The Great Influenza (26 page)

But the phenomenon is complex. The increase in killing efficiency does not continue indefinitely. If a pathogen kills too efficiently, it will run out of hosts and destroy itself. Eventually its virulence stabilizes and even recedes. Especially when jumping species, it can become less dangerous instead of more dangerous. This happens with the Ebola virus, which does not normally infect humans. Initially Ebola has extremely high mortality rates, but after it goes through several generations of human passages, it becomes far milder and not particularly threatening.

So passage can also weaken a pathogen. When Pasteur was trying to weaken or, to use his word, 'attenuate' the pathogen of swine erysipelas, he succeeded only by passing it through rabbits. As the bacteria adapted to rabbits, it lost some of its ability to grow in swine. He then inoculated pigs with the rabbit-bred bacteria, and their immune systems easily destroyed it. Since the antigens on the weak strain were the same as those on normal strains, the pigs' immune systems learned to recognize (and destroy) normal strains as well. They became immune to the disease. By 1894, veterinarians used Pasteur's vaccine to protect 100,000 pigs in France; in Hungary over 1 million pigs were vaccinated.

The influenza virus is no different in its behavior from any other pathogen, and it faces the same evolutionary pressures. When the 1918 virus jumped from animals to people and began to spread, it may have suffered a shock of its own as it adapted to a new species. Although it always retained hints of virulence, this shock may well have weakened it, making it relatively mild; then, as it became better and better at infecting its new host, it turned lethal.

Macfarlane Burnet won his Nobel Prize for work on the immune system, but he spent the bulk of his career investigating influenza, including its epidemiological history. He noted an occasion when passage turned a harmless influenza virus into a lethal one. A ship carrying people sick with influenza visited an isolated settlement in east Greenland. Two months after the ship's departure, a severe influenza epidemic erupted, with a 10 percent mortality rate; 10 percent of those with the disease died. Burnet was 'reasonably certain that the epidemic was primarily virus influenza' and concluded that the virus passed through several generations (he estimated fifteen or twenty human passages) in mild form before it adapted to the new population and became virulent and lethal.

In his study of the 1918 pandemic, Burnet concluded that by late April 1918 'the essential character of the new strain seems to have been established.' He continued, 'We must suppose that the ancestral virus responsible for the spring epidemics in the United States passaged and mutated' . The process continued in France.'

Lethality lay within the genetic possibilities of this virus; this particular mutant swarm always had the potential to be more pestilential than other influenza viruses. Passage was sharpening its ferocity. As it smoldered in the roots, adapting itself, becoming increasingly efficient at reproducing itself in humans, passage was forging a killing inferno.

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On June 30, 1918, the British freighter
City of Exeter
docked at Philadelphia after a brief hold at a maritime quarantine station. She was laced with deadly disease, but Rupert Blue, the civilian surgeon general and head of the U.S. Public Health Service, had issued no instructions to the maritime service to hold influenza-ridden ships. So she was released.

Nonetheless, the condition of the crew was so frightening that the British consul had arranged in advance for the ship to be met at a wharf empty of anything except ambulances whose drivers wore surgical masks. Dozens of crew members 'in a desperate condition' were taken immediately to Pennsylvania Hospital where, as a precaution against infectious disease, a ward was sealed off for them. Dr. Alfred Stengel, who had initially lost a competition for a prestigious professorship at the University of Pennsylvania to Simon Flexner but who did get it when Flexner left, had gone on to become president of the American College of Physicians. An expert on infectious diseases, he personally oversaw the sailors' care. Despite Stengel's old rivalry with Flexner, he even called in Flexner's protegé Paul Lewis for advice. Nonetheless, one after another, more crew members died.

They seemed to die of pneumonia, but it was a pneumonia accompanied, according to a Penn medical student, by strange symptoms, including bleeding from the nose. A report noted, 'The opinion was reached that they had influenza.'

In 1918 all infectious disease was frightening. Americans had already learned that 'Spanish influenza' was serious enough that it had slowed the German offensive. Rumors now unsettled the city that these deaths too came from Spanish influenza. Those in control of the war's propaganda machine wanted nothing printed that could hurt morale. Two physicians stated flatly to newspapers that the men had not died of influenza. They were lying.

The disease did not spread. The brief quarantine had held the ship long enough that the crew members were no longer contagious when the ship docked. This particular virulent virus, finding no fresh fuel, had burned itself out. The city had dodged a bullet.

By now the virus had undergone numerous passages through humans. Even while medical journals were commenting on the mild nature of the disease, all over the world hints of a malevolent outbreak were appearing.

In London the week of July 8, 287 people died of influenzal pneumonia, and 126 died in Birmingham. A physician who performed several autopsies noted, 'The lung lesions, complex or variable, struck one as being quite different in character to anything one had met with at all commonly in the thousands of autopsies one has performed during the last twenty years. It was not like the common broncho-pneumonia of ordinary years.'

The U.S. Public Health Service's weekly
Public Health Reports
finally took notice, at last deeming the disease serious enough to warn the country's public health officials that 'an outbreak of epidemic influenza' has been reported at Birmingham, England. The disease is stated to be spreading rapidly and to be present in other locations.' And it warned of 'fatal cases.'

Earlier some physicians had insisted that the disease was not influenza because it was too mild. Now others also began to doubt that this disease was influenza - but this time because it seemed too deadly. Lack of oxygen was sometimes so severe that victims were becoming cyanotic - part or all of their bodies were turning blue, occasionally a very dark blue.

On August 3 a U.S. Navy intelligence officer received a telegram that he quickly stamped
SECRET
and
CONFIDENTIAL.
Noting that his source was 'reliable,' he reported, 'I am confidentially advised' that the disease now epidemic throughout Switzerland is what is commonly known as the black plague, although it is designated as Spanish sickness and grip.'

Photographic Insert

1. William Henry Welch, the single most powerful individual in the history of American medicine and one of the most knowledgeable. A wary colleague said he could 'transform men's lives almost with the flick of a wrist.' When Welch first observed autopsies of influenza victims, he worried, 'This must be some new kind of infection or plague.'

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2. Welch and John D. Rockefeller Jr. (on the right) together created the Rockefeller Institute for Medical Research (now Rockefeller University), arguably the best scientific research institution in the world. Simon Flexner (on the left), a Welch protegé, was the institute's first head; he once said that no one could run an institution unless he had the capacity to be cruel.

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3. Flexner brought the mortality rate for the most common bacterial meningitis down to 18 percent in 1910 without antibiotics. Today, with antibiotics, the mortality rate is 25 percent.

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4. A dense jungle-like growth of epithelial cells covers a healthy mouse trachea.

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5. Only seventy-two hours after infection the influenza virus transforms the same area into a barren and lifeless desert. White blood cells are patrolling the area, too late.

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