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Only a trickle of people moved back and forth between Haskell and Funston, but a river of soldiers moved between Funston, other army bases, and France. Two weeks after the first case at Funston, on March 18, influenza surfaced at both Camps Forrest and Greenleaf in Georgia; 10 percent of the forces at both camps would report sick. Then, like falling dominoes, other camps erupted with influenza. In total, twenty-four of the thirty-six largest army camps experienced an influenza outbreak that spring. Thirty of the fifty largest cities in the country, most of them adjacent to military facilities, also suffered an April spike in 'excess mortality' from influenza, although that did not become clear except in hindsight.
At first it seemed like nothing to worry about, nothing like the measles outbreak with its pneumonic complications. Only in Haskell had influenza been severe. The only thing at all worrisome was that the disease was moving.
As Macfarlane Burnet later said, 'It is convenient to follow the story of influenza at this period mainly in regard to the army experiences in America and Europe.'
After the pandemic, outstanding epidemiologists searched military and civilian health records in the United States for any signs of uncommon influenza activity prior to the Funston outbreak. They found none. (The warning published about Haskell misstated the date, incorrectly putting it after Funston.) In France there had been some localized flare-ups of influenza during the winter, but they did not seem to spread and behaved like endemic, not epidemic, disease.
The first unusual outbreaks in Europe occurred in Brest in early April, where American troops disembarked. In Brest itself a French naval command was suddenly crippled. And from Brest the disease did spread, and quickly, in concentric circles.
Still, although many got sick, these outbreaks were, like those in the United States, generally mild. Troops were temporarily debilitated, then recovered. For example, an epidemic erupted near Chaumont involving U.S. troops and civilians: of 172 marines guarding headquarters there, most fell ill and fifty-four required hospitalization - but all of them recovered.
The first appearance in the French army came April 10. Influenza struck Paris in late April, and at about the same time the disease reached Italy. In the British army the first cases occurred in mid-April, then the disease exploded. In May the British First Army alone suffered 36,473 hospital admissions and tens of thousands of less serious cases. In the Second Army, a British report noted, 'At the end of May it appeared with great violence' . The numbers affected were very great' . A brigade of artillery had one-third of its strength taken ill within forty-eight hours, and in the brigade ammunition column only fifteen men were available for duty one day out of a strength of 145.' The British Third Army suffered equally. In June troops returning from the Continent introduced the disease into England.
But again the complications were few and nearly all the troops recovered. The only serious concern (and it was serious indeed) was that the disease would undermine the troops' ability to fight.
That seemed the case in the German army. German troops in the field suffered sharp outbreaks beginning in late April. By then German commander Erich von Ludendorff had also begun his last great offensive - Germany's last real chance to win the war.
The German offensive made great initial gains. From near the front lines Harvey Cushing, Halsted's protegé, recorded the German advance in his diary: 'They have broken clean through' .''The general situation is far from reassuring' . 11 P.M. The flow of men from the retreating Front keeps up.' 'Haig's most disquieting Order to the Army' ends as follows: 'With our backs to the wall, and believing in the justice of our cause, each one of us must fight to the end. The safety of our homes and the freedom of mankind depend alike upon the conduct of every one of us at this moment.''
But then Cushing noted, 'The expected third phase of the great German offensive gets put off from day to day.' 'When the next offensive will come off no one knows. It probably won't be long postponed. I gather that the epidemic of grippe which hit us rather hard in Flanders also hit the Boche worse, and this may have caused the delay.'
Ludendorff himself blamed influenza for the loss of initiative and the ultimate failure of the offensive: 'It was a grievous business having to listen every morning to the chiefs of staff's recital of the number of influenza cases, and their complaints about the weakness of their troops.'
Influenza may have crippled his attack, stripped his forces of fighting men. Or Ludendorff may have simply seized upon it as an excuse. British, French, and American troops were all suffering from the disease themselves, and Ludendorff was not one to accept blame when he could place it elsewhere.
In the meantime, in Spain the virus picked up its name.
Spain actually had few cases before May, but the country was neutral during the war. That meant the government did not censor the press, and unlike French, German, and British newspapers (which printed nothing negative, nothing that might hurt morale) Spanish papers were filled with reports of the disease, especially when King Alphonse XIII fell seriously ill.
The disease soon became known as 'Spanish influenza' or 'Spanish flu,' very likely because only Spanish newspapers were publishing accounts of the spread of the disease that were picked up in other countries.
It struck Portugal, then Greece. In June and July, death rates across England, Scotland, and Wales surged. In June, Germany suffered initial sporadic outbreaks, and then a full-fledged epidemic swept across all the country. Denmark and Norway began suffering in July, Holland and Sweden in August.
The earliest cases in Bombay erupted on a transport soon after its arrival May 29. First seven police sepoys who worked the docks were admitted to the police hospital; then men who worked at the government dockyard succumbed; the next day employees of the Bombay port fell ill, and two days later men who worked at a location that 'abuts on the harbor between the government dockyard and Ballard Estate of the Port Trust.' From there the disease spread along railroad lines, reaching Calcutta, Madras, and Rangoon after Bombay, while another transport brought it to Karachi.
Influenza reached Shanghai toward the end of May. Said one observer, 'It swept over the whole country like a tidal wave.' A reported half of Chungking lay ill. It jumped to New Zealand and then Australia in September; in Sydney it sickened 30 percent of the population.
But if it was spreading explosively, it continued to bear little resemblance to the violent disease that had killed in Haskell. Of 613 American troops admitted to the hospital during one outbreak in France, only one man died. In the French army, fewer than one hundred deaths resulted from forty thousand hospital admissions. In the British fleet, 10,313 sailors fell ill, temporarily crippling naval operations, but only four sailors died. Troops called it 'three-day fever.' In Algeria, Egypt, Tunisia, China, and India it was 'everywhere of a mild form.'
In fact, its mildness made some physicians wonder if this disease actually was influenza. One British army report noted that the symptoms 'resembled influenza' but 'its short duration and absence of complications' created doubt that it was influenza. Several different Italian doctors took a stronger position, arguing in separate medical journal articles that this 'febrile disease now widely prevalent in Italy [is] not influenza.' Three British doctors writing in the journal The Lancet agreed; they concluded that the epidemic could not actually be influenza, because the symptoms, though similar to those of influenza, were too mild, 'of very short duration and so far absent of relapses or complications.'
That issue of 'The Lance't was dated July 13, 1918.
In March and April in the United States, when the disease began jumping from army camp to army camp and occasionally spreading to adjacent cities, Gorgas, Welch, Vaughan, and Cole showed little concern about it, nor did Avery commence any laboratory investigation. Measles was still lingering, and had caused many more deaths.
But as influenza surged across Europe, they began to attend to it. Despite the articles in medical journals about its generally benign nature, they had heard of some worrisome exceptions, some hints that perhaps this disease wasn't always so benign after all, that when the disease did strike hard, it was unusually violent - more violent than measles.
One army report noted 'fulminating pneumonia, with wet hemorrhagic lungs' (i.e., a rapidly escalating infection and lungs choked with blood) 'fatal in from 24 to 48 hours.' Such a quick death from pneumonia is extraordinary. And an autopsy of a Chicago civilian victim revealed lungs with similar symptoms, symptoms unusual enough to prompt the pathologist who performed the autopsy to send tissue samples to Dr. Ludwig Hektoen, a highly respected scientist who knew Welch, Flexner, and Gorgas well and who headed the John McCormick Memorial Institute for Infectious Diseases. The pathologist asked Hektoen 'to look at it as a new disease.'
And in Louisville, Kentucky, a disturbing anomaly appeared in the influenza statistics. There deaths were not so few, and (more surprisingly) 40 percent of those who died were aged twenty to thirty-five, a statistically extraordinary occurrence.
In France in late May, at one small station of 1,018 French army recruits, 688 men were ill enough to be hospitalized and forty-nine died. When 5 percent of an entire population (especially of healthy young adults) dies in a few weeks, that is frightening.
By mid-June, Welch, Cole, Gorgas, and others were trying to gather as much information as possible about the progression of influenza in Europe. Cole could get nothing from official channels but did learn enough from such people as Hans Zinsser, a former (and future) Rockefeller investigator in the army in France, to become concerned. In July, Cole asked Richard Pearce, a scientist at the National Research Council who was coordinating war-related medical research, to make 'accurate information concerning the influenza prevailing in Europe' a priority, adding, 'I have inquired several times in Washington at the Surgeon General's office' (referring to civilian Surgeon General Rupert Blue, head of the U.S. Public Health Service, not Gorgas) 'but no one seems to have any definite information in regard to the matter.' A few days later Cole showed more concern when he advised Pearce to put more resources into related research.
In response Pearce contacted several individual laboratory scientists, such as Paul Lewis in Philadelphia, as well as clinicians, pathologists, and epidemiologists, asking if they could begin new investigations. He would act as a clearinghouse for their findings.
Between June 1 and August 1, 200,825 British soldiers in France, out of two million, were hit hard enough that they could not report for duty even in the midst of desperate combat. Then the disease was gone. On August 10, the British command declared the epidemic over. In Britain itself on August 20, a medical journal stated that the influenza epidemic 'has completely disappeared.'
The 'Weekly Bulletin' of the Medical Service of the American Expeditionary Force in France was less willing than the British to write off the influenza epidemic entirely. It did say in late July, 'The epidemic is about at an end' and has been throughout of a benign type, though causing considerable noneffectiveness.'
But it went on to note, 'Many cases have been mistaken for meningitis' . Pneumonias have been more common sequelae in July than in April.'
In the United States, influenza had neither swept through the country, as it had in Western Europe and parts of the Orient, nor had it completely died out.
Individual members of the army's pneumonia commission had dispersed to perform studies in several locations, and they still saw signs of it. At Fort Riley, which included Camp Funston, Captain Francis Blake, was trying to culture bacteria from the throats of both normal and sick troops. It was desultory work, far less exciting than what he was accustomed to, and he hated Kansas. He complained to his wife, 'No letter from my beloved for two days, no cool days, no cool nights, no drinks, no movies, no dances, no club, no pretty women, no shower bath, no poker, no people, no fun, no joy, no nothing save heat and blistering sun and scorching winds and sweat and dust and thirst and long and stifling nights and working all hours and lonesomeness and general hell - that's Fort Riley Kansas.' A few weeks later, he said it was so hot they kept their cultures of bacteria in an incubator so the heat wouldn't kill them. 'Imagine going into an incubator to get cool,' he wrote.
He also wrote, 'Have been busy on the ward all day - some interesting cases'. But most of it influenza at present.'
Influenza was about to become interesting.
For the virus had not disappeared. It had only gone underground, like a forest fire left burning in the roots, swarming and mutating, adapting, honing itself, watching and waiting, waiting to burst into flame.
The 1918 influenza pandemic, like many other influenza pandemics, came in waves. The first spring wave killed few, but the second wave would be lethal. Three hypotheses can explain this phenomenon.
One is that the mild and deadly diseases were caused by two entirely different viruses. This is highly unlikely. Many victims of the first wave demonstrated significant resistance to the second wave, which provides strong evidence that the deadly virus was a variant of the mild one.
The second possibility is that a mild virus caused the spring epidemic, and that in Europe it encountered a second influenza virus. The two viruses infected the same cells, 'reassorted' their genes, and created a new and lethal virus. This could have occurred and might also explain the partial immunity some victims of the first wave acquired, but at least some scientific evidence directly contradicts this hypothesis, and most influenza experts today do not believe this happened.
The third explanation involves the adaptation of the virus to man.
In 1872 the French scientist C. J. Davaine was examining a specimen of blood swarming with anthrax. To determine the lethal dose he measured out various amounts of this blood and injected it into rabbits. He found it required ten drops to kill a rabbit within forty hours. He drew blood from this rabbit and infected a second rabbit, which also died. He repeated the process, infecting a third rabbit with blood from the second, and so on, passing the infection through five rabbits.
Each time he determined the minimum amount of blood necessary to kill. He discovered that the bacteria increased in virulence each time, and after going through five rabbits a lethal dose fell from 10 drops of blood to 1/100 of a drop. At the fifteenth passage, the lethal dose fell to 1/40,000 of a drop of blood. After twenty-five passages, the bacteria in the blood had become so virulent that less than 1/1,000,000 of a drop killed.
This virulence disappeared when the culture was stored. It was also specific to a species. Rats and birds survived large doses of the same blood that killed rabbits in infinitesimal amounts.
Davaine's series of experiments marked the first demonstration of a phenomenon that became known as 'passage.' This phenomenon reflects an organism's ability to adapt to its environment. When an organism of weak pathogenicity passes from living animal to living animal, it reproduces more proficiently, growing and spreading more efficiently. This often increases virulence.
In other words, it becomes a better and more efficient killer.
Changing the environment even in a test tube can have the same effect. As one investigator noted, a strain of bacteria he was working with turned deadly when the medium used to grow the organism changed from beef broth to veal broth.
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.
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.'
Written by John M. Barry in "The Great Influenza",Penguin Group, USA, 2009,excerpts part 4, chapter 14 & 15. Digitized, adapted and illustrated to be posted by Leopoldo Costa.
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