IELTS Academic Reading Practice Test 333

Medicine in the late nineteenth century could offer very little to a patient with an infectious disease. Surgeons could cut and physicians could prescribe rest, fresh air and opium, but against the bacteria and other organisms that cause illness they had almost nothing. Paul Ehrlich, born in 1854 in the Silesian town of Strehlen, was convinced that this would change. As a medical student in Breslau, Strasbourg and Leipzig he became fascinated by the way certain dyes stained particular tissues while leaving others untouched.

His reputation was made in Berlin, where he worked at the Charité hospital. When Robert Koch announced in 1882 that he had identified the bacterium that causes tuberculosis, Ehrlich showed that the organism could be made visible with a staining method he had developed, and Koch accepted the demonstration. Ehrlich then turned to how the body defends itself.

He proposed that cells carry chemical side chains that can lock onto a toxin, and that the body produces more of these chains once it has met the toxin, an early version of the theory of antibodies. In 1908 he and the Russian zoologist Elie Metchnikoff shared that year's Nobel Prize for physiology or medicine.

Out of this work grew the idea for which Ehrlich is best remembered. If a dye could attach itself to one kind of cell but not to another, he reasoned, the same principle might be turned against disease. It should be possible, he argued, to design a chemical that would attack the organism responsible for a disease while leaving the patient's own cells unharmed. He called such a substance a magic bullet, and he gave the name chemotherapy to the treatment of infection with synthetic chemicals, a term that later acquired a narrower meaning.

The disease he chose to attack was syphilis, then widespread and greatly feared. In 1905 the German researchers Fritz Schaudinn and Erich Hoffmann identified the organism responsible, a corkscrew-shaped bacterium known as a spirochaete, which is extremely difficult to grow in the laboratory. For centuries the standard treatment had been mercury, given as an ointment, by injection or as a vapour. It was unreliable and deeply unpleasant, and the metal itself was poisonous, so patients were often damaged by the cure as well as by the disease.

Ehrlich's team concentrated on compounds of arsenic, which were already being used against the parasites that cause sleeping sickness. His institute in Frankfurt, the Georg-Speyer-Haus, had been founded in 1906 with a donation from Franziska Speyer, the widow of a banker, to provide Ehrlich with a laboratory of his own. The chemists, led by Alfred Bertheim, made hundreds of arsenic-based compounds, each of which was given a number, and the bacteriologists tested them one after another on infected animals. Progress was slow, and Ehrlich's ambition was demanding: he wanted a substance that would cure in a single dose, without relapse and without serious harm.

In 1909 a young Japanese bacteriologist, Sahachiro Hata, arrived in Frankfurt. He brought with him a technique for infecting rabbits with the syphilis organism, which made systematic testing possible for the first time. The team went back through the numbered compounds, and compound 606, which Bertheim had made in 1907, proved strikingly effective: the animals' sores healed and the organism disappeared from their tissues. The substance was soon named Salvarsan. Before the end of 1909 it had been tried on a small number of patients, and the results were encouraging enough for the team to move quickly.

In the spring of 1910 Ehrlich announced the results at a congress of internal medicine in Wiesbaden, and the German chemical company Hoechst began to manufacture the drug. Salvarsan was a yellow powder that had to be dissolved in an alkaline solution immediately before use, and the resulting liquid, which was unstable, had to be injected into a vein. Supplies were limited at first, because manufacture on a large scale proved difficult, and patients often needed a series of injections spread over many weeks.

Worse, the drug was toxic. Many patients suffered nausea and rashes, some suffered damage to the liver, and a number of deaths were reported. A fierce argument broke out in the German medical press, remembered as the Salvarsan war, between doctors who believed that the compound had been released before it had been properly tested and those who considered the criticism unfair. Ehrlich, who had always insisted that a drug must be judged by the ratio between the dose that cures and the dose that kills, defended his work vigorously. In 1912 his team introduced a modified compound, Neosalvarsan, which dissolved more easily and was gentler on patients, though it was regarded as rather less potent.

Ehrlich died in 1915, before the treatments he had pioneered were superseded. Salvarsan and its successors remained the main weapon against syphilis for three decades, until penicillin became widely available in the 1940s. By then the magic bullet had become a general principle of drug development, and the idea of attacking a disease at a specific molecular target lies behind much of modern pharmacology, including the targeted therapies used against cancer. Ehrlich's insistence on measuring both benefit and harm, and his belief that chemistry could be made selective, outlasted the arsenic compounds that first demonstrated it.

At the summit of Mount Everest the air pressure is roughly a third of what it is at sea level. The proportion of oxygen in the atmosphere does not change with height — it remains about 21 per cent — but because the air is thinner, each breath contains fewer oxygen molecules, and the pressure that drives oxygen into the blood is lower. Physiologists call the result hypobaric hypoxia. For a climber, the consequence is that every step demands deliberate effort, and the body's ability to deliver oxygen to muscle and brain becomes the factor that limits performance. Acclimatisation is the set of changes that partly close the gap between supply and demand.

The first response begins within minutes. Chemoreceptors in the carotid arteries of the neck detect the fall in the oxygen pressure of arterial blood and signal the brainstem to increase ventilation. Breathing becomes deeper and, at rest, noticeably faster. This reflex is remarkably effective at restoring the oxygen content of the blood, but creates a problem of its own: rapid breathing washes carbon dioxide out of the blood, making it more alkaline, and the resulting alkalosis blunts the signal that drives breathing. The immediate response therefore levels off well before it has done all it could.

Within a day or two the kidneys intervene. They reduce the amount of bicarbonate — the alkaline buffer — that they return to the blood and excrete more of it in the urine. The blood becomes more acidic again, the brake on breathing is released, and ventilation can climb further. This renal adjustment is among the most important steps in acclimatisation, and explains why the first two or three days at altitude feel so unpleasant. It has costs too: the increased urine output adds to dehydration, and the loss of plasma water thickens the blood.

Meanwhile the kidneys respond to low oxygen by releasing erythropoietin, a hormone that instructs the bone marrow to make more red blood cells. Over one to three weeks the number of red cells and the concentration of haemoglobin rise, increasing the blood's capacity to carry oxygen. This is the adaptation most often cited, but it carries a penalty. More red cells make the blood more viscous, so the heart must work harder to pump it, and among people who live permanently at altitude the result can be a dangerous rise in the blood pressure of the lungs. The body is trading one kind of strain for another.

Other adjustments are subtler and less well understood. The capillary network around muscle fibres appears to become denser, shortening the distance oxygen must travel from blood to tissue. The chemistry of the red cell alters too, changing the readiness with which haemoglobin releases its oxygen. There is also evidence that muscles become more efficient, extracting more work from each molecule of oxygen, and that at extreme altitude muscle tissue itself is gradually lost. How these changes fit together, and which of them actually determines performance, remains disputed; studies examining one factor at a time have produced inconsistent results.

For some people acclimatisation fails. Acute mountain sickness — headache, nausea, exhaustion — affects a large minority of those who ascend quickly, and in a small proportion it progresses to two conditions that can kill: high-altitude pulmonary oedema, in which fluid leaks into the lungs, and high-altitude cerebral oedema, in which the brain swells. Neither is reliably predicted by fitness, age or previous performance, and the only certain treatment is to descend. Because early symptoms are easy to dismiss, mountaineers are taught to treat a persistent headache at altitude as a warning rather than an inconvenience.

Populations that have lived for millennia on high plateaus show how far adaptation can go. Andean communities in Peru and Bolivia have larger lungs and higher haemoglobin concentrations than people at sea level, and in middle age they are prone to a chronic form of mountain sickness. Tibetans differ. They breathe more at rest and do not raise their haemoglobin much, and have done so for so long that the difference is written into their genes. Variants of two genes, EPAS1 and EGLN1, are unusually common in Tibetans, and the version of EPAS1 they carry appears to have come from an extinct human relative, the Denisovans.

Much of this comes together at the level of a single molecular switch. When oxygen is scarce, a protein called hypoxia-inducible factor, or HIF, escapes the destruction that normally follows its production and accumulates, switching on a wide range of genes: those for erythropoietin, for new blood vessels and for enzymes that alter metabolism. The discovery of how cells sense and respond to oxygen earned three scientists the Nobel Prize in Physiology or Medicine in 2019. Drugs that enhance the response have been developed to treat anaemia in kidney disease, while drugs that block it are of interest in cancer, where tumours exploit the same machinery to grow.

None of this makes rapid ascent safe. The usual advice is to gain height slowly above about 3,000 metres, adding a day of rest for every further 1,000 metres, and to descend if symptoms worsen. Acclimatisation is temporary as well: at sea level the changes fade within a few weeks.

Hardly a week passes without a politician or a management consultant observing that hospitals would work better if they were run like businesses. On the face of it the claim is hard to resist. Hospitals employ thousands of people and buy everything from hip joints to diesel; if a supermarket can move goods to its shelves more cheaply than a hospital can deliver sterile instruments to an operating theatre, something has gone wrong. Yet the same claim provokes fury among clinicians, who point out that a patient is not a customer and that a hospital which is failing cannot simply be allowed to close.

The case for business methods is strong, and it does not depend on any particular view about markets. Studies that score hospitals on ordinary managerial practices — whether anyone is responsible for a budget, whether processes are standardised, whether performance is measured — find that better-managed hospitals tend to have lower death rates and shorter stays. Simple disciplines borrowed from industry, such as checklists for surgical teams and logistics for supplies, have saved lives and money. Where hospitals have been insulated from such scrutiny, waste and variation have flourished: the same operation performed by two surgeons in the same building can cost very different amounts.

The case for business purposes is much weaker, because a hospital is not a normal business. A market works when customers can choose, judge what they are buying and pay for it themselves. Patients arriving by ambulance can do none of these things. They cannot tell whether the surgeon is competent, and in most systems a third party — an insurer or the state — pays the bill. Where hospitals compete for patients, therefore, they tend to compete on what can be advertised and easily measured. Competition of this kind rewards the visible rather than the important.

There is a further problem, which economists call selection. If a hospital is paid for each operation it performs, the sensible strategy is to take the patients who are quick and cheap to treat and leave the complex, unprofitable ones to somebody else. A patient with several chronic conditions, or one who needs social care before discharge, becomes a financial liability. Systems that rely on competition must therefore spend a great deal of effort on rules to prevent this, and the rules themselves generate paperwork and fresh distortions.

Measurement, too, has a darker side. When a single number becomes the test of success, people manage the number rather than the thing it was meant to measure. Targets for waiting times in emergency departments have been followed, in several countries, by reports of patients waiting in ambulances outside the building, because the clock began only when they were wheeled through the door. None of this is evidence that staff are dishonest. It is evidence that a hospital under pressure will direct its effort towards whatever is being counted.

Hospitals also depend on something that business thinking finds hard to model: the willingness of staff to do more than they are paid for. A nurse who stays late to comfort a frightened patient, a junior doctor who telephones a relative after a shift — these are the behaviours that make an institution humane, and they are not produced by incentives. There is a respectable argument, associated with the social researcher Richard Titmuss, that paying people for what they would otherwise give freely can weaken the willingness itself.

None of this means that clinicians should be left alone. Professional autonomy has its own history of failure. For decades doctors were trusted to judge their own work, and in several countries the results were wide, unexplained variation in practice, poor infection control and a reluctance to investigate colleagues. Scandals in which appalling care went unchallenged for years were, at root, failures of accountability. Business thinking has done real service here, by insisting that outcomes be published, that complaints be counted, and that someone answer for the quality of what is done. The question is not whether hospitals should be accountable, but to whom and for what.

What business thinking cannot supply is the signal that tells a firm whether it is succeeding. A company knows it is doing well if customers buy its products and it makes a profit. A hospital cannot abandon its unprofitable patients, and its success cannot be expressed in money alone, because the point of the exercise is health, not revenue. In the absence of a profit signal, hospitals need substitutes: clinical audit, outcome registers and measures that include what patients say about their own recovery. The danger is that the substitutes are treated as if they were the real thing.

My conclusion is therefore not that hospitals should be shielded from business thinking, but that they should adopt its methods while rejecting its purposes. Budgets, supply chains, standardised processes and published results should all be borrowed without embarrassment. Profit, competition for its own sake and the treatment of patients as customers should not, because they point an institution away from the people it exists to serve. A hospital is best understood as an organisation that must be run with commercial discipline in the service of a purpose that is not commercial at all.