The Pandemic Century
Page 3
In the late Victorian and Edwardian period, pneumonia was perhaps the most feared disease after tuberculosis and nearly always fatal, particularly in the elderly or those whose immune systems were compromised by other diseases. Prominent victims included the ninth president of the United States, William Henry Harrison, who died one month after his inauguration in 1841, and the Confederate general Thomas Jonathan “Stonewall” Jackson, who died of complications of pneumonia eight days after being wounded at the Battle of Chancellorsville in 1863. Little wonder then that Sir William Osler, the so-called father of modern American medicine, dubbed pneumonia the “Captain of the Men of Death.”
When contracted in childhood measles usually results in a rash and high fever accompanied by a violent cough and sensitivity to light, but in the case of the camp-acquired measles cases the symptoms were far more severe. The outbreaks produced the highest infection rates the army had seen in ninety-seven years and were often accompanied by an aggressive bronchopneumonia. The result was that between September 1917 and March 1918, more than 30,000 American troops were hospitalized with pneumonia, nearly all as a result of complications of measles, and some 5,700 died. The extent of the outbreaks astonished even battled-hardened doctors, such as Victor Vaughan, the dean of the University of Michigan’s School of Medicine and a veteran of the Spanish-American War. “Not a troop train came into Camp Wheeler (near Macon, Georgia) in the fall of 1917 without bringing one to six cases of measles already in the eruptive stage,” he wrote. “These men had brought the infection from their homes and had distributed its seed at the state encampment and on the train. No power on earth could stop the spread of measles through a camp under these conditions. Cases developed, from one hundred to five hundred a day, and the infection continued as long as there was susceptible material in the camp.”
By the spring of 1918 the War Department was being lambasted by Congress for shipping recruits to training camps before facilities were fully ready and under conditions that failed to meet basic standards of public health, and by July the department had appointed a pneumonia commission to investigate the unusual prevalence of the disease in the large cantonments. The commission read like a future who’s who of American medicine, and included Eugenie L. Opie, the future dean of Washington University School of Medicine; Francis G. Blake, who would go on to become professor of internal medicine at Yale University; and Thomas Rivers, who would become one of the world’s leading virologists and director of the Rockefeller University hospital in New York. Assisting them in the surgeon general’s office with the rank of commanders were Victor Vaughan and William H. Welch, the dean of Johns Hopkins School of Medicine and then the most famous pathologist and bacteriologist in America, and Rufus Cole, the first director of the Rockefeller University Hospital and a specialist in pneumococcal disease. Together with his assistant Oswald Avery, Cole would direct laboratory investigations of the pneumonia outbreaks and train medical officers in the correct techniques for culturing the bacteria and making serums and vaccines. Meanwhile, keeping a watch over their endeavors would be Simon Flexner, the head of Rockefeller Institute and a former student and protégé of Welch.
WHILE AMERICAN PHYSICIANS were worrying about camp-acquired measles and pneumonia cases, medics in the British Army were becoming concerned about another respiratory disease. Labeled “purulent bronchitis” for want of a better term, the disease had broken out at Etaples in the bitterly cold winter of 1917, and by February 156 soldiers were dead. The initial stages resembled ordinary lobar pneumonia—a high fever and the expectoration of blood-streaked sputum. But these symptoms soon gave way to a racing pulse accompanied by the discharge of thick pale yellow dollops of pus, suggesting bronchitis. In half these cases death from “lung block” followed soon after.
Another striking feature was cyanosis. This condition occurs when a patient becomes breathless because the lungs can no longer transfer oxygen efficiently to the blood and is characterized by a dusky purple-blue discoloration of the face, lips, and ears (it is oxygen that turns blood in the arteries red). However, in the case of the Etaples patients, their breathlessness was so acute that they tore off their bedclothes in distress. At autopsy, the pathologist, William Rolland, was shocked to find a thick, yellowish pus blocking the bronchi. In the larger bronchi, the pus was mixed with air, but when he cut a section through the smaller tubes he wrote, “the pus exudes spontaneously . . . with little or no admixture of air.” This explained why the attempt to relieve patients’ symptoms by giving them piped oxygen had been of little use. Etaples was not the only army camp where this peculiar disease appeared. In March 1917 a similar outbreak had occurred at Aldershot, “The Home of the British Army,” in southern England. Once again the disease proved fatal to half those it infected, the signature feature being the exudation of a yellowish pus followed by breathlessness and cyanosis. In the cyanosed patients, physicians noted, “no treatment that we have been able to devise appears to do any good.” To some, the short shallow breathing recalled the “effects of gas poisoning,” but later the bacteriologists and pathologists who examined the Aldershot and Etaples cases became convinced it had been a type of influenza. Flu had long been recognized as trigger for bronchial infections. During influenza epidemics and the seasonal outbreaks of the disease which occurred every fall and winter, epidemiologists were accustomed to seeing a spike in respiratory deaths, particularly among the very young or elderly sections of the population. But for young adults and those below the age of seventy, flu was considered more of a nuisance than a mortal threat to life, and convalescents were frequently viewed with suspicion.
WE MAY NEVER KNOW whether the outbreaks at Etaples and Aldershot were flu, but in March 1918 another unusual respiratory outbreak visited a large army camp—this time at Camp Funston in Kansas. Initially, physicians thought they were seeing another wave of camp-acquired pneumonias, but they soon revised their opinion.
The first casualty was supposedly the camp cook. On March 4, he woke with a splitting headache and aches in his neck and back and reported to the base hospital. Soon, one hundred other members of the 164th Depot Brigade had joined him, and by the third week in March more than 1,200 men were on the sick list, forcing Fort Riley’s chief medical officer to requisition a hangar adjacent to the hospital for the overflow. The illness resembled classic influenza: chills followed by high fever, sore throat, headache, and abdominal pains. However, many patients were so incapacitated that they found it impossible to stand up; hence the malady’s nickname, “knock-me-down fever.” Most of the men recovered within three to five days, but, disturbingly, several went on to develop severe pneumonias. Unlike the pneumonias after measles, which tended to localize in the bronchi, these postinfluenzal pneumonias frequently extended to the entire lobe of a lung. In all, such lobar pneumonias had developed in 237 men, roughly one-fifth of those hospitalized, and by May there had been 75 deaths. As Opie and Rivers discovered the following July when the pneumonia commission eventually arrived to conduct an investigation, there were other disturbing features, too: after the initial epidemic had petered out in March there had been further outbreaks in April and May, each one corresponding to the arrival of a new group of draftees. Not only that, but men transferred to camps in the East appeared to carry the disease with them, and when many of these same men joined the American Expeditionary Force and mingled freely with soldiers sailing for Europe, they sparked further outbreaks on board Atlantic troopships. The pattern continued when the transports arrived at Brest, the main disembarkation point for American troops, and disgorged their cargo. “Epidemic of acute infectious fever, nature unknown,” reported a medical officer at a US Army hospital in Bordeaux on April 15. As at Funston, the initial cases were mild but by June thousands of Allied troops were being hospitalized, and by August alarm was mounting. “These successive outbreaks tended to be progressively more severe both in character and extent, which would speak for an increasing virulence of the causative agent,” observed Alan M. Ch
esney, a medical officer at an AEF artillery training camp in Valdahon.
Chesney’s was a rare example of concern. In the summer of 1918 no one had experienced a pandemic of influenza for twenty-eight years. Compared to typhus, a deadly blood-borne disease spread by lice that lived in soldiers’ clothing, or the septicemia that bred in gunshot and shrapnel wounds, influenza was a trifling infection from the point of view of army medical officers. Civilian physicians regarded flu with similar disdain, particularly the British, who had long considered influenza a suspect Italian word for a bad cold or catarrh.* Besides, after nearly five years of brutal trench warfare which had already claimed the lives of tens of thousands of Europeans, and with two million Allied troops now dug in in northern France and Flanders, officers had more pressing issues on their minds. “Quite 1/3 of the Batt. and about 30 officers are smitten with the Spanish Flu,” the poet Wilfred Owen informed his mother, Susan, disdainfully in a letter from a British Army camp in Scarborough, North Yorkshire, in June. “The thing is much too common for me to take part in. I have quite decided not to! Imagine the work that falls on unaffected officers.”
Owen was wrong to be so complacent. Between the summer of 1918 and the spring of 1919, tens of thousands of soldiers and millions of civilians would be mown down by Spanish flu (so-called because Spain was the only country not to censor reports of the spreading epidemic) as the disease ricocheted between America and northern Europe before engulfing the entire globe. In the United States alone, some 675,000 Americans would perish in the successive waves of flu; in France, perhaps as many as 400,000; in Britain, 228,000. Worldwide, the death toll from the Spanish flu pandemic has been estimated at 50 million—five times as many as died in the fighting in World War One and 10 million more than AIDS has killed in thirty years.
One reason Owen and others were so relaxed about influenza was that in 1918, medical scientists were confident that they knew how the disease was transmitted. After all, in 1892 Richard Pfeiffer, the son-in-law of Robert Koch, the German “father” of bacteriology, had announced that he had identified the disease’s “exciting cause,” a tiny Gram-negative bacterium he dubbed Bacillus influenzae. Pfeiffer’s “discovery” came at the height of the so-called Russian influenza pandemic and made headline news around the world, fueling expectations that it would only be a matter of time before scientists trained in German laboratory techniques had produced a vaccine. Never mind that other researchers were not always able to isolate “Pfeiffer’s bacillus,” as the bacterium was popularly known, from the throat washings and bronchial expectorations of influenza patients. Or that it was notoriously difficult to cultivate the bacteria on artificial media and it often took several attempts to grow colonies of sufficient size so that the small, spherical, and colorless bodies could be visualized through a microscope using special dyes. Or that despite inoculating monkeys with the bacillus, Pfeiffer and his Berlin colleague, Shibashuro Kitasato, had so far been unable to transfer the disease, thereby failing the test of Koch’s fourth postulate. As far as most medical authorities were concerned, Pfeiffer’s bacillus was the etiological agent of influenza and that was that. Rare was the man of science who dared to challenge the authority of Koch and his disciples by expressing unease at the failure to find the bacillus in each and every case of influenza.
Perhaps that explains why, on arriving at Camp Funston in July, Opie, Blake, and Rivers had ignored the fact that researchers had failed to find Bacillus influenzae in 77 percent of the pneumonia cases, or that the bacillus had also been isolated from the mouths of one-third of the healthy men, i.e., those who had not shown any signs or symptoms of influenza.† Instead, they tried to make sense of the higher pneumonia attack rates observed among African American draftees from Louisiana and Mississippi, an incidence they attributed to racial differences between white and “colored” troops. This was despite observing that the units that had suffered most severely from postinfluenzal pneumonias were the ones that were new to the camp and who had only been at Fort Riley for three to six months, and that a greater proportion of the African American draftees came from rural areas. For the most part, the survey was dull, repetitive work and Blake soon found himself longing for a change of scene. As he complained to his wife on August 9, “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.”
Very soon Opie, Blake, and Rivers would get orders to leave Kansas, only to be thrust into a far worse hell when they found themselves in the midst of a raging epidemic of influenza and pneumonia at Camp Pike, Arkansas. They were spared the worst hell of all, however.
IN AUGUST 1918, Clifton Skillings, a twenty-three-year-old farmer from Ripley, Maine, boarded a southbound Boston train. Like thousands of other American men of fighting age, Skillings had received his draft papers a few weeks earlier and had now been ordered to report for duty to Camp Devens. Alighting at Ayer, he fell into step with other draftees dressed in their Sunday best and began striding toward the camp, with a trooper on horseback leading the way. To the eyes of the Boston men, Ayer was a “hick town.” Whether Skillings thought it so he does not say, but to judge by his letters and his postcards he did not care particularly for the food. “We had your beans at noon but they are not like the beans you get at home,” he complained to his family on August 24. “It makes me think of mixing up dog food.” Skillings immediately fell in with a group from Skowhegan, Maine, but was amazed to learn that the camp included men from midwestern states such as Minnesota. “There is a good many thousand men in this campground. It seems awful funny to see nothing but men . . . I wish you folks could come in & look around.” Four weeks later the size of the camp and the quality of food is the least of his concerns, however. “Lots of the boys are sick and in the hospital,” he wrote home on September 23. “It is a disease. Some [thing] like the Gripp . . . I don’t think I will get it.”
It’s not known where the fall wave of influenza originated. It could have been incubating in America over the summer, but more likely it was introduced by troops returning from Europe. From an ecological point of view, northern France was a vast biological experiment—a place where large masses of men from two continents converged and mingled freely with men from a host of other nations, including Indian soldiers from the Punjab, African regiments from Nigeria and Sierra Leone, Chinese “coolies,” and Indochinese laborers from Vietnam, Laos, and Cambodia. One theory is that the second wave began with an outbreak at a coaling station in Sierra Leone at the end of August, from whence it spread rapidly to other West African countries and to Europe via British naval vessels. Another is that the bug was already in Europe, hence the prepandemic waves recorded in Copenhagen and other northern European cities in July.
In the United States, the fall wave had first announced itself toward the end of August at Commonwealth Pier in Boston, one of the main entry points for returning AEF troops, when several sailors were suddenly taken ill. By August 29, fifty had been transferred to the Chelsea Naval Hospital, where they came under the care of Lieutenant Commander Milton Rosenau, a former director of the US Public Health Service’s Hygienic Laboratory and member of Harvard Medical School. Rosenau isolated the sailors in an effort to contain the outbreak, but by early September US naval stations in Newport, Rhode Island, and New London, Connecticut were also reporting significant numbers of influenza cases. At around the same time, Devens saw an increase in pneumonia cases. Then, on September 7, a soldier from Company B, 42nd infantry, was admitted to the base hospital with “epidemic meningitis.” In fact, his symptoms—runny nose, sore throat, and inflammation of the nasal passages—were consistent with influenza, and when the following day twelve more men from the same company fell ill with similar symptoms, doctors had
no hesitation in labeling it a “mild” form of Spanish influenza. It would not remain mild for long.
When a parasitic organism meets a susceptible host for the first time, it triggers an arms race between the pathogen and the host’s immune system. Having never encountered the pathogen before, the immune system is initially blindsided and takes time to mobilize its defenses and launch a counterattack. With nothing to stop it, the pathogen tears through the host’s tissue, invading cells and multiplying at will. At this stage, the parasite resembles a child with a tantrum. With no one and nothing to discipline it, its tantrum can easily escalate and its behavior can become increasingly virulent. Eventually, in the most extreme cases of all, its rage may become all-consuming. This is usually bad news for the host. From a Darwinian point of view, however, the parasite does not want to kill its host; its primary objective is to survive long enough to escape and infect a new susceptible. In other words, the death of the host is a bad strategy for a parasite, an “accident” of biology if you will. A far better survival strategy over the long term is to evolve in the other direction, toward avirulence, resulting in an infection that is mild or barely detectable in the host. But in order for that to happen, the immune system must first find a way of taming the parasite.