One of the most important secrets for a long and happy life is knowing who your friends are. If you can’t tell who you can rely on, and who will take the first opportunity to stab you in the back, you won’t last long.

The importance, and the difficulty, of distinguishing friend from foe is never greater than when dealing with bacteria. Many are beneficial, most are harmless, and others are virulent pathogens. Family resemblances are little help in distinguishing friend from foe. E coli  0157, which is just one strain of the Escherichia coli species has caused a fatal food poisoning outbreak in Scotland in recent weeks, and is a fairly common cause of serious illness in man. But other strains of E coli  live harmoniously in our digestive tracts, and may even help us.

“As a human, we tend to think that all these bacteria are out to assault us” says Jonathan Saunders, professor of microbiology at Liverpool University, “but most of them are extremely beneficial. They just see us as a source of food, and many of the bacteria in our intestines do us a lot of good, helping us to digest food and even making vitamins for us” he says.

E coli 0157 causes severe disease because it carries a deadly weapon, a toxin that splits mammalian cells open. According to Tom Baldwin, of the Institute for Infections and Immunity at the University of Nottingham the toxin has exactly the same effect in the body as ricin, the poison made famous by umbrella-wielding Bulgarian assassins. But according to Saunders, for the bacteria the toxin is not really a weapon. It’s more like a kitchen knife than a dagger, “it’s just a mechanism to release food” he says.

It’s more complicated than that. Not all E coli 0157 carry weapons “the toxin gene is carried by a virus that infects the bacterium” says Saunders.”So it could potentally infect other strains” . Even then, possession of the weapon will not be enough for a safe conviction. “Some strains of bacteria make the toxin but do not cause disease.” he says. “Virulence is caused by a combination of factors.”

Paul Williams, director of the Institute for Infections and Immunity at Nottingham University, is emphatic about this. “It’s crucially important to remember that virulence is multifactorial” he says. “It depends on a whole series of mechanisms.” The pathogen has to colonise its host, it may have to fight off resident microorganisms, it needs mechanisms for avoiding host defences, it has to invade cells, and it has to spread to other hosts. Blocking the mechanisms it uses for any of these activities will block virulence, Williams says

For many pathogens that, like E coli {italics}, colonise the intestinal tract, foecal oral contamination is the commonest mode of spread, so causing diarrhoea is an obvious tactic for the bacteria to find new hosts. But it also means that routine precautions – purification of drinking water, care in cooking meat, storing cooked meat separately from raw meat, and cleanliness – can effectively block spread.

The same cannot be said of the other virulent bacterium that has hit the UK headlines in recent weeks, Neisseria meningitidis [correct] {italics}, also known as meningococcus, causes meningitis. Its invasion route begins in the upper respiratory tract, where it is very common, according to Saunders “about 10 per cent of adults are carrying some form of meningococcus” he says.

In order to cause disease, the meningococcus has to colonise the blood and eventually the membranes that surround the brain. Whether or not it can do so depends on our immune system, according to John Heckels of the Department of Microbiology at Southampton General Hospital. We acquire immunity to dangerous strains of meningococcus by encountering their less dangerous cousins. Babies are particularly at risk, Heckels says. They inherit antibodies from their mothers, but these tend to decline before the baby can make its own antibodies, resulting in a peak in vulnerability to meningitis at about six months of age.

Meningococcus is not resistant to antibiotics, Baldwin says, but once it has invaded, killing the bacteria releases the toxins that they contain which can cause further damage. Vaccination, which primes the immune system to recognise the bacterium as an enemy and attack it before it invades the blood is a better approach.

A successful vaccine has to recognise the bacterium, even though it may conceal its distinctive foreign proteins under a bland cloak. Group B meningococci, which are responsible for 60 per cent of meningitis cases in the UK, have a capsule of sialic acid- a carbohydrate that is a normal constituent of the body and so elicits no immune response. Heckels and Baldwin are both developing vaccines that will enable the immune system to see through the cloak and kill the bacterium before it has a chance to unsheath its dagger.