Allies and Enemies: How the World Depends on Bacteria (15 page)

Medical microbiologist Stuart Levy has warned that overzealous

cleaning with disinfectants merely increases the opportunity for bacteria to develop resistance. Might disinfectant-and antibiotic-resistant superbugs share their best defenses with each other by exchanging genes? Such sharing seems implausible because the chemicals in cleaning products (bleach, quaternary ammonium compounds) differ from large antibiotic molecules. Yet bacteria eject these chemicals much the same way they expel antibiotics: They use a pumplike mechanism. The term “pump” can be misleading. Bacterial

antibiotic efflux pumps use transporters inside the cell. When an

antibiotic enters the cell through a receptive pore in the bacterium’s

outer membrane, the transporter moves toward the antibiotic and locks onto it. A bacterial protein (called a fusion protein) then recognizes the transporter now reconfigured by the antibiotic and swiftly carries the complex out through another pore. As long as bacteria have the nutrients needed to build transporters and fusion proteins, they can resist antibiotics by excreting them. Because the transporter

must recognize all or part of the antibiotic for this system to work, chemists try to construct unique antibiotics, and biologists seek new natural substances that will throw a monkey wrench into the antibiotic efflux pump. If molecular biologists discover that the chemical

pump and the antibiotic pump are one and the same, a new super—

superbug may be around the corner, able to resist disinfectants as well as it resists antibiotics. No one yet knows which side will win the race to perfect resistance or a perfect drug.

Surely the rise in antibiotic resistance has made a difference to

the bacteria that have always lived in harmony with their host. When

the body’s good bacteria cause infection, they do so because circumstances change to invite them in. These circumstances usually have to

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allies and enemies

do with a weakened or immature immune system, mainly in groups

of people considered “high-risk” individuals:

· Chronic, debilitating disease

· Drug or alcohol abuse

· Poor nutrition

· Pregnancy

· Old age

· Young age (infants and children under 12 years)

· HIV/AIDS

· Organ transplantation

· Cancer chemotherapy or radiation.

Each of the stressors listed here increases the dangerous cycle of

antibiotic-resistance causing infection that requires antibiotics, leading to more resistance. One of the prevalent bacteria on the body, Staphylococcus aureus, has already become one of the most multidrug-resistant microbes known. Because S. aureus is both a health risk and a prominent member of the body’s normal flora, good personal hygiene usually trumps antibiotics, disinfectants, and other weapons from the antimicrobial armory (see Figure 3.2).

Drug companies have for the past decade introduced fewer and

fewer new antibiotics. Because “all the easy antibiotics have been discovered,” research into new natural or synthesized compounds has grown more difficult and more expensive. Companies that once led in antibiotic production have now decreased the money they spend on

new antibiotic research. The combination of skyrocketing research costs and patents that limit the profit-earning future of drugs has left doctors with a shrinking armamentarium against infectious disease.

Entrepreneurs have tried colloidal silver, copper, zinc, magnesium, medicinal herbs (cloves, echinacea, garlic, oregano, turmeric, and thyme), citrus oils, tea tree extracts, and grapefruit seed extract. I have tested most of these substances on laboratory cultures, and they do possess antibacterial activity. But inhibiting bacteria in a laboratory is much easier than stopping bacteria in nature or in the body. In a laboratory, bacteria are at their most vulnerable to damage because

antibiotics work best on rapidly multiplying cells. In nature, bacteria

chapter 3 · “humans defeat germs!” (but not for long)

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turn on defensive mechanisms and slow their growth. Both actions take away some of the power of antimicrobials.

Figure 3.2 Court at No. 24 Baxter Street, ca. 1890. Photographer Jacob Riis captured life in one of New York City’s tenement slums. Similar living conditions exist today worldwide. Poor nutrition and faulty hygiene have contributed to germ transmission throughout history. (Courtesy of Museum of the City of New York, Jacob A. Riis Collection) A new generation of antibiotics may yet emerge. If they do, they

will probably come from the ocean. In the past decade scientists have

recovered marine bacteria, algae, sponges, coral, and microscopic invertebrates that produce novel antibiotics. The new marine antibiotics might soon replace current antibiotics that are losing the battle against Staph infections, gonorrhea, strep, tuberculosis, and nosocomial infections.

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allies and enemies

The history of medicine

2000 BCE—Here, eat this root.

1000 CE—That root is heathen. Here, say this prayer.

1850 CE—That prayer is superstition. Here, drink this potion.

1920 CE—That potion is snake oil. Here, swallow this pill.

1945 CE—That pill is ineffective. Here, take this penicillin.

1955 CE—Oops...Bugs mutated. Here, take this tetracycline.

1960-1999 CE—Thirty-nine more “oops.” Here, take this more

powerful antibiotic.

2000 CE—The bugs have won! Here, eat this root.

—Anonymous (2000)

4

Bacteria in popular culture

Bacteria and viruses are silent, invisible, and multiply inside the body.

Sometimes they mutate; sometimes they kill. No one could blame a

novelist for making microbes into antagonists for a hero to overcome.

Bacteria have for decades infiltrated popular culture, and the arts offer a surprising number of lessons on disease as well as Earth ecology. As important, the arts have communicated people’s fears and conceptions of bacteria. Misconceptions about bacteria in movies and novels reveal how people view germs. The perceptions of bacteria give insight into the effects bacteria have had on society and events in the past.

Popular culture, regardless of the century, has understandably

made more of deadly pathogens and given less credit to the environmental microbes that make the planet livable. The exaggerations and

falsehoods regarding pathogens in the arts enlighten us to the perceptions of bacteria that have persisted through the years.

Bacteria and art

Europe’s Black Plague influenced art and mirrored changing attitudes toward disease and death. Early 14th-century paintings before the plague depicted serene country life, the hunt, and the upper classes. The church often influenced the work—Heaven and Hell received almost equal focus—but artists seldom made death appear

violent or cruel. When the Black Death tightened its grip on upper

and working classes alike, artwork reflected the somber mood. As the

plague and its toll continued with no end in sight, European artists

conveyed only the tragic and painful outcomes society faced. Heaven

and Hell no longer shared equal billing; the jaws of Hell seemed to

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allies and enemies

gape everywhere. Europe’s 14th century painting in fact displays a multitude of deathbed scenes.

Hidden behind the images was an oppressive darkness that

Y. pestis
brought to the continent. The plague microbe had developed no special traits that allowed it to emerge with regularity and unhin—dered in Europe for five centuries. Crowded cities, poverty, misinfor—

mation, and perhaps too much faith in a powerless clergy and medical

profession made the plague into the scourge that changed history.

These same factors, more or less, exist today.

The Black Death also affected artists’ lives in an unexpected way.

Because the disease interrupted invasions on Europe by Barbarian tribes, small and large European towns had time between epidemics

to develop creative pursuits. Artists, skilled artisans, and architects became proficient in their crafts, and they rose to professional stature and enhanced level of respect in society.

No one at the time of the Black Death had a notion as to its cause.

Antoni van Leeuwenhoek would not view bacteria in a microscope for another three centuries. Historians gleaned from artwork the mis—

ery that
Y. pestis
caused. Paintings showed pale, weak subjects fallen to the ground where they had stood. Often crowds of the sick and dying shuffled past the corpses. Almost every account of the plagues from Justinian’s through the Great Plague of London in 1665

described bodies piling up in the streets. These accounts and the art

of the period captured not only the despair of the surviving but also

their challenges. Paintings and writings described townspeople haul—

ing bodies to distant funeral pyres by handling the dead with long sticks or poles, trying to avoid too-close contact with the contagion.

Bacteria in the performing arts

A familiar rhyme thought to have originated during London’s Great

Plague in 1665 has developed different versions in various languages

and cultures over time, but all convey the same message:

Ring around the rosey,

A pocketful of posies.

Ashes, ashes.

We all fall down!

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A microbiologist living in the Middle Ages but armed with today’s

knowledge of bubonic plague might revise the rhyme to a less lyrical:

Red rash encircling the bulbous swelling of the skin,

A supply of medicinal herbs.

Burn the deceased in funeral pyres.

We all die from the plague sooner or later.

The plague struck down its victims within hours. A healthy person infected with
Y. pestis
in the morning could be dead by nightfall.

But plague epidemics grew less frequent between the 15th and 19th

centuries—the reason for this has not been fully explained. As the plague disappeared, another disease haunted society, and thus

entered the arts. Tuberculosis (TB), known as consumption into the

early 1900s, is thought to be humanity’s oldest disease. The lengthy

and debilitating illness causes a slow decline in many of the people

who do not receive treatment.
M. tuberculosis
takes 24 hours to divide in two, and TB thus develops very slowly in an infected person.

M. tuberculosis
’s curved rods reach no more than 4
ì
m long and

0.3
ì
m wide. These stringy bacteria travel through the air in moisture

droplets expelled by the cough of an infected person. The droplets called bioaerosols can drift in the air for several feet before being inhaled by a new host. Once inhaled, as few as five M. tuberculosis cells begin an infection by infiltrating the air sacs, or alveoli, of the lungs. The host’s immune system responds to the presence of the foreign entity by sending macrophage cells to the site of infection. The macrophages engulf
M. tuberculosis
as they do all other foreign matter with the intent of decomposing it. But macrophages cannot kill M. tuberculosis . Some of the bacteria hide inside the macrophage and ride with it through the lymph system to other organs. Other M. tuberculosis cells stay in the lungs and multiply. The intensifying infection prompts the immune system to double its efforts, and so an increased inflammatory reaction develops in an effort to kill the infection. As a result, the body’s immune system causes more harm than the bacterium.