Virusphere. Frank Ryan

to others, through coughing and sneezing, for a period of anything from one to three weeks.

      There is an adage that colds will not kill you. This is largely true, but colds can make children more liable to sinusitis and otitis media, a nasty bacterial infection of the middle ear. Colds can also precipitate asthma in people constitutionally prone to it, and they can provoke secondary bacterial chest infections in people suffering from cystic fibrosis or chronic bronchitis. Nevertheless, the salutary consolation is that, in the great majority of human infections, the rhinovirus eventually passes on by and we make a complete recovery.

      Is there anything we can do to minimise the risk of contracting that cold – or is there any effective treatment when we are afflicted?

      In Roman times, Pliny the Younger recommended kissing the hairy muzzle of a mouse as a remedy for colds. Benjamin Franklin was more sensible, suggesting that exposure to cold and damp in the atmosphere was responsible for the development of a cold. He also recommended fresh air and avoiding the exhaled air of other people. More modern times have seen a veritable cornucopia of quack remedies for prevention or treatment of colds. One of the most popular was vitamin C, championed by the distinguished American chemist, Linus Pauling. But alas, when subjected to scientific scrutiny it proved no more effective than the mouse’s whiskers. Perhaps we should focus more on common sense? Colds are contracted from the coughs and sneezes of infected people. People in congested offices, or even relatives who find themselves ill at home, should follow the old adage: trap your germs in a handkerchief. If an individual is deemed to be at a particularly high risk from a cold, wearing a virus-level face mask would certainly reduce the likelihood of infection when exposed to an infectious source.

      A pertinent question remains: why, then, if our immune system has come to recognise and react to the rhinovirus, are we still susceptible to further colds during our lifetime? In fact, there are roughly 100 different ‘serotypes’ of the rhinovirus, so immunisation to any one type would not provide adequate protection from the others. Added to this is the fact that serotypes are capable of evolving so that their antigenic properties are apt to change.

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       A Plague Upon a Plague

      In 1994 the East African nation of Rwanda erupted onto the world’s news and television screens when a simmering civil war between the major population of Hutus and minority population of Tutsis erupted into a genocidal slaughter of the minority population. But despite the deaths of half a million Tutsis, the Hutu perpetrators lost the war, causing more than two million of them to flee the country. Roughly half of these fled northwest, across the border of what was then Zaire, these days the Democratic Republic of the Congo, where they ended up around the town of Goma. Up to this point Goma had been a quiet town of some 80,000 people, nestling by Lake Kivu in the lee of a volcano. Goma now found itself overwhelmed by a desperate torrent of refugees, carrying everything from blankets to their meagre rations of yams and beans. Two hundred thousand arrived in a single day, confused, thirsty, hungry and homeless. They camped on doorsteps, in schoolyards and cemeteries, in fields so crowded that people slept standing up. Agencies from the world’s media flocked to the vicinity, reporting the chaos and the urgent need for shelter, food and water.

      A reporter for Time magazine estimated that the volume of refugees needed an extra million gallons of purified water each day to prevent deaths from simple thirst, meanwhile the rescue services were managing no more than 50,000. Desperate people foraged for fresh water, scrabbling hopelessly in a hard volcanic soil that needed heavy mechanical diggers to sink a well or a latrine. Human waste from the relief camps fouled the waters of the neighbouring Lake Kivu, creating the perfect circumstances for the age-old plague of cholera to emerge. Within 24 hours of confirmation of the disease some 800 people were dead. Then it became impossible to keep count.

      Viruses are not the only cause of plagues, which include a number of lethal bacteria, such as the beta-haemolytic streptococcus, tuberculosis and typhus, as well as some protists, which cause endemic illnesses such as malaria, schistosomiasis and toxoplasmosis. Cholera is a bacterial disease, caused by the comma-shaped Vibrio cholerae. The disease is thought to have originated in the Bengal Basin, with historical references to its lethal outbreaks in India from as early as 400 CE. Transmission of the germ is complex, involving two very different stages. In the aquatic reservoir the bug appears to reproduce in plankton, eggs, amoebae and debris, contaminating the surrounding water. From here it is spread to humans who drink the contaminated water, where it provokes intense gastroenteritis, which proves rapidly fatal from massive dehydration as a result of the fulminant ‘rice-water’ diarrhoea. This human phase offers a second reservoir for infection to the bug. If not prevented by strict hygiene measures, the extremely contagious and virulent gut infection causes massive effluent of rice-water stools that are uncontrollable in the individual sufferer, so that they contaminate their surroundings, and especially any local sources of drinking water, leading to a vicious spiral of very rapid spread and multiplication of the germ.

      During the nineteenth century, cholera spread from its natural heartland, provoking epidemics in many countries of Asia, Europe, Africa and America. The massive diarrhoeal effluent of cholera is unlike any normal food poisoning. An affected adult can lose 30 litres of fluid and electrolytes in a single day. Within the space of hours, the victims go into a lethargic shock and die from heart failure.

      The English anaesthetist, John Snow, was the first to link cholera with contaminated water, expounding his theory in an essay published in 1849. He put this theory to the test during a London-based outbreak around Broad Street, in 1854, when he predicted that the disease was disseminated by the emptying of sewers into the drinking water of the community. Snow’s thoughtful research led to the civic authorities throughout the world realising the importance of clean drinking water. Today the life of an infected person can be saved by very rapid intravenous replacement of fluid and electrolytes, but the size of the outbreak around Lake Kivu, and the relative paucity of local medical amenities, limited the clinical response. The situation was made even worse by the recognition that the cholera in the Rwandan refugee camps was now confirmed as the 01-El Tor pandemic strain of Vibrio, known to be resistant to many of the standard antibiotics. This presented immense problems for the medical staff from local health ministries and those arriving from the World Health Organization. Even though the response was one of the largest relief efforts in history – involving the Zairian armed forces, every major global relief agency and French and American army units – the spread of cholera was too rapid for their combined forces to take effect.

      Three weeks after the outbreak began, cholera had infected a million people. Even with the modern knowledge and the desperate efforts of civic and medical assistance, the disease is believed to have killed some 50,000. It is hard to believe that so resistant a plague bacterium as the Vibrio cholerae might itself be prey to another microbe. But exactly such an attack, of a mystery microbe upon the cholera vibrio, had been recorded in a historic observation by another English doctor close to the very endemic heartland of the disease, a century before the outbreak at Lake Kivu.

      In 1896 Ernest Hanbury Hankin was studying cholera in India when he observed something unusual in the contaminated waters of the Ganges and Yamuna Rivers. Hankin had already discovered that he could protect the local population from the lethal ravages of the disease by the simple expedient of boiling their drinking water before consumption. When, in a new experiment, he added unboiled water from the rivers to cultures of the cholera germs and observed what happened, he was astonished to discover that some agent in the unboiled waters proved lethal to the germs. It was the first inkling that some unknown entity in the river waters appeared to be preying upon the cholera bacteria.

      Hankin probed the riddle further. He found that if he boiled the water before adding it to the cholera germ cultures this removed the bug-killing effect. This suggested that the agent that was killing the cholera germs was likely to be of a biological nature. He needed to know if it was another germ – sometimes germs antagonised one another – or if it was something completely different, a truly mysterious agent, that was killing the germs. Hankin decided that he would set up a