The influenza epidemic at San Quentin was unremarkable given conditions at the prison. Resident physician Dr Leo Stanley had been appalled at the lack of hygiene when he arrived in 1913. ‘The ventilation was abominable, the beds were crowded together, air space was extremely limited,’15 he wrote, in his account of the outbreak. Stanley was particularly concerned about the spread of tuberculosis, a major killer at the time, and also reflected the prejudices of his age by expressing disgust at the lack of racial segregation. ‘Whites, Negroes and Indians commingled here indiscriminately,’16 he wrote, and the ‘surroundings were extremely sordid’.17 Despite his evident shortcomings, Stanley became an apparently model prison doctor, devoting himself to his work. With a team of four paid assistants, and inmate clerks and nurses, Stanley developed an efficient treatment system, with prisoners lined up in ‘pill lines’ morning and afternoon.18 It was Stanley who, in his efficient way, chronicled the onset of influenza at San Quentin when it first arrived in April 1918.
The first outbreak at San Quentin began on 13 April when a prisoner, henceforth referred to as Prisoner A, arrived from Los Angeles county jail, where a number of other inmates had been ill. Prisoner A had been sick before he arrived at San Quentin, suffering from ‘pains over his body accompanied by fever’.19 When he entered San Quentin, Prisoner A ‘mingled with the 1,900 men who were congregated in the yard on Sunday, April 14, ate in the general mess with them, and at night was locked in the receiving room with about 20 other newcomers’.20 Prisoner A’s condition deteriorated the following day and he was admitted to the prison hospital with ‘a temperature of 101, chills, and an aching sensation in the back and bones’.21 From this time on until 26 May, San Quentin underwent an epidemic of unusual severity, with 101 patients admitted to the hospital, of whom seven developed broncho-pneumonia, and three died.
The epidemic was at its height on Tuesday 23 April, when eight new cases were hospitalized; a further sixteen were admitted the following day, 24 April. On these two days, about half of the prison population was ill. According to Stanley,
the records show that whereas ordinarily only 150 to 200 men call each day at the hospital for treatment, consultation, and advice, on these days 700 and 750 appeared.22
Instead of the usual number of from 3 to 7 being excused from work on account of sickness, at this time there were from 25 to 62. All of these men excused from their ordinary tasks were quite ill, having temperatures ranging from 100 to 101, with pains in the back and severe prostration. They should have been placed in the hospital, but it was impossible to put them there on account of lack of facilities. They were allowed to stay in the open air and were not permitted to go to their cells until evening, because, it was believed that this unusual disease might be increased by confinement in stuffy rooms during the day.23
This move reveals one of the early treatment methods for influenza victims. Although doctors had no real understanding of influenza, there remained the prevailing Victorian conviction that fresh air was beneficial to patients, hence the countless entreaties encouraging families of flu victims to open a window.
Stanley was genuinely astonished by the number of flu victims at San Quentin, particularly as he maintained a profound belief that many prisoners faked their symptoms in order to avoid work details. In his memoirs, Stanley reflected on his capacity to ‘distinguish the malingerer, the malcontent, and the hypochondriac’24 although the ‘talent I developed for recognizing faked illnesses has won me a fair share of hatred … I have been pictured as a medical sadist, gloating over tortured victims.’25 As far as Stanley was concerned, this was the price he paid for being a stern, but fair, prison physician.26
But on this occasion, the men at San Quentin were genuinely sick. Although many prisoners who were obviously unwell carried on with their work, so many were ill that in ‘the jute mill, tailor shop, furniture factory, and foundry it was almost impossible to keep up operations, and the governor considered a complete shutdown’.27
Stanley’s article indicates how rapid the onset of influenza was. ‘The weather at this time was warm and balmy, with much sunshine, and the men who felt ill were allowed to leave the mills for periods to go outside. Many felt too ill to return to work and lay down on the ground in the sunshine.’28
The epidemic at San Quentin gradually subsided, but in retrospect Stanley believed that over 500 of the prisoners were ill. Noting that ‘the disease reached its height on Tuesdays and Wednesdays of the second and third weeks’,29 Stanley put forward an explanation. Every Sunday morning, the prisoners were permitted to watch a ‘moving-picture show’, with two screenings, one at eight o’clock and the other at ten. The room in which screenings were shown were partly underground, poorly ventilated, artificially lit and always ‘tremendously crowded’.30 Almost all of San Quentin’s 1,900 prison population attended, and before the morning was over the room was ‘moist, warm, and foul with smoke and human odours’.31 Fans had been installed, but they were not efficient, and there was no time to air the room between shows. One body of prisoners entered the room as soon as the other left. Some prisoners remained for both shows.
Were these movie shows the ground zero of the San Quentin epidemic? Stanley seemed to think so.
Assuming that this respiratory infection attacked its victims at the Shows on Sunday, it would seem that there was an incubation period of from 36 to 60 hours, which produced the sudden illness on the following Tuesday or Wednesday. A typical history of many of the cases is that on Sunday they visited the show, and that on Tuesday or early Wednesday they were seized with headache, fever, chills, bone ache, severe prostration, and sometimes nausea. It seems probable that the epidemic was started and introduced in this prison by the new arrival from Los Angeles, for he was the first one ill, and others became sick shortly after he arrived.32
Stanley admitted that Prisoner A associated closely with the other men, and could probably have passed on the disease by droplet infection. Stanley was also one of the first doctors to notice the peculiar trademarks of this specific strain of flu, including ‘becoming dyspnoeic [distressed breathing], cyanotic [blue due to low oxygen in the blood], and often expelling a thin, sanguineous fluid from the lungs’.33 Stanley also noted another aspect of the disease which had hitherto gone unrecorded: the repeat effect, during which patients would appear to recover, before relapsing and being readmitted. ‘In this epidemic 9 per cent of the cases, after two or three days, had a subsidence of all symptoms and were discharged from the hospital, but in about 10 days returned with a recrudescence.’34
As it would later demonstrate to vicious effect, this new strain of influenza was colour blind and attacked all, regardless of race and creed. At San Quentin, victims were 73 per cent white, 18 per cent Mexican, 6 per cent African American and 3 per cent Chinese. A number of patients attacked by the influenza were so weakened that, according to Stanley, they developed tuberculosis, of which one died.
Stanley’s hypothesis that Prisoner A spread the flu among his fellow prisoners appears to be convincing. But this hypothesis also raises issues about the treatment of Prisoner A from the time of his arrival. If, as Stanley stated, Prisoner A was already suffering from conventional flu, he should have been quarantined to stop the flu spreading. Instead, he was allowed to mix freely with his fellow prisoners and even attend a full house movie screening in a badly ventilated room. Was this carelessness, or was there another factor at play?
In his study of Dr Leo Stanley, the historian Ethan Blue makes it clear that Stanley was no ordinary prison doctor. Dr Leo Stanley was a eugenicist who later became famous for a bizarre series of medical experiments conducted upon the prison population of San Quentin. These included medical experiments of dubious ethical value, including attempting to treat older, ‘devitalized men’ by replacing their testicles with transplants from livestock and recently executed convicts. ‘The practice was known as rejuvenation, the idea being that an aging man could have his testosterone levels renewed by having th
e testicles of a younger man implanted into him.’35 Stanley had already begun the rejuvenation experiments in 1918, five years after taking the post at San Quentin. But Dr Stanley was concerned with more than restoring the virility of flagging older men. Motivated by his eugenicist beliefs, Dr Stanley wanted to remedy what he considered to be ‘the plight of white masculinity in a country increasingly inhabited by a melting pot of races and ethnicities’36 by encouraging white men to reproduce and so-called ‘undesirables’ to undergo sterilization.
Given Stanley’s propensity for experimentation, it does not seem beyond the bounds of possibility that he allowed Prisoner A from Los Angeles County Jail to mix with the prisoners of San Quentin. The prison offered the perfect opportunity for a smart physician to watch the progress of the disease in laboratory conditions. Dr Stanley’s observations about the spread of influenza throughout San Quentin remains an important source. Whether he deliberately tampered with the conditions in order to conduct an early medical experiment is a matter for conjecture, but it remains a convincing theory. Stanley certainly got more than he bargained for with this virulent strain of influenza.
Meanwhile, in the world outside San Quentin, the deadly new strain of influenza began to take its toll, silently, invisibly. The disease remained under the radar in the United States, breaking out here and there with sudden, dramatic impact and then vanishing again. Beyond the careful, record-keeping military and the diaries of strange Dr Stanley, its impact was hard to judge. By the early summer of 1918, the ‘first wave’ of influenza appeared to have receded.
In Europe it was a different story. Influenza was having a catastrophic effect on the war effort, impacting on both sides. One young American’s story gives us some idea of the conditions and shows us what it was like for a man from the comparatively safe haven of mainland US confronted with the suffering in the Old Country.
In Cittadella, Italy, Second Lieutenant Giuseppe Agostoni was tending a 25-year-old soldier in an army hospital. A second-generation Italian-American, Agostoni had watched powerlessly as influenza had devastated his regiment. He and his comrades had never witnessed anything like it. Men were coughing up blood and choking to death on their pus-filled lungs; their faces turned blue and their laboured breathing produced a duck-like quack. In an effort to do something, anything, Agostoni drew out a syringe and attempted to draw blood from the soldier’s arm, rationalizing that draining some of his blood might relieve the congestion. But instead, the blood clotted after 10cc; it had become black and gummy, viscous as tar.37 He did not know it, but as Agostoni gazed hopelessly at his dying patient, similar scenes were being enacted across the entire continent of Europe. He was not alone, but he was just one man in a massive struggle against an invisible enemy: Death, and its sinister agent, the deadly disease with no name.
CHAPTER FOUR
THE INVISIBLE ENEMY
AS THE GERMAN army was launching its massive attack on France in spring 1918, both sides were being attacked by the lethal new strain of influenza. The Allies and the Germans did not realize it at the time, but they were dealing with an enemy mightier than any man-made army.
The German army had launched its attack on France with the conviction that it would win the Great War. With Russia having withdrawn from the war, the Germans were able to deploy over one million experienced men and 3,000 guns to the Western front, where Germany had numerical superiority. Thirty-seven infantry divisions were placed at the Western Front, with another thirty in reserve. In several sectors, the British and French were outnumbered by the German forces by a ratio of four to one.1
While the French position was desperate, the British army had sustained serious losses at the battle of Passchendaele. The Germans, knowing that the Allies were depleted, knew that their main hope of success depended on attacking early before the arrival of the American forces.2
Initially, it seemed as if the Germans were winning, gaining over 1,250 square miles of French soil within four months. By May 1918, the German army had reached the Marne River, and its heavy artillery was within range of Paris. As a result, more than one million people had already fled the French capital.3
But, as the Germans attacked, an invisible enemy was creeping through the Allied Expeditionary Force in France, with doctors and pathologists reporting a widespread fever in Rouen and Wimereux in the ‘ill-famed Ypres salient, where disease of all sorts seemed to flourish’.4 This development obviously raised concerns as the British and the newly arrived American forces on the Western front braced themselves for a major assault from the Germans.
Although other military diseases such as typhoid had been contained, and the British army was in relatively good physical shape despite four years of war, outbreaks of influenza were a regular occurrence. But there was something different about this one.
A rash of articles in medical journals attests to the sudden onset of this epidemic and how it differed from normal influenza. Doctors were intrigued and dismayed by this development, which resisted the traditional classification of ‘la grippe’ or ‘trench fever’. There was clearly something different about this new condition. While Hammond and Rolland had proposed their theory of ‘purulent bronchitis’ for the disease they had witnessed at Étaples, there was considerable disagreement as to the aetiology of this new disease.
While the British Expeditionary Force was succumbing to the mystery illness, reports emerged in March 1918 that influenza had struck the American Allied Expeditionary Force (AEF) crossing the Atlantic to serve in France. In March, 84,000 American ‘doughboys’ had set out for Europe, unaware that influenza had travelled with them on their troopships. The 15th US Cavalry was hit by a pneumonia epidemic on the voyage to Europe, suffering thirty-six cases and six deaths. Private Harry Pressley, who had survived the influenza epidemic at Camp Dix, was among those on board. Private Pressley’s buddy, Cid Allen, who had been forced to carry on drilling at Camp Dix despite his obvious illness, died two days out. Private Pressley never found out whether his friend was buried at sea, or in France.5
By the end of March, as the killer flu continued its remorseless progress through the ranks, one of its most distressing features, acute cyanosis, had become a regular occurrence. On 1 April 1918, American nurse Shirley Millard wrote in her diary: ‘We are swamped with influenza cases. I thought influenza was a bad cold, something like the grippe, but this is much worse than that. These men run a high temperature, so high that we can’t believe it’s true, and often take it again to be sure … When they die, as about half of them do, they turn a ghastly dark grey and are taken out at once and cremated.’6
Despite this disturbing development, the Allies rejoiced at the arrival of their American reinforcements. On 13 April 1918, VAD Vera Brittain looked on as a large contingent of troops arrived at Étaples and a cry went up from the nurses: ‘Look! Look! Here are the Americans!’7
I pressed forward with the [other nurses] to watch the United States physically entering the War, so god-like, so magnificent, so splendidly unimpaired in comparison with the tired, nerve-racked men of the British army. So these were our deliverers at last, marching up the road to Camiers in the spring sunshine. There seemed to be hundreds of them, and in the fearless swagger of their proud strength they looked a formidable bulwark against the peril looming from Amiens.8
The tragic truth was that, although there were already outbreaks of influenza in France, the magnificent doughboys had unwittingly brought another, more virulent strain of the disease with them from the home. On 15 April, the first cases of epidemic influenza in the AEF appeared at a camp near Bordeaux, one of the chief disembarkation ports for American troops.9 Those handsome, healthy farm boys were to pay the price for America’s entry into the war. In the words of epidemiologist Dr Vaughan: ‘City dwellers acquire some degree of immunity to respiratory diseases because they live in an atmosphere frequently or constantly bearing these infections. Country boys are more highly susceptible to the respiratory disease.’10
Influenza killed these young men in their thousands. Indeed, by the end of the war, more Americans would have died from Spanish flu than perished in the war. When Vera Brittain and her comrades greeted the doughboys with such enthusiasm, little did they know that many of these youths were doomed.
Colonel Alfred Soltau of the British Army Medical Service noted that the first outbreaks ‘occurred in the ill-famed Ypres salient, an area where disease of all sorts seemed to flourish’.11 Initially, Colonel Soltau regarded this development impassively; influenza had always been a constant feature of army sick lists.12 As the epidemic spread, the colonel still saw no cause for alarm, but instead found a name for this malaise, christening it ‘three day fever – three days’ incubation, three days’ fever, and three days’ convalescence’.13 Apart from the high rate of patients, he concluded that this illness gave ‘very little cause for anxiety’.14
By the end of May, the first wave of infection had died down, but it recurred dramatically in early June, in rapidly mounting numbers, reaching its height in the third week.
As far as Colonel Soltau was concerned, the most disturbing aspect of the epidemic was that as the epidemic increased in numbers, it became more virulent. While the earlier patients had recovered swiftly and seldom experienced complications, the second onset brought an increasing number of respiratory complications. In June it was estimated that of the cases admitted to the special influenzal centres, some 2 per cent developed serious pulmonary lesions, of whom a very considerable proportion died. This was particularly the case in patients suffering from ‘any old-standing renal lesion. In such cases a rapid increase in the renal inadequacy and a profound toxaemia led almost invariably to a fatal termination.’15
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