The Pandemic Century
Page 7
It is perhaps also worth remarking that as doubts about the etiological role of B. influenzae grew, so pathologists took care to distinguish between lung lesions attributable to commensal bacteria and those due to the presumed, though as yet unproven, virus of the epidemic. By the mid-1920s, this was a view that Welch was also coming to endorse. Addressing a meeting of public health officials in Boston in 1926, Welch said that the idea that influenza was due to an “unknown virus” had much to recommend it, and he now thought that “when there was a lesion of the lung . . . it was attributable to the virus, the real influenza virus, not general respiratory manifestations.” He had also been struck by the “crowding together” of soldiers at the base hospital at Devens, an occurrence that he thought increased patients’ risk of exposure to other organisms and was “largely responsible for the enormous extent of the disease.”
Unlike in 1918, today it is possible to study the virus in the laboratory using a process called reverse genetics. Beginning in 2005, this is exactly what scientists have done, reassembling the virus in Biosafety Level Four facilities and then challenging mice and other test animals. The resurrected virus kills mice in three to five days and causes a severe lung inflammation reminiscent of the lesions reported by doctors in 1918. It also replicates very efficiently in bronchial epithelial cells. Indeed, so striking is the virulence of the 1918 virus in animal models that some virologists argue that infection with the virus alone could have triggered the rapid onset pneumonias and symptoms of cyanosis described by pathologists in 1918 and that it is unnecessary to invoke secondary bacterial invaders. One suggestion is that the pneumonias and symptoms of cyanosis may have been due to an overly exuberant immune response involving the release of proinflammatory cells called cytokines. This phenomenon—known as a “cytokine storm”—was implicated in the deaths from Acute Respiratory Distress Syndrome (ARDS) that followed the H5N1 bird flu outbreaks in Southeast Asia in the early 2000s, and has also been observed with other epidemic viruses such as SARS.
Whether or not these pneumonias were primarily viral or bacterial, or a mixture of both, does not answer the question why the Spanish flu proved so deadly to young adults in the prime of life, however. Here, present-day science has several hypotheses but no good answers. One suggestion is that older age groups enjoyed greater protection because they had previously been exposed to a similar virus. This fits with serological evidence suggesting that people born between 1830 and 1889 were also exposed to an H1. It was only after 1890 that this virus was replaced by a new pandemic virus, the Russian H3. In other words, those aged thirty-eight and over would have already possessed some antibodies to the H1N1 Spanish flu, and in the case of the very elderly—those born in 1834 and who had been infants when they first encountered an H1—this protection would have been considerable.
Another suggestion is that the virus that was to become the Spanish flu (in a scenario where it acquired avian genes around 1915) may have begun life as an H1 that emerged shortly after 1900. This could have been critical for those born in the first years of the twentieth century and who would have been eighteen or younger at the time the pandemic struck, as it is thought that early life infection with influenza results in an immunological “blind spot.” Usually referred to as “original antigenic sin,” the idea is that antibodies to the first-encountered flu strain are more readily “recalled” and produced at the expense of new antibodies specific to newer flu strains. It is even possible that through a process known as antibody-dependent enhancement, the older immune response might aid the virus to evade the body’s defenses and infect cells more readily. However, while the advantage of such hypotheses is that they help explain why, no matter where the flu struck, the mortality fell most heavily on twenty-to-forty-year-olds, most experts feel that without knowing the precise genetic identity of the 1890 virus and the viruses that came before and after, and the precise immunological profiles of the affected age groups, these hypotheses are somewhat speculative. As David Morens, a medical epidemiologist who works closely with Taubenberger, points out, it is equally possible that the W-shaped mortality pattern could be due to some as yet unidentifiable environmental exposure peculiar to young adults at the time. We just do not know. Indeed, for all that new molecular techniques and a better understanding of the ecology and immunology of flu have brought new insights into the patterns of pandemics, Taubenberger and Morens argue that “we have moved ever further from certainty about the determinants of, and possibilities for pandemic emergence.” It is this uncertainty that makes flu—and the 1918 pandemic in particular—such an enigmatic and enduring object of scientific interest and source of anxiety.
But perhaps for the last word on the pandemic we should leave North America and turn to someone who viewed the spreading global morbidity and mortality from the periphery. In 1919, at the age of twenty, Frank Macfarlane Burnet was studying medicine at the University of Melbourne when he suffered an attack of influenza. Thankfully, the illness proved mild. Nevertheless, it left an indelible impression, igniting a lifelong fascination with flu and with what Burnet called “the natural history of infectious disease.” In 1931, Burnet arrived at the National Institute for Medical Research in London on a two-year fellowship to study the burgeoning new field of virus diseases. His arrival coincided with the discovery that ferrets could be infected with influenza, and on his return to Melbourne in 1934 he pioneered the technique for growing the virus in chick egg embryos. This would be the first in a series of contributions to influenza research by Burnet—research that would see him investigate variations in virulence between newly isolated and chick-cultivated viruses and lay the ground for future genetic insights into the emergence of pandemics. Intrigued by Nicolle and Lebailly’s findings in Tunis in 1918, in 1941 Burnet also conducted a series of trials in macaques, challenging the monkeys with several strains of egg-propagated virus. Although none of the monkeys developed a fever or other signs of illness when infected intranasally, several became ill when Burnet injected the virus directly into their trachea, and at autopsy one showed signs of extensive bronchopneumonia. However, it was the epidemiology of influenza that fascinated Burnet most, and the more he studied the patterns of morbidity and mortality in 1918, the more convinced he became that it was the concentration of recruits from rural and urban districts in overcrowded barracks that held the key to the pandemic’s unusual characteristics. Like Welch and the members of the pneumonia commission, Burnet was persuaded that the emergence of Spanish flu was, as he put it, “intimately linked to war conditions,” and that it was the immunological profiles of American recruits, followed by their transfer to northern France, where they were able to mix freely with men from other nations, that accounted for the extreme virulence of the virus and the unusual age profile of its victims. “If the early American epidemics supplied the initial spark for the pandemic we can be certain that it was fanned into a flame in Europe,” Burnet concluded. But what struck Burnet as possibly even more significant from an immunological point of view was how many people had been unaffected by the pandemic. Thus two-thirds of the population had escaped infection altogether, and the overall mortality, as a measure of the total population, had been just 2 percent. While that was twenty-five times higher than in a normal flu season, it was far lower than the mortality rate seen during outbreaks of cholera and pneumonic plague in the nineteenth century, and went some way to explaining why, except for at the height of the killing wave in October, when hospitals had been flooded with pneumonia cases and the deaths had become impossible to ignore, the pandemic had not provoked greater fear and panic. Yes, influenza had briefly presented as “some new kind of plague.” But by November 1918 and the declaration of the armistice it was already once more on its way to becoming a perennial seasonal ailment. Unfortunately, that would not be true of other twentieth- and twenty-first-century epidemics caused by similar ecological imbalances and environmental disturbances.
* Influenza derives from the Latinate Italian phrase in
fluenza coeli, meaning “influence of the heavens.”
† Today the bacillus is referred to as Hemophilus influenzae.
‡ Chick egg embryo cultivation is still the principal means of making flu vaccines.
CHAPTER II
PLAGUE IN THE CITY OF ANGELS
“The word ‘plague’ had just been uttered for the first time.”
—ALBERT CAMUS, The Plague
On October 3, 1924, Dr. Giles Porter, a Los Angeles city health officer, was called to the home of a railroad worker in the heart of the Mexican quarter. A few days earlier, Jesus Lajun and his fifteen-year-old daughter, Francisca Concha Lajun, had fallen ill at their apartment at 700 Clara Street, and both were now running high temperatures. Francisca also had a spasmodic, rattling cough, while Jesus had a nasty swelling on his groin. Porter attributed Jesus’s swelling to “venereal adenitis” due to syphilis, while Francisca’s symptoms of fever and coughing, he thought, were most likely due to influenza. “This child was not considered to be in a serious condition,” he recorded in his report. But Porter was wrong and two days later Luciana Samarano, the owner of a nearby boarding house who had been nursing Francisca, became so concerned about the girl’s condition that she called an ambulance. Francisca died en route to Los Angeles General Hospital, a pathologist later listing the cause of death as “double pneumonia.” For an otherwise healthy teenager to suffer a severe attack of pneumonia was a highly unusual occurrence, but Clara Street was surrounded by brickyards and gas and electrical works, and even in fine weather the air was choked with pollutants. Taking into account the unpleasant odors emanating from the nearby meatpacking plants, it came as little surprise that Mexicans were the only people prepared to live in the environs of Clara Street or that a young life had been taken prematurely.
Built in 1895 on a vacant plot near the Los Angeles River, Clara Street had originally been an affordable white middle-class neighborhood, but as the city expanded and a land and building boom brought a demand for brick makers and cheap agricultural labor, the Italian residents had moved out and the area had been colonized by Hispanics and migrant workers from south of the border. By 1924 some 2,500 Mexicans were packed into the 307 houses in and around Clara Street, an eight-block area bounded on the east by the Southern Pacific Railroad, on the west by Alameda Street, and on the south by Macy Street. Overcrowding was rife. Many, such as Samarano’s home at 742 Clara Street, had been subdivided into “apartments” or transformed into boarding houses in which up to thirty people resided at a time. Other guests bedded down in shacks appended to the rear of the simple clapboard dwellings. People were not the only lodgers. The crawl spaces beneath the floorboards also provided sanctuary for rats and, on occasion, ground squirrels. In short, it was a world away from the Los Angeles described by realtors as the city “of eternal youth—a city without slums.”
In the 1920s, Los Angeles had a population of one million and was one of the fastest growing urban centers in the United States. Billed as the “climatic capital of the world,” the city was in the midst of a real estate boom as Americans tired of the harsh midwestern winters and the overcrowded conditions in cities in the East flocked to Southern California, attracted by the promise of a new life in a land blessed by oil, palm trees, abundant farmland, and sunshine. Most of these settlers made for the new bedroom communities with names like “Petroleum Gardens” that were springing up on reclaimed desert just beyond the city limits. By contrast, Hispanics tended to congregate in Macy District—as the Mexican quarter was officially known—or the adjacent Mariana and Belvedere Gardens districts.
By 1924, Los Angeles’s Hispanic population totaled around 22,000, and the signs of their labor were everywhere: it was Mexican hands, toiling in the clay pits adjacent to the Los Angeles River, that had fashioned the bricks for the high rises transforming L.A.’s skyline, and it was Mexicans who kept the grocery stores stocked with fresh fruit and vegetables and who scrubbed the floors of the swank downtown hotels. Yet for the city’s majority Anglo-Saxon population, these brown-skinned inhabitants of the City of Angels were all but invisible. Sure, there may have been concerns from time to time about the diseases they were presumed to carry, or the demographic implications of the burgeoning Hispanic birthrate, but as Harry Chandler, the owner of the antiunion Los Angeles Times, and a prominent Californian landowner and power broker, reassured Congress: Mexicans “do not intermarry like the negro with white people. They don’t mingle. They keep to themselves. That is the safety of it” (emphasis added).
Seven days after Francisca Lajun’s death, her father Jesus also succumbed to the mysterious infection. Then, five days later, Luciana Samarano was admitted to County General, dying on October 19 of “myocarditis” or heart disease (six months’ pregnant at the time, Luciana’s unborn child died with her). The next casualties were Samarano’s husband, Guadalupe, followed by several mourners who had attended Luciana’s wake, which, as per Catholic tradition, saw relatives filing past the open casket and kissing the corpse to pay their respects. As with Francisca Lajun, Guadalupe’s death was listed as “double pneumonia.” By now, several other people who had attended Luciana’s wake had also fallen ill with similar symptoms. However, it was only on October 29 that the hospital dispatched its chief resident, Dr. Emil Bogen, to investigate. Bogen’s first stop was a house at 343 Carmelita Street in Belvedere Gardens. “In the middle of the room,” Bogen recalled, “an old Mexican woman was lying on a large double bed, crying between paroxysms of coughing, while along the wall was a couch on which was seen a Mexican man of about 30 years of age, restless and feverish, but not coughing.” Several other people were also present, and one agreed to act as Bogen’s interpreter. Bogen was told that the man had fallen sick the day before, that he had a pain along his spine, and that he was running a temperature of 104 degrees. He also had red spots on his chest. The old woman, meanwhile, “had been coughing for the past two days, expectorating a profuse bloody sputum, and had loud, coarse rhonchi.”
Bogen arranged for the couple to be transferred to an ambulance, then went with the interpreter to the adjacent house where another man and his wife and daughter were ill with similar symptoms. The wife informed Bogen that she felt better than previously while the daughter “insisted that she was not sick, only a little tired.” Within three days, however, both the woman and the girl were in a critical condition at County General, and the woman’s husband was dead. Only later did it emerge that he was Guadalupe Samarano’s brother, Victor, and that both he and his wife had recently attended the wake at 742 Clara Street. There, Bogen found four desperately sick boys between the ages of four and twelve, the recently orphaned sons of Luciana and Guadalupe. “The four boys were brought to the hospital that same night, and during the following day six more cases were admitted from that neighborhood,” he recorded. “Soon after admission they developed signs of a severe pneumonia, with bloody expectoration and marked cyanosis.”
Samarano’s home would subsequently be labeled the “death house.” In all, thirty-three people who had attended Luciana’s wake or who were related to the Samaranos or who had lodged at 742 Clara Street would contract plague, and thirty-one would die. The sequence of illnesses was laid out in an official report in which the casualties were listed according to their initials and their relationship to “L.S.” or “G.S.” After the Samaranos, the next casualty was “J.F.,” or Jessie Flores, a family friend and next door neighbor who had nursed Luciana. Then came two of the couple’s sons by different marriages, and both Luciana and Guadalupe’s mothers. Even the family priest, Father Medardo Brualla, contracted the disease. Brualla had gone to 742 Clara Street on October 26 to administer the last rites to Guadalupe and Jessie, but a few days later he was also expectorating bloody sputum, and by November 2 he was dead.
After Guadalupe’s death, unsuspecting health officials had released his body so that his family could pay their respects. Once again, they held the service at 742 Clara Street, and once again, mourners who
attended the wake fell ill soon after. By October 30, some twelve people were in critical condition at County General. It was one of these, Horace Gutiérrez, a cousin of Luciana Samarano, who would provide the crucial evidence that would alert health officials to the identity of the pathogen and plunge the Los Angeles Chamber of Commerce and city hall into panic. In his summary, Bogen records that Horace had arrived at the hospital at around the same time as the four Samarano boys, and, shortly after, had developed the same symptoms of pneumonia accompanied by bloody expectorations and cyanosis. As cyanosis had been a signature symptom of the Spanish influenza and the epidemic was still fresh in physicians’ memories, the immediate suspicion was flu. In the end, however, the cases were attributed to “epidemic meningitis.” Only the hospital’s pathologist, Dr. George Maner, thought differently, suggesting that perhaps they were dealing with plague. Later, Maner decided to check his intuition by taking a sputum sample from Gutiérrez and examining it under a microscope. What he saw filled him with dread. Gutiérrez’s sputum was packed with tiny rod-shaped bacteria that looked distinctly like the images Maner had seen in textbooks of Pasteurella pestis, the bacterium of plague. Unsure of the bacteria’s morphology and wanting to get a second opinion, Maner approached his predecessor as chief of pathology at Los Angeles General, a Scotsman by the name of Roy Hammack. Hammack had previously served in the Philippines, where he had treated several cases of plague, so he had the advantage of having seen the bacillus before. “Beautiful!” he supposedly exclaimed when he espied the familiar rod-shaped bacteria through his microscope. “Beautiful but damned.”