IELTS Academic Reading Practice Test 343

In 1928 a child whose breathing muscles had been paralysed had almost no chance of survival. The lungs themselves were often healthy; it was the muscular machinery of breathing that had failed. Although a doctor might clear an airway or squeeze a hand pump for a few minutes, nobody could keep that effort going for days. What such patients needed was a machine that would take over the work of breathing and continue for as long as the body required. The device that answered this need was built at Harvard, and it became one of the most recognisable objects in twentieth-century medicine.

Enclosing a patient in a box and altering the pressure of the air around the body was not a new idea. In the 1870s the French physician Eugène Woillez constructed a rigid chamber in which a patient lay with the head outside while air was pumped out and allowed back in. His apparatus was described in medical journals but never came into general use, and other inventors proposed similar devices over the following decades. The principle was sound enough. If the pressure around the chest is lowered, the chest expands and air flows into the lungs through the nose and mouth without anything being inserted into the airway. What had been missing was a machine reliable enough to be left running for weeks beside a desperately ill patient.

Philip Drinker (1894–1972) came to the problem from an unusual direction. Trained as an engineer, he spent his working life at the Harvard School of Public Health, where he specialised in industrial hygiene, the study of dust, fumes and ventilation in mines and factories. Measuring the air that workers breathed had given him a practical understanding of pumps, valves and airtight seals. In the late 1920s he turned this experience to artificial respiration and, with a colleague, Louis Agassiz Shaw, built a machine that worked.

The first version was a horizontal metal cylinder roughly two metres long, mounted on legs. The patient lay on a mattress inside, with the head outside and the neck sealed by a rubber collar, and portholes fitted with rubber sleeves allowed nurses to reach in. An electric pump drew air out of the tank, so the pressure inside fell below that of the room; the chest rose and air was drawn into the lungs. A valve then let air back in, the pressure returned to normal and the patient breathed out. The rate could be adjusted, usually to between twelve and eighteen breaths a minute.

The machine was first used on 12 October 1928 at the Children's Hospital in Boston. The patient was an eight-year-old girl whose breathing had failed, and she was close to death when she was placed inside. Within minutes of the pump starting she regained consciousness and her colour returned. Her recovery was short-lived, for she died a few days later of pneumonia, but news that the machine could keep a paralysed patient breathing travelled quickly; doctors in other cities wrote to ask how the device was made. The girl had been paralysed by polio, a viral infection that in a small minority of cases destroys the nerve cells controlling the muscles of breathing.

Demand grew as polio epidemics returned each summer. Warren E. Collins, a Boston maker of scientific instruments, began producing the machines to Drinker's design, and hospitals across the United States installed them. During outbreaks whole wards were filled with rows of tanks, each with a patient's head visible at one end, while nurses moved between them checking pressures and turning dials. In the worst American epidemic, in 1952, nearly 58,000 cases of polio were reported, and demand for the machines outstripped supply.

Drinker did not have the field to himself. In 1931 John Haven Emerson, an inventor working in Cambridge, Massachusetts, produced a respirator that was cheaper to build, lighter and easier to open for nursing care. Drinker brought a legal action, but the courts did not uphold his claim, and Emerson's design spread widely. The competition probably helped patients, since it brought the price down and encouraged improvements such as clearer windows and quieter pumps.

The tank had serious drawbacks. Nurses could examine a patient only through the sleeves, turning a patient was difficult, and some found the confinement frightening. The machines were heavy and hard to move, and they were poorly suited to anyone who needed surgery or complicated drug treatment, since almost everything had to be done through the portholes. Then in 1952, during a severe epidemic in Copenhagen, an anaesthetist named Bjørn Ibsen showed that air could instead be forced into the lungs through a tube inserted into the trachea, with medical students squeezing bags by hand to keep patients alive. Mortality among the most severely affected patients fell sharply, and the episode is often described as the beginning of the modern intensive care unit.

Negative-pressure ventilation did not vanish at once. Some patients continued to use iron lungs at home for the rest of their lives, and smaller versions, including shells that fitted over the chest, remained in use; variations on the idea are still employed for a small number of people with long-term weakness of the breathing muscles. By the 2000s, however, only a handful of long-term users of the tanks were left. Drinker died in 1972, having seen his machine save thousands of lives, and although modern hospital ventilators work on a different principle, they owe a great deal to it.

Only female mosquitoes bite. Males feed on nectar and plant juices and never take blood, while a female needs the protein and iron in blood to develop her eggs; most species must take such a meal before they can lay. That single requirement explains the persistence with which she hunts, and it is also why mosquitoes are such effective carriers of disease: the mouthparts that draw blood can pass parasites and viruses from one person to the next. How a mosquito locates a host has been studied for more than a century, and the answer turns out to be a sequence of senses, each useful at a different distance.

The first cue is the air we exhale. Every breath contains carbon dioxide at a concentration far above that in the atmosphere, and mosquitoes detect it with nerve cells housed on the maxillary palps, a pair of short appendages beside the mouthparts. These receptors are extremely sensitive: an insect can notice very small changes in carbon dioxide concentration, and can respond to a plume of exhaled air from tens of metres away. Tiny fluctuations in concentration then help her to judge direction, and she flies upwind towards the source. Carbon dioxide alone, however, is not enough to make her bite. A trap baited with the gas will attract mosquitoes, but far fewer than a human being does, which tells researchers that other signals must also be involved.

As she gets closer, the mosquito begins to read the chemistry of the skin. Human skin releases a mixture of more than a hundred compounds, among them lactic acid from sweat, ammonia and various fatty acids, and some of these are produced not by the body itself but by the bacteria that live on its surface. The mixture differs from one person to another, which is one explanation for a familiar observation: some people are bitten far more often than others in the same room. Body size matters, because larger people exhale more carbon dioxide, and pregnancy has been linked to increased attractiveness, probably for the same reason. Studies of blood group have produced inconsistent results, and most researchers regard them as inconclusive.

Warmth provides the next signal. Once she is within about a metre of a person, the mosquito can sense the heat radiating from the skin, using temperature-sensitive nerve cells on the antennae. A warm object at roughly body temperature is attractive even when no odour is present, although on its own it is a weak lure. Moisture matters too, because a small insect risks drying out, and the humid layer of air next to human skin is a reliable sign that a host is close. In still air this layer stays close to the body, so a mosquito that flies into it is very near its target, and receptors that respond to humidity help to keep her oriented as she makes her final approach.

Sight plays a part at the shortest range. A mosquito's compound eyes are poor by human standards, but they are good enough to pick out a dark shape against a lighter background, particularly if the shape is moving. This is why people dressed in dark colours are often bitten more than those in pale clothing. Laboratory experiments have shown that carbon dioxide and body odour make a mosquito more responsive to visual features, so that the eyes take over as the other cues fade with proximity. Under a dark sky, however, vision is of little use, and the remaining senses must do the work alone.

No single cue is sufficient, and the insect appears to combine them in a rough order of priority: carbon dioxide first, then skin odour, then heat, moisture and vision. Quite how the brain weighs these signals is still not understood. A further channel was reported in 2024, when researchers found that Aedes aegypti can detect infrared radiation, the heat given off by the skin, from a distance of up to about seventy centimetres. Infrared on its own did not attract the insects, but combined with carbon dioxide and human odour it produced a much stronger response than either cue alone. Why individuals differ so greatly in how often they are bitten remains equally unresolved: the bacteria on the skin, the gases in a person's breath and their body temperature all seem to matter, but no test can yet predict who will prove most attractive.

Understanding these senses is not merely academic. Traps used to monitor mosquito populations are baited with carbon dioxide, often from a cylinder or from fermenting sugar, together with a chemical copy of skin odour; the better the bait imitates a person, the more reliable the count. Repellents work on the same system. DEET, developed for the United States army in 1946 and used by the public from the 1950s, does not kill mosquitoes; it appears to interfere with their sense of smell, although the exact mechanism is still argued over. Other compounds, including picaridin and a substance derived from lemon eucalyptus, offer alternatives. None of them would be needed if we understood precisely why a mosquito chooses one sleeping body rather than another.

Dengue infects an estimated 100 to 400 million people every year, and malaria still kills more than half a million, most of them young children in sub-Saharan Africa. Control has rested for decades on insecticides, bed nets and drugs, and all three are being weakened by resistance. It is hardly surprising, therefore, that attention has turned to the insects themselves. Mosquitoes can now be engineered so that they no longer transmit a virus, or so that their numbers collapse. The question is no longer whether this is technically possible; it is when, where and under whose authority such insects should be released.

Two approaches are involved, and they are very different. The first is self-limiting. Oxitec, a company spun out of the University of Oxford in 2002, engineered males of Aedes aegypti, the mosquito that carries dengue, Zika and yellow fever, to carry a gene that kills their offspring before they reach adulthood. The insects are reared with the antibiotic tetracycline, which switches the lethal gene off; the males are then released, they mate with wild females, and the young die. The second is a gene drive, in which a genetic change is designed to copy itself into almost every offspring, so that it spreads through a population without further releases, potentially suppressing the species or making it unable to transmit disease.

These technologies are often discussed as though they were the same thing, and that is a mistake. A self-limiting strain is a sophisticated version of the sterile insect technique, in which radiation-sterilised males have been released against agricultural pests for decades. Its effect is meant to end when the releases end: the introduced genes are expected to dwindle and disappear from the population within a few generations, although a study in Brazil found traces of them persisting for longer. A gene drive has no such brake. Once released it is designed to keep going, crossing roads, fences and frontiers, and there is no practical way of recalling it.

The evidence from self-limiting releases is growing. Males have been released on Grand Cayman at the end of the 2000s, in Malaysia, Panama and Brazil, and, after several years of public argument, in the Florida Keys in 2021. In the Brazilian town of Juazeiro, the company reported reductions of more than 90 per cent in the target mosquito. Such figures are encouraging, but they need to be read with care: most of the trials have been organised and paid for by the companies that make the insects, few have been assessed by independent groups, and the published studies have generally been small.

The argument in favour rests on the scale of the burden. Dengue fills hospitals during the rainy season, and no drug acts against the virus itself. Aedes aegypti is not native to the Americas; it spread there over centuries of shipping and is now thoroughly at home in tropical cities, breeding in water tanks, discarded tyres and flower pots. Suppressing an invasive species that transmits disease is a more modest aim than eradicating a native one, and it could reduce the volume of insecticide sprayed in densely populated areas, where spraying is unpopular and often incomplete.

The risks are harder to state with confidence, and that is precisely the problem. Aedes aegypti is eaten by some birds, bats and dragonflies, and adults of both sexes visit flowers for nectar, so they may play a minor part in pollination. What would happen if the species were suppressed over large areas is not known; surveillance in places where it has been reduced has been too limited to reveal ecological effects, and other mosquitoes, including Aedes albopictus, might occupy the space left behind. Aedes albopictus also carries dengue. Uncertainty of this kind is an argument for caution, not for paralysis.

Governance is the weakest part of the picture. Gene drives do not respect borders, and no international agreement yet sets rules for organisms designed to spread. The Cartagena Protocol on Biosafety, negotiated in 2000, was written with crops and contained laboratories in mind, not insects that travel on the wind. In the United States the modified mosquito has been handled under laws intended for pesticides, while other countries have their own procedures, and the guidance published by the World Health Organization is voluntary. Some releases have drawn vocal local opposition; others have passed with little public comment. What is missing is a settled principle that those who live where the insects would be released should have a genuine say.

Meanwhile, a rival method has produced the strongest evidence of all, and it is not genetic modification in the usual sense. Mosquitoes infected with Wolbachia, a group of bacteria common in insects, are less able to support dengue virus, and when they are released they pass the bacteria on to their offspring. In a large randomised trial in the Indonesian city of Yogyakarta, this approach reduced dengue cases by about 77 per cent. That is a higher standard of proof than anything yet reported for a modified mosquito.

None of this means that genetic engineering should be abandoned. The self-limiting strains have a reasonable safety record so far, their effects are reversible, and the diseases they target are serious enough to justify controlled trials. My own view is that they should proceed, but only where independent monitoring is in place, where the results are published whatever they show, and where the communities affected have agreed. Gene drives are another matter: no such insect should be released in the wild until international rules exist, and until research in contained laboratories has answered the questions that field trials cannot.