IELTS Academic Reading Practice Test 359

The cinchona is an evergreen tree that grows on the eastern slopes of the Andes, from Colombia southwards to Bolivia. Its bark is intensely bitter, and the peoples of the region are known to have used it for centuries to treat fevers, long before Europeans reached South America. The Quechua word for the bark, kina, is usually said to be the origin of the Spanish quina, from which the name quinine derives.

According to a story repeated in almost every account of the tree, the bark reached Europe through the Countess of Chinchón, the wife of a Spanish viceroy in Peru, who is said to have fallen ill with fever in the late 1630s and to have been saved by a local remedy. The tale gave the tree its scientific name, since Carl Linnaeus called the genus Cinchona in the countess's honour. Historians who have examined the records, however, doubt the story, noting that the dates do not fit and that no contemporary document mentions such a cure. What is certain is that by the middle of the seventeenth century the bark was being shipped to Spain in quantity.

The bark was carried to Europe by members of the Society of Jesus, who were active as missionaries in South America, and for generations it was known simply as Jesuit's bark or Peruvian bark. Its reception was not always warm. In Protestant countries the association with the Jesuits made physicians suspicious, and some regarded the enthusiasm for a foreign remedy as a fashion rather than a treatment. The medicine's champions included an Englishman named Robert Talbor, whose secret preparation was credited with saving the life of Charles II in 1679. Talbor later treated the heir to the French throne and sold his recipe to Louis XIV for a very large sum.

Demand grew, but supply was precarious. The trees grew slowly and were harvested by stripping the bark, which killed them, and the bark collected from different species and at different seasons varied greatly in strength. Adulteration was common, and a physician had no way of knowing how much active ingredient a powder contained. The trees were confined to a narrow band of mountain forest, and the Spanish crown tried to keep the trade under its control.

The decisive advance came in Paris in 1820, when two chemists, Pierre Joseph Pelletier and Joseph Bienaimé Caventou, isolated the principal active substance from cinchona bark and named it quinine. They showed that the bark contained several related alkaloids, of which quinine was the most important, and their work allowed the drug to be produced in standard doses for the first time. Quinine was not a gentle medicine. Taken in effective amounts it causes ringing in the ears, headache and nausea, a cluster of symptoms that became known as cinchonism; nor was it cheap, since it could be obtained only from bark.

The obvious solution was to grow cinchona elsewhere. In the 1850s a Dutch botanist, Justus Hasskarl, brought seeds and seedlings from South America to the island of Java, where plantations were soon established. British collectors working for the government in India, among them Clements Markham, arranged for cinchona plants to be sent from Peru to India in the 1860s, and plantations were established in the Nilgiri hills and in Ceylon. The Dutch plantations were built on a species that proved unusually rich in quinine; by the early twentieth century Java was producing the great majority of the world's supply.

Quinine's great value was against malaria, a disease transmitted by mosquitoes and caused by a parasite that multiplies inside red blood cells. Quinine kills the parasite while it is in the blood, which relieves the fever and can save the life of a patient with severe disease. It does not, however, prevent infection. Nor does it eliminate the dormant forms that some species of parasite leave in the liver. The drug is extremely bitter, and for centuries it was taken dissolved in wine, water or spirits; British soldiers in India are said to have mixed it with soda water, sugar and gin to make it palatable, a habit often credited with the origin of the gin and tonic.

Because quinine came almost entirely from Java, the Second World War exposed a dangerous dependence. When Japanese forces occupied the island in 1942, the Allies lost access to most of the world's supply and were forced to develop synthetic alternatives. The German chemical industry had already produced synthetic antimalarials in the 1930s; one of them, mepacrine, carried the Allied armies through the war, and another, chloroquine, came into wide use soon afterwards. For a time after 1945 it seemed that quinine might be retired altogether, but the parasite developed resistance to chloroquine and the drug was gradually abandoned in most of the world. A new medicine, artemisinin, was extracted from a Chinese plant in the 1970s, and one of the scientists responsible, Tu Youyou, later received the Nobel Prize in Physiology or Medicine.

Quinine has never quite disappeared. The World Health Organization still recommends it for severe malaria where the preferred artemisinin-based treatments are unavailable, usually in combination with an antibiotic. Cinchona is still cultivated, mainly in Indonesia and parts of Africa, and its bark remains the source of most of the world's medicinal quinine, though much of what is produced now goes into flavouring rather than medicine. In Peru the tree is a national symbol, appearing on the country's coat of arms.

Malaria is caused by single-celled parasites of the genus Plasmodium, of which five species routinely infect people. The deadliest by far is Plasmodium falciparum, responsible for most of the deaths, and those deaths occur overwhelmingly in young children in sub-Saharan Africa. The parasite's life is unusually complicated. It alternates between a human being and a female mosquito of the genus Anopheles, and passes through a series of distinct forms, each adapted to a particular place in the body. Working out this sequence took decades of patient laboratory research, and it explains both why the disease is so severe and why it has proved so difficult to control. The World Health Organization estimates that there were roughly 250 million cases and more than 600,000 deaths in 2022.

Infection begins when an infected female mosquito, probing the skin for a blood meal, injects saliva containing thread-like cells called sporozoites. A mosquito may deliver only a few dozen of them, and they do not remain in the blood for long. Within about half an hour most have left the circulation and entered cells of the liver, where antibodies cannot reach them. Because the parasite is by then inside a host cell rather than free in the plasma, the immune system has little opportunity to attack it. This is the phase of the disease that produces no symptoms at all: a person can carry the parasite without the slightest sign of illness. Inside a liver cell the parasite takes over the cell's machinery and begins to make copies of itself.

The liver stage is a period of explosive multiplication. A single sporozoite becomes a schizont, a bag containing tens of thousands of merozoites, the form that will invade red blood cells. In P. falciparum this takes about a week, after which the host cell bursts and releases its cargo into the bloodstream. Two species, P. vivax and P. ovale, add a further complication. Some of their parasites become dormant hypnozoites that remain in the liver for months or even years, waking to cause a relapse long after the original illness has been treated. These sleeping forms are invisible to most antimalarial drugs, which is why vivax malaria can return again and again.

Once in the blood, merozoites invade red blood cells and the cycle of replication begins again. Inside a cell the parasite feeds on haemoglobin and grows, then divides into up to two dozen new merozoites, which burst out and invade fresh cells. For P. falciparum, P. vivax and P. ovale the cycle takes about 48 hours; for P. malariae it takes 72. The parasites tend to develop in step with one another, so that huge numbers of cells rupture at almost the same moment. The debris released triggers a surge of inflammatory signals, and this synchrony is what produces the characteristic rhythm of fever, chills and sweating that recurs every second or third day. Because the cycle is repeated without pause, a patient with untreated falciparum malaria can lose a substantial proportion of their red cells within days.

Plasmodium falciparum has evolved an additional trick. Shortly after invading a red blood cell, it pushes a protein called PfEMP1 onto the cell's surface, where it forms small sticky knobs. These knobs make the infected cell adhere to the lining of small blood vessels, so that it is carried out of the circulation rather than through the spleen, the organ that would otherwise destroy damaged red cells. The parasites therefore accumulate in the capillaries of the brain, the lungs, the kidneys and the placenta. In the brain this can cause swelling, coma and death, a condition known as cerebral malaria, while in pregnancy it leads to anaemia and low birth weight. This single adaptation accounts for much of the difference in danger between falciparum malaria and the other forms.

Not all parasites continue to multiply asexually. A small proportion develop into sexual forms, male and female gametocytes, which circulate in the blood and are harmless to their host. They are, however, the stage on which the whole life cycle depends. When a mosquito bites an infected person it takes up gametocytes along with the blood; in the insect's gut they fuse to form a zygote, which burrows into the gut wall and grows into a cyst. After ten days or so the cyst releases sporozoites that travel to the salivary glands, ready to be injected into the next person. The speed of this process depends on temperature: below about 16°C the parasite cannot complete its development in the mosquito, which is one reason malaria is confined to warm regions.

Much remains uncertain. People who survive repeated infections gradually acquire partial immunity, so that adults in areas of intense transmission may carry the parasite with few symptoms, but this protection is slow to develop and fades when exposure stops. A vaccine directed at the sporozoite's circumsporozoite protein, known as RTS,S, was recommended by the World Health Organization in 2021, and a second, R21, followed in 2023. Both reduce cases substantially in young children, but they protect only part of the time and neither prevents infection altogether. Drug resistance is a persistent problem: resistance to chloroquine spread from Asia to Africa in the late twentieth century, and partial resistance to artemisinin, marked by mutations in a gene called kelch13, has since appeared in East Africa. Each of these difficulties can be traced back to the parasite's biology: its ability to hide in the liver, to alter the proteins on the surface of the cells it occupies and to reproduce in enormous numbers.

In 1980 the World Health Organization declared that smallpox had been eradicated. The last natural case had occurred three years earlier, in Somalia, and the campaign that achieved this had taken little more than a decade. The total bill is usually put at around $300 million, a sum that looks modest beside the value of the lives that would otherwise have been lost. Polio is nearly gone, guinea worm is close, and malaria and tuberculosis are the subject of ambitious international targets. The question that follows is blunt: who should pay?

The strongest argument for wealthy countries paying is that eradication is a global public good. A country that eliminates a disease protects its neighbours as well as itself, and no single country can finish the job alone, because the last cases usually occur in the poorest and most remote places, where surveillance is hardest. Eradication also has an economic logic that control lacks: vaccination campaigns must be continued indefinitely, whereas eradication is a one-off investment that ends. Economists who have tried to value the benefits have generally found returns far in excess of costs, although such calculations depend heavily on assumptions about the value of a life and the future behaviour of the disease.

The second argument is moral and does not require arithmetic. Malaria, tuberculosis and diarrhoeal disease kill millions of people every year, and most of those deaths could be prevented with tools that already exist and cost very little. Oral rehydration salts, insecticide-treated bed nets and a course of antibiotics are cheap. If a child's death can be prevented for the price of a few dollars, the fact that the child was born in a poor country is hard to defend as a reason for doing nothing.

The third argument is self-interest, and the COVID-19 pandemic made it vivid. Infectious diseases do not observe borders, and a pathogen circulating anywhere is a threat everywhere. Rich countries discovered that they could not vaccinate their way out of a pandemic while the virus continued to replicate in unvaccinated populations elsewhere. The same logic applies to drug resistance: every untreated infection is an opportunity for a parasite or bacterium to acquire resistance, and resistance eventually arrives in wealthy hospitals. Spending on disease control abroad can therefore be understood as spending on domestic security.

Against all this, critics raise objections that deserve to be taken seriously. The first concerns effectiveness. Aid can weaken the relationship between a government and its citizens, because a state that is not responsible for financing its own health services has little incentive to make them work. Disease-specific programmes can distort national priorities, drawing nurses away from clinics into campaigns and leaving the routine system weaker than before. Promises are also broken: rich countries have repeatedly pledged to spend 0.7 per cent of national income on development assistance, and only a handful have consistently met the target, while African governments that signed the Abuja Declaration in 2001, promising to devote 15 per cent of their budgets to health, have mostly fallen short.

A second objection is that eradication is a gamble with other people's money. Campaigns consume a growing share of resources as they approach the last cases, and failure is expensive. The attempt to eradicate yaws in the 1950s and 1960s was abandoned when the disease proved harder to finish than expected, and the parasites that cause malaria belong to several species, each with its own habits, which makes the goal far more difficult than it was for a single virus.

A third objection is political. Programmes designed in Geneva or Washington reflect the priorities of those who pay for them, and the diseases that attract money are not always the diseases that cause the most suffering. A neglected tropical disease that disables people slowly may attract less attention than a virus that threatens travellers. Critics also point out that the language of eradication, with its military metaphors, encourages donors to believe that complex health systems can be fixed by a single intervention. These are real dangers, but they are arguments about how money should be spent, not about whether it should be given.

The debate between vertical campaigns and horizontal health systems is often presented as a choice. It is not. The smallpox campaign trained a generation of surveillance workers and left behind laboratory networks that were used for decades. The polio infrastructure in Nigeria now carries other vaccines and other messages. What matters is whether a campaign is designed to leave something behind, and whether it is planned and led by the country in which it takes place.

My own view is that the case for rich countries paying is overwhelming, but the case for their paying without conditions is not. Financing should be long-term and predictable, since a campaign that stops halfway wastes everything already spent; it should include money for laboratories, staff and data systems, not only for drugs and vaccines; and the countries affected should set the priorities. Eradication should be attempted where the biology makes success plausible, not where the announcement makes a good headline. On those terms, the obligation is clear enough.