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.

Fast transport and slow deaths

The factors that influence the spread and/or limitations of disease can often be quite unexpected, and in some cases, the causes remain unknown.

The delivery of tea to England by fast ship may have kept the English drinking tea, which constrained them to boil their water to make the tea, which killed the bacteria that caused cholera and other diseases. On the other hand, fast transport also caused some curious outbreaks of disease.

Airport malaria is a known phenomenon today, where people close to airports may very occasionally catch malaria when an infected mosquito emerges from an aircraft and draws blood from somebody before it dies. That sort of thing was far less likely in the days of steamships, but not impossible, even with a sailing ship like the barque Hecla, which once carried yellow fever to Wales.

Hecla reached Swansea with a cargo of copper ore from Cuba on 8 September 1865, and did not raise the quarantine flag. The ship had left one crewman, dead of yellow fever in Cuba, and she was under-crewed due to three deaths at sea that were put down to yellow fever.

Another sailor, James Saunders, died just after landing, and doctors judged this to be yellow fever, so his body was immediately buried in a tar sheet, his house was cleared and disinfected with lime wash and chloride of lime, and his clothing and bedding were destroyed.

Nobody had any idea that the disease was spread by mosquito bites, so the ship’s water supply, almost certainly complete with mosquitoes in all stages of life, was left unexamined. The ship’s owners resisted moving the ship, and while it was disinfected, though it later moved after locals intimated that it might mysteriously catch fire. This removal would have had no effect on the mosquitoes, though the fire would have curtailed the outbreak.

Before the outbreak ran its course, at least 27 people fell ill with yellow fever and 15 of them died, while there were a few other “possibles”, but how did a tropical disease reach Wales? Yellow fever and its mosquitoes had travelled from Africa to the Caribbean with African slave ships and been established there, but non-tropical Wales was safe from any permanent threat from yellow fever, back then.

The ship travelled in warm weather that let the mosquitoes survive, and it arrived in warm weather, which allowed the mosquitoes to spread, briefly into parts of Swansea. Still, in these days of global warming and climate change, who can say what the future might hold?

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In China in the late 19th century, political unrest was common, but new technology brought hope to some of China’s urban poor. They could take steam trains into rural areas to shoot, kill and skin ground rodents, and take the skins back to the city for sale. In an age before plastics, skins were always saleable, and if the local people had silly traditions, like not shooting a sick-looking animal, the city slickers saw those animals as fair and easy game.

Bubonic plague is a disease that harms rodents, fleas and humans. A flea bites an infected mammal, gets an infection that blocks its bloodsucking apparatus, so the next time it tries to feed, some of the plague bacteria “blow back” into the new food source, and so the disease spreads. When a host dies, fleas move to any other warm body—like the person skinning the old rodent host.

The hunters caught fast steam trains back to the city before they fell ill, and from there, bubonic plague infected rats in the city, either from the hunters or from fleas that were still in the fur of the skins. Over time, some of the rats found their way onto fast steam ships that went around the world from Chinese ports.

In earlier times, plague usually killed the rats before sailing ships reached port, but steamships bustled from port to port, and sooner or later, some of the rats made it to the other end, found their way ashore to die, and shared their fleas and their ills. Indian ports were hit, along with those in Sydney, San Francisco, Madagascar, Paraguay, South Africa and more. In every port, people died because of fast ships.

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There is fairly wide agreement that the spread of HIV was brought about by long-haul truck drivers in Africa making use of prostitutes along the way, followed by an entry into the more general population of the western world, thanks to jet aircraft. The world got lucky with SARS, as my next two posts will explain.

Strange armour

Curiosities from the scrap folder

A Cork Ship.—The Mobile papers report the arrival of a great curiosity at that city, a vessel made entirely of cork, which is lying at one of the wharves. That she will never sink may be true enough, but the other claim of the Mobilians, that “she will last forever,” requires some proof.
— Scientific American, April 28, 1866, p. 276.

Charles Atherton was the Chief Engineer at Her Majesty’s Royal Dockyard, Woolwich. When he wrote to The Times in January 1859 about his idea for filling vessels with of light material, up to the waterline, people paid attention. Essentially, he wanted to ensure that no matter how badly holed a ship was, it would never settle lower in the water, because no shot, no reef, no ram could harm the bottom layer. Gunboats, floating-batteries and mortars would all become unsinkable, so long as the guns and crew survived. Suitable solids might be:

…cork shavings, light wood sawdust, rush stems, cotton waste, flocks, hemp, and other lightweight material, which, by the aid of a solution of gutta percha or other chemical process, would form a solidifying mass, so tough that it could not be knocked to pieces by shot, and so light that it would only be one half the specific gravity of water, and therefore, unsinkable, however perforated by shot… 

— The Times Wednesday, Jan 12, 1859; pg. 6; Issue 23201; col E.

While he was concerned with warships withstanding fire, if Atherton’s solution had been applied to the “unsinkable” Titanic, it would have stayed afloat. The usual maritime practice of putting heavy items as low as possible, in order to move the centre of gravity down is an effective way of enhancing stability, but it takes a toll by increasing a vessel’s sinkability.

At the end of the year, Scientific American mentioned the scheme, but the writer said that cork would not suit, because heated shot could set fire to it, but that a suitable material ought to be able to be found. Half a century on, most lifeboats were fitted with sealed cork-filled compartments and self-draining seacocks to keep them afloat under the worst of conditions, but armour and armour-plating became the preferred solutions.

Mind you, if you knew where to look, the idea had been around for quite a while. The New York Times reported on an old patent in 1862, giving the date of issue as March 19, 1814. (‘The First Iron-Clad’, New York Times, May 30, 1862.)

The following day’s issue of Scientific American stated that a plan for a ball-proof vessel had been patented, “forty-eight years ago”. In each case, the patentee is said to be one Thomas Gregg, and the thrust of the report in each case was the same, that the idea behind the Merrimac (a Confederate ironclad warship) was by no means new.

It has to be said that this was during the US Civil War, and there is no evidence in the on-line records of the US Patent Office of Mr Gregg or his design. Perhaps it was a piece of wartime propaganda? The design and the illustration from Scientific American appeared again in 1889 in the Pittsburgh Dispatch, in an article sponsored by Gregg’s family.

It was in the early years of ironclad-mania that the attempt was made to dress warships up in sheepish clothing. In the 1860s, Australian wool growers were shearing huge flocks, and there must have been some fear of a glut. How their hearts must have sung when they heard that the Royal Navy was testing compressed wool as a way of blocking shot that hit their ships.

The plan was apparently to give ships a fleecy coat of pressed wool, 10 or 12 feet thick. Sadly, the graziers’ hopes were dashed when after tests, The Times reported in March 1864 that “the experiment of Wednesday proved the wool rather more permeable to shot than almost any other novelty that has yet been fired at.”

Every ship that sails the oceans represents a compromise. Sailing vessels had to trade off a reduction in strength from thinner hulls in order to float higher and sail faster—or to carry more cargo. A broad-beamed vessel would carry more cargo, but it would wallow along, losing time. That brings me to shipwrecks, and I shall go there next.

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