IELTS Academic Reading Practice Test 309

In the 1840s the Vienna General Hospital was one of the largest medical institutions in Europe, and its maternity department was divided into two separate clinics. Founded in 1784, the hospital treated patients from across the Austrian Empire. The First Clinic was staffed by medical students, the Second by trained midwives. The two were otherwise similar in size and in the patients they admitted, yet their records told a starkly different story: in the First Clinic, women who gave birth were several times more likely to die than those in the Second. The difference was so widely known that some women begged to be admitted to the second department, and stories circulated of women giving birth in the street on the way to the hospital rather than risk the first.

The illness that killed them was puerperal fever, a devastating infection of the womb and the bloodstream that could begin within hours of delivery. A woman might develop a high temperature and severe abdominal pain, and within a day or two she could be dead. Doctors of the period had many explanations: overcrowding, poor ventilation, poisonous vapours in the air, and even the shame of unmarried motherhood. None of these could account for the fact that a hospital divided into two departments produced such different results, and in bad months the First Clinic lost close to one woman in ten.

Ignaz Semmelweis, a Hungarian-born physician who joined the First Clinic as an assistant in 1846, became preoccupied with the question. He examined the statistics month by month and considered one explanation after another, ruling out overcrowding, ventilation, climate and the behaviour of the patients themselves. The difference between the two departments, he became convinced, lay not in the women, who were broadly alike, but in what the staff carried on their hands. It was an idea that few of his colleagues were prepared to entertain.

The medical students of the First Clinic spent part of each day in the mortuary, where they dissected the bodies of women who had died of puerperal fever, and then went upstairs to examine women in labour. The midwives of the Second Clinic did no such work. In 1847 a friend and colleague of Semmelweis, Jakob Kolletschka, died after his finger was cut during an autopsy, and the record of his illness resembled what Semmelweis saw in the dying mothers. Semmelweis concluded that particles from the corpses were being carried on the hands of the students from the mortuary to the delivery room.

In May 1847 he ordered every student and doctor in the First Clinic to wash his hands in a solution of chlorinated lime before entering the wards. The effect was dramatic. Within a few months the death rate fell from around one in ten to little more than one in a hundred, and the fever very nearly disappeared from the department. Semmelweis extended the practice to instruments and bedding. He also observed that women who had delivered outside the hospital, on their way to the ward, rarely developed the fever, which fitted his theory neatly.

Yet the reaction of his superiors was not gratitude. Chlorine had a pungent smell, handwashing took time, and the suggestion that gentlemen were killing their patients was deeply unwelcome. Semmelweis's appointment at the clinic was not renewed in 1849, and in 1850 he left Vienna for Hungary, where he later became professor of obstetrics in Pest. There he continued to apply his methods and to gather statistics, and his later writings reported similarly encouraging results. He also corresponded with physicians elsewhere in Europe, urging them to adopt chlorinated lime, but he won few converts while he lived.

His statistical methods were criticised and his manner was said to be difficult, and his great work on the cause and prevention of childbed fever did not appear until 1861. The book was not well received. Much of the medical establishment in Vienna and elsewhere remained attached to the miasma theory of disease, in which infection was thought to arise from foul air rather than from contact between people. Others accepted the statistics but disputed the explanation, arguing that the chlorine had simply removed the offensive smell that was the true cause of illness. Semmelweis responded to criticism with anger and public letters, which did little to persuade his opponents.

His own health declined. He suffered what contemporaries described as a breakdown, and in 1865 he was taken to an asylum in Vienna, where he died on 13 August at the age of 47, apparently from an infection that had entered a wound. He never saw his ideas accepted, and to many of his contemporaries his name stood for a career wasted on a delusion.

Vindication came from elsewhere. In the 1860s and 1870s the work of Louis Pasteur and Robert Koch established that many diseases are caused by microorganisms, and Joseph Lister's antiseptic methods, introduced in surgery in 1867, showed that killing germs could save lives. Handwashing then became a standard example of a simple measure that saves many lives. Today hand hygiene remains one of the most effective defences against infections acquired in hospital, yet studies of compliance show that doctors and nurses still wash less often than they should. The physician who counted the dead in Vienna is now remembered as a pioneer of infection control, and a medical university in Budapest now bears his name.

The human body hosts countless microbes, most of which do no harm. The immune system nevertheless maintains a standing defence, and it works in two quite different ways. The first, usually called the innate response, is fast and blunt: barriers such as the skin and the lining of the airways, together with cells that attack anything that looks foreign, go into action within minutes. The innate response cannot tell one virus from another, however, and it does not improve with practice. The second, the adaptive response, takes days to get going, but it is precise, and it leaves behind the cells that give the whole system its memory.

When a virus enters the body, sentinel cells called dendritic cells take up fragments of it and travel through the lymph vessels to the nearest lymph node. There they display these fragments on their surface, and T cells that happen to recognise them are activated. The lymph nodes, which swell during an infection, act as the meeting place where the cells of the adaptive system are introduced to the enemy. Without this step, the rest of the response cannot begin.

A second population, the B cells, each carry on their surface a receptor that binds to a particular shape on the surface of the pathogen. When a B cell meets a shape it fits and receives confirming signals from helper T cells, it is activated and begins to divide. Most of its descendants become plasma cells, which are factories for antibodies: proteins that attach to the pathogen, neutralise it and mark it for destruction. Antibody molecules are produced in enormous numbers, and their concentration in the blood can rise a thousandfold within a week or two of a first infection.

Inside the lymph node, dividing B cells pass through a structure called a germinal centre, where a remarkable process of trial and error takes place. The genes that encode their receptors mutate at a very high rate, and the resulting cells compete to bind to antigen displayed by other cells. Those that bind weakly die; those that bind more tightly are kept alive and divide again. Over a few weeks the population is refined so that its antibodies fit the pathogen more closely, a process known as affinity maturation. From the germinal centre emerge two long-lived kinds of cell: memory B cells, which circulate quietly, and plasma cells that settle in the bone marrow and continue to release antibodies for years.

T cells have their own memory. Helper T cells, which coordinate the response, and killer T cells, which destroy infected cells, both give rise to memory populations that persist long after the infection has cleared. Some of these cells remain in the blood and the lymph nodes, but others take up residence in the tissues where the germ was first met — the lungs, the gut, the skin — and respond within hours if it returns. These tissue-resident cells are thought to be particularly important in the defence of the surfaces through which most infections enter.

The practical consequence is speed. In a first infection, the adaptive response needs roughly one to two weeks to reach its peak, and the person may be ill throughout. In a second infection with the same pathogen, memory cells are already present in large numbers. They multiply and produce antibodies within a few days, often before symptoms appear, and the infection may be stopped altogether.

Memory can last for an extraordinarily long time. When researchers tested survivors of the 1918 influenza pandemic ninety years later, survivors in their nineties and older still had antibodies that neutralised the virus that had infected them as children. People vaccinated against smallpox decades earlier have likewise been found to retain memory B cells and T cells, even when antibody levels in their blood had fallen. Antibodies themselves are short-lived proteins, but the cells that make them are not, and the marrow can keep releasing them at a low level for a lifetime.

Why some vaccines produce this kind of durable protection and others do not is still not fully understood. Vaccines against measles and smallpox are both based on live viruses and give immunity that lasts for decades. Vaccines made from inactivated toxins, such as those against tetanus and diphtheria, protect the individual well but generate fewer long-lived plasma cells, so booster doses are recommended at intervals. The acellular pertussis vaccine, used in many countries against whooping cough, protects for a time, but its effect on transmission appears to fade within a few years.

There are also limits on what memory can do. Measles is unusual in that infection can damage the memory that already existed: studies have found that children who recover from measles lose antibodies against other infections they had previously met, a phenomenon sometimes called immune amnesia. Researchers are also still trying to identify simple measurements, known as correlates of protection, that reliably show whether an individual is still protected. Antibody levels are the usual guide, but they are an imperfect one, because memory T cells and long-lived plasma cells can hold a line that a blood test does not reveal.

For new pathogens the picture is harder still. Much of what is known about immune memory comes from viruses long established in humans, and a first encounter with a virus shapes the response in ways that subsequent exposures do not entirely undo, a phenomenon known as imprinting. How far that matters for new vaccines, and how long the memory they create will last, are questions that only time and very large studies can answer.

Every autumn, in a growing number of countries, a small group of children is turned away from school because their parents have not had them vaccinated. Some of these families have simply missed appointments; others have decided, often after reading material online, that the vaccines are not worth the risk. The question such cases raise is not whether vaccination is a good thing, which the evidence settles overwhelmingly in favour of, but whether the state may require it. My answer is a qualified yes: compulsion is defensible for a short list of serious diseases, provided that it is designed with care.

Mandates are not a modern invention. In England and Wales, an Act of 1853 made smallpox vaccination compulsory for infants, and later legislation extended the requirement to older children. The result was a long campaign of resistance, with demonstrations, pamphlets and prosecutions, and in 1898 Parliament allowed parents who objected on grounds of conscience to obtain a certificate exempting them. In the United States, the Supreme Court upheld compulsory vaccination in 1905, during a smallpox outbreak in Massachusetts, and school-entry requirements have existed in most states for decades. Two lessons follow. Mandates work only when the public accepts them, and they can be withdrawn or softened when they do not.

The strongest argument for compulsion is indirect protection. A highly infectious disease such as measles will spread through a community unless a very large proportion of its members are immune; the figure usually quoted for measles is around 95 per cent. Below that level, outbreaks occur, and the people who suffer are not only those who refused. Newborn babies are too young to be vaccinated, and some children cannot be: those receiving treatment for cancer, those with certain immune deficiencies, and those who have had a severe reaction to a previous dose. These children depend entirely on the immunity of those around them. To send an unvaccinated child into a classroom is, in effect, to ask other families to carry a risk on that child's behalf.

The second argument is about consequences. An outbreak closes schools, disrupts families and consumes the time of health services that are already stretched. Yet the cost of an outbreak is a reason to raise vaccination rates, not by itself a reason to use the law. Only if every less coercive measure has failed does the balance tip towards compulsion, and it is worth asking what a government would have to show before it reached that point.

Against compulsion there are three serious objections. The first concerns consent. Vaccination means piercing the skin of a child who cannot agree to it, in order to protect that child and others, and a liberal society should be reluctant to use the power of the state in this way. The second concerns trust. Vaccines are not risk-free: serious reactions are rare but real, and in many countries the families affected receive little or no compensation. When a government compels a medical intervention, it takes on a duty to support those who are harmed by it. The third concerns backlash, since some researchers argue that heavy-handed requirements can entrench opposition, and a mandate that raises uptake among the hesitant while hardening a small minority against all vaccination may do more harm than good.

A further objection is fairness. Requirements are usually enforced through exclusion from school or through the withdrawal of child-related payments, as in Australia, where family payments were made conditional on vaccination in 2016. Both penalties fall hardest on families with the least money and the least time to negotiate a complicated system. An unvaccinated child excluded from lessons is punished for a decision made by an adult. And a requirement introduced without adequate access — appointments that fit around work, reminders, a doctor within reach — penalises people for obstacles that the state itself has failed to remove.

This is why the design of a mandate matters more than its existence. A defensible scheme has three features. It applies only to diseases that are serious, that spread readily and against which the vaccine blocks transmission effectively. It exempts children with a genuine medical reason, on a doctor's assessment rather than a parent's assertion, and it offers no exemption on grounds of personal belief. And it guarantees that vaccination is free, easy to obtain and not conditional on anything else the family needs.

The choice of which vaccines to require is as important as the choice to require any. A mandate should not extend to vaccines that protect the individual well but do little to stop transmission, because a requirement is hardest to justify when the risk to others is small. For measles the case is strong: the disease is among the most infectious known, two doses of the vaccine are highly effective, and the protection of children who cannot be vaccinated depends on very high coverage. For a vaccine whose effect on transmission fades within a few years, the argument from protecting others is correspondingly weaker.

Where does that leave the question in my title? Compulsion is justified, but only narrowly: for measles and a small number of comparable diseases, for children at school age, with medical exemptions and no financial penalties, and only where the health system has made vaccination genuinely easy to obtain. Outside those limits, persuasion, information and good access are both more ethical and, in the long run, more effective. A mandate is a blunt instrument, and it should be used as a last resort rather than a first.