Smoking Ears and Screaming Teeth - Trevor Norton (2010)
The Desire for Disease
‘Physicians of the utmost fame
Were called at once, but when they came
They answered, as they took their fees,
There is no cure for this disease’
– Hilaire Belloc
In the early nineteenth century it was inadvisable to be downwind of a city, for its streets were paved not with gold but with ‘malignant effluvia’. Every day twenty-three tonnes of horse droppings were removed from London’s two most fashionable shopping streets. Elsewhere, no one bothered. The fate of garbage was to accumulate and rot. There was no system for removing waste. In Leeds, for example, half the streets had no drains. In one area of the city there were only two privvies for 400 people. The local authority removed the accumulated effluent from just thirty houses – it required seventy cartloads.
Festering slums were breeding grounds for diseases. Edwin Chadwick’s monumental report into the ‘sanitary conditions’ of the working class in 1842 revealed that labourers and mechanics in Manchester had a life expectancy twenty years shorter than rural labourers in the surrounding countryside. Fifty-seven per cent of the children of Manchester’s poor never saw their fifth birthday. The gentry also fared better. They could expect to live well into their forties, whereas a labourer was lucky to see his twentieth birthday. As a Tory politician made clear, the lot of the poor ‘must always be eating, drinking, working and dying’. But if the workers became diseased and died prematurely, their families were flung onto the street and became reliant on the state. Worse still, how could the well-to-do avoid catching the dreadful diseases intended for the poor?
Medics had little knowledge of how diseases were transmitted from one person to another. Probably it was through personal contact with the sick or perhaps from their bed linen or utensils. It was easy for the wealthy mill owner to avoid sharing the slum dweller’s spoon, but there was a more pernicious mechanism at work.
The medical profession firmly believed that decay did not merely produce a bad odour but also airborne poisons – malicious ‘miasmas’ carried by the wind. Malaria, for example, means ‘bad air’. Since ‘all smell is disease’ courtrooms were crammed with bowls of flowers whose scent would nullify the dangerous stench of prisoners.
The Houses of Parliament sat beside the fetid river Thames and the ‘Great Stink’ of 1858 shut down the seat of government to spare the ‘nasally tortured’ members. Perhaps from fear of being ‘miasmatised’ the House voted substantial funds to begin the construction of a network of sewers to carry the city’s waste down to the lower reaches of the river.
This was undoubtedly the largest single contribution to London’s future health, but it was not the smell of the river that had to be feared. Should you fall from London Bridge, it would be far better to drown quickly than to be rescued to die slowly from some dreadful disease. Yet the majority of citizens got their drinking water from the river.
A worldwide epidemic of cholera began in India in 1817 and lasted for almost twenty years, leaving mountains of corpses in its wake: forty million died in India alone; one in every twenty Russians perished. A succession of pandemics followed with high death tolls in Hungary, Japan and the United States. Three thousand pilgrims to Mecca died in a single night. In Britain there wasn’t a city that escaped. Prompt action to deal with outbreaks was often impeded by merchants and other ‘interested parties’ who vociferously denied that cholera had arrived in their city. Medical authorities condemned people of ‘gross and unexampled ignorance or shameful venality who … continue to deny the existence of an unusual disease, until the choked graveyards bear witness to the deplorable fact’. Even some doctors were accused of ‘perverting and concealing facts which militate against their respective theories’. Perhaps ‘when desolation and death thicken around … reason becomes silent’, or the unreasonable become deaf.
Cholera strikes like a hammer. A seemingly healthy person can collapse and be swamped in vomit and pints of diarrhoea. One woman was stricken so suddenly that she fell into the fire. In Paris cholera struck a society ball with couple after couple collapsing mid-waltz. It was said that some were hastily buried, still in their evening gowns.
The lucky ones died within hours. Many of those who clung to life turned blue or black and succumbed to extreme dehydration. When they had no more fluid to void, they expelled fragments from the lining of their gut. The pain was ‘like a sword put in on one side of the waist and drawn through, handle and all’. It is a ghastly way to die.
In 1832 a Dr Latta showed that patients with cholera could be saved by ‘copious injections of saline fluids into the veins’. Sadly, other physicians continued to do the opposite, giving purges and vomit-inducers to patients who were expelling vast quantities of water from every aperture, presumably ‘to assist in hurrying them to the grave’.
Countries were powerless to halt the disease’s spread. Troops were stationed on their borders to keep out possible carriers. Ports quarantined ships from infected areas. At the beginning of the voyage of the Beagle, Darwin was prevented from landing in Tenerife ‘by fears of our bringing the cholera’.
Diverse ‘cures’ and preventative measures were tried. Medics had great faith in ‘distracting’ the disease by applying severe irritants to the patient’s skin. One remedy involved blowing hot air under the bedclothes – to such good effect that it set fire to the bed. Patients were given a ‘flannel cummerbund’ or swathed in bandages like a mummy and told to inhale toxic fumes of mercury. They should also drink ‘tonics’ containing ammonia and nitric acid or strychnine, and eat beef and peas boiled in chlorine.
There were ‘official’ days of fasting and humiliation to beg God to erase the pestilence. But if cholera was indeed a punishment for our sins, it was strange that during cholera epidemics prisons were the safest places in the land. Others who benefited were healthy tramps who turned up on the doorsteps of grand houses to announce that they were oozing with cholera and demand money to go away.
The greatest beneficiary was a London clergyman who established a life insurance scheme during a cholera outbreak in 1877. He gambled that most people didn’t catch the disease and many of those that did survived. The premiums were only a penny a week, but he later retired a rich man when the Prudential had become a million-pound business.
Attempts were made to ‘clear the air’ of miasmas: towns were shrouded in smoke billowing from barrels of burning tar, citizens were deafened by the sound of mortars being fired heavenward every hour. It was even suggested that gunpowder should be exploded in bedrooms. These methods proved as effective as Joseph Addison’s country gent who nailed shut his gate to keep out the crows.
Although the Board of Health favoured the miasma theory, a puzzling feature of cholera was that it didn’t fit the airborne scenario. Sometimes among people living in close proximity and breathing the same air some contracted the disease while others didn’t. Also, since the gut was affected first, the causal agent was perhaps ingested rather than inhaled.
That was certainly the belief of John Snow, a doctor who had trained at the Hunterian School of Medicine in Soho. He was a successful physician and by means of experiments on animals and himself he had invented an inhaler that delivered a regulated dose of anaesthetic to the patient. By removing much of the uncertainty from anaesthesia he became the expert in the field. It was he who gave chloroform to Queen Victoria to ease her deliveries.
Snow had been in Sunderland during England’s first cholera epidemic and became seriously involved with the disease when there was an isolated outbreak in London in 1849. Within ten days almost six hundred people died in a small area of Soho. Florence Nightingale, a young nurse at the local hospital, could do nothing but watch them die. Karl Marx, a local resident, described Soho as ‘a choice district for cholera’.
In the first-ever epidemiological study Snow plotted where every victim lived and discovered that all those who caught cholera had drunk water from the Broad Street pump. None of the seventy workers at the Broad Street brewery fell ill because the brewery had its own well. Free beer was also available to employees and we now know that beer is poisonous to the organism that causes cholera. The local workhouse also had its own well and only five of its 535 inmates died of cholera. Removing the handle from the pump accelerated the decline of the outbreak. Later, the water supply to the pump was found to be contaminated from a leaking cesspool in a cellar only a few yards away.
In a later study Snow discovered that the incidence of cholera was fourteen times higher in areas of the city where the drinking water came from the Southwark and Vauxhall Company compared with those communities supplied by the Lambeth Company. Both the companies got their water from the river, but the Southwark and Vauxhall obtained their supply downstream from a large sewage outfall, whereas the Lambeth Company pumped up water from above the discharge. Dickens was right when he wrote: ‘Look at the water. Smell it! That’s wot we drinks. How do you like it?’
Although he couldn’t name the causal organism, Snow had no doubt that cholera was a waterborne disease originating from contaminated drinking water. It did not convince everyone – in fact, it convinced hardly anyone. When he pleaded for the handle to be removed from the Broad Street pump, ‘not a member of his own profession, not an individual in the parish believed that Snow was right’. Nor was there great enthusiasm for public health measures. The Times declared that as a nation ‘we prefer to take our chance with cholera … than be bullied into health … There is nothing a man hates so much as being cleaned against his will, his pet dung heaps cleared away … It is a positive fact that many have died of a good washing … no longer protected by dirt.’ A cleric railed against failing to give God credit for catastrophes and ‘explaining away the Lord’s visitation into a carnal matter of drains’. Snow died young in 1858 and it would be a generation before he was credited with his major discovery.
Diehard miasmatists were determined not to be persuaded. Even The Lancet published several articles dismissing Snow’s conclusions. His sternest critic was a German chemist called Max Pettenkofer, whose achievements so far had been developing a method for separating platinum from gold, improving the quality of German cement and producing red Bavarian glass. On his appointment as Professor of Medical Chemistry at the University of Munich he turned his attention to improving public health and exploring the connection between disease and the environment. His idea was that the unhygienic conditions endured by the poor rendered them more susceptible to miasmas.
When cholera broke out in Munich in 1854 Pettenkofer mapped the geography of the victims, just as John Snow had done in London. He claimed that the majority of the deaths occurred in low-lying damp areas and he amplified this into a grand theory. Fresh air permeated into these damp soils and instigated an unspecified chemical reaction to produce a poisonous miasma. He didn’t attempt to isolate or identify this deadly emanation.
Elsewhere others were finding a very different cause of disease. Louis Pasteur in Paris and Robert Koch in Berlin were independently developing what became known as the germ theory of disease. Pasteur demonstrated that decay was not merely a chemical reaction; it was mediated by microbes and could be arrested by pasteurisation (repeated heating and cooling). He also developed a vaccine for rabies.
Koch, his bitter rival, developed microscopes that allowed him to see and characterise these tiny bacteria. He was a brilliant microbial detective. He and his team tracked down the microbes responsible for anthrax, gonorrhoea, leprosy, pneumonia, typhoid and syphilis. He also produced a set of rules by which the causal agent of a disease could be established:
1. Isolate the bacterium from an infected animal.
2. Culture it in the laboratory. For this job Koch’s assistant Julius Petri invented the Petri dish.
3. Demonstrate that the microbe produces the symptoms of the disease when injected into a healthy animal.
4. Finally, re-isolate the microbe from the infected animal.
The problem with cholera was that it didn’t infect animals, only people, so it was difficult to experiment with. Both Pasteur and Koch sent teams to Egypt during an epidemic to study the disease. The co-leader of Pasteur’s team died of cholera.
When the Egyptian outbreak waned Koch went on to India where cholera was always available. He isolated from both live and dead victims a tiny comma-shaped bacterium that he called Vibrio cholerae. He had found the cause of cholera.
Max Pettenkofer was not impressed. He scoffed at those who ‘confine themselves to the behaviour of the comma bacteria in test tube or plate’. He conceded that the bacterium might play some role, but the disease could only develop if certain environmental factors were favourable such as the ‘right’ soil – no matter that several researchers had examined the soil where outbreaks were rife and found that it wasn’t the ‘right’ type. Koch also showed that the cholera bacterium was present in the water supply drunk by victims. And in Hamburg, where either side of the same street had a different water supplier, only those on the contaminated side fell ill. It was, as Snow had asserted, a waterborne disease.
When Koch referred to him disparagingly as ‘Herr Localist’, Pettenkofer could take no more. In 1893 he requested a sample of Vibrio cholerae and Koch’s laboratory obliged. Pettenkofer had no intention of studying the bacteria; he had a far more dramatic experiment in mind. Propelled by the certainty that he was right, he would put Koch in his place.
When Pettenkofer had been young he had had theatrical ambitions. In Goethe’s Egmont he had played the unsuccessful lover who feigns to swallow poison but wisely refrains. This time the seventy-four-year-old professor in love with his theory held the flask of bacteria aloft and announced to his assembled colleagues: ‘Even if I deceived myself and the experiment endangered my life, I should face death calmly, for it would not be a thoughtless or cowardly suicide. I should die in the cause of science.’ To the horror of his audience he drank the contents of the flask.
He suffered severe stomach cramps and diarrhoea that lasted for a week. These were symptoms of cholera but relatively mild. How did he cheat death? Did a concerned colleague heat the culture to make it less virulent or was it a less dangerous strain, or was he just lucky? In epidemics many people contract the disease but don’t die.
Pettenkofer sent a note to Koch boasting that: ‘Herr Doctor Pettenkofer has now drunk the entire contents … and is happy to be able to assure Herr Doctor Professor Koch that he remains in his usual good health.’
He was convinced he had disproved ‘once and for all’ the idea that drinking water could spread cholera. He rejected all this ‘zealous comma-hunting’ for without the ‘cholera miasm’ from the soil the bacterium was harmless. But he was swimming against a rising tide. His theories were progressively discredited by everyone except his former students. Even fellow professors in Germany dismissed them as ‘nonsensical’ or ‘the product of an inventive imagination … built on drastic hypotheses that are entirely contradicted by the real facts’.
Pettenkofer’s case highlights the danger inherent in medical research reliant on trying to find correlations between external factors and specific diseases. Because in the incident that he investigated cholera was more prevalent in damp places, Pettenkofer leapt to the conclusion that damp soil was implicated in causing the disease and then devised a theory to explain how. The problem is that correlations frequently occur between totally unrelated factors. For example, the number of pigs reared in the United States followed the same trends as the production of pig iron. This did not necessarily indicate that pigs provided the raw material for ingots. In Britain there was found to be a correlation between the number of TV licences bought and the incidence of mental illness. Was this proof that TV addled the brain or that only the mentally impaired bought licences? Or was it just a chance correlation of unrelated things? The news is full of reports such as that natives of Tuscany use more olive oil and drink more red wine than the British, and have a lower incidence of heart disease. So should we get oily and drunk to prevent heart attacks? There may be dozens of reasons why Tuscans suffer less from cardiac problems: unlike the Brits they don’t consume two million tonnes of chips every year, or think that taking a deep breath is a form of exercise. One could argue that a heart attack isn’t such a bad way to go compared to the horrors that may lie in wait should your heart keep going.
For his undoubted achievements in the field of public health Pettenkofer was rightly rewarded with a gold medal from the British Institute of Public Health. In Germany he was elevated to the aristocracy as His Excellency Max von Pettenkofer. But even these honours failed to quench his bitterness as the support for his theory of infection proved to be as insubstantial as a miasma.
Nine years after he had risked his life by tasting cholera, His Excellency conducted his final experiment by putting a revolver to his temple and pulling the trigger.
Had Pettenkofer sacrificed himself to cholera he would not have been alone among self-experimenters. Curiosity has killed more than cats.
In 1885 Daniel Carrión, a Peruvian medical student who was studying a skin disease called verruga, inoculated himself with blood from a patient’s ‘wart’. He was soon dangerously ill and it became clear that he was suffering from a fatal blood disease called Oroya fever. Daniel realised his plight, as a friend had recently died of the same disease, but he also appreciated what he had discovered. ‘This is the evident proof,’ he said, ‘that Oroya fever and the verruga have the same origin.’ Within weeks twenty-six-year-old Daniel was dead and the physician who had initially discouraged him from experimenting but had then assisted him was arraigned for murder, although he was later acquitted. Daniel was acclaimed in Peru and there is a statue of him in Lima.
The search to determine how yellow fever was transmitted was also not without casualties. As with so many epidemic diseases, yellow fever influenced history. Had Napoleon’s Caribbean army not been decimated by the fever, which prompted the sale of Louisiana and a vast amount of other land, North America might well have become French.
Yellow fever damages the liver, causing jaundice. The blood fails to clot and leaks into the stomach to be regurgitated as black vomit. The illness is often fatal within days. Clearly not a disease to messed with, but that didn’t stop the researchers. Although there was no evidence that carers caught the fever from their patients, often relatives merely abandoned sufferers for fear of contracting the disease. In 1804 Stubbins Ffirth, an American medical student, decided to determine that it was contagious. He slept alongside fever patients who were ‘attended by black vomit’ and ensured that he received ‘the breath of patients in my face’. But he had only just begun to explore the encyclopaedia of unpleasantness.
Black vomit may not be everyone’s cup of tea, but Ffirth spent hours inhaling the vapour from simmering vomit until he felt too nauseous and faint to continue. Although a dog he had injected with black vomit died within minutes, he injected it into his own veins and into deep cuts on his arms. He smeared his body with blood, sweat and urine, and drank the saliva, blood and vomit of infected patients. As someone who declines a second helping of black pudding, Ffirth’s appetite for black vomit wins my admiration.
He didn’t catch the disease, and therefore wrote a reassuring article: ‘I hope these experiments will have a tendency to allay … that great fear which some have … as it is at least doubtful whether it is ever communicated from one person to another by means of contagion.’
After all Ffirth’s ordeals, the publication of his results had little influence for he had not shown what caused the disease. Almost a century later the cause was still unknown and there was concern over the high death rate of troops in the Spanish–American War. An American army medical team led by Walter Reed was dispatched to Cuba to discover how the disease was transmitted.
Mosquitoes were suspect as they were being implicated in the transmission of malaria and filariasis (elephantiasis). Yellow fever doesn’t occur in animals so there was no choice but to experiment on humans. In Cuba, where yellow fever was endemic, it would be almost impossible to find many non-infected volunteers and urgency was in the air as experts from the Liverpool School of Tropical Medicine had arrived on a similar mission. The team also had ‘a grave sense of responsibility … which the conscientious observer must always feel, even with the full consent of the subjects to be experimented upon’. So they made a pact that they would all consent to experiment on themselves. No sooner was this agreed than Reed, the team leader, departed for Washington.
The procedure was simple. Mosquitoes were placed on the arms of patients with yellow fever and were then used to infect the experimenter. The first to submit to this was a bacteriologist called Jesse Lazear, but he didn’t develop any symptoms. Next in line was an Englishman, James Carroll, who had studied medicine in the United States. He had a wife and four children. Earlier he had been a guinea pig in tests of an experimental vaccine against typhoid, but by accident the inoculum still contained live bacteria and seven out of the twelve volunteers went down with typhoid. Carroll had avoided infection, but this time he was not so fortunate. Within days he was seriously ill with yellow fever and his appearance shocked his colleagues. His yellowed eyes were bloodshot, and he became feverish and too weak to stand.
Although Carroll’s life had been in the balance, Lazear, who was later described as being ‘oblivious of self’, was exposed again to infected mosquitoes to confirm the findings, which he did with a vengeance. He was soon spurting black vomit, and there was fear in his eyes before he became delirious. Within twelve days he was dead. He was thirty-four years old. His pregnant wife received a telegram that merely stated: ‘Dr Lazear died at eight p.m. this evening.’ She hadn’t even been told that he was ill.
The report of their findings was published in record time, only two months after Lazear’s death. Reed wrote: ‘The mosquito serves as the intermediate host for the parasite of yellow fever, and it is highly likely that the disease is only propagated through the bite of this insect.’ The experts weren’t convinced and the press were scornful. According to the Washington Post: ‘Of all the silly and nonsensical rigmarole about the yellow fever that has yet found its way into print … the silliest beyond compare is to be found in the arguments and theories engendered by the mosquito hypothesis.’
So the experiments continued, this time with local volunteers, each of whom was given $100 in gold, with an extra $100 if they caught the fever. Those rejected wept with disappointment. Some volunteers had to sleep for three weeks in the pyjamas and bed sheets soiled by yellow fever patients and with their heads resting on pillows covered with a towel soaked in a patient’s blood. None of the volunteers caught the fever, which merely replicated Ffirth’s results from similar ordeals ninety-three years earlier.
To identify the causal organism volunteers were injected with infected blood that had been filtered to remove all bacteria. They still became feverish, because the microbe responsible was a virus (although no one knew this at the time), which is much smaller than a bacterium and could pass through the filter.
Others were injected with blood from a mildly infected patient in the hope that this would act as a vaccine conferring some immunity. These injections killed a young nurse. Two soldiers also died and another became so incapacitated that only public donations saved this ‘soldier who gave himself to science’. All volunteers had to sign a cunningly worded waiver indicating that he might develop a fever which ‘endangers his life to a certain extent, but it being entirely impossible to avoid the infection during his stay in this island, he prefers to take the chance of catching it intentionally …’
Walter Myers, one of the Liverpool team, also died of yellow fever and Carroll never fully recovered his health. Sadly, Carroll and Lazear received little recognition for the risks they took, whereas Reed, the team leader who was a thousand miles away at the time of the fateful experiments, was lauded as a valiant pioneer and his name was immortalised in the Walter Reed Military Hospital in Washington. Perhaps the moral is that it is far better to write up the report than to take part in the experiments.
Yellow fever was not eradicated from the United States until 1905 and remains a serious threat in the tropics. The causal virus has now been identified, but once the disease has taken hold there is no cure. Mass vaccination is effective, but in 2008 a shortage of vaccine compromised the campaign worldwide.
Even when a vaccine is developed it may not be well received. A British Army doctor called Almroth Wright developed a vaccine against typhoid fever. Existing vaccines involved giving the patient a mild infection of typhoid to stimulate the body’s defences. Unfortunately, sometimes the ‘mild’ typhoid killed the patient. Wright’s idea was to inject dead typhoid bacteria in the hope of fooling the immune system into thinking it was under attack, thus producing immunity with no risk of getting infected by the inoculation. The only problem was that to test whether or not it was effective, the body had to be challenged with the real disease. So in 1897 Wright and ten of his laboratory assistants injected themselves with the vaccine and then with typhoid. It worked.
The new vaccine was issued to British troops departing to fight in the Boer War. Such was their suspicion of the injections that boxes of vaccine were flung into the sea. As a consequence only four per cent of the soldiers benefited from the vaccine and 9,000 died from typhoid. Even today 600,000 people die every year for want of a vaccination.
Prejudice against new findings that challenge existing beliefs is not a thing of the distant past. When I was young it seemed to me that not only my father but all my mates’ fathers suffered from duodenal ulcers. Every doctor knew they were caused by stress, smoking, bad diet, alcohol. The treatment was to take antacids or have major surgery.
In the early 1980s Barry Marshall, an Australian microbiologist, teamed up with a pathologist called Robin Warren to document the bacteria living in the human gut. They found that one species, Helicobacter pylori, was invariably present in patients suffering from duodenal ulcers and also in seventy-five per cent of those with stomach ulcers. Could it be the causative organism?
To find out, Marshall slid a tube down his throat into his stomach and removed fragments of the stomach lining. These were examined to ensure that he didn’t have either a gut infection or Helicobacter. After allowing time to let the gut wall heal he swallowed a culture of the bacterium. He had, of course, taken precautions before doing so. Firstly, he didn’t inform the hospital ethics committee in case it refused permission and secondly, he didn’t tell his wife until after he had taken the draught. She guessed anyhow when within days he became listless and began vomiting. To add insult to self-inflicted injury, his wife informed him that his breath was ‘putrid’. A series of biopsies of his gut tissue revealed severe inflammation (gastritis) that precedes ulceration. Fortunately he cleared up the problem with an antibiotic. Marshall and Warren went on to show that when the Helicobacter bacteria were eliminated, symptoms of gastric ulcers vanished within days and the ulcers began to heal even in patients who had suffered from them for decades. Yet it was thirteen years after Marshall’s experiment before this treatment became widely available in western hospitals. During that time perhaps hundreds of thousands of patients were given the wrong drugs or underwent unnecessary surgery.
At first critics scoffed at the idea that gastric ulcers were an infection since everyone knew they were the result of a chemical imbalance. As for bacteria living in the stomach, it was far too acid an environment for that. Worst of all, perhaps, Marshall was a junior doctor at the time and neither he nor Warren was a gastroenterologist. What did he know about such matters?
Well, sufficient to be awarded the Nobel Prize for medicine in 2005.
A mosquito caught in the act of transmitting one disease or another.