Officials investigating an outbreak of avian flu in Suffolk in February 2007. Turkeys were culled to prevent the spread of the virus. © REUTERS/Luke MacGregor

Five diseases that are worse than Ebola

It's chikungunya and flu we ought to dread
September 17, 2014

Are you at risk from Ebola? Not in the United Kingdom, unless you eat monkey meat smuggled from Africa. Nevertheless, the name fills us with dread. With mortality rates ranging from 50 per cent to 95 per cent, no specific treatment and no preventive measures better than wearing Marigolds and a pair of spectacles, this is not unreasonable. Smallpox engendered the same emotions of fear and panic, even though at worst it only killed 25 per cent and there was a vaccine that worked, was cheap to make and easy to deliver.

I comment on microbiological matters. The massive recent publicity about Ebola has been good for my business. It has also stimulated us to ask what other horrible things are out there. Might there even be things lurking closer to home? And could surprises be just around the corner?

The last question is easy to answer. Yes, there will be surprises. But by definition it isn’t possible to say anything more. All that we can do is be ready for them. Bacteria and viruses have no brains, but sometimes they seem to be more cunning than the microbiologists and epidemiologists whose job it is to understand their weaknesses in order to fight them. And without doubt, microbes have no difficulty in outwitting politicians.

Consider E.coli O104:H4. This is by far the nastiest E.coli for humans. It has emerged recently, a millennium bug that has only been found in the 21st century and never before. It is a hybrid. It has the genes from E.coli O157 that code for the toxins that have made this particular E.coli the scourge of vendors of rare burgers in the United States, and petting farm owners and bad butchers in the UK; it has genes from enteroaggregative E.coli, a common cause of diarrhoea in children in developing countries.

A 15,000kg batch of fenugreek seeds contaminated with O104 left Egypt by sea in November 2009. The sealed container was offloaded at Antwerp, went on to Rotterdam by barge and then by road to Germany. In February 2010, 75kg arrived at an organic farm in Lower Saxony. The seeds sprouted in late spring 2011. Soon afterwards, in early May, people in Hamburg started to fall ill with violent gastroenteritis. Diarrhoea was often bloody. Many developed the haemolytic uraemic syndrome, in which the kidneys fail, blood cells are damaged, and in severe cases the brain is damaged and the heart fails. The outbreak continued for a month. By its end 4,075 had fallen ill, 908 had developed the haemolytic uraemic syndrome, and 53 had died. The German epidemiologists struggled. Women were affected more commonly than men, and when asked, yes, they had eaten salads. So salads it was. E.coli bacteria capable of causing gastroenteritis were found on two Spanish cucumbers. The Hamburg health minister went public. The Spanish cucumber industry went into meltdown.

But cucumbers and the E.coli on them had nothing to do with the outbreak. A detailed restaurant study compared cases of those affected and non-ill control cases by looking at receipts, menus, dish ingredients and photographs taken by groups in restaurants that happened to show food on plates. The victims had eaten fenugreek sprouts (often unknowingly, because they were only a garnish); the controls had not. But the outbreak was over before the official investigating it was able to say, “It’s the sprouts!”

Sometimes our preparedness is aided by accident. When Chernobyl blew up on 25th April 1986, tracking the spread of radioactivity on the wind was an uncertain science. In response, the Met Office developed a mathematical system for predicting the long distance travel, dispersion, and persistence of radioactivity. It was very useful after Fukushima in March 2011, when a nuclear power plant in Japan was hit by a tsunami.

In August 2007, a Numerical Atmospheric-dispersion Modelling Environment, or “NAME” as it is now called, was run to assess the risk that Belgian midges infected with the Bluetongue virus might be blown over the sea to England. Bluetongue is a virus that affects cloven-hoofed animals. It is spread by midge bites. There are many different types. They have numbers—2, 4 and some others occur in southern Europe. For climatic reasons the midge that spreads them only lives in the south, but has been slowly moving north, probably because of global warming. But in 2006, type 8 surprised everyone by taking off in northern Europe. It could do this because it is spread by northern kinds of midge. In August 2007 there were cases in Ostend. NAME was run. It predicted that Belgian midges would be blown across the North Sea to Suffolk. Cases were detected there in late September. NAME helped by pointing to the areas that should be targeted for animal vaccination. Control measures worked. The last case in the UK occurred in 2008.

Bluetongue only infects animals. So does the Schmallenberg virus. This is fortunate for us, because it damages the brains and joints of foetuses. Lambs are its main target. It was first identified in November 2011 in samples from animals at Schmallenberg, a spa town in North Rhine Westphalia. Since then it has spread across Europe. It is also spread by midge bites. The midges have blown across from the continent to infect animals in England, and the virus has spread north to Scotland.

So far in Britain we have been lucky with insect-borne human diseases. An outbreak of yellow fever in Swansea in 1865 was spread by mosquitoes that flew into town from a Cuban ship, and an outbreak of bubonic plague in Glasgow in 1900-01 by fleas that had bitten infected ship rats. Both outbreaks were small, local and short-lived.

Will our good fortune hold? It is not possible to say. If a virus evolved that was nastier for humans and transmissible by our midges or mosquitoes, we could be in big trouble. The same might happen if the biting habits of mosquitoes changed.

The West Nile virus surprise is the example. Discovered in 1937, for many years it caused mild illnesses in Africa, Israel and the south of France. In the mid-1990s it became significantly more virulent, causing encephalitis and meningitis. In 1999 it came to New York, causing 62 cases and 7 deaths.

The arrival of West Nile took all the US experts by surprise. It first declared itself in June by killing crows in Queens and the Bronx. Two months went by before the human infections started. Linking the two took time. The wrong virus (St Louis Encephalitis, a relatively common one in the US) was blamed. The right identification was not made until the end of September. Helped by bird migration, West Nile swept rapidly across the continent; in 2002 there were 4,156 cases and 284 deaths. It now occurs in every state.

The virus is spread by the bites of Culex pipiens mosquitoes. The US type bites birds (which are a reservoir for the virus) and humans. The UK has two types. One breeds in human artefacts like water butts, paddling pools and garden ponds. It bites only birds. The other lives in warm subterranean places. It is common in the London Underground. It is a vicious biter of humans. Mosquito geneticists think that the US Culex pipiens is a hybrid of these two types. Could this hybridisation happen here? Yes, it could. But such an event wouldn’t be necessary for another mosquito-borne virus to establish itself in the UK.

Chikungunya virus, although not fatal, causes severe joint pain, headaches and rashes. It occurs in Africa and Asia and has recently spread to the West Indies. About one case a week is reported in the UK in returning travellers. A recent mutation in the virus means that it can be spread by the Asian tiger mosquito, Aedes albopictus, which in the last three decades has spread worldwide. It reached Italy in 1999, is now established there, and was responsible for spreading chikungunya in Ravenna in 2007. It was brought there by someone infected in India. Mosquito bites then spread it, causing 205 cases. Aedes albopictus hasn’t come to Britain, yet. But it is showing signs of adaptation to colder climates, ours is scheduled to get warmer, and it breeds in water butts and garden ponds.

HIV (human immunodeficiency virus) is also comparatively new. It had probably moved from monkeys to humans before the 1950s, although the first cases were recognised in 1981 in the US. About 100,000 people in the UK are infected, mostly men who have sex with men and heterosexuals from sub-Saharan Africa. More than 20 per cent of them do not know it, and are several times more likely to transmit the virus to their partners than those who have a diagnosis. Half of the newly diagnosed cases in the UK seek medical help when they are in the late stages of disease. In England the local authorities with the highest prevalence of diagnosed infections are London, Brighton and Hove, Salford, Manchester, Blackpool and Luton, and in Scotland, Edinburgh. Treatment with antiretroviral drugs reduces the risk of transmission by more than 90 per cent.

Other sexually transmitted diseases are also important. In England in 2013, chlamydia caused 208,755 infections, 73,418 people had ano-genital warts, 32,279 had ano-genital herpes, and 29,291 had gonorrhoea. The unpleasant surprise is that syphilis was diagnosed in 2,970 men and 279 women. The surprise is not the gender gap. It is nearly as big for gonorrhoea, because with both bacteria the immediate and short- term effects of infection in women are often clinically silent. The surprise is that syphilis is still so common, because it is as sensitive to penicillin as it was in the 1940s. “Serosorting,” where men seek other men with the same HIV status as themselves for unprotected sex, and oral sex, considered to be relatively safe regarding HIV transmission but an effective way of transmitting syphilis, have helped to keep it going.

One can avoid catching sexually transmitted diseases by being celibate, using a condom and so on. STDs are far less common in older people, although in the past medical students were taught to remember that every bishop was once a divinity student because the long-term complications of syphilis often didn’t show themselves until decades after the initial infection.

We can protect ourselves from food poisoning by eating well- cooked burgers and buying pasteurised milk. Our drinking water does not infect us with typhoid or cholera because we no longer draw it from wells contaminated with our faeces and then consume it in its natural state. But the challenge from viruses spread on the wind and in other ways is still very big.

Norovirus infects about three million UK residents every year. It does not kill very often. That is just as well, because there is no specific treatment and no vaccine. The virus particle is tough. It can survive for many days in the environment. It is resistant to most disinfectants. Only a very small number of virus particles are needed to start an infection. And the hallmark of an infection is projectile vomiting. This often happens without warning. The virus is in the vomit. It is also in the diarrhoea. The great majority of cases recover quickly. Norovirus can be looked on as the common cold of the bowels. It is important not because of its individual impact, but because it is so common and because of its impact on groups of individuals kept close together and on the function of the places where they are staying, like patients in hospitals, prisoners in jails and passengers on cruise liners.

Influenza is different. Unlike norovirus, environmental contamination is not an important route of spread. The virus is not very tough. The main way that infection spreads is by breathing in virus particles coughed out by sufferers. And it kills quite often; the pregnant and the elderly are particularly at risk. The big worry is a repeat of 1918-19, when a new virus spread world-wide, causing a pandemic that killed about 40m people. Pandemics happen when new influenza viruses emerge with a combination of new genes coding for the virus structures attacked by our immune system so any pre-existing immunity no longer protects, and old genes allow them to grow in our cells. They are hybrids. The new genes come from bird or pig influenza viruses and the old ones from human viruses. It is very hard for humans to be infected with bird influenza H5N1, but when they are, the mortality rate is as high as with Ebola. Virologists became concerned that if H5N1 hybridised with a human virus, a pandemic strain as nasty—or even nastier—than the 1918-19 virus might emerge. Plans were made to cope with this eventuality. In the UK a big exercise, known as “Winter Willow,” was held in early 2007. It informed a plan that was published by the Department of Health and the Cabinet Office in November 2007. In April 2009 a new virus did emerge, swine flu. But the virus had not read the plan, which considered H5N1 to be a plausible component (it was not) and that it was most likely to emerge from southeast Asia, the Middle East or Africa (it came out of Mexico). And against expectations it caused a mild illness, and mainly affected young people. At the peak of the first wave of cases in July, the mathematical modellers were predicting up to 65,000 deaths. But after the end of the second wave, in March 2010, 457 had died. Maybe the next pandemic will be caused by a much more virulent virus. Nobody knows. But the response to swine flu showed that the international surveillance system set up in the 1940s still works well, that we can make a vaccine in real time, and that we can successfully treat those close to death. But flu should still worry us. Your life might be saved, but only by venovenous ECMO, a procedure in which blood is taken via a tube in the groin to an oxygenator and returned though another tube in the neck while at the same time you are being mechanically ventilated.

Flu comes and goes in an unpredictable way. It gets commoner every winter. But the biggest risk from infection that we face is from our own bugs. The commonest cause of infection after surgery is Staphylococcus aureus; 30 per cent of us carry it up our noses. And we have to die of something. In 2012 flu/pneumonia was registered as the sixth commonest cause of male deaths in England and Wales and the fourth commonest in women. The only cancer that caused death more often was lung cancer in men. The commonest cause of pneumonia is the pneumococcus, which also lives in our noses and throats. The good news is that there is an effective single-shot vaccine against it. The bad news is that then we will have to die of something else.

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