Allies and Enemies: How the World Depends on Bacteria (11 page)

Soper had all but called Mary Mallon an evil genius and put equal

blame on upper class women who brought people like Mary into their

homes. He irrationally likened them all to murderers. In 1928, he told the
New York World
, “She knew that when she cooked she killed people, and yet she deliberately sought employment as a cook.” In fact, Mary Mallon never believed she had made anyone sick. Soper fought the prevailing beliefs of the day to stop the Typhoid Mary outbreaks. He also spearheaded the inspection of New York’s sewers, water supply, and garbage pickup and became an advocate for good personal hygiene and community sanitation as the best ways to break

the transmission of pathogens.

I thought of Mary Mallon in 1998 at a San Francisco crafts festi—

val. Waiting in the lunch line, I noticed a young woman behind the

salad-mixing station. During a lull in the action, she fished around in her mouth with her fingers and cleaned her teeth. She then plunged

her unwashed, gloveless hands into a trough of lettuce, mixing the leaves and scooping out salad. I stepped out of line and said to her,

“Do you realize you just contaminated all that salad with your dirty

hands?” She looked confused at first then glanced at the lettuce.

“Good,” I thought, “I’ve taught someone about hygiene and averted a

possible health disaster.”

In 1909, New York quarantined Mallon on an island in the East

River. Miserable, angry, and convinced she had nothing to do with typhoid, she lamented her role as “a peep show for everybody.” After

her release Mary changed her name and began cooking again, this time at Sloane Maternity Hospital. By 1915, she had caused 25 new

cases of typhoid until a health inspector spotted her in the hospital

kitchen. Police took Mary back to the island where she died in 1938.

Unlike other pathogens,
S. typhi
lacks multiple strains of varying virulence; the species is fairly uniform the world over.
S. typhi ’s survival rests on asymptomatic carriers who efficiently spread the pathogen through a population. Research has not yet uncovered all of the secrets of typhoid susceptibility in those who are asymptomatic.

In carriers the bacteria multiply in the gallbladder, bile duct, and intestines, and then spread in drinking water and food contaminated

with miniscule bits of fecal matter, a more common occurrence than

most people think. I had no more success in convincing the salad

chapter 2 · bacteria in history

57

vendor to change her hygiene habits than Soper had with Mallon because no one wants to believe they disseminate contamination.

Because of the prevalence of fecal bacteria everywhere, people

would be wise to take a bacteriocentric view of the world, “seeing”

bacteria on the places they exist even though they remain invisible.

Suspicious foods, dirty floors, or murky water shout the presence of

bacteria as do people who avoid washing their hands. In the 1970s,

bacteriocentricity helped solve one of modern epidemiology’s most puzzling outbreaks.

Joseph McDade

Mid-July in Philadelphia is sticky, sweaty, and heavy with odors that

seem to seep from the concrete. In 1976, the 70-year-old Bellevue Stratford on South Broad Street opened its doors to 4,000 World War

II Legionnaires in town for their annual convention. An influenza outbreak that had killed a soldier in nearby Fort Dix, New Jersey, that

summer put many of the visitors on edge, especially because the virus

resembled one that took 40 million lives in 1918 to 1919, the worst single flu outbreak in history. The Legionnaires and hotel staff likely took extra care washing their hands and staying on guard for the sounds of sneezing or coughing. But trouble came from a different direction.

The Bellevue Stratford’s air conditioning system had developed a

thick biofilm in the condensation-wetted distribution lines. There, amoeba, a type of protozoa, multiplied in the moist habitat they need

for survival, feeding on the biofilm. Hidden inside the amoeba lived a

bacterium that most microbiologists did not know existed. Because of

the biofilm, the air conditioning vents began to emit moisture droplets filled with microbes.

No one knew they were inhaling contaminated air. Hotel guests

and even people who had strolled past the building’s open doors became congested and weak, developed muscle pain and headaches,

and suffered with diarrhea. The dreaded flu virus obviously had returned and with it, near panic—someone blamed the communists.

Congress ordered into place an emergency vaccination program, but

the year closed with few weapons against the mysterious disease.

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allies and enemies

During the holidays, Joseph McDade from the Centers for Disease Control and Prevention (CDC) stared into his microscope

searching blood samples from the hotel’s guests for
Rickettsia bacteria. Rickettsia bacilli would be easy to miss because it lives only inside other cells, such as human cells. Weary with eyestrain he went to a holiday celebration, but for McDade, bacteria were more com—pelling than office parties. He returned to his laboratory and re-examined the Legionnaires’ samples. In the early hours he spotted a cluster of bacilli inside white blood cells. The bacteria were not stubby, short rods of 1
ì m like Rickettsia, however, but long thin rods stretching to 10
ì m or more.

McDade had found a new species, Legionella pneumophila. The

CDC unraveled the bacteria’s pathology. L. pneumophila enters the lungs and then infects the bloodstream. The immune system releases cells called macrophages for the specific purpose of destroying infectious agents such as bacteria, but like Rickettsia, Legionella is a “stealth pathogen.” L. pneumophila slips inside macrophages and multiplies in the phage’s cytoplasm. A new generation of cells bursts

free and continues the infection cycle. Microbiologists had noted bacteria that fit L. pneumophila’s description years earlier, but the microbe’s finicky growth requirements made laboratory studies almost impossible.

Clinical microbiologists deal with a short list of stealth pathogens

in addition to Rickettsia and Legionella, including the foodborne pathogens Listeria monocytogenes, Shigella flexeri, and Salmonella enterica, and mycoplasmas. L. monocytogenes invades the epithelial cells lining the digestive tract, and when in the bloodstream is one of the few bacteria that cross the blood-brain barrier. Severe cases of lis-teriosis therefore damage the central nervous system. Salmonella and Shigella usually stay in the digestive tract.

On the front

Microbes have played a part in war before the Tartars deployed their

unique bioweapon. Prior to the introduction of antibiotics, minor battlefield injuries led to about half of all wartime deaths. Marginal food, lack of sleep, and emotional stress reduced soldiers’ ability to fight chapter 2 · bacteria in history

59

infection. Without treatment of infected wounds, pathogens could enter the bloodstream and multiply—a condition called sepsis—and

then infect major organs. Some pathogens stay at the wound site and

cause severe infection there. Badly injured skin contains oxygen-free

pockets in the tissue, which promotes the growth of anaerobes such

as
Clostridium perfringens
, the cause of gas gangrene. Before World War II small scratches caked with soil and left untreated presented the risk of amputation or death.

Virulence factors aid the infection process. Some bacteria rely on

only one approach, such as
Mycoplasma
that produces hydrogen per-oxide and ammonia, both toxic to the body’s cells. After the two compounds damage cells lining the respiratory tract, Mycoplasma enters lung tissue.
Staphylococcus aureus , by contrast, uses a battery of weapons: · Coagulase enzyme clots the blood surrounding a wound and

protects the bacteria from the body’s immune defenses.

· Nuclease enzyme breaks up exudates in the wound and thus

helps the bacteria’s mobility.

· Hemolysins lyse red blood cells, causing anemia and weakened

body defenses.

· Hyaluronidase enzyme degrades the binding material between

human cells to aid passage of the pathogen throughout the

body.

· Protein A binds the body’s antibodies and renders them

inactive.

· Streptokinase enzyme activates a series of steps in blood clot destruction, allowing the bacteria to escape a clotted area.

Two champions of proper medical care died a few years before

the First World War. British nurse Florence Nightingale called for reforms in treating combat injuries. During her service in the Crimean War, she reported on the diseases, poor food, and unsanitary conditions in medical hospitals. Her 1,000-page report compiled in 1858 convinced her superiors that the British Army was needlessly losing soldiers to treatable injuries. During the same period in Britain, surgeon Joseph Lister insisted that surgeries required sterile 60

allies and enemies

conditions and wounds must be kept clean with antiseptics. Lister used carbolic acid as an antiseptic; several years would pass before less irritating chemicals came into use.

Sterility and antiseptics were new ideas when war began in 1914.

Not all surgeons wanted to put chemicals on patients’ skin, and they

initially resisted using antiseptics. A second, more revolutionary, defense against infection soon surfaced. Microbiologist Felix

d’Herelle had tried to fight a locust outbreak by infecting the insects with bacteria. He presumed that if a similar agent attacked pathogenic bacteria, it would fight infectious disease. d’Herelle knew that some microbiologists had discovered a substance in their bacterial cultures that infected and killed other bacteria. With little idea of the material’s identity, d’Herelle began collecting liquid medium from affected cultures. By 1917, he was using it to cure hundreds of cases of dysentery by injecting patients with his “antagonistic microbe.”

Not until 1939 with the advent of electron microscopes did microbiology learn of bacteriophages, viruses that infect only bacteria. The

treatment called phage therapy would be superseded by antibiotics in

the next decade, but for a short period in history phages played the

part of the magic bullet.

The consequences of war, upheaval of home life, and the creation

of mass refugee migrations hampered sanitation and personal

hygiene. The common body lice
Pediculus humanus
infested almost everyone in World War I. The lice carried the typhus bacterium Rickettsia prowazekii. This microbe behaves like a virus by living as a parasite inside other cells. The lice ingested R. prowazekii when they bit an infected person and after an incubation of six days they became infective to others. Unlike the plague, which spread via flea bites, typhus spread when lice defecated on the skin and the bacteria entered the body through a wound.

Typhus would blanket Europe and become an epidemic second

only to the Black Death in fatalities. In Serbia, 20 percent of the population contracted typhus and 60 to 70 percent of those people died.

Disease became so devastating to Austria, the Balkans, Russia, and Greece that the Central Powers delayed some maneuvers for fear of

wiping out their own armies. At the close of the war, a four-year epidemic struck Russia and would kill half of the 20 million people who

had been infected with typhus.

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61

Many in the German army that invaded Poland to start World

War II carried memories of the typhus outbreaks. Entering the third

year of occupation, Polish physicians Eugene Lazowski and Stanislaw

Matulewicz devised a way to stop some of the carnage and deporta—

tions to work camps. They knew that the
Proteus
strain OX19 looked similar to
R. prowazekii to the body’s immune system. They thus began injecting healthy residents of the town of Rozvadow with killed OX19 cells. This ersatz vaccine induced the production of antibodies

against the typhus bacterium. Lazowski and Matulewicz had created a

fake typhus epidemic.

The Germans may have had suspicions of the isolated outbreak.

A German medical team arrived in Rozvadow in 1942 to assess the

situation, but their doctors so feared infection that they skipped giving physical exams; they collected blood samples and hurried back to

Berlin. The antibodies in the samples convinced the German army to