IELTS Academic Reading Practice Test 312

Rabies is one of the oldest diseases known to medicine, described in ancient texts from Egypt, Greece and India. It is caused by a virus carried in the saliva of infected animals, usually dogs, and passed on when they bite. Once the virus reaches the brain and the first symptoms appear — restlessness, an inability to swallow, convulsions — the patient almost always dies. A bite from a rabid dog was a common injury in the nineteenth century, and doctors had tried for centuries to help those who came to them. Their remedies, which included washing the wound and then burning it with a hot iron, had little effect.

In the 1880s the person best placed to change this was not a doctor at all. Louis Pasteur, born in 1822, had trained as a chemist and had become famous for showing that micro-organisms cause fermentation and decay, an idea that undermined the long-held belief in spontaneous generation. His work had already made him one of the most celebrated scientists in France. He had also turned the insight to practical use. In 1879 he produced a vaccine against chicken cholera, and in 1881 he demonstrated publicly that vaccinated sheep and cattle survived anthrax, a disease that had been ruining French flocks.

Rabies was far harder. Pasteur could see the micro-organisms of anthrax through a microscope, but the agent of rabies was too small for any instrument then available, and he could not grow it in a laboratory culture. He was therefore unable to produce it in quantity or to weaken it by the methods he had used before. Working with Émile Roux, he established that the infectious material was concentrated in the nervous system, in the brain and spinal cord of infected animals, rather than only in the saliva. That finding was crucial, because it gave him a source of the agent that he could dry and measure.

The two men then devised an ingenious solution. Healthy rabbits were infected, and after they died their spinal cords were removed and suspended in dry air inside a jar containing a substance that absorbed moisture. The longer a cord was left, the weaker its power to cause disease became, a process that Pasteur called attenuation. If a dog was given an injection from a heavily dried cord and then, on successive days, injections from cords that had been dried for shorter periods, its body appeared to learn to resist material of full strength. Dogs treated in this way survived a bite that would otherwise have killed them.

By 1885 Pasteur had a method that worked in animals and no idea whether it would work in people. He was not a physician, and under French law the treatment of patients was not open to him. He could also see that if someone died after he had intervened, his reputation and the young science of vaccination might not survive. On 6 July 1885 the decision was taken out of his hands. A woman from Alsace brought her nine-year-old son, Joseph Meister, to his laboratory in Paris. The boy had been bitten on the hand and both legs by a rabid dog, and there was no reason to expect that he would live.

Pasteur hesitated, and discussed the case with two physicians, Alfred Vulpian and Jacques-Joseph Grancher; Grancher gave the injections, since Pasteur himself could not. He then began a series of injections, each containing material stronger than the last, and continued for ten days. The boy did not develop rabies. Pasteur reported the case cautiously that autumn. Soon afterwards a teenage shepherd from the Jura was brought to him after being bitten while protecting younger children from a dog, and he recovered as well.

News of the recoveries travelled quickly, and by the end of the year patients were arriving from other countries. Not all of them lived, and Pasteur was accused of experimenting on desperate people and of hastening deaths that rabies would have caused anyway. In reply he insisted that every case had been hopeless before treatment began. His critics were not entirely silenced, but letters from bitten people begging for help made the argument difficult to sustain. In 1888 an international subscription paid for the opening of the Institut Pasteur in Paris, a centre for research and for treatment.

Pasteur died in 1895, but the idea he had pursued in the dried spinal cords of rabbits proved more durable than his particular preparation. Attenuation — deliberately using a weakened form of a pathogen to teach the body to defend itself — became one of the foundations of immunology. Modern rabies vaccines, grown in cells and given after a bite as a course of injections together with antibodies, are a world away from the dried cords of 1885. Yet they follow the same logic. Rabies still kills tens of thousands of people each year, mostly in Asia and Africa, where the source is almost always a rabid dog and treatment is often out of reach.

The boy from Alsace did not disappear from the story. Joseph Meister remained in Paris and was later employed as a caretaker at the institute whose founding his survival had helped to justify. He worked there for many years, a modest link between a desperate experiment and the vaccine programmes that followed.

Most people, asked which organ keeps them upright, would probably name the muscles of the legs or the eyes. In fact the crucial structure is a pair of organs no larger than the last joint of a finger, buried deep in the temporal bone on each side of the skull. The inner ear is best known as the home of the cochlea, the coiled, fluid-filled duct that turns sound into nerve impulses. Beside it lies a second and older system, the vestibular apparatus, which reports every tilt, turn and acceleration of the head. Unlike hearing, balance is a sense we are rarely aware of until it fails.

The most conspicuous parts of the vestibular apparatus are three loops of membrane, the semicircular canals. They rise from a central chamber and lie roughly at right angles to one another. Each contains a fluid, endolymph, and each ends in a swelling, the ampulla, where a ridge of hair cells rises into a gelatinous flap called the cupula. When the head rotates, the bony canals turn with it, but the fluid, because of its inertia, lags behind. The moving fluid pushes the cupula sideways and bends the hair cells beneath it. Because the three canals lie in different planes, a rotation in any direction is detected by at least one of them, and the brain can reconstruct the movement from the pattern across all three.

Rotation is only half the problem, since the brain must also know which way is down. This is the work of two sacs, the utricle and the saccule. The utricle lies roughly horizontally and the saccule vertically. Each contains a patch of hair cells, the macula, covered by a membrane on which rest hundreds of tiny crystals of calcium carbonate, known as otoconia. When the head tilts, gravity pulls the crystals and the membrane slides across the hair cells below. The same mechanism registers the sudden forward acceleration of a bus, which feels to these organs much like a backward tilt of the head.

Whatever the stimulus, the conversion into a nerve signal is the task of the hair cells. Each carries at its upper surface a bundle of fine projections, the stereocilia, arranged in order of height, together with a single longer projection, the kinocilium. The bundle projects into the endolymph, a fluid that is unusual in containing a high concentration of potassium rather than sodium. When the bundle is deflected towards the kinocilium, small channels in the cell membrane open, potassium flows in and the cell becomes depolarised. This releases a neurotransmitter that excites the endings of the vestibular nerve, which carries the message to the brain.

The brain does not simply record these signals. It uses them, together with information from the eyes and from stretch receptors in the muscles and joints, to build a working model of where the head is and how it is moving. Some of the resulting reflexes are extremely fast. The vestibulo-ocular reflex, for example, turns the eyes in the opposite direction to the head whenever it moves, so that the image on the retina stays steady. The pathway involved has only three nerve cells between ear and eye, which allows the correction to begin within a few thousandths of a second.

Most of the time this machinery operates unnoticed. When it malfunctions, the result is unmistakable. Vertigo, the illusory sense that the room is spinning, arises when the two ears send contradictory reports, and it can be severe enough to cause vomiting. The commonest cause is benign paroxysmal positional vertigo, in which a few otoconia become detached and drift into one of the semicircular canals, most often the posterior canal. Certain movements of the head then produce a brief, violent sensation of spinning. The condition can usually be cured in a clinic by a sequence of guided head movements that manoeuvres the loose crystals back into the utricle.

Another disorder, Ménière's disease, produces episodes of vertigo lasting hours, together with fluctuating hearing loss and ringing in the ears. It is associated with a build-up of pressure in the endolymph, although why this happens in a particular person remains unclear. Motion sickness has a different explanation. In a car or on a ship the eyes may report a stationary interior while the vestibular system reports constant movement. Faced with signals that do not match, the brain responds in some people with nausea, sweating and pallor.

Several questions remain open. Researchers cannot yet explain why some people are far more susceptible to motion sickness than others. Nor can they say why the brain's attempt to recalibrate itself after injury, known as vestibular compensation, succeeds well in some patients and poorly in others. Unlike those of birds and fish, the hair cells of the human inner ear are not replaced after they are lost. Infections, certain drugs and ageing therefore erode balance, and poor balance is one of the main reasons older people fall. Experimental vestibular implants, which stimulate the nerve directly, have been tested in a small number of patients, but how much benefit they offer over the long term is not yet known.

Few public health policies divide opinion as sharply as paying people to look after themselves. A scheme might offer shopping vouchers to a pregnant woman who stops smoking, or a cash prize to someone who loses weight. A third might enter everyone who attends a clinic for a vaccination into a lottery. To some this is a sensible use of public money, since prevention is cheaper than treatment and advice alone changes little. To others it is bribery, an insult to personal responsibility and a reward for behaviour that most people manage without payment. I think the practice can be justified, but on narrower grounds than its supporters usually offer, and only if schemes are designed with unusual care.

The case for trying something is strong. Habits such as smoking, heavy drinking and inactivity are resistant to information alone; decades of health campaigns have shifted behaviour far less than their authors hoped. The attraction of an incentive is that it competes on equal terms with the immediate pleasures that make unhealthy behaviour attractive. A voucher for a drug-free urine sample, a standard technique in addiction treatment known as contingency management, offers a reward today rather than a benefit years away. That logic is not sentimental; it accepts that people weigh costs and benefits, sometimes impatiently.

The evidence is better than critics assume and weaker than enthusiasts claim. Reviews of contingency management consistently find that it reduces drug use while payments continue, and it is among the better-supported treatments for stimulant dependence. Trials of payments for weight loss have found modestly greater losses among those paid, and schemes offering vouchers to pregnant smokers in Britain have reported higher quit rates than ordinary cessation services. Almost every review, however, reaches the same sober conclusion: the effect is generally small to moderate and tends to fade once the money stops. Payments appear to work as a temporary scaffold rather than a cure.

The commonest objection is that payment is coercive. This is a word that needs care. Offering somebody money to do something is normally the opposite of forcing them: it enlarges their choices. Yet the objection becomes serious when the sum is large relative to the recipient's income, or when the alternative is the loss of a benefit on which a family already depends. A modest voucher is an offer; a payment that determines whether a family eats this week is closer to pressure. Any honest defence of incentives has to acknowledge that the same sum means different things to different people.

A second objection is that payment is paternalistic, an attempt to buy behaviour that adults should choose for themselves. Here I part company with the critics. The state already bears much of the cost of unhealthy behaviour, through hospitals and sickness benefits, and it already shapes choices with taxes, advertising rules and the design of public spaces. A payment is simply a more explicit instrument. The more interesting worry is that rewards may crowd out people's own reasons for changing. Someone paid to quit may come to see the change as something done for money rather than for health, and may relapse once the payments end. Some studies have found such effects and others have found none. The possibility deserves respect, but it is not a settled finding, and it argues for good design rather than abandonment.

Questions of fairness are harder to answer. Who is paid? A scheme that rewards success will tend to reward those who were already most able to succeed. Payments can also penalise the people who need most help. A person with a disability, a mental illness or three jobs is less able to meet a target, and a scheme that punishes failure adds a second disadvantage to the first. There is a broader risk, too. Money for individual behaviour can quietly shift responsibility away from the conditions in which people live, such as cheap unhealthy food, insecure housing or streets with nowhere safe to walk. Responsibility then falls on the individual who is expected to cope with them.

Design, then, matters more than the principle. Small, frequent and immediate rewards attached to a specific act, such as attending an appointment or taking a dose of medicine, work better than large prizes for a distant outcome such as losing fifteen kilograms. Outcomes depend on biology and luck as well as effort, and paying for them can feel like a lottery. Incentives should be time-limited, offered alongside support, and given to everyone eligible rather than only to those judged likely to succeed. They should also be evaluated, which is rare: many schemes are launched with publicity and quietly discontinued without any proper assessment.

So where does that leave the question? I would defend payment for a narrow range of behaviours. The act should be clear, the sum modest and the scheme time-limited, and payment should be understood as an addition to, never a replacement for, taxes, regulation and the shaping of environments. Paying someone to attend a clinic is not an admission that advice has failed; it is an acknowledgement that advice was never sufficient on its own. What I would resist is the larger claim, increasingly heard, that financial incentives are the modern answer to chronic disease. They are a tool, and a limited one.