IELTS Academic Reading Practice Test 404

In the winter of 1925 Nome was a small town on the Seward Peninsula of Alaska. Its port was sealed by ice for most of the year, and its only reliable link with the outside world was the railway running north from the ice-free port of Seward to Nenana, in the interior; beyond Nenana lay 674 miles of winter trail. Nome had a hospital and several nurses but only one physician, Curtis Welch, and its isolation meant that a serious epidemic would have to be fought with whatever supplies were already on hand.

Diphtheria is caused by a bacterium, Corynebacterium diphtheriae, which settles in the throat and releases a powerful toxin. The infection forms a thick grey membrane that can block the airway, and the toxin attacks the heart and nerves, so that a child may survive the fever only to die of heart failure a week or two later. Antitoxin does not kill the bacteria; it neutralises the poison already circulating, and must therefore be given early, before the toxin binds to the tissues. A vaccine had recently been developed, but none had reached Nome.

In December 1924 Welch began to see children with sore throats and fever. He suspected diphtheria but hesitated to use his small stock of antitoxin, most of which was out of date, and hoped the illness would prove to be something milder. The question was settled in January, when a young boy died and others quickly followed. Welch placed the town under quarantine and sent radio telegrams appealing for antitoxin, but radio could not deliver a parcel, and the nearest supply was hundreds of miles away.

Antitoxin was a product of the new science of immunology. In 1890 Emil von Behring, working with Shibasaburo Kitasato in Berlin, showed that the blood serum of animals injected with weakened diphtheria toxin could protect other animals against the disease. To make the treatment, horses were immunised with gradually increasing doses of toxin until their blood contained large quantities of antibodies; they were then bled, and the serum separated and purified. In 1901 Behring became the first person to be awarded the Nobel Prize for medicine, and by the 1920s antitoxin had sharply reduced deaths from diphtheria in European cities.

A search of Alaskan hospitals produced a stock in Anchorage, but much of it had passed its expiry date and some had been damaged by frost, so only a fraction was usable. This portion, of about 300,000 units, was packed and put on a train north on the night of 26 January 1925. The railroad's staff cleared the line and drove the locomotive through the drifts, reaching Nenana on 27 January. A fresh consignment from Seattle was to follow, but it could not arrive for days.

The territorial governor had two options. Aircraft were available and pilots volunteered, but open-cockpit biplanes in an Alaskan winter, with no airfields along the route, were thought too risky. The governor chose the mail trail instead: a relay of dog teams, with fresh mushers and dogs waiting at roadhouses, so that the serum could travel day and night. The trail from Nenana to Nome was 674 miles long, and twenty mushers and about 150 dogs took part, in temperatures that fell below −40 °C and in gales that filled the trail with drifting snow.

The most experienced musher was Leonhard Seppala, a Norwegian who had come to Alaska during the gold rush and become one of its finest dog drivers. His lead dog, Togo, was small and stubborn and had seemed unpromising as a puppy. Seppala's team travelled east from Nome to meet the serum, covering the longest distance of any team in the relay, and on the return journey Togo led the team across the sea ice of Norton Sound in darkness and a blizzard, taking a line that Seppala could not see. Togo covered well over 200 miles during the relay, and Seppala gave the dog much of the credit.

The last leg fell to Gunnar Kaasen, whose team was led by a black-and-white dog named Balto. Kaasen drove through a night in which he could not see his lead dog, and at one point the sled was blown over and the package of serum buried in a drift; he found it by searching with his hands. He reached Nome at about half past five on the morning of 2 February, five and a half days after the serum had left Nenana. It was thawed and administered the same day.

Diphtheria continued to spread for a time, and the second consignment from Seattle was still needed, but the epidemic was brought under control within weeks. The number of deaths is usually given as five, although published accounts differ. What is not in doubt is that a town of some 1,400 people, cut off from the world for months, had escaped a disaster that could have killed many more children.

Balto became a national celebrity, and a bronze statue of him was unveiled in Central Park in December 1925; Togo, by contrast, was little known outside Alaska until much later. In 1973 a long-distance race, the Iditarod, was established along part of the old mail trail in memory of the run. The wider legacy was medical: the episode persuaded Alaskan towns to keep antitoxin in stock, and vaccination, introduced in the 1920s, gradually turned a common childhood killer into a rarity in rich countries.

An itch is not simply a mild pain. For much of the twentieth century, doctors regarded itching as a lesser version of pain. Work over the past three decades has overturned that view. Itch has its own dedicated nerve fibres, its own chemical messengers and its own relay stations in the spinal cord, and the scratching it provokes has consequences of its own. Understanding why we itch means following a signal from the skin to the brain and back again.

The best-known cause is histamine. When the skin is stung by an insect or brushed by a stinging nettle, mast cells in the tissue release histamine, which binds to receptors on the ends of sensory nerves and makes them fire. The same chemical is released in hives, the raised rash of allergic reactions. Histamine itch has a characteristic appearance: a raised wheal surrounded by a red flare, produced as blood vessels dilate and fluid leaks into the tissue. Antihistamine tablets, which block the receptor, deal with this kind of itch effectively.

Not all itch is histamine itch, however. Cowhage, a tropical plant whose seed pods are covered in fine hairs, has been used for centuries to provoke itching. Its active ingredient proved to be an enzyme, mucunain, that splits proteins. In the 1990s researchers recorded the activity of single nerve fibres in volunteers given histamine or cowhage. The two substances excited different populations of fibres. Histamine-sensitive fibres fired slowly and were linked to the spreading flare, while the fibres that responded to cowhage fired in brief bursts at scattered points beneath the inserted hairs and ignored histamine entirely.

Most persistent itching is not caused by histamine at all, which is why antihistamines disappoint so many patients. Chronic itch is a common feature of kidney disease, especially in people receiving dialysis, and of liver disease, in which bile acids accumulate in the blood. It is also the defining symptom of atopic dermatitis, the commonest form of eczema. In that condition much of the sensation is driven by interleukin-31, a signal released by immune cells that acts directly on sensory neurons. Doctors describe such itch as antihistamine-resistant, and the search for other targets has driven much of the recent research. Antibody treatments that block the signal have reduced itching in clinical trials.

Whatever the chemical, itch signals converge on the spinal cord. In the late 2000s a team at Washington University in St Louis identified a small population of neurons in the dorsal horn of mice that carry the itch signal upwards. The cells use a molecule called gastrin-releasing peptide as their messenger. When the cells were destroyed, the animals stopped scratching in response to itch-producing substances, while their responses to painful heat and pressure were unchanged. Pain and itch, it seemed, run on separate lines.

Scratching offers relief, and the oldest explanation for it is the gate-control theory proposed in 1965. Signals from large, fast fibres carrying touch and pressure can close a 'gate' in the spinal cord and block the passage of slower signals. Scratching produces a mild, brief pain, and this activity competes with the itch signal in the same relay station. Relief follows within seconds and the urge subsides, at least for a while. The theory was proposed before anyone had mapped itch neurons, but it still explains why a hard rub can quiet a mosquito bite.

The relief does not last, because scratching sets off a second, less helpful process. The pain of scratching prompts the release of serotonin, a messenger used widely in the brain and spinal cord. Serotonin acting on the spinal neurons that carry itch makes them more excitable, so the itch returns more strongly than before and the person scratches again. This loop, the itch-scratch cycle, is central to eczema and to other conditions in which the skin is repeatedly broken. Mice in which serotonin signalling was blocked scratched far less than normal mice.

Brain imaging has added a further piece. When histamine is applied to a volunteer's skin inside a scanner, the anterior cingulate cortex and the insula become active. Scratching reduces activity in both, and it switches on the brain's reward circuits, which is part of why the relief feels pleasurable. Itch is contagious as well: watching someone scratch makes many people itch and scratch themselves.

Scratching is not harmless. Fingernails break the skin barrier, and the gaps they leave allow bacteria to enter, which is why scratched eczema so often becomes infected. Repeated scratching also thickens the skin, a change called lichenification, and in some people it produces hard, itchy lumps known as prurigo nodularis. Dermatologists therefore treat the habit as part of the disease, and much of their advice aims to interrupt the cycle before the skin is damaged.

Because antihistamines fail in most chronic itch, treatment borrows from other branches of medicine. Low doses of antidepressants, and gabapentinoids developed for nerve pain, damp down overactive sensory fibres and help some patients. Emollients that repair the skin barrier reduce the itch of eczema by keeping irritants out, and topical steroids calm the inflammation beneath. Behavioural treatment matters too: in habit-reversal therapy, patients learn to notice the moment before they scratch and to substitute another action. The benefit of such programmes is modest but measurable, and they are now a standard part of care.

Every few years a story appears about a dog that has detected a disease its owner's doctors had missed. A pet that repeatedly sniffs at a mole, a labrador that refuses to leave the side of someone later found to have cancer, a spaniel that alerts its owner minutes before a diabetic emergency: such accounts are gripping, and they suggest that medicine is ignoring a powerful sense that humans lack. Reactions tend to divide sharply. Some people treat the stories as proof that dogs can diagnose illness; others dismiss them as coincidence dressed up as science. Neither response is reasonable, because the question at issue is not whether dogs can detect a smell, but whether their performance is reliable enough to be used in patient care.

The biology is not in dispute. A dog's nose contains many times more receptor cells than a human's, and a much larger proportion of its brain is devoted to processing smell. Dogs can follow a trail days old and pick out one odour from a mixture in which it is present at extraordinarily low concentration. Disease can plausibly give them something to detect, because illness alters metabolism, and the altered chemistry is exhaled or excreted in breath, sweat and urine as a set of volatile organic compounds. What a dog responds to is probably a pattern of such compounds rather than a single molecule.

The scientific literature began with an anecdote. In 1989 a brief report in a British medical journal described a dog that had repeatedly sniffed at a mole on its owner's leg; the mole proved to be a malignant melanoma. A more systematic study followed in 2004, when a British team trained dogs to choose between urine samples from people with bladder cancer and samples from healthy volunteers. The dogs did far better than chance, but they were also wrong often enough that no clinician would have relied on them alone.

The pandemic produced the largest test of the idea. Dogs were trained on samples of sweat or saliva and deployed in pilot schemes at airports in several European and Middle Eastern countries, where they were asked to identify arriving passengers who might be infected. Some teams reported accuracy that sounded remarkable. Reviews of the work were less enthusiastic: many studies used small numbers of samples, few were fully blinded, and the ways in which samples were collected and stored varied so much that results could not easily be compared. No airport replaced laboratory testing with a dog.

One of the most intriguing lines of research began not with a dog but with a person. A retired nurse in Scotland, Joy Milne, noticed that her husband had acquired a faint musky smell years before he was diagnosed with Parkinson's disease, and she later found the same smell on other patients. Researchers at the University of Manchester have since analysed the oils on the skin of people with the condition and identified changes in the mixture of compounds there. This is the pattern that makes the field worth taking seriously: a remarkable nose, human or canine, points chemists towards molecules they would not otherwise have looked for.

The central difficulty is one that psychologists have understood for more than a century. Early in the twentieth century a horse called Clever Hans appeared to solve arithmetic problems, until a careful investigation showed that he was responding to tiny, involuntary movements of his questioner's posture and face. Dogs are equally attentive to people, and a handler who knows which sample is the right one may give the answer away without intending to. Trials must therefore be double-blind, with neither handler nor experimenter aware of the correct sample. Many published studies claim to be, but independent assessments have found that blinding was often incomplete or poorly described.

There are practical obstacles too. Training a detection dog takes many months, and the animal works for only short periods before it tires; its working life is perhaps eight or nine years, after which the investment is lost. Hospitals are cautious about animals in clinical areas because of the risk of transmitting infection. And dogs are now competing with machines. Electronic noses, which use sensors to detect volatile compounds, are improving steadily, and they do not need walks, rest or a handler. Machines may well take over much of the routine work.

Yet the case for dogs is not merely sentimental. In places where laboratories and trained technicians are scarce, a dog team may be a realistic option where a mass spectrometer is not; field studies have examined dogs as a way of screening for malaria and other infections in exactly such settings. The comparison, however, has to be like for like. A dog that finds most cases but also flags many healthy people is not necessarily better than a simple laboratory test, and the anxiety and unnecessary treatment caused by false alarms must be counted in the balance.

My own view is that the most valuable role for detection dogs is not as a clinical test but as a research instrument. Their noses can tell chemists where to look, as the Parkinson's work shows, and that is a genuine contribution. As a screening tool, however, the evidence is not yet strong enough, and the businesses now selling cancer detection sessions to the public should be regulated rather than encouraged. Well-designed trials are worth funding; claims made ahead of the evidence are not.