The SARS case

It will possibly be my last book, but Not Your Usual Science is going to be HUGE, close to 1.5 million words, equal to a dozen 'airport books', the thick tomes you buy to read on a long flight. It collects together many of the articles and essays that I have generated over the past 35 years, covering science, how science works and how what we now call science was put together. It even includes some of the blog entries that have appeared here. In due course, it will be released as an e-book.

Here's a small taste of it...

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This news story was mostly written in the first few weeks of the SARS outbreak. I have left it as I wrote it, at a time when we had no idea what the future would be. It was a scary time.

SARS is the abbreviation for Severe Acute Respiratory Syndrome. It is still a comparatively new disease in human beings, first recognised in late February, 2003, in Hanoi, Vietnam. It is caused by a coronavirus, either one that arose from several other coronaviruses recombining, or more probably, an unknown coronavirus that made the transfer from an animal host to humans.

The first recorded case was in November 2002, when a businessman from the city of Foshan in the southern Chinese province of Guangdong (formerly Canton) may have been the first victim. Guangdong Province, an agricultural area with a population of 75 million, has thousands of farms with large and small animals, a subtropical climate, and rainfall of about 2 metres (80 inches) per year.

(The problem was later shown not to involve farm animals. It took seven years to show, in 2013, that initial suspicions were correct: the SARS virus transferred to humans from horseshoe bats.)

A physician from Guangdong Province became ill in February 2003 while staying on the ninth floor of a hotel in Hong Kong. Twelve guests later became infected, including at least seven who stayed in rooms on the ninth floor. These hotel guests subsequently became the index patients who transported the disease to Vietnam, Singapore, Canada, Ireland, and the United States.

The severity of the disease, combined with its rapid spread along international air-travel routes, prompted WHO to set up a network of scientists from 11 laboratories around the world to try to identify the causal agent and develop a diagnostic test.

In a remarkably short period of time, the coronavirus was identified as the likely cause of SARS, and within days, a number of the strains of the virus had been sequenced, a major triumph for international collaboration in a world increasingly riven by violence and war.

Results of work in the different labs were shared in real time via a secure web site, on which microscopy pictures, protocols for testing, and polymerase chain reaction (PCR) primer sequences were also posted. Findings were discussed in daily teleconferences. Progress was aided through sharing between laboratories of samples and test materials.

The network identified a coronavirus, consistently detected in samples of SARS patients from several countries, and conclusively named it as the causative agent of SARS. They added that the strain was unlike any other known member of the genus coronavirus.

The main observation from the sequencing was that the virus was not mutating rapidly. That was taken to indicate that the human immune system was having little effect on the virus, as any immune challenge would favour more rapid selection of mutant forms.

Coronaviruses are found everywhere and cause illness in many animals, including pigs, cattle, dogs, cats, and chickens. They have been associated with upper respiratory infections and sometimes pneumonia in humans.

Genetic changes occur frequently, and the closeness of humans to animals in rural southern China may have caused a recombinant animal virus to become an accidental tourist, crossing species to humans and leading to an epidemic among highly mobile and susceptible populations globally. Different viruses in this group cause devastating epizootics (animal epidemics) of respiratory or enteric (gut) disease in livestock and poultry.

Comparison of isolates of the coronavirus from infected patients and from the natural host could reveal how the virus jumped to humans. If they could find how it jumped to humans, researchers would have tried to discover if the coronavirus had an original host. If there was no animal reservoir, there would be a better chance of eliminating the virus from humans, but in either case, it was important to identify the source.

In May 2003, it appeared that the probable reservoir was civet cats, bred and sold for eating, a delicacy in southern China. This might have explained the lower mortality rates in China, if many of the potential victims have already encountered a similar virus.

By late May, reports were coming in that some of those engaged in breeding civet cats appeared to have antibodies to a SARS-like coronavirus, but there were odd inconsistencies in the official data released by Chinese authorities.

It is possible that the Chinese authorities may have been lying, engaging in a massive cover-up. As the disease outbreak fizzled out, Singapore and Canada had the disease under control, showing that it could be blocked and stopped, but cases were multiplying in Taiwan, which was showing a mortality pattern more like that seen in Canada (16.4%), Hong Kong (15%) and Singapore (14.1%).

By May 22, Taiwan’s mortality rate was 12.4%, and this was expected to increase, because there was a ‘lag effect’ as the outbreak was controlled. In the final lag phase, old cases are still dying while no new cases are added. One of the puzzles was the low mortality reported from China other than Taiwan, where the figure, by May 22, 2003, had only reached 5.7%, up from 4.8% in mid-May.

We will never know, now, but significantly for the cover-up advocates, in China alone, there was no final upward jump in mortality as the disease fizzled out. The easiest explanation is that somebody was fabricating the statistics.

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So how does SARS spread? Large-droplet transmission seems to be important in the spread of SARS, suggesting a requirement for intimate contact with a patient. Against that, the unusually rapid transmission suggests that airborne transmission through droplet nuclei, less than 10 micrometres in diameter can occur.

Such droplet nuclei, which are key in the transmission of influenza, measles, and tuberculosis, allow the organisms to reach the alveoli of the lungs of contacts directly. Alternatively, viral contamination of the water supply or contacted surfaces might be important in some places.

The evidence is that close contact is generally required for infection to take place. As one expert put it, “You only get it by coming face to face with someone with the virus. You won’t pick it up in the street.”

The infection rates per capita were far lower, for example, than for normal influenza, and there was an age bias in the death figures. The fatality rate was 13.2% for patients under the age of 60, but as high as 43.3% for those over the age of 60, according to an article in The Lancet at the time.

So next time there's an outbreak of anything in China, be worried.