Natural Defense: Enlisting Bugs and Germs to Protect Our Food and Health
208
Natural Defense: Enlisting Bugs and Germs to Protect Our Food and Health
208eBook
Available on Compatible NOOK devices, the free NOOK App and in My Digital Library.
Related collections and offers
Overview
Fortunately, scientists are finding new solutions that work with, rather than against, nature. Emily Monosson explores science’s most innovative strategies, from high-tech gene editing to the ancient practice of fecal transplants. There are viruses that infect and bust apart bacteria; vaccines engineered to better provoke our natural defenses; and insect pheromones that throw crop-destroying moths into a misguided sexual frenzy. Some technologies will ultimately fizzle; others may hold the key to abundant food and unprecedented health. Each represents a growing understanding of how to employ ecology for our own protection.
Monosson gives readers a peek into the fascinating and hopeful world of natural defenses. Her book is full of optimism, not simply for particular cures, but for a sustainable approach to human welfare that will benefit generations to come.
Product Details
| ISBN-13: | 9781610917209 |
|---|---|
| Publisher: | Island Press |
| Publication date: | 06/20/2017 |
| Sold by: | Barnes & Noble |
| Format: | eBook |
| Pages: | 208 |
| File size: | 2 MB |
About the Author
Read an Excerpt
Natural Defense
Enlisting Bugs and Germs to Protect Our Food and Health
By Emily Monosson
ISLAND PRESS
Copyright © 2017 Emily MonossonAll rights reserved.
ISBN: 978-1-61091-718-6
CHAPTER 1
Natural Allies: Our Bacterial Protectors
FIVE YEARS AGO, Tim Stoklosa caught a cold. He was twenty-six at the time, his lungs compromised by muscular dystrophy, a neurodegenerative condition that he has managed for much of his life. Because Tim lacked the ability to cough and clear his lungs, colds predictably led to pneumonia. This time around, it was silent pneumonia. Tim was given Augmentin, a powerful combination of penicillin and clavulanic acid, an enzyme inhibitor aimed at amoxicillin-resistant bacteria. As a so-called broad-spectrum antibiotic, it kills not only harmful bacteria but also plenty of beneficial species that make their home in our gut. For many of us, a few cups of yogurt or some probiotics help rebuild that microscopic community.
But ten days after Tim's first course of Augmentin, his fever continued and he developed stomach upset. He was given another course. It didn't help. "Finally," says his mother, Karen Anderson, a single mom who has devoted a large part of her life to Tim's health, "one nurse figured he had C. diff." Clostridium difficile is a potentially lethal infection of the colon. Though the bug may lurk in our guts without causing harm, it is also a notorious opportunist often acquired in the hospital; in the past few years, a particularly dangerous strain has emerged. Wiping out the beneficial gut flora provides the pathogen with the perfect opportunity to set up shop. "When you have C. diff," says Karen, "it is like the lining of your colon is coming out of you. It's horrifying." Infection with C. diff is a direct consequence of waging chemical warfare against a community of bacteria when our real aim is just to target a few troublemakers. Not only is Clostridium an opportunist, but it is particularly difficult to eradicate from the body and from hospital surfaces. Some strains are antibiotic-resistant, and all can form spores — capsules capable of resisting chemical treatment and which can lie in wait for months for just the right conditions to go forth and multiply.
To combat Tim's infection, doctors prescribed a course of Flagyl (metronidazole). It seemed to do the trick. But as soon as the drug left his body, the C. diff returned. Next up was vancomycin. In many cases it is the one remaining weapon in the antimicrobial arsenal — a so-called drug of last resort. Tim was on and off "vanco" for over a year. But the resilient bug held its ground. After each ten-day course, C. diff returned. "Tim is in a wheelchair, on a ventilator," says Karen, "and he's tolerated the treatments and the ongoing C. diff. He's tough." But as the infection dragged on, Tim and Karen became more and more desperate for an actual cure.
Tim isn't alone. The bug causes nearly half a million infections in the United States alone, with nearly 30,000 patients succumbing within a month of diagnosis. Most affected are the elderly and the immunocompromised, but cases are increasingly occurring in the very young who have had no prior antibiotic exposure. In the industrialized world, C. diff is the leading cause of hospital-acquired diarrhea and colitis. The pathogen is on the rise — and we are to blame. When we destroy a functioning and diverse ecosystem, we cannot expect it to rebuild itself as it was. Yet that is what we do every time we use broad-spectrum antibiotics.
My own kids were prescribed round after round of bacteria-busting drugs for all sorts of common childhood ills. Even with some background in microbiology, I gave little thought to the havoc caused by those antibiotics; I just wanted my child cured (whether or not the antibiotics, which are not effective against viruses, did the trick). My son Sam slurped his first dose of sticky, sweet, bubblegum-flavored amoxicillin in 1994. He was six months old. On average, kids in the United States will have had twenty courses of antibiotics by the time they reach adulthood. "You must have felt awful, that first time you gave Sam antibiotics," commented an ecologist friend who teaches about evolution and resistance. His own two-year-old had recently become fussy and had begun pulling at his ears, a situation that would have sent me running to the pediatrician for a fix. "You basically annihilated his bacteria." But I didn't feel awful, I felt relieved.
Five years and several ear infections later, I was teaching medical microbiology to nursing students. It was a "get to know the enemy" kind of class. We examined one pathogen after another: its life history, how and where it attacked, how quickly it reproduced, its favorite conditions, and how a patient might respond to it — the signs of infection. One day the students had an opportunity to become acquainted with some of their own bacteria. They swabbed their skin, mouth, or whatever body bit they dared, inoculated petri dishes, and popped the dishes into an incubator set at body temperature. Days later, like a container of sour cream forgotten in the back of the refrigerator, the plates were covered with growth. Trillions of bacteria piled up in colonies initiated from single cells. There were glistening white dots; globular egg-yolk-like mounds; salmon-colored bubbles. Tiny studded colonies grew next to those with undulating edges or wrinkles. Others oozed across the plates like phlegm. No two plates were alike, each displaying an incredible diversity of microscopic life rendered visible by sheer numbers. Most of the bacteria on those plates wouldn't bother us, and many are beneficial. But some, given the opportunity, would make us sick. Even as the students marveled at the number of species growing on and within their bodies, no one thought to ask what happens when we poison the whole lot of the bacteria in an attempt to eradicate a few.
The bacteria on those plates represented a small fraction of the microbiota (bacteria, viruses, fungi, and other organisms) cohabiting the students. If we could take a teaspoon of liquid from our stomach — an organ once thought to be sterile — it would contain several thousand bacteria; if we were to do the same in our colon it would be more like 100 billion. Our gut — from intake to exit ramp — has a surface area equal to the floor space of an efficiency apartment, and it is coated with bacteria. Skin has the surface area of a playground's four-square court, though it too plays host to a universe of microscopic life. Our bodies support thousands of different bacterial species, and we carry around more bacterial cells than human cells. Most of those bacteria have shared their lives with humans for eons. Some pass from mother to child. The first time I fed Sam that amoxicillin, I didn't know that I would also be killing off bacteria that likely descended from my own microscopic flora. When he was born, he picked up my bacteria as he made his way from uterus to vagina and into the world, and he ingested still more as he latched on to my breast, hungry for mother's milk. Much of this natural microbial ecosystem was disrupted months later with a single teaspoon of pink liquid.
We pay little attention to these casualties, the harmless and beneficial bacteria lost alongside the pathogens. Plenty of us pull through just fine, eventually recolonized by survivors or other sources of bacteria. Some of us may benefit from probiotics, mixtures of living bacteria that are able to reseed the bacterial turf. And then there are others, like Tim, for whom the cost of disrupting this microbial ecosystem can be life-threatening. Roughly seventy years ago, we began using antibiotics on an industrial scale. Yet we are only now realizing the destruction we have wrought upon our own vital ecosystems. How can that be?
MicroGenetics
Within and upon our bodies, microbes outnumber our own cells. Just in terms of bacteria alone, according to a cell-for-cell recent estimate, our bodies are roughly one part human and one part bacterium. These microbial species intermingle, form biofilms, spit out toxins, have sex, and produce clone after clone. Our lives depend upon an invisible diversity of bacteria, fungi, protozoa, and viruses, but we know little of these microscopic allies. We knew practically nothing of them until the seventeenth century, when Dutch draper and scientist Antonie van Leeuwenhoek discovered "animalcules" under his microscopes. Fashioned from lenses originally intended to help distinguish good textiles from bad, Leeuwenhoek's microscopes introduced humanity to the bustling world of microbial life. It would be another 200 years until German physician Robert Koch developed his elegant "postulates" of disease causation, providing criteria to link a disease to a particular microbe, before medical microbiology finally hit its stride. Within a few years, diseases like anthrax and tuberculosis could be pinned on specific bacteria. Applying Koch's postulates required isolating and growing pure bacterial colonies. A drop of blood, saliva, or even soil was smeared across a nutrient-rich agar, and within a day or so pinprick colonies began to bloom as individual bacteria divided again and again until visible colonies emerged. Culturing and identifying bacteria is an art that has changed little since Koch's day. Walk into a microbial laboratory today and you are hit with the smell of agar and nutrient broth like a blast of concentrated chicken soup.
Until recently, our knowledge of microbes remained limited to those species we could capture and culture: an estimated 2 percent of bacterial life. But from that fraction we learned that bacteria have circular chromosomes (unlike plants, animals, and humans, whose chromosomes are linear), that fungal cells are much like our own, that chemicals excreted by bacteria and fungi can be used as antibiotics, and that bacteria can trade genetic information directly from one microbe to another. We also learned that all life — whether bacterium, barnacle, bed bug, or human being — shares a genetic code. Just four different molecules — guanine, cytosine, thymine, and adenine, denoted by G, C, T, and A — spell out the proteins that build our cells and provide directions for their production, in large part making us what we are.
Since the early decades of the twentieth century, scientists have understood that DNA was somehow responsible for carrying traits from one generation to the next. This realization led to a whirlwind of discovery. By mid-century, Rosalind Franklin, George Watson, and Francis Crick revealed the very structure of DNA: the now-familiar winding ladder of paired bases known as the double helix. A few years later, in 1957, Crick proposed that the genes encoded by DNA directed the synthesis of proteins by controlling the order in which amino acids link together. Within the next two decades, scientists were learning how to cut DNA apart and paste it together — the first steps toward genetic engineering. Yet, as exciting as the advances were, sequencing DNA, or determining the precise order of those bases, remained a tedious process. Scientists could read enough code to sequence the amino acid building blocks of proteins, but decoding a simple virus remained beyond reach. Scientists were limited to browsing the children's section of the genome library while dreaming of Tolstoy and Proust. But now, new technology is providing access to almost every book in life's library, augmenting what we know about everything from genetics to evolution, ecology, and microbiology. And this knowledge is fueling a revolution that promises new solutions to age-old problems, both in the hospital and on the farm.
The key to genetic speed-reading began with advances by teams led by Walter Gilbert and graduate student Allan Maxam at Harvard University, and Fred Sanger at Cambridge University in England. Working nearly simultaneously, both groups made breakthrough discoveries that, relatively rapidly, allowed scientists to bring order to life's A's, T's, G's, and C's. (The work garnered Gilbert and Sanger a Nobel in 1980; it was Sanger's second.) Though their approaches differed, their efforts kick-started the present era of genetic sequencing. Genes, which may run as long as 10,000 bases, could finally be deciphered in a reasonable amount of time, enabling scientists to read the paragraphs of life. But still, the full story remained beyond their reach. Pages were out of order. And much of the "literature" seemed garbled: a tangle of genetic gibberish that scientists labeled "junk DNA." Progress was still relatively slow. But meanwhile, another technology that would change the world was also developing rapidly: computer science.
In the 1970s, when Gilbert and Sanger were working out their techniques, each bit of information had to be transferred from laboratory notebook to computer punch cards and then typed up for publication while scientists spent days and nights waiting for results. It was tedious and expensive. Even so, DNA sequences were proliferating at such a fast clip that the National Institutes of Health (cosponsored by various health institutes including the National Cancer Institute, along with the Departments of Energy and Defense) created GenBank: the world's first computerized database for the code of life. Over the course of just a few years, as ease of sequencing combined with increased access to computing power, and as punch cards gave way to magnetic tapes, the size of the database grew more than twenty-fold. By 1985, GenBank held around 5,700 sequences — decoded stretches of DNA describing bits of viruses, plants, and animals that constitute some of the first genetic representations of life on earth. At that time there were 570 bacterial sequences, or a total of nearly 700,000 base-pairs (pairs of the letters G, C, T, and A). These were bits of sequenced DNA from bacteria, but not wholly sequenced bacteria. Despite all the decoding and reporting, gaps remained. As the twentieth century was coming to a close, no living organism had been fully sequenced.
Hemophilus influenza — a pneumonia-causing microbe possibly similar to the bug that forced Tim onto antibiotics — would be the first organism fully sequenced. Craig Venter and others cracked its genetic code in 1995, translating the 2,000 protein-encoding genes and nearly 2 million base-pairs. It would be the first "fully translated" book in life's genomic library. But five years earlier, an even more audacious project had begun: the Human Genome Project, one of the largest global biological collaboratives at the time. Initiated by the US Department of Energy, the National Institutes of Health, and international collaborators, the project had been creeping along. The slow pace, combined with differences in opinion about methodologies, frustrated Venter, who was fast becoming a sequencing revolutionary. Pushing the pace of discovery, Venter founded Celera, a privately funded company. In 2001, the Human Genome Project and Celera published simultaneously in separate journals a first "draft" of the human genome. Humans had finally cracked their own code.
Sequencing the human genome pushed genetic sequencing technology from a sluggish, labor-intensive, and expensive prospect to an automated process where, for pennies, tens of thousands of DNA base-pairs can be sequenced in a few hours or even minutes. "What used to take thousands of culture plates, now takes one tube. For five bucks, 100 different populations are revealed," says one microbial ecologist who for decades has isolated and cultured soil microbes one population at a time. Much of the publicly available genetic data is deposited into GenBank, which now holds information for hundreds of thousands of species. It is the place to go if you're looking for a sequence or have one to report. The vast majority belong to microbes: bacteria, viruses, archaea (bacteria-like organisms). Sequences for tens of thousands of bacterial species (some genomes more complete than others) are now available.
For decades we have known that we are more than just an organized collection of animal cells. But new sequencing technologies are empowering microbiologists to seek out life beyond the limits of the agar, revealing complex microbiomes in humans, soils, the deep sea, extreme environments, and elsewhere. The library is open, with billions of books to be read. But there are stark differences between reading and understanding. We may be able to speed-read genomes, but the attributes of each newly discovered virus or fungi or bacterium remain to be teased out of masses of data. What fuels their growth? With whom do they associate? Under what conditions might they become pathogenic — or beneficial? Metagenomics, the sequencing of all the genomic DNA in a community, can help.
By providing unprecedented insights into microbial communities, metagenomics is changing how we think about life on earth and elsewhere. Focusing on the single microbe is no longer sufficient. Just as humans live in neighborhoods that are defined neither by the delinquent who steals change from unlocked cars nor by the generosity of the neighbor who shares her homegrown tomatoes, but rather by the rich diversity therein, so too microbes exist in complex communities. The more we know about who does what, the better. Metagenomics not only opens the door but may someday provide insights into what makes a community hum, and what may rip it apart. It is the next step in the genetic technology revolution, and it is already shaking things up in a big way. Metagenomic technology "gives us the ability to explore the microbial world in much higher resolution," says Jack Gilbert, a microbial ecologist at the University of Chicago and founder of the Earth Microbiome Project. Gilbert explains, "It's like looking at the stock market. If we only had information about the market at the end of each day we'd have a low-resolution understanding of how things change. It's all about fluid dynamics in space, time, metabolism, and functional composition." Metagenomics is enabling us to capture ecology in motion, both in our bodies and in the world at large. That is a powerful thing because we are now realizing that, despite all their benefits, our antibiotics and antimicrobials have their downside. Wholesale destruction of bacteria, whether in the human body or the agricultural field, can be profoundly disruptive.
(Continues...)
Excerpted from Natural Defense by Emily Monosson. Copyright © 2017 Emily Monosson. Excerpted by permission of ISLAND PRESS.
All rights reserved. No part of this excerpt may be reproduced or reprinted without permission in writing from the publisher.
Excerpts are provided by Dial-A-Book Inc. solely for the personal use of visitors to this web site.
Table of Contents
PrefaceChapter 1. Natural Allies: Our Bacterial Protectors
Chapter 2. Natural Allies: How the Smallest of All Can Help Feed the World
Chapter 3. The Enemy of Our Enemy is Our Friend: Infecting the Infection
Chapter 4. The Enemy of Our Enemy is Our Friend: Replacing Pesticides with Nature’s Chemistry
Chapter 5. Provocation: GMOs and the Science of Protecting Plants, Naturally
Chapter 6. Provocation: The Next Generation of Vaccines
Chapter 7. Know Thine Enemy: Diagnosing Crop Disease Goes High Tech
Chapter 8. Know Thine Enemy: The Future of Diagnostics
Epilogue