The pharmaceutical arms race with microbes is unwinnable. We have to learn that successful diseases need us to surviveby Jerome Burne / July 20, 2001 / Leave a comment
imagine what life is like for a virus or bacteria infecting the human body. You have a series of problems. You must get in, evade the sentinels of the immune system, make as many copies of yourself as possible and then, most importantly, get passed on to a new host. Failure at any stage will mean a decline in the numbers of your particular gene combination in the gene pool. Success means that your numbers will grow.
It is not a difficult exercise, yet thinking about microbes in this way has the potential to transform our ideas about diseases and how best to treat them. Paul Ewald, a professor of biology at Amherst College, is one of the few researchers in the world looking at infection from an evolutionary point of view. In his book just published in the US-Plague Time-he claims that the failure of the medical profession to understand the forces involved in pathogen evolution has meant a short-sighted concentration on genetic causes of disease and on ever more powerful drugs. Evolutionary medicine, on the other hand, explains why the influenza pandemic of 1918 is unlikely to happen again and suggests it is possible to domesticate certain microbes so they become less harmful, rather than engaging in an unwinnable pharmaceutical arms race.
“Microbiologists don’t normally think about viruses and bacteria in evolutionary terms,” says Ewald, “which is why they miss something important.” Go back, for a moment, to being a microbe. Let’s suppose you’ve successfully entered your human host and you are reproducing furiously, numbers doubling by the minute. Trouble is, this has a very damaging effect on the body you are in. Your host takes to his bed and within a day or so is dead. This is a disaster for you because you’ve failed the final stage-none of your offspring have gone on to infect anyone else. Now imagine there is a rival strain of your type of infection that doesn’t reproduce so aggressively. Its host doesn’t feel so bad and so dutifully goes in to work where-let’s assume you are an airborne infection, such as flu-he sneezes over dozens of people and infects them.
This trade-off between how aggressive an infection is and how effectively it is passed on, is crucial to Ewald’s ideas about taming pathogens. The simple rule is that when transmission is easy, it pays microbes to reproduce as fast as possible and not to worry about the effect on the host. But make transmission harder and the infection becomes milder because the host has to be kept alive, and preferably active, to increase the chances of transmission.
In a series of experiments that Ewald ran in South America, he showed this process at work. Cholera is passed on by faeces getting into the drinking water supply. Dirty water makes transmission easy, so the strains of cholera bacteria that reproduce fast are the most successful and that means a high mortality rate for the hosts. But Ewald found that in countries which had cleaned up their water supply, the strains of cholera that infected people were much milder.
The balance between virulence and ease of transmission has implications for diseases closer to home too. Millions are spent every year to detect the latest variation in the flu virus. This is fuelled by the fear that a super virulent strain is going to emerge like the one that killed millions worldwide in the wake of the first world war.
What that fear ignores is that a virulent bug needs easy transmission. Filthy trenches and hospitals provided just such conditions. “There is never just one type of flu virus around, instead there are competing genetic combinations,” says Ewald. “Depending on the conditions, certain ones will be successful while others won’t.” It’s a brave claim because the consequences of being wrong in this case could be horrendous.
The evolutionary perspective also throws new light on the problem of the antibiotic resistant bug Staphylococcus aureus, which can infect wounds in hospitals. About 30 per cent of us carry a version of Staph, but only a tiny number are effected. So why does this bacteria suddenly become so virulent in hospital? “The logic of the evolutionary perspective,” says Ewald, “is that it is because Staph gets access to an effective means of transmission-unwashed hands and poor hygiene.” So the obvious and money-saving option, rather than trying to knock it out with ever more potent drugs, is just to institute more rigorous cleaning procedures. Not as dramatic as a new antibiotic, but more effective.
Ewald’s even more controversial claim is that we have been approaching the big killers like heart attacks and cancer in the wrong way. They are, he claims, largely the work of microbes. The general assumption is that infectious diseases are acute. But since the early 1990s, when it was finally accepted that ulcers, long believed to be the result of stress, were actually the work of the bacteria Helicobator pylori, pathogens have been linked to a growing number of long term illnesses. Bacteria and viruses have been implicated in arthritis, gall stones, heart attacks, some forms of leukaemia and breast cancer-at least in mice.
Ewald has been roundly attacked by microbiologists for going way beyond the evidence. But if he’s right, all the emphasis on a healthy lifestyle-exercise, large amounts of fruit and vegetables, a little red wine-may turn out to be the western equivalent of charms to ward off the plague. The good news is that the bugs’ eye view opens up a host of new approaches to dealing with diseases, the causes of which have so far remained a mystery.