IELTS Academic Reading Practice Test 403

Tetanus has been recognised for as long as medicine has kept records. The disease begins with stiffness in the jaw — hence its familiar name, lockjaw — and can spread to produce violent muscle spasms that arch the patient's back and, in the worst cases, stop the breathing. Ancient medical writings describe it, and nineteenth-century surgeons knew that it followed wounds, particularly deep puncture injuries contaminated with soil. Even a scratch from a garden fork could be enough. What they did not know was what caused it. The death rate was extremely high, and no treatment existed beyond quiet, darkness and hope.

The first clue came in 1884, when a young German physician named Arthur Nicolaier injected samples of garden soil into mice and found that the animals developed the symptoms of tetanus. He examined them under the microscope and saw rod-shaped bacteria, but he could not grow the organism in the laboratory. Others tried and failed as well. The reason, it later emerged, is that the tetanus bacterium is anaerobic: it can multiply only where there is no oxygen, and the culture methods of the period exposed it to air.

The person who solved the problem was Kitasato Shibasaburo, a Japanese physician who had trained at the medical school in Tokyo and who came to Berlin in 1885 to work in the laboratory of Robert Koch, the bacteriologist who had identified the causes of tuberculosis and cholera. In 1889, Kitasato succeeded in growing the tetanus organism in pure culture, using sealed vessels from which oxygen had been removed.

The culture was a technical achievement of the first order. Koch's laboratory was then the most important centre of bacteriology in the world, and the new technique gave researchers there, for the first time, an unlimited supply of the organism to study and experiment with.

His cultures revealed a slender bacillus carrying a round body at one end. These bodies were spores: dormant forms that the bacterium builds when conditions are hostile, and that allow it to survive for years in soil, resistant to heat, drying and many disinfectants. Spores explain both why tetanus is so difficult to eradicate from farmland and why an infection can begin from a wound so small that the patient never noticed it. Deep tissue, starved of oxygen by damaged blood vessels, provides the conditions in which the spores revive.

Kitasato went further. Working with cultures that had been passed through filters fine enough to hold back the bacteria themselves, he found that the clear fluid that came through could still produce the symptoms of tetanus in animals. The conclusion was startling. The damage was done not by bacteria spreading through the body but by a poison — a toxin — that they released. Tetanus, in other words, was a form of poisoning, and the bacteria responsible could remain at the site of the wound. It followed that a treatment might be aimed at the toxin rather than at the bacterium.

In Berlin, Kitasato worked alongside Emil von Behring, a German physician with an interest in immunity. In 1890, the two men reported an experiment that became a landmark. They immunised rabbits and other animals with small, carefully controlled doses of the toxin, then took blood from the immunised animals and separated the serum from the cells. When this serum was injected into other animals, those animals withstood doses of tetanus toxin that would otherwise have been fatal. Immunity, it appeared, was carried in the blood fluid rather than in the cells. The paper appeared in December 1890 in the Deutsche Medizinische Wochenschrift.

The finding launched what became known as serum therapy. A substance in the blood — later called an antibody — could neutralise a toxin, and it could be transferred from one animal to another. Behring applied the same reasoning to diphtheria, a disease that was then killing large numbers of children, and diphtheria antitoxin became the first effective treatment for it. Physicians could now do something they had never done before: intervene in a disease after the poison had entered the body. The work is often described as the beginning of immunology as a practical science, and it depended heavily on Kitasato's cultures and on the serum experiments the two men designed together.

In 1901 Behring received the first Nobel Prize in Physiology or Medicine for this work. Kitasato was not included. Whether he should have been is still argued over. Many historians of medicine note that the tetanus experiments rested on Kitasato's cultures and on his demonstration of the toxin; others point out that Behring had been pursuing the idea before the collaboration began and had applied it to a disease of far greater significance in Europe. What is not disputed is that the paper of 1890 had two authors.

Kitasato returned to Japan in 1892 and founded an institute for the study of infectious diseases in Tokyo, which became a leading centre of research. In 1894, during an outbreak of plague in Hong Kong, he identified the bacterium responsible, working independently and almost simultaneously with the Swiss-French bacteriologist Alexandre Yersin; the organism is now named Yersinia pestis. Antitoxin against tetanus entered medical practice, and its use in the treatment of wounded soldiers became standard in the First World War. Kitasato was made a baron and died in 1931, having seen the idea he had helped to establish become the basis of modern immunology.

The bacterium responsible for tetanus, Clostridium tetani, lives in soil and in the intestines of animals, where it does no harm. In the presence of oxygen it cannot multiply; exposed to air it survives only as a spore, a dehydrated package of genetic material with a tough coat. Spores can persist in dry soil, dust and on rusty metal for years, which is why the disease has never been eradicated and why it remains a danger after floods, earthquakes and other disasters that scatter soil and disrupt medical services. For an infection to begin, spores must be pushed deep into tissue where the blood supply is poor and oxygen scarce, as in a puncture wound from a nail.

Once conditions allow, the spores revive and the bacteria multiply, releasing tetanospasmin, the protein that causes every symptom of the disease. Measured by weight, it is among the most poisonous substances known; a quantity too small to see can kill an adult. Yet the toxin does not act at the wound. It must first find its way into the nervous system, and it does so without ever travelling freely in the blood — a fact that took researchers decades to establish.

The toxin enters the very nerve fibres that serve the injured muscle, at their endings in the tissue. From there it is carried inside the axon, the long thread that conducts impulses, back towards the cell body in the spinal cord. This journey is not fast: the toxin advances perhaps a few centimetres a day, which is one reason why the symptoms of tetanus appear only after an interval of days. Botulinum toxin, produced by a close relative of the tetanus bacillus, acts at the junction between nerve and muscle, blocking the signals that tell muscles to contract and producing a limp paralysis. The two poisons are chemically similar; the site at which each acts decides whether the patient goes limp or goes rigid.

Tetanospasmin is built in two parts. One, the heavy chain, attaches to the surface of a nerve ending and enables the other part to enter. The second, the light chain, is an enzyme that works only in the presence of zinc. Once inside the cell it seeks out a particular protein of the machinery that allows small packets of neurotransmitter to fuse with the membrane and release their contents. Having cut this protein, the toxin leaves the cell unable to communicate. The effect is permanent for that nerve ending: recovery requires the growth of new terminals, which is why the illness lasts for weeks even when the toxin has long since disappeared.

What makes tetanus so distinctive is the identity of the cells the toxin attacks once it reaches the spinal cord. It enters the small interneurons whose task is to restrain the motor neurons, the cells that command muscles to contract. These interneurons release the transmitters GABA and glycine, the nervous system's main brakes. With the brakes removed, motor neurons fire continuously and without coordination. The result is the rigidity and violent spasms that characterise the disease: the clenched jaw of lockjaw, the fixed grin known as risus sardonicus, and the arched back of opisthotonus. The toxin also disturbs the autonomic nerves that control heart rate, blood pressure and sweating, which is one reason why severe cases are so difficult to manage.

The interval between injury and illness is usually between three days and three weeks. A short incubation period is a bad sign, because the toxin has less distance to travel. Treatment has three aims, and none of them is straightforward. The wound is cleaned and dead tissue removed, so that no more toxin is produced. Antitoxin, in the form of human immunoglobulin, is given to neutralise poison that is still in the bloodstream; it cannot undo damage already done inside nerve cells. And the patient is kept alive while the nervous system recovers, with sedatives, muscle relaxants and, in severe cases, mechanical ventilation. Even with modern intensive care, a proportion of patients die, and in settings without such facilities the figure is far higher.

Several questions remain open. Why do some patients develop only a localised form of the disease, with stiffness confined to the limb that was injured, while others progress within days to generalised spasms? The difference is thought to reflect the amount of toxin produced and the route it takes, but the explanation is not settled. Nor is it clear how much toxin travels in the bloodstream rather than along nerves, or how far the disease in humans differs from that in other species: dogs and cats appear far less susceptible than people or horses, for reasons that are still being investigated. The answers would matter, because they would help clinicians predict which patients are likely to deteriorate.

Meanwhile, the toxin has acquired a second life as a laboratory instrument. Its ability to enter nerve endings and travel backwards along axons makes it a valuable tracer: researchers attach markers to a harmless fragment of the molecule and use it to map which neurons connect to which. Modified forms that cannot cause illness are also being explored as delivery vehicles, carrying drugs or genetic material into cells of the nervous system that are otherwise hard to reach. And the disease itself is now largely preventable. Tetanus toxoid, a chemically inactivated form of the toxin, was developed in the 1920s and remains part of routine childhood immunisation in most countries; where coverage is high, cases have become rare.

Health systems in rich countries face a squeeze: populations are ageing, treatments are becoming more expensive, and the tax revenue that pays for care is not keeping pace. In this climate a proposal that surfaces regularly is that patients should contribute to the cost of treating conditions they could have avoided. Smokers with lung disease, heavy drinkers with liver damage, people who are seriously overweight: the list of examples is easy to draw up, and the underlying idea has an obvious appeal. If someone's choices have added to the bill, why should everyone else pay it? My answer, after weighing the arguments, is that the idea is far more attractive in principle than it could ever be in practice.

The case in favour rests on two principles that deserve respect. The first is fairness. Insurance works by pooling risk, and a pool is stable only while its members believe that contributions are roughly commensurate with need. Where people see others behaving in ways that predictably increase the cost of care, resentment grows and willingness to pay falls. The second principle is respect for agency. Treating adults as though their decisions were irrelevant to their health is patronising; charging them, supporters argue, treats people as agents who make choices rather than as passive victims of circumstance. On this view a charge is not a punishment but a price.

The difficulty lies in establishing what a patient could have avoided. Most common diseases have many causes, and a single behaviour is rarely decisive. Even for smoking, the habit most tightly linked to a specific illness, many people who smoke never develop lung cancer, and a substantial minority of cases occur in people who have never smoked. The epidemiologist Geoffrey Rose pointed out a related paradox: the great majority of cases of a disease often arise among the many people whose risk is only slightly raised, not among the few at high risk, simply because the former group is so large. A policy that aims at the visibly reckless will therefore miss most of the burden it claims to address.

There is also a question about incentives. Prices do change behaviour: tobacco taxes reduce smoking, especially among the young, and alcohol taxes reduce consumption. But the effect depends on the price being paid at the moment of choice. A bill arriving years after the behaviour began cannot alter the decision it is said to penalise, because the patient is already ill and has no further choice to make. Prospective prices shape behaviour; retrospective charges merely redistribute the cost. Evidence on charging for care itself is not encouraging. The RAND Health Insurance Experiment, a large American study begun in the 1970s, found that when patients paid part of the cost they used fewer services, including services they needed.

Fairness, moreover, cuts both ways. Risk factors are not distributed at random. Smoking, obesity and harmful drinking are consistently more common among people with less education and lower incomes, and they are concentrated in neighbourhoods where cheap, energy-dense food is easy to buy and safe places to exercise are scarce. Mental illness, which is strongly associated with smoking, is itself unequally distributed. A charge levied on the consequences of behaviour would therefore fall most heavily on those with the least money and the least capacity to change. A policy that widens inequality in order to promote responsibility has lost sight of what fairness means.

Practically, someone has to decide which conditions qualify. Injuries from skiing and rugby? A patient who forgot to take a preventive medicine, and another who could not afford it? Someone who ignored advice to lose weight, and someone who was never offered help? Every judgement requires a doctor to sit in judgment on a patient's life, and a consultation in which the physician is also the assessor is a consultation in which embarrassing facts are less likely to be disclosed. Schemes of this kind do exist: in the United States, some employers are permitted to charge employees who smoke substantially more for their health insurance. Whether such arrangements improve health, as opposed to raising revenue, is disputed.

There are better instruments. The most effective measures against the diseases of lifestyle have changed the environment in which choices are made rather than the individual making them: clean indoor air laws, advertising restrictions, plain packaging, and taxes on tobacco, alcohol and sugary drinks. Such measures are criticised as regressive, since the poor pay a larger share of their income in tax. The objection has force, but the health gain from reducing consumption is also concentrated among the poor, and the revenue can be used to fund the services they use. Support for individuals — help to stop smoking, treatment for addiction, accessible advice — does more, pound for pound, than penalties.

So where does that leave the question? I would not charge patients for the treatment of conditions that are said to have been avoidable. The administrative burden would be considerable, the attribution of blame would be arbitrary, and the people most likely to be billed would be those least able to pay. That does not mean that behaviour is irrelevant or that anything goes. It means that the price should be paid at the point of purchase, where it can still influence what is bought, rather than at the hospital bedside, where it influences nothing except whether a sick person seeks help. No arrangement will be perfectly fair; the aim should be one that is not systematically unfair.