IELTS Academic Reading Practice Test 313

Tuberculosis was the leading cause of death in Europe during the nineteenth century. The disease was so familiar that it was known simply as consumption, because of the way it seemed to consume those it attacked. Its cause was disputed. Many doctors attributed it to inherited weakness, others to damp housing and foul air, and some to the workings of a person's constitution. That a single kind of living organism might be responsible was an idea that few were prepared to accept.

Robert Koch was born on 11 December 1843 in Clausthal, a mining town in the Harz mountains of what is now Germany. He studied medicine at the University of Göttingen and, after serving as a medical officer in the Franco-Prussian war, became a district physician in Wollstein, a small town in the province of Posen. It was there, far from any university laboratory, that he began the work that would transform medicine. Working with a microscope his wife had given him and with equipment he improvised himself, he set out to identify the organism responsible for anthrax, a disease then devastating cattle and sheep.

Anthrax was a good subject for such a study, because the disease was easy to recognise in animals and its course could be followed. Koch injected material from infected animals into mice, grew the bacteria outside the body, and showed that the disease could be transmitted again and again from one host to another. He also found that the bacteria could form resistant resting bodies, or spores, which allowed them to survive in soil for years and explained why outbreaks kept returning to particular fields. In 1876 he travelled to Breslau to demonstrate his findings to Ferdinand Cohn, a distinguished botanist. Cohn was impressed, and the young country doctor's reputation began to spread.

In 1880 Koch was appointed to the Imperial Health Office in Berlin, where he had better equipment and a small team. With a small team, including Julius Petri, who later gave his name to the shallow glass dish, he developed a way of growing bacteria on the surface of solid culture media rather than in liquid, which made it possible to separate different species from a mixture and obtain pure cultures. The first solid medium was gelatin, but gelatin melted at the temperature of the human body and was digested by many bacteria, so it was replaced by agar, a setting agent derived from seaweed.

Tuberculosis was a far harder problem. Koch began by infecting guinea pigs with material from people who had died of the disease, keeping the animals isolated so that he could test whether tuberculosis was truly infectious. The animals developed the disease, and their tissues contained the same organisms. To make the bacteria visible, Koch stained them with methylene blue and then added a brown dye that coloured the surrounding material, so that the blue bacilli stood out against a background of brown tissue. On 24 March 1882 he told the Berlin Physiological Society that tuberculosis was caused by a bacterium, which he called the tubercle bacillus.

The announcement was received with astonishment and, in some quarters, disbelief. Some pathologists doubted that a single organism could be responsible for a disease with so many forms, and others argued that the bacteria were a consequence of the illness rather than its cause. The evidence, however, was difficult to resist, and within a few years Koch's conclusions had been confirmed in laboratories across Europe. If tuberculosis was infectious, it could be prevented, and the ventilation of homes and the isolation of the sick acquired a new urgency. Sanatoria were built in many countries for patients who could afford them.

Koch's next assignment came from the German government. Cholera had been spreading out of Asia for decades, and its cause was as uncertain as that of tuberculosis. In 1883 Koch led an expedition to Egypt and then, when the outbreak there subsided, to India, where he examined patients in Calcutta. There he identified a comma-shaped bacterium, later named Vibrio cholerae, in the intestines of the sick, and he found the same organism in a water tank used by local households, a discovery that supported the view that cholera was spread through contaminated water.

Koch's later career was not an unbroken success. In 1890 he announced a remedy for tuberculosis, prepared from cultures of the bacillus, which he called tuberculin. He claimed that it could halt the disease, and the announcement created enormous excitement, but the substance was not a cure and caused severe reactions in some patients. Koch declined at first to reveal how it was made, which damaged his reputation and led to bitter disputes with other physicians. Tuberculin was eventually used instead as the basis of a skin test for exposure to the disease, in modified forms that are still employed today.

Koch received the Nobel Prize in Physiology or Medicine in 1905, and he died in 1910 at a sanatorium in Baden-Baden. His most important legacy was not a single discovery but a method: the systematic linking of a particular microbe to a particular disease, later formalised in the rules known as Koch's postulates. Koch is also remembered in the date of his announcement, 24 March, now observed as World Tuberculosis Day.

The liver lies in the upper right of the abdomen, protected by the lower ribs, and weighs about one and a half kilograms in a healthy adult. It stores sugar as glycogen and releases it between meals, makes most of the proteins that circulate in the blood, produces the bile needed to digest fat, and holds reserves of iron and several vitamins. It also processes almost every drug, food additive and environmental chemical that enters the body, converting them into forms that can be removed.

Nothing absorbed from the gut travels directly to the rest of the body. The veins of the stomach and intestines merge into a single large vessel, the portal vein, which carries their contents to the liver. Roughly three-quarters of the blood entering the organ arrives by this route, loaded with nutrients and with whatever else has been swallowed. Only after passing through the liver does this blood return to the heart and reach the brain, the muscles and other organs. The arrangement, known as first-pass metabolism, means that the liver inspects most of what we absorb before anything else does.

The first stage of that inspection is a set of reactions collectively called phase I. Its most important agents are the cytochrome P450 enzymes, a large family of proteins embedded in the smooth endoplasmic reticulum inside the cell. These enzymes add oxygen to molecules, typically turning a fat-soluble compound into a slightly more water-soluble one. That is a useful step towards excretion, but it has a cost: the products are often more chemically reactive than the substances they came from, and occasionally more toxic.

Phase II reactions deal with the products. The cell attaches a small, water-soluble group to the molecule, a process known as conjugation. The commonest group is glucuronic acid, but sulfate, acetate and glutathione are also used, and the choice depends on the substance and on the enzymes a person has inherited. Conjugation usually makes a compound far more water-soluble and far less biologically active, so that it can be carried safely to the kidneys. The same enzymes act on hormones and bile acids as well as on foreign chemicals.

The finished products leave by two routes. Water-soluble compounds pass into the blood and are filtered out by the kidneys. Larger or fat-soluble ones are pumped into bile, a greenish fluid that the liver produces continuously. Between meals bile is diverted into the gallbladder, a small sac below it, where it is concentrated; when fat arrives in the intestine, the gallbladder contracts and releases it. Bile carries away cholesterol, which would otherwise crystallise, as well as the pigments formed when red blood cells are broken down.

Old red blood cells are dismantled in the spleen after about four months. Their haemoglobin is broken down, and one of the products is bilirubin, a yellow pigment. Bilirubin does not dissolve in water, so it travels in the blood attached to albumin, a protein made by the liver. The liver takes it up, attaches glucuronic acid and releases the result into bile. If the liver is damaged, or if the duct that carries bile away is blocked, bilirubin accumulates in the blood and then in the tissues: the whites of the eyes and the skin turn yellow, a condition known as jaundice.

Alcohol shows the system under strain. Ethanol is converted to acetaldehyde by alcohol dehydrogenase, and acetaldehyde is a toxic substance that produces flushing, headache and nausea. A second enzyme, aldehyde dehydrogenase, normally clears it within minutes, turning it into acetate, which the tissues can use as fuel. Heavy drinking disturbs the balance. The liver produces more of a P450 enzyme that also acts on ethanol, and acetaldehyde builds up faster than it can be removed. The consequences include fat accumulating in liver cells, inflammation and, over the years, the scarring known as cirrhosis.

Paracetamol offers a clearer example of a mechanism going wrong. At normal doses, most of the drug is joined to glucuronic acid or sulfate, while a small fraction is oxidised by cytochrome P450 into a reactive compound. This compound is neutralised at once by glutathione, a molecule that the liver holds in reserve. In an overdose the two safe pathways become saturated, so a larger share of the drug takes the oxidative route. The reactive compound then binds to proteins in liver cells, and the damage can progress to liver failure. The standard treatment, given early enough, is N-acetylcysteine, which restores the supply of glutathione.

Protein presents a different problem. Amino acids that are not needed are broken down, and the nitrogen they contain is released as ammonia, which is toxic to the brain. The liver converts ammonia into urea in a series of reactions known as the urea cycle; urea is harmless and highly soluble. The kidneys then remove it and excrete it in urine. When the liver fails, ammonia and other nitrogenous compounds accumulate in the blood, and they are thought to contribute to hepatic encephalopathy, the confusion and drowsiness that accompany severe liver disease.

A great deal of what is sold as liver support rests on shaky ground. Products described as detoxifying or cleansing the liver have rarely been tested in controlled trials, and the organ needs no help to carry out the reactions described above; it performs them continuously. Some herbal preparations, far from protecting the liver, are themselves a recognised cause of injury. Genetic differences in the P450 enzymes also mean that people metabolise the same drug at very different rates, and the gut microbiome may influence how the liver responds.

In 2023, junior doctors in England walked out of hospitals for days at a time, and their senior colleagues soon followed. Similar disputes have erupted in Kenya, India, Nigeria and South Korea, where thousands of trainee doctors resigned over plans to admit more students to medical school. Each conflict has its own history, but the underlying question is the same: should people whose work is to preserve life be permitted to withdraw it? My answer is that they should, but only within limits that are clearly defined in advance and enforced by law.

The argument against is easy to state. A patient in an emergency has not chosen the timing of their illness and cannot take their custom elsewhere; a person waiting for cancer surgery has no way of knowing whether the delay will matter. Doctors are also granted extraordinary privileges: a monopoly over the diagnosis and treatment of disease, the power to prescribe dangerous drugs and, in most countries, a large measure of self-regulation. With those privileges comes a reciprocal obligation. Police officers and firefighters are often forbidden by law from striking, precisely because the public cannot do without them, and it is argued that doctors belong in the same category. On this view, a strike is not simply a bargaining tactic but a betrayal of the trust on which the profession depends.

Yet the case for a right to strike rests on principles that are not easily dismissed. Doctors are employees, and like other employees they bargain over pay, hours and staffing. In many health systems the most serious threat to patients is not a short strike but chronic understaffing, exhausted staff and equipment that does not work. Clinicians who have no lawful way of pressing such grievances may watch conditions deteriorate for years. It is also worth asking who benefits from a prohibition. A ban hands governments a considerable advantage: they can allow wages to fall and vacancies to grow, knowing that the workforce has no lawful means of reply.

What does the evidence say about the effect on patients? The answer is more surprising than either side usually admits. Reviews of doctors' strikes in several countries have found that most were not associated with a clear rise in deaths, and a few reported a fall, probably because elective operations were postponed and only urgent cases were admitted. These findings should be treated with caution. Mortality is a crude measure: it says nothing about pain, disability or the anxious months spent on a waiting list. Strikes are usually brief, and emergency cover is normally maintained. Where services have been withdrawn for months, the picture is likely to be worse, though reliable data are scarce.

If a right exists, its boundaries matter more than the principle. Three conditions seem to me essential. The first is a guaranteed level of emergency care, defined in advance and agreed with an independent body, so that nobody is left without treatment for a condition that threatens life or sight. In practice this means cover at roughly the level of a public holiday such as Christmas Day, when hospitals run on a skeleton staff anyway. The second is notice: employers, patients and ambulance services need time to rearrange appointments. The third is that the most vulnerable departments, including intensive care, maternity and dialysis, should never be emptied.

Beyond these safeguards lies a question about how disputes should be settled. Strikes are a blunt instrument, and the threat of them is sometimes used to extract concessions that have little to do with patient care. A better arrangement would oblige both sides to submit unresolved disputes to arbitration conducted by an independent panel, with a published timetable and a duty to accept the outcome. Doctors' organisations have sometimes resisted this, fearing that an arbitrator would favour the government, and governments have resisted it for the opposite reason. Neither objection is unreasonable, which is itself a sign that the mechanism would be roughly even-handed. The alternative, in most countries, is bargaining in which the threat of harm is the main source of leverage.

Outright prohibition, then, is the wrong response. It would not remove the grievances that produce strikes; it would drive them into forms that are harder to see and harder to regulate, such as mass resignations, refusal of overtime and the emigration of trained staff. It would also make it easier for a government to neglect a health service, because the political cost of doing so would fall. A sensible legal framework should instead distribute obligations. Doctors should be required to maintain emergency cover and give notice; employers and ministers should be required to negotiate in good faith and to accept arbitration.

My conclusion is therefore a qualified one. The right to strike is not absolute, and any claim that doctors may withdraw their labour without limit mistakes a professional privilege for a licence. But a blanket ban is equally mistaken. It treats adults who have chosen a demanding career as though they had surrendered the ordinary rights of citizens, and it leaves the people best placed to identify dangerous conditions in hospitals with no lawful way of saying so. A right exercised under strict conditions, with emergency care protected and disputes referred to independent arbitration, protects patients better than either extreme. The task for legislators is to write those conditions carefully, and to hold both doctors and governments to them.