10% Human: How Your Body’s Microbes Hold the Key to Health and Happiness. Alanna Collen

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СКАЧАТЬ 1978, Janet Parker became the last person on Earth to die of smallpox. Just 70 miles from the place where Edward Jenner had first vaccinated a young boy against the disease with cowpox pus from a milkmaid, 180 years earlier, Parker’s body played host to the virus in its final outing in human flesh. Her job as a medical photographer at the University of Birmingham in the UK would not have put her in direct jeopardy were it not for the proximity of her dark room to the laboratory beneath. As she sat ordering photographic equipment over the telephone one afternoon that August, smallpox viruses travelled up the air ducts from the Medical School’s ‘pox’ room on the floor below, and brought on her fatal infection.

      The World Health Organisation (WHO) had spent a decade vaccinating against smallpox around the world, and that summer they were on the brink of announcing its complete eradication. It had been nearly a year since the final naturally occurring case of the disease had been recorded. A young hospital cook had recovered from a mild form of the virus in its final stronghold of Somalia. Such a victory over disease was unprecedented. Vaccination had backed smallpox into a corner, ultimately leaving it with no vulnerable humans to infect, and nowhere to go.

      But the virus did have one tiny pocket to retreat to – the Petri dishes filled with human cells that researchers used to grow and study the disease. The Medical School of Birmingham University was one such viral sanctuary, where one Professor Henry Bedson and his team were hoping to develop the means to quickly identify any pox viruses that might emerge from animal populations now that smallpox was gone from humans. It was a noble aim, and they had the blessing of the WHO, despite inspectors’ concerns about the pox room’s safety protocols. With just a few months left before Birmingham’s lab was due to close anyway, the inspectors’ worries did not justify an early closure, or an expensive refit of the facilities.

      Janet Parker’s illness, at first dismissed as a mild bug, caught the attention of infectious disease doctors a fortnight after it had begun. By now she was covered in pustules, and the possible diagnosis turned to smallpox. Parker was moved into isolation, and samples of fluid were extracted for analysis. In an irony not lost on Professor Bedson, his team’s expertise in identifying pox viruses was called upon for verification of the diagnosis. Bedson’s fears were confirmed, and Parker was moved to a specialist isolation hospital nearby. Two weeks later on 6 September, with Parker still critically ill in hospital, Professor Bedson was found dead at his home by his wife, having slit his own throat. On 11 September 1978, Janet Parker died of her disease.

      Janet Parker’s fate was that of many hundreds of millions before her. She had been infected by a strain of smallpox known as ‘Abid’, named after a three-year-old Pakistani boy who had succumbed to the disease eight years previously, shortly after the WHO’s intensive smallpox eradication campaign had got under way in Pakistan. Smallpox had become a significant killer across most of the world by the sixteenth century, in large part due to the tendency of Europeans to explore and colonise other regions of the world. In the eighteenth century, as human populations grew and became increasingly mobile, smallpox spread to become one of the major causes of death around the world, killing as many as 400,000 Europeans each year, including roughly one in ten infants. With the uptake of variolation – a crude and risky predecessor of vaccination, involving intentional infection of the healthy with the smallpox fluids of sufferers – the death toll was reduced in the latter half of the eighteenth century. Jenner’s discovery of vaccination using cowpox in 1796 brought further relief. By the 1950s, smallpox had been all but eliminated from industrialised countries, but there were still 50 million cases annually worldwide resulting in over 2 million deaths each year.

      Though smallpox had released its grip on countries in the industrialised world, the tyrannical reign of many other microbes continued in the opening decade of the twentieth century. Infectious disease was by far the dominant form of illness, its spread aided by our human habits of socialising and exploring. The exponentially rising human population, and with that, ever-greater population densities, only eased the person-to-person leap that microbes needed to make in order to continue their life cycle. In the United States, the top three causes of death in 1900 were not heart disease, cancer and stroke, as they are today, but infectious diseases, caused by microbes passed between people. Between them, pneumonia, tuberculosis and infectious diarrhoea ended the lives of one-third of people.

      Once regarded as ‘the captain of the men of death’, pneumonia begins as a cough. It creeps down into the lungs, stifling breathing and bringing on a fever. More a description of symptoms than a disease with a sole cause, pneumonia owes its existence to the full spectrum of microbes, from tiny viruses, through bacteria and fungi, to protozoan (‘earliest-animal’) parasites. Infectious diarrhoea, too, can be blamed on each variety of microbe. Its incarnations include the ‘blue death’ – cholera – which is caused by a bacterium; the ‘bloody flux’ – dysentery – which is usually thanks to parasitic amoebae; and ‘beaver fever’ – giardiasis, again from a parasite. The third great killer, tuberculosis, affects the lungs like pneumonia, but its source is more specific: an infection by a small selection of bacteria belonging to the genus Mycobacterium.

      A whole host of other infectious diseases have also left their mark, both literally and figuratively, on our species: polio, typhoid, measles, syphilis, diphtheria, scarlet fever, whooping cough and various forms of flu, among many others. Polio, caused by a virus that can infect the central nervous system and destroy nerves controlling movements, paralysed hundreds of thousands of children each year in industrialised countries at the beginning of the twentieth century. Syphilis – the sexually transmitted bacterial disease – is said to have affected 15 per cent of the population of Europe at some point in their lifetime. Measles killed around a million people a year. Diphtheria – who remembers this heart-breaker? – used to kill 15,000 children each year in the United States alone. The flu killed between five and ten times as many people in the two years following the First World War than were killed fighting in the war itself.

      Not surprisingly these scourges had a major influence on human life expectancy. Back then, in 1900, the average life expectancy across the whole planet was just thirty-one years. Living in a developed country improved the outlook, but only to just shy of fifty years. For most of our evolutionary history, we humans have managed to live to only twenty or thirty years old, though the average life expectancy would have been much lower. In one single century, and in no small part because of developments in one single decade – the antibiotic revolution of the 1940s – our average time on Earth was doubled. In 2005, the average human could expect to live to sixty-six, with those in the richest countries reaching, again on average, the grand old age of eighty.

      These figures are highly influenced by the chances of surviving infancy. In 1900, when up to three in ten children died before the age of five, average life expectancy was dramatically lower. If, at the turn of the next century, rates of infant mortality had remained at the level they were in 1900, over half a million children would have died before their first birthday in the United States each year. Instead, around 28,000 did. Getting the vast majority of children through their first five years unscathed allows most of them to go on and live to ‘old age’ and brings the average life expectancy up accordingly.

      Though the effects are far from fully felt in much of the developing world, we have, as a species, gone a long way towards conquering our oldest and greatest enemy: the pathogen. Pathogens – disease-causing microbes – thrive in the unsanitary conditions created by humans living en masse. The more of us we cram onto our planet, the easier it becomes for pathogens to make a living. By migrating, we give them access to yet more humans, and in turn, more opportunity to breed, mutate and evolve. Many of the infectious diseases we have contended with in the last few centuries originated in the period after early humans had left Africa and set up home across the rest of the world. Pathogens’ world domination mirrored our own; few species have as loyal a pathogenic following as us.

      For many of us living in more developed countries, the reign of infectious diseases is confined to the past. Just about all that remain of thousands of years of mortal combat with microbes are memories of the sharp prick of our childhood СКАЧАТЬ