IELTS Academic Reading Practice Test 386

River blindness, or onchocerciasis, begins with the bite of a blackfly. The insects breed in fast-flowing water, so the disease is concentrated among communities that farm the fertile land beside rivers. Each fly may carry larvae of a parasitic worm, Onchocerca volvulus, which enter the body through the bite wound and grow into adult worms that live for years, coiled in nodules beneath the skin. The adults release millions of microscopic offspring, called microfilariae, which migrate through the skin and the eye. When these larvae die, they provoke intense inflammation: unbearable itching, rashes and disfigurement and, in the eye, damage that slowly destroys the sight. In the worst-affected parts of West Africa, whole villages near the most productive rivers were abandoned because so many adults became blind.

In the early 1970s a Japanese microbiologist, Satoshi Ōmura, working at the Kitasato Institute in Tokyo, began a systematic search for new compounds produced by bacteria of the genus Streptomyces. These soil organisms were already the source of many antibiotics, and Ōmura's team collected thousands of soil samples from across Japan, culturing the bacteria and testing what they secreted. One sample, taken from soil near a golf course, contained a strain that would prove unusually productive.

Ōmura sent cultures to the American pharmaceutical company Merck, where a team led by William Campbell tested extracts against parasitic worms in laboratory animals. Most extracts did nothing. One, however, cleared the parasites at extraordinarily low doses, and the compound responsible was isolated and named avermectin. Merck's chemists then altered the molecule slightly, removing a double bond, to produce a derivative that was more potent and safer for mammals. The result, ivermectin, was introduced for animal health in the early 1980s and soon became one of the most widely used veterinary medicines in the world.

A human use was less obvious. The drug is poorly absorbed from the gut, but this mattered little for river blindness, because the microfilariae live in the skin and the eye rather than deep inside the body. A single dose removed almost all of them within weeks, relieving the itching and halting the damage to the eye, and the effect lasted for months. Ivermectin does not kill the adult worms, which can survive in their nodules for a decade or more, so treatment has to be repeated. Yet destroying the larvae has a second benefit: a treated person is no longer a source of infection for the flies that bite them, so transmission within a community falls.

Here was the difficulty. The people who needed the drug were among the poorest in the world, subsistence farmers in remote areas who could pay nothing for it, and no ordinary market existed. In 1987 Merck announced that it would supply ivermectin free of charge, for as long as necessary, to any country that asked for it and could not afford to buy it. The drug was given the brand name Mectizan, and the arrangement became known as the Mectizan Donation Program.

Distributing a medicine to millions of people scattered across difficult terrain was another matter. The solution devised in the 1990s was community-directed treatment: trained volunteers in each village kept records, calculated doses with a simple height measure, handed out tablets and reported side effects. Because the drug is taken only once a year, the system could be attached to other village activities, and the cost per person treated stayed very low.

Coordination came from international bodies. The Onchocerciasis Control Programme, launched in 1974 with the World Health Organization as its executing agency, had first attacked the blackfly itself, spraying breeding sites in rivers from helicopters. Its original aim was less to treat individuals than to free fertile river valleys for cultivation, and it was financed by a group of international donors. From the 1990s it added the distribution of ivermectin, and the African Programme for Onchocerciasis Control, which ran from 1995 to 2015, extended mass treatment to many more countries. Where spraying and treatment were combined, transmission fell sharply.

One complication became apparent as treatment spread. In parts of central Africa, people are often infected at the same time with another worm, Loa loa, which lives in the blood and is also carried by biting flies. In a small number of people with very heavy Loa loa infections, ivermectin can provoke a severe and sometimes fatal reaction in the brain. Health workers therefore had to learn to identify communities where the risk was too high, and in some areas treatment was suspended or supervised more closely.

The results have nevertheless been striking. In the Americas, where the disease was confined to a few isolated communities, transmission has been eliminated, and Colombia, Ecuador, Mexico and Guatemala have all been certified free of it by the World Health Organization. In parts of Africa, notably in Uganda, mass treatment has also been stopped in areas where transmission appears to have been interrupted. Elsewhere the disease persists and will require many more years of annual distribution.

The discovery brought Ōmura and Campbell a share of the 2015 Nobel Prize in Physiology or Medicine, with the committee citing the extraordinary benefit the drug had brought to human and animal health. It was a rare case of a medicine developed for livestock becoming, in a different form and at no charge, one of the most important public-health tools in the tropics.

Around a quarter of the world's population is thought to carry a parasitic worm. The infections they cause, among them schistosomiasis, hookworm disease, lymphatic filariasis and river blindness, are rarely dramatic in the way that a bacterial infection can be, but they are extraordinarily persistent. A single schistosome may live in a person's blood vessels for a decade, and some filarial worms survive for fifteen years or more. Such longevity is remarkable, because these animals are large, extracellular and constantly exposed to an immune system designed to destroy invaders.

The immune system's usual weapons are poorly suited to the task. Phagocytes, the cells that digest microbes, cannot swallow an animal that may be centimetres long. Antibodies can bind to a worm's surface, but the surface is renewed so quickly that the antibody is often shed before it can do damage. Worms are also animals rather than microbes, and many of their molecules closely resemble our own, so the immune system has difficulty recognising them as foreign at all. The result is a stand-off that may last for years.

The first line of defence for a worm is its own body surface. The outer layer of a nematode, called the cuticle, is a tough, cross-linked structure that resists both enzymes and antibodies, and it is replaced as it wears out. Flukes such as Schistosoma, which live inside blood vessels, take a different approach. Their outer surface is a continuous living layer that is constantly renewed, so that antibodies bound to it are simply discarded and replaced with new material. The parasite also absorbs molecules from its host onto this surface, including blood group antigens and proteins of the immune system itself, so that it appears to be clothed in the host's own identity.

A second strategy is to live where the immune system cannot easily follow. Adult filarial worms lodge in the lymphatic vessels, where the flow of fluid makes them difficult to attack, and larvae of Trichinella encyst inside muscle cells and can remain there for years. Some worms also alter the tissue around them, building a capsule of host collagen that shields them from immune cells. Location alone, however, would not be enough if the worms did not also produce molecules that actively interfere with the response.

That interference is chemical. Hookworms secrete anticoagulants that keep blood flowing while they feed, and inhibitors that block the enzymes immune cells use to digest them. Other worms release molecules that mop up the reactive oxygen compounds produced by inflammatory cells, or that block the complement system, a cascade of proteins that normally punches holes in foreign cells. Some parasites shed decoy molecules that occupy the antibodies which would otherwise bind to the worm itself. In laboratory experiments, a single one of these secreted proteins can be enough to dampen inflammation.

Perhaps the most sophisticated tactic is to manipulate the immune system's own control mechanisms. Chronic infection drives the response towards a state in which regulatory T cells, whose normal job is to stop the immune system attacking the body's own tissues, become more numerous and more active. This keeps inflammation around the worm in check, which suits the parasite, but it also affects the response to everything else. Several studies have found that people with heavy worm burdens may respond less strongly to some vaccines, and that treating the infection can improve those responses.

Filarial worms, the group that includes the agents of river blindness and elephantiasis, carry an additional complication: they depend on bacteria. Almost all of them harbour Wolbachia, an intracellular bacterium passed from one generation to the next and apparently required for the worm's development and reproduction. When the worms die, it is often the release of Wolbachia, rather than the worm itself, that triggers the worst inflammation. This partnership has given medicine a route of attack: courses of ordinary antibiotics kill the bacteria and, over months, sterilise and gradually kill the adult worms, though far more slowly than the drugs normally used against them.

If worms are so successful, why do people living in affected areas eventually develop some resistance? In communities where transmission is intense, adults typically carry fewer and smaller worms than children, and after treatment people are often less heavily reinfected than they were the first time. But this protection takes years to develop, is partial and depends on continued exposure; it is not the solid, lasting immunity that a vaccine aims to produce. The difficulty for vaccine designers is that the worms suppress exactly the responses a vaccine would try to stimulate, and the surface molecules a vaccine might target vary between life stages.

Today much of the research runs in two directions. One aims to find ways of blocking the molecules that let worms survive, whether by vaccines or by drugs that interfere with them. The other turns the parasite's inventions to medicine's advantage. Because worm proteins are so effective at calming inflammation, several groups are investigating whether copies of them could treat conditions in which the immune system attacks the body, and small trials have deliberately infected volunteers with hookworm larvae to study the effect on inflammatory bowel disease and coeliac disease. The results so far are mixed and the approach remains experimental, but the interest is easy to understand: after millions of years of learning to live inside a host, worms have become experts in the art of not being attacked.

Every year, hundreds of millions of tablets reach patients in low-income countries without any money changing hands. Ivermectin for river blindness is donated by Merck, albendazole for lymphatic filariasis by GSK, praziquantel for schistosomiasis by Merck KGaA, azithromycin for trachoma by Pfizer, and the combination of drugs that cures leprosy by Novartis. These are not minor contributions. Entire programmes of disease control, coordinated by the World Health Organization, depend on them. Yet the arrangement raises a question that is rarely asked aloud: should the supply of medicines that people cannot live without rest on the goodwill of private companies?

The defenders of donation point out that these diseases have almost no commercial market. A company that manufactures a product for people who earn a few dollars a day will never recover what it spends, and for decades the result was that nothing was done at all. Donations, on this view, have made elimination programmes possible at a speed that public funding could not have matched, and the drugs have reached places where governments and aid agencies had failed to go. The arrangement is best understood not as charity but as a division of labour: industry makes the medicine, international agencies decide who receives it, and local health services deliver it.

It would be naive, though, to imagine that companies gain nothing. The medicines donated are usually old ones whose patents have expired, so the true cost is the cost of manufacture, which for a tablet may be a few cents. In exchange, a company earns goodwill, access to field data and relationships with ministries that may later buy other products. Whether this is cynical or simply honest is a matter of taste. The more important point is that the arrangement aligns the interests of shareholders and patients only for as long as it suits the shareholder.

Critics make a sharper argument. The diseases that attract donations, they observe, are largely those for which a company already has a suitable product. Conditions for which no such product exists, or where the profitable market lies elsewhere, remain neglected. The decision about which disease is worth solving is taken not by the ministry of health in an affected country but by a committee in a corporate headquarters. Donation, on this view, does not correct the priorities set by the market; it reproduces them, with a charitable gloss. A medicine that is convenient for a company to give away is not necessarily the medicine that patients most need.

There is also the question of what a donation actually pays for. A tablet is useless without a nurse to prescribe it, a vehicle to carry it, a warehouse to store it and a system to report the rare but serious side effects. These costs fall on ministries of health that are already stretched, and in some countries the arrival of free drugs has reduced the pressure to fund distribution properly. Critics argue that the value of a donation should be judged against the whole cost of treatment, of which the medicine itself may be a small proportion.

Then there is the fragility of the arrangement. A pledge of as much as is needed, for as long as it is needed, is a promise rather than a contract. Programmes have continued for many years, but they survive at the discretion of a board; a merger, a restructuring or a change of leadership could end one, and patients who depend on a tablet every year have no remedy. No major programme has yet been abandoned in this way, but nothing in the arrangements guarantees that one will not be.

Ministries of health in affected countries take a different view again. Most welcome the drugs, and many officials describe the programmes as among the most effective forms of assistance they receive. The same officials point out, however, that a donation gives them little say over the product, the timetable or the packaging, and that a free medicine can make it harder to negotiate lower prices for the drugs they must buy themselves. Dependency, they note, is not only a matter of money; it is a problem of planning.

What would a more durable system look like? Pooled procurement, in which countries buy medicines together and bargain for lower prices, has worked well for vaccines and for the treatment of HIV. Tiered pricing, in which companies charge according to a country's income, is another option, though it has proved difficult to police when cheap products are resold in richer markets.

Advance agreements, in which a buyer guarantees a market in return for a low price, are a further possibility, though they require negotiating skills that many small states do not possess. Above all, money for delivery must come from somewhere, and it is more likely to come from a government budget or an international fund than from a company's charitable budget.

None of this is an argument for refusing the tablets. Where people are at risk of blindness or elephantiasis, a donation that prevents suffering is obviously justified, and the companies that have made such commitments deserve credit. But a donation should be understood as a bridge, not a foundation: useful for crossing a gap, dangerous if mistaken for solid ground. The test of a donation programme is therefore not how generous it is but whether it is designed, from the start, to make itself unnecessary.