IELTS Academic Reading Practice Test 315

Before the 1860s, an operation was only the beginning of a patient's ordeal. Surgeons worked in their ordinary clothes, often in crowded wards where the air was heavy with the smell of wounds. A limb might be amputated in minutes, but the cut surface was then left to heal as best it could, and a large proportion of patients who survived the operation itself died days later of infection. The condition was known as hospital gangrene, and it could spread through a ward with terrible speed.

Joseph Lister, born in 1827, grew up in a household where careful observation was taken for granted. His father, Joseph Jackson Lister, was a wine merchant who devoted his leisure to the microscope and whose work on lens design helped to make the instrument a reliable tool for biologists. The son trained in medicine at University College London and then moved to Edinburgh, where he worked as assistant to the surgeon James Syme and married Syme's daughter, Agnes. In 1860 he was appointed Regius Professor of Surgery at Glasgow.

At the time, most surgeons assumed that wound infection arose either from foul air, or miasma, or spontaneously from the damaged tissue itself. Lister was not convinced. He had noticed that a clean wound protected from dirt healed differently from one that was exposed, and in the early 1860s he read the work of Louis Pasteur, who had shown that fermentation and putrefaction were produced not by spontaneous generation but by microorganisms carried in the air. If microbes made wine sour and milk turn, Lister reasoned, they could equally well make a surgical wound suppurate.

What he needed was a substance that would kill such organisms without destroying the tissue, and a clue came from an unexpected source. Carbolic acid, a chemical obtained from coal tar, was being used in the town of Carlisle to disinfect sewage, and Lister learned that cattle grazing on the treated fields remained healthy and that the smell of the sewage disappeared. If the acid could destroy the organisms responsible for decay in sewage, it might do the same in a wound. It was also cheap and had a numbing effect on the skin.

In August 1865 a boy of eleven was brought to the Glasgow Royal Infirmary with a compound fracture of the leg, in which the broken bone had pierced the skin. Injuries of this kind were almost always fatal: the wound became septic, the limb was amputated, and the patient died. Lister cleaned the wound, applied a piece of lint soaked in carbolic acid, and covered it with a dressing that excluded air. Days later the wound looked healthy rather than inflamed. The boy recovered and the leg was saved.

Lister treated further cases and in 1867 published his reasoning and his results in a series of papers in The Lancet under the title 'On the Antiseptic Principle in the Practice of Surgery'. The change in his wards was striking. In the years before he adopted the method, roughly 45 per cent of his amputation patients died; afterwards the figure fell to about 15 per cent. He also learned to treat the silk threads, or ligatures, with which he tied off bleeding arteries, so that they would not carry infection deep into the wound.

The method was demanding. Dressings had to be changed with carbolic acid, instruments and hands were washed in it, and the wound was kept covered between changes. From the 1870s Lister added a spray, worked by hand, that filled the air of the operating theatre with a fine vapour of carbolic acid, in the belief that organisms floating in the air were a danger. The chemical had drawbacks: it irritated the skin, left surgeons' hands rough and sore, and the spray made everything in the room damp.

Not everyone was persuaded. The germ theory was still contested, and some senior surgeons dismissed the notion that invisible organisms could do such damage, arguing that Lister's results came from the extra cleanliness of his wards rather than from the acid. Others found the ritual of the spray absurd and the technique too slow for a busy hospital. In Britain, and especially in London, acceptance was slow. German surgeons, by contrast, took up the antiseptic method relatively quickly, and visitors travelled from abroad to watch Lister operate.

In 1877 Lister moved to King's College London, where he continued to operate and to train a new generation of surgeons in his methods. Honours followed: he was made a baronet in 1883 and a peer in 1897, and he served as President of the Royal Society from 1895 to 1900. By the end of the century the argument in Britain was effectively over, although surgical practice was already changing in ways that went beyond his own technique.

Antisepsis, the killing of organisms in and around the wound, was eventually replaced by asepsis, the attempt to keep them out altogether. From the 1880s surgeons began to sterilise instruments, dressings and gowns with steam, and rubber gloves, adopted in the United States in the 1890s, protected both the patient and the surgeon's hands. The carbolic spray was abandoned. Yet the principle Lister had established, that infection is caused by living organisms and can be prevented, transformed surgery. He died in 1912, by which time an operation that had once been a gamble had become a calculated risk.

A tooth is often imagined as a small white lump of bone, but it is a living structure with a blood supply and a nervous system of its own, and it is built from four distinct tissues. The part that shows above the gum is the crown; the part below, which is hidden and which may divide into two or three branches, is the root. The crown is covered by enamel, and beneath the enamel lies a much thicker layer of dentine, which continues into the root. In the centre of the tooth is the pulp, a soft tissue containing nerves and blood vessels. The root itself is coated with cementum, and it is held in a socket in the jawbone by the fibres of the periodontal ligament.

Enamel is the hardest tissue in the human body, harder than bone, because almost all of it is mineral: some 96 per cent by weight, mostly crystals of a calcium phosphate mineral similar to the substance of rocks. It is also translucent, so the colour of a tooth comes largely from the dentine underneath. Enamel is formed once, before a tooth erupts, by cells that then disappear. It contains no living cells of its own and no blood vessels, and it therefore cannot repair itself. A chip or a worn surface stays as it is, and the body has no way of replacing what has been lost.

Dentine, which makes up most of the bulk of a tooth, is softer and more yellowish, and it is a composite material: crystals of mineral bound in a mesh of collagen, the protein found in skin and tendon. It is pierced from the pulp to the enamel by enormous numbers of microscopic channels called tubules, each far narrower than a human hair. Fluid moves within these tubules, and the movement is detected by nerve endings in the pulp. This is why a tooth with worn enamel, or a small cavity, can be painfully sensitive to cold drinks or to a sudden breath of air.

The pulp keeps the tooth alive. It carries the blood vessels that supply oxygen and nutrients, and the nerves that register temperature and pain, and its cells continue to lay down dentine throughout life, slowly narrowing the pulp chamber as a person ages. If decay reaches the pulp, the tissue becomes inflamed and then infected, which is why an untreated cavity can end in a severe toothache and an abscess. Around the root, the cementum is thin and bone-like, while the periodontal ligament, a sheet of fibres less than a millimetre thick, suspends the tooth in its socket and absorbs the forces of chewing.

Decay begins with plaque, a sticky film that forms on the surface of a tooth within hours of brushing. Plaque is not a single organism but a community, a biofilm in which hundreds of species of bacteria live and interact. Some of these bacteria feed on sugar from the diet and convert it into acid, and the acid begins to dissolve the mineral of the enamel surface. When the acidity at the surface falls below a certain level, roughly pH 5.5, the fluid around the crystals becomes undersaturated and mineral is lost, a process called demineralisation. Saliva can neutralise acid and wash plaque away, but its capacity to do so is limited, and the flow rises during a meal while it almost ceases at night.

Demineralisation is not in itself a disaster, because saliva contains calcium and phosphate and can supply them back to the enamel, so that mineral is continuously being lost and restored. The balance tips when acid attacks are frequent. The first visible sign is a dull white patch on the enamel, which can still be reversed. Once the surface collapses, however, a cavity has formed, and the damage is permanent. Decay then spreads more quickly through the softer dentine and can reach the pulp within a year or two of the first lesion.

Fluoride shifts the balance in the tooth's favour. When it is present in the mouth in small amounts, it is incorporated into the surface crystals, forming a mineral that dissolves less readily in acid, and it also encourages calcium and phosphate to return to demineralised areas. This is the reasoning behind fluoride toothpaste and behind the addition of fluoride to drinking water, which began in the 1940s in North America and has since been adopted by many cities around the world. Dentists also emphasise the frequency of sugary snacks rather than the total quantity eaten.

Much remains uncertain. Some people eat a great deal of sugar and develop few cavities, while others with careful habits lose tooth after tooth, and nobody can yet explain the difference fully. Researchers now describe the plaque community as an ecosystem, in which a shift in acidity or in diet can favour destructive species over harmless ones, and the aim of treatment is increasingly to manage that community rather than to destroy it entirely. Whether a vaccine, or the deliberate introduction of harmless bacteria, will one day make caries a rare disease is not known. Caries is nonetheless among the most common conditions in the world, and the basic mechanism by which sugar becomes acid and acid becomes a hole is among the best understood processes in dentistry.

Screening means testing people who feel well in order to find a disease before it produces symptoms. The idea has an obvious appeal. If a cancer or a damaged blood vessel is detected at an early stage, treatment ought to be simpler, gentler and more successful, and the patient ought to live longer. This is the reasoning behind the leaflets that arrive with an invitation to a mammogram or a bowel test, and it is a reasoning few of us are inclined to question. A woman told that a shadow on her scan was found early feels fortunate, and a service that reports more cases detected appears to be doing its job. Yet the appeal rests on an assumption: that finding a disease early is the same thing as changing its course.

Because that assumption is not always true, public health bodies have long insisted that screening should meet strict conditions. The best-known list was drawn up by two doctors, James Maxwell Glover Wilson and Gunnar Jungner, in a report for the World Health Organization published in 1968. They argued that the condition being sought should be an important health problem, that its natural history should be understood, that there should be a recognisable early stage, that an accepted treatment should exist, and that the test itself should be acceptable to the population. They added that the chance of physical or psychological harm from the test should be smaller than the chance of benefit, and that the cost of finding a case should be weighed against the cost of treating it.

Some programmes satisfy these conditions comfortably. In many countries every baby is offered a blood test taken from the heel within days of birth, which detects a rare inherited condition called phenylketonuria. Babies with the condition cannot process one component of ordinary protein, and if it is left untreated the result is severe and permanent intellectual disability; once it is identified, a carefully controlled diet allows the child to develop normally. Cervical screening is a comparable case. The test finds abnormal cells that may, years later, become cancerous, and a small procedure removes them before they do. In countries with organised programmes, deaths from cervical cancer have fallen substantially since they were introduced.

Screening also has costs, and they fall on people who are not, by definition, ill. A test may be positive when no disease is present, and the consequences of a false positive are not trivial: further investigations, some of them uncomfortable or carrying small risks, weeks of anxiety, and occasionally an operation that proves to have been unnecessary. In a population where a condition affects one person in a thousand, even an accurate test will produce more false alarms than true discoveries. A negative result can mislead as well, offering reassurance to someone whose disease was missed. And a test may find an abnormality that would never have troubled the person at all.

This last problem has a name: overdiagnosis. It occurs when screening detects a cancer or other condition that is growing so slowly, or not at all, that it would never have caused symptoms or shortened the patient's life. The patient is then treated, with all the accompanying risk, for a disease that did not need treating. Treatment of such a tumour may mean the removal of a whole organ and lifelong medication. A striking illustration comes from South Korea, where ultrasound screening for thyroid cancer was introduced in the late 1990s. The number of thyroid cancers diagnosed rose enormously, yet deaths from the disease stayed much the same.

Such findings help to explain why screening statistics can be treacherous. Lead-time bias arises because a disease diagnosed early appears to have been survived for longer, even when the moment of death is unchanged: someone found to have a cancer five years before symptoms would have appeared is credited with five extra years of survival, although nothing has been gained. Length bias arises because screening is more likely to pick up slow-growing disease, which is by nature less dangerous. For both reasons, a rise in five-year survival after screening may reflect earlier diagnosis rather than saved lives.

Money is another consideration. A national screening programme must be paid for, and the staff and equipment it uses cannot be used for anything else. Where a health service has a fixed budget, extending screening to a new group or a new disease means that something else is not done. A programme that detects many cases is often reported as a success, whatever it costs. There is also evidence that screening is taken up most readily by people who are already advantaged, so that a programme offered to everyone can widen the gap in health between rich and poor rather than narrowing it.

None of this means that screening is a bad idea. The heel test and cervical screening save lives and prevent suffering, and few people would wish to be without them. What it means is that screening is a tool with harms as well as benefits, and that each programme must be judged on whether it does more good than harm, for whom, and at what cost. That judgment should rest on evidence from fair trials, and the people invited to be screened should be told honestly what is known and what is not. More testing is not the same as better health.