of antibiotics and overreliance on C-sections are problems that urgently need resolution.

Solutions vary from the personal—the attitudes we embrace and the decisions we each can make—to the institutional—the kinds of policies the medical establishment or government should make and what kinds of research need to be prioritized. Sometimes the distinctions between personal and institutional blur, as in the case of antibiotics.

First we must curb our appetites for these powerful drugs. This is the biggest, simplest, and most achievable step we can take in the short term. It won’t turn back the clock, but it could help slow the daily carnage to our microbial diversity.

Each of us can take personal responsibility for how to deal with antibiotics. Tell your doctor that you want to wait a few more days before taking amoxicillin for the cough that has lasted a week. Or you want to wait another day before you get a prescription for your child with a head cold. Resist pushing your physician for a quick fix to mitigate your anxiety. Without parental pressure, your doctor can make a better judgment about the need for an antibiotic.

Inform your dentist that you don’t want to take antibiotics unless he or she can convince you that the benefits outweigh the potential risks. The axiom of good medicine (and dentistry) is “do no harm.” Because we were not properly calculating the harm from antibiotics, they were above scrutiny. Many dental diseases are best managed by operative intervention and oral hygiene measures.

Stop using so many sanitizers on yourself and on your kids. While the key ingredient in these products, triclosan, is not an antibiotic, it kills bacteria on contact. What’s wrong with good old soap and water? I use sanitizers only when I’m in the hospital seeing patients and during flu season. Most of the bacteria on my skin have been living with me for years. I know them, and they know me. I might pick up bacteria from other people, say on the pole in the subway car. Of course, I don’t put my fingers in my mouth after touching that pole, but I don’t use sanitizers either. I worry that I’ll remove good bacteria, the ones that help me fight the bad bacteria that come my way.

Back to the question of what to do when your child is sick. I’m not saying wait and see in every instance. Sometimes children are quite ill and should be examined immediately. They are fussy, run high fevers, and gasp for breath. Or they are listless and don’t respond normally to light or sounds. Their bellies may be swollen. They may have severe diarrhea or a terrible rash. These are true emergencies.

At a time like this, parents should carefully reconstruct the daily events leading up to the onset of symptoms and tell the physician everything they recall. After the exam, which may include blood tests and X-rays, many acutely ill children will need antibiotics immediately to avoid permanent injury or to save their lives. It would be a terrible mistake for a doctor to delay such treatment out of concern for causing collateral damage to resident microbes. Serious bacterial infections will always be with us.

Doctors thus face a conundrum: antibiotics are vital and yet way too many—more than 41 million courses in 2010—are being prescribed annually to U.S. children. Most kids don’t need them.

Pediatricians and other health-care providers must be trained to think twice before prescribing antibiotics. They need to carefully weigh each situation. Is this a dangerous infection or, more likely, is it a mild one that will go away by itself in the vast majority of children?

This judgment call is not a simple task. It can take years of experience to conduct truly careful examinations. For the doctor in a hurry, it’s far easier to write a prescription for everyone who walks in the door with a runny nose, sore throat, or red ear drums. It’s more time-consuming for a doctor to examine a child carefully, to discuss with a parent why the antibiotic should be withheld, to answer questions, to explain the danger signals, and to say “call me in the morning if things don’t get better.”