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In China, Killing the Viral Messenger

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Wendy Orent writes frequently about emerging infections and is the author of the forthcoming book "Plague: The Mysterious Past and Terrifying Future of the World's Most Dangerous Disease."

Civet cats -- more like ferrets than our house cats, prized by some Chinese for their “wild” taste (and restorative effect on flagging male libidos) -- were electrocuted, strangled, drowned and boiled in China by the thousands last week. This was because some were infected with a virus genetically similar to human severe acute respiratory syndrome, or SARS, a new disease that swept across the world last year and may be reemerging. One confirmed and three probable cases of human SARS have appeared again in Guangdong province in China, where SARS first broke out.

The slaughter of the civets, followed by a huge campaign to rid the province’s capital of rats, is an attempt to quell the emergence at its source. This sounds, initially, like a good idea: destroying infected animals to stem the disease before SARS can spread again.

Killing off the reservoir is an old strategy, though it doesn’t always work. The plague, essentially a rodent disease caused by the germ Yersinia pestis, is an old human nemesis. In the territory of the former Soviet Union, colonies of burrowing rodents, called marmots, harbor the most lethal and explosive plague strains in the world. Soviet plague-control institutes tried for decades to eliminate the disease by killing marmots with the poison chloropicrin. But they found that, within a few years, the marmots -- and the plague -- came back. On the ground that poisoning caused “unjustifiable harm to nature,” as plague expert Igor V. Domaradskij put it, the baiting ended.

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In 1997, an outbreak of avian flu triggered the slaughter of more than a million chickens in Hong Kong. The strain infected 18 people and killed six, including a 3-year-old boy who had handled a sick chicken at a petting farm. Because those avian flu strains did not spread from person to person, slaughtering the chickens ended the outbreak. Several subsequent epidemic outbreaks of avian flu in Hong Kong and in Vietnam were similarly contained.

According to Nancy Cox, a flu expert at the Centers for Disease Control and Prevention, there are two reasons for killing all those chickens: protecting the poultry industry and preventing human disease. Bird flu spreads quickly; culling sick flocks effectively prevents the destruction of many more chickens, much as huge herds of cattle are destroyed to stop the spread of foot-and-mouth disease. But how much of a risk to people does chicken flu represent?

“The more times such transmission occurs between birds and people,” says Cox, “the greater the probability of a more dangerous strain emerging. If you mix avian and human flu genes in an infected person, you could get a transmissible disease.”

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Possibly. The great flu pandemic of 1918, variously reported to have killed between 20 million and 100 million people, may have been caused by such a mix. But was 1918 just an accident, an event that, having happened once, could easily happen again through random changes in the bird-flu genome or by mixing bird flu with human -- or perhaps pig -- influenza genes?

According to infectious-disease expert Paul W. Ewald of the University of Louisville, another 1918 flu isn’t very likely. More is involved in a lethal pandemic than the accidental mixing of genes or the introduction of a novel germ into the human species. A dangerous pandemic must be both virulent and transmissible, a combination that doesn’t evolve very often. If a disease kills too quickly, it’s unlikely to spread effectively; sick people die before they spread the disease. The lethal 1918 flu could maintain itself because of the close quarters under which it evolved: Soldiers packed together in barracks, in trenches, in trains, in trucks, dying men mixed with healthy ones, all of them shuttled together from place to place, country to country. It wasn’t the 1918 flu for nothing; the conditions that allowed that virulent, transmissible strain to evolve started to die out as the war ended. The infection burned across the world and vanished.

Avian flu, which during the last month has killed four people in Vietnam, isn’t a good candidate for such a lethal pandemic. It still shows no signs of spreading among people, and probably won’t if avian flu patients can be kept in isolation and their earlier contacts carefully watched. As for SARS, it never became much of a human pathogen, either; last year’s strains only spread late in the disease’s course, when people were already ill and not very mobile. The most transmissible human respiratory infections, such as measles, spread in their early stages, while the patient is walking around, coughing and sneezing. A disease that transmits after the patient is hospitalized or immobile from illness is much less likely to become a serious pandemic threat -- except in conditions like those in 1918.

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Furthermore, according to an analysis published in the British medical journal Lancet by epidemiologist Stephen Ng, the single most explosive instance of SARS transmission, in which more than 200 people were infected from a single common source, was probably produced by roof rats tracking infectious material shed by a sick man throughout the upper floors of his apartment building, and not by direct person-to-person contact.

Late transmission proved, ultimately, to be SARS’ Achilles’ heel. Arresting the spread of the disease through isolation and quarantine drove last year’s strains into extinction.

The new cases of SARS are something of a mystery. Only one of the suspected cases has any apparent connection with civets. This case is of a waitress who works in a restaurant that keeps live, wild animals stacked in cages until patrons select them for dinner. But the only confirmed SARS case, that of a television producer, insists he has had no contact with civets at all.

If there is no clear link between patients and civets, why destroy 10,000 animals? Virologist Stephen Morse of Columbia University puts it this way: “In general, to kill them out is not a sustainable strategy. At this point, it’s an indication of our desperation. It’s a desire to show that things are being done.”

And what’s being done may cause us more harm than good. Morse points out that destroying the civets also destroys evidence vital to our understanding of SARS’ ecology, about which we know almost nothing. SARS, unlike avian flu, may have been a low-level, undetected presence for years in China, where the intermingling of animals and humans is extensive, and where many people have surely died -- as they do in the West -- of uninvestigated, unreported pneumonia. It may be common for these strange coronaviruses, the cause of SARS, to come from some animal reservoir, infect one or two people and then die out. Perhaps we only noticed SARS when it evolved, however ineffectively, the ability to spread among human populations; breaking that chain of transmission stopped the evolution of the strains into a more effective human disease.

Killing birds in Hong Kong or Vietnam may be a useful strategy, killing civets a pointless waste. But in either case, it’s less the introduction of disease into the human species we have to fear; it’s the evolution of those diseases into efficient human pathogens. Whether we are speaking of flu or SARS or some other, yet-unknown, threat, stopping the person-to-person transmission cycle should be our top priority. It’s not really the threat outside we have to fear; it’s the diseases -- like smallpox, like AIDS -- allowed to take up residence among us that become our real enemies.

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