England's chief medical officer on why the drugs don't work

Large-scale resistance to antibiotics is inevitable, yet new antibacterials aren't emerging. Why?

The Drugs Don’t Work: a Global Threat
Sally C Davies, with Jonathan Grant and Mike Catchpole
Penguin Specials, 112pp, £3.99

Professor Dame Sally Davies, England’s chief medical officer, likens the impending crisis in antimicrobial drug resistance to global warming. In both instances scientists foresee a problem and can offer solutions. In neither case is our response anywhere near sharp enough, Davies fears. Acting on antibiotic resistance should be the easier of the two; no one has a vested interest in denying the risk. Why then are we stumbling towards a selfmade but preventable calamity?

Alexander Fleming is credited with discovering antibiotics. In the summer of 1928, while working at St Mary’s hospital in London, he went on holiday and left an open plate of bacteria behind. Returning to work, he found a fungus growing on the plate that had killed the bacteria with a chemical that he named penicillin. In 1930s Oxford, Howard Florey and Ernst Chain produced enough penicillin to prove its healing ability. The penicillin production programme that followed during the Second World War is a classic tale of ingenuity under adversity. By engaging American pharmaceutical companies, the Allies were able to cure soldiers of otherwise fatally infected wounds.

Bugs create chemicals to kill other bugs as part of an aeons-old microbial arms race, so drug-hunters turned to soil microbes to help fight a range of diseases. Streptomycin, discovered in America in 1943, even cured tuberculosis, one of mankind’s greatest afflictions. Today, however, roughly a third of the world’s population still carries TB. Of the nearly 9,000 cases reported in the UK in 2011 hundreds of sufferers were resistant to at least one drug. Half a dozen cases carried incurable, “extensively drug-resistant” strains of TB. Cholera, leprosy, typhoid fever and syphilis all remain global scourges. Just last year several people in Edinburgh died after inhaling legionnaire’s disease-causing bacteria. Dozens of Germans died in 2011 after eating beansprouts contaminated with E coli.

Luckily, for now at least, we can still treat most bacterial infections, but some bacterial cells can yield over a billion progeny in just 24 hours. Genetic mutations stimulating drug resistance are inevitable. Cases of penicillin resistance appeared almost immediately: methicillin, a more stable derivative of penicillin, enjoyed only a few years of success before resistance emerged. Methicillin-resistant Staphylococcus aureus (MRSA) now kills hundreds in British hospitals every year.

Yet new antibacterials aren’t emerging. The reasons for this are primarily economic. Antimicrobial agents are usually given in shortterm doses. Compare that to statins, taken by affluent westerners with high cholesterol over decades. Most antibiotics are also off-patent, which has driven prices down. The estimated $1bn it costs to develop a drug inflates the cost of new medicines. Cash-strapped health services will use cheaper, old drugs until their utility is all but gone.

Davies fears that time might come quickly. Resistance genes are flourishing out there and bacteria are remarkably happy to share their genes. The widespread imprudent use of antibiotics has created perfect conditions to select those resistance genes and global air travel can carry resistant bugs around the world in hours.

Davies offers possible solutions. Fifteen years ago the pharmaceutical industry had largely abandoned diseases of the poor – malaria, tuberculosis, sleeping sickness, bilharzia and so on. An anti-sleeping sickness drug, called eflornithine, was even about to be withdrawn because sufferers couldn’t pay for it. When eflornithine was shown to prevent unwanted hair growth, however, pharmaceutical companies fell over themselves to produce it. Economics dictated that a drug could be made to “treat” unwanted facial hair but not to save lives. New models were needed to combat diseases of the poor. Groups such as the Medicines for Malaria Venture and Drugs for Neglected Diseases Initiative emerged to help promote drug development. A decade on, the first new drugs are poised to appear. The pharmaceutical industry itself, though, is in crisis and shedding staff at an alarming rate.

If a pestilential Armageddon really is upon us, a cynical company might gamble on huge profits, getting new antimicrobials ready for when the competition fails. But the economic models won’t shift until the evidence becomes overwhelming. Davies also talks of incentivisation – a £50m prize to develop a new antibiotic, for instance. Given development costs, $1bn would be more realistic. Yet even that’s a snip compared to the taxpayers’ bank bailouts. Surely saving life trumps life savings. Whatever it takes, though, action is needed now. The big pharmaceutical companies continue to abandon their anti-infective programmes and with them goes the expertise and capacity that will be needed when the crisis hits.

Michael Barrett is Professor of Biochemical Parasitology at the University of Glasgow

Who decides which drugs are made, and which ones we have access to? Image: Getty

This article first appeared in the 30 October 2013 issue of the New Statesman, Should you bother to vote?

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Paul Auster's 4 3 2 1 is by turns rewarding and maddening – just like life

Auster’s epic new novel of immigration, politics and consciousness is rich but imperfect.

It’s a cliché, or a joke: the immigrant who arrives in the New World from the Old Country, to be greeted by an official who promptly renames him, mishearing the strange tongue that the arrival speaks. Paul Auster’s new novel begins: “According to family legend, Ferguson’s grandfather departed on foot from his native city of Minsk with one hundred rubles sewn into the lining of his jacket, travelled west to Hamburg through Warsaw and Berlin, and then booked passage on a ship called the Empress of China, which crossed the Atlantic in rough winter storms and sailed into New York Harbor on the first day of the twentieth century.”

Ferguson’s grandfather is called Isaac Reznikoff. Another Russian Jew advises him that it will be wiser to give his name as “Rockefeller” to the official. “You can’t go wrong with that.” But when it is his turn, “the weary immigrant blurted out in Yiddish, Ikh hob fargessen (I’ve forgotten)! And so it was that Isaac Reznikoff began his new life in America as Ichabod Ferguson.”

A joke or a fable: the way that so many stories begin in America, the stories of those who sailed past the Statue of Liberty and the words inscribed on its base, words to welcome the tired, the poor, those masses yearning to breathe free. And so Auster, in his first novel in seven years, presents the reader with an Everyman, Ferguson-who-is-not-Ferguson, not the man who stepped off the Empress of China but his grandson, Archibald Isaac Ferguson, the cranky protagonist and hero of this tale.

Ichabod begat Stanley and Stanley begat Archie, who was born, like his creator, in Newark, New Jersey, in 1947. This nearly 900-page epic is a Bildungsroman, though it would be more accurate to call it a Bildungs-Bildungs-Bildungs-Bildungsroman, because Archie’s story is told not once but four times. There are that many versions of the protagonist: in each version, his life takes a different turn, and so everything that follows is altered.

Auster is something of a prophet in exile in his own land. His brand of existentialist postmodernism – in which characters with the author’s name might appear, in which texts loop back on themselves to question the act of writing, in which the music of chance can be heard loud and clear – has sometimes found greater favour in Europe than it has in his native United States. For example, City of Glass, the 1985 meta-detective novel that forms part of The New York Trilogy, will be adapted for the stage here this year.

But City of Glass, like all of Auster’s previous books, is a slender novel. The New York Trilogy as a whole comes in at just over 300 pages. Where much of Auster’s work is elliptical, 4 3 2 1 can be overwhelming, but that is precisely the point. The author creates a vast portrait of the turbulent mid-20th century by giving his protagonist this series of lives. The book is divided into sections that clearly mark which Ferguson we are getting: 1.1, 1.2, 1.3 or 1.4.

Yet there is nothing supernatural about this journey lived and relived, as there was in Kate Atkinson’s Life After Life. The only magic involved is the magic of the novelist’s imagination, which allows both writer and reader to juggle realities as if they were balls in the air.

However, it is not as if one Ferguson is midshipman and another a circus performer, or one a loudmouth and another shy and retiring. The strength of this novel is that Ferguson remains himself while events shift around him, changing the course of his life. Ferguson’s father dies, or Ferguson’s father lives but divorces his mother, Rose. What happens then? Rose is a talented photographer; does she continue her work when Stanley prospers and they move to the suburbs, or does she take up golf and bridge? Ferguson is a good student, always a writer: does he go to Princeton or Columbia? What’s the difference between translating poetry in a Paris attic and working as a journalist for the Rochester Times-Union?

At its best, 4 3 2 1 is a full immersion in Ferguson’s consciousness, which, perhaps, is a consciousness not too far removed from Auster’s. His protagonist’s youth is wonderfully, vividly conveyed. Even if you don’t care about baseball, you’ll come to care about it because Ferguson does. The details of the young Ferguson’s life are carefully and lovingly created: the powder-blue Pontiac that his mother drives, the pot roast and cheese blintzes served at the Claremont Diner in Montclair, New Jersey – and  the floorboards in an old house that creak when two young lovers make their way between their separate rooms in the middle of the night. Auster builds a world of heartfelt, lived-in detail.

But this is a novel of politics, too. Ferguson is a young man during the tumult of the late 1960s, when dozens were killed and hundreds injured during riots in Newark in 1967; when students at Columbia occupied the campus in protest over the war in Vietnam; when young men such as Ferguson could be drafted to fight in that war.

It is in this last third of the novel that the book flags a little, as lists of events tumble on to the page: one paragraph contains the My Lai massacre, the killing of the Black Panther Fred Hampton and the Rolling Stones concert at Altamont. At times, history lessons threaten to overwhelm the narrative, and Ferguson’s story/stories lose the texture and particularity that have made them so compelling. And its ending is abrupt, a tying-up of loose ends that fragments on the final page.

But then lives – real lives – have strange, abrupt endings, too. This is a rich, imperfect book, often rewarding, occasionally maddening. Again, like life, or at least if we’re lucky.

4 3 2 1 by Paul Auster is published by Faber & Faber (880pp, £20)

Erica Wagner is a New Statesman contributing writer and a judge of the 2014 Man Booker Prize. A former literary editor of the Times, her books include Ariel's Gift: Ted Hughes, Sylvia Plath and the Story of “Birthday Letters” and Seizure.

This article first appeared in the 19 January 2017 issue of the New Statesman, The Trump era