Not really a plague, but not just hype: The cases of necrotising fasciitis provide a shocking reminder of the power of disease. Steve Connor and Nick Cohen report

IT WAS a big week for something so small it can slip through the eye of a needle as easily as a ping-pong ball through goalposts. The 'flesh-eating' bug Streptococcus pyogenes has officially struck 15 people this year, but unofficially it has affected a lot more. The media exposure the bacterium has received - many doctors say over-exposure - has brought a torrent of reports of necrotising fasciitis, the gangrenous condition caused by the bug which can dissolve flesh and kill within 48 hours.

A sensation somewhere between morbid fascination and genuine panic seized the country as case after case of infection from a bacterium previously known only to the students of medical textbooks dominated the news. The Daily Star ran the headline 'Killer Bug Ate My Face' and the rest of the media coverage was only slightly less dramatic.

Many took the scare personally. Patrick Fergusson, a retired London doctor, received a call on Wednesday from an old patient who was in France. 'He was due to come back for surgery but had heard of a new virus sweeping Britain and wondered whether the killer germ made it dangerous,' said the doctor. 'I reassured him it was entirely safe. But I gather he will still elect to have the operation in France.'

Scientists have generally reacted to the fuss with contempt. Streptococcus pyogenes is not Aids; not a new plague to terrify the modern world. The first record of it may even date back to Hippocrates, the father of medicine. Twenty-three centuries ago in ancient Greece he described a man, Griton of Thasus, who 'while still on foot and going about, was seized with a violent pain in the great toe'. Delirious fevers, swellings and flesh that was 'blackened by mortification' killed the unfortunate Griton two days later.

Ever since, doctors have seen the effects of the bacterium. In late 20th-century Britain there has been a steady succession of cases, tragic but mercifully small in number. Nothing which was reported last week, not even the cluster of cases in Gloucestershire, nor the alleged second cluster in Chichester, has changed that fact.

All the evidence showed, the scientific authorities agreed, that there was no cause for concern. As Diana Walford, director of the Public Health Laboratory Service, declared: 'The public should be reassured that there is no 'killer bug' sweeping the country.'

Norman Begg, deputy director of the Communicable Diseases Surveillance Centre at Colindale, north London, said all diseases show some annual variation from one year to the next and an extra five cases this year hardly constituted an epidemic. 'Given this intense publicity I think if we weren't seeing an increase (in reported cases) there would be something wrong,' he said.

Dr Begg and, indeed, virtually every scientist who has studied the bacterium criticised the media. 'The press coverage certainly isn't in the public interest,' he said. 'The nature of the reporting has frightened and confused.'

Another Colindale scientist, Robert George, described the reporting as sensationalist and distressing to victims' families. 'It's all a great hype,' added Professor Peter Borriello, a bacteriologist at the Queen's Medical Centre at Nottingham Univeristy. 'There is an element of irresponsibility and culpability somewhere. The story broke in Gloucestershire because whoever gave the story out was either misinformed or had what they said distorted.'

ALMOST none of the theories advanced in the press in the past two weeks to explain what was happening stood up to scrutiny, the scientists insisted. There is no evidence, for example, that the usually innocuous microbe, which in most cases does little more than cause sore throats, has mutated into a new more vicious form. All that has happened is that some types (or strains) of the bacterium have made fatal attacks as they have always done. Potentially lethal types of the bacterium may possibly be becoming more common, scientists concede, but the case for this is far from proven.

There is no evidence either that there is an epidemic caused by one patient passing the bacterium to another. The victims did not know each other. Most of the deaths this year, even in Gloucestershire, have been caused by different types of the bacterium. The deaths are, in other words, unrelated.

And even the term 'super-bug', widely batted about during the week, is inappropriate. This is a word sometimes used by scientists, but it describes bacteria that are resistant to antibiotics. This microbe is not.

And yet the scare is not wholly confected. In its heavy-handed way the press has touched a raw nerve both in the scientific establishment and the public consciousness. There may not be any clear answers in all this, but there is are some pressing questions.

For whatever reason, the number of reported cases has increased. The Government's Public Health Laboratory Service in Colindale, which collects reports of infectious diseases from around the country, saidit can confirm 15 cases of necrotising fasciitis resulting from the streptococcus bacteria since 1 January.

The service admitted that there are at least as many more 'probable cases'. Normally, only 10 cases are confirmed each year. The 15 confirmed cases in the first half of this year - ignoring the probable cases still to be confirmed - means the reporting rate for necrotising fasciitis has doubled since January.

Virginia Bottomley, the Health Secretary, Professor Borriello, Dr Begg and the managers of Colindale may, rightly, assure the public that this is nothing to panic about. But other experts, while agreeing that there is little evidence of a significant increase in cases, are critical of the methods used to track the disease in the country.

David Seal, an expert on necrotising fasciitis at Glasgow University, said the figure of about 10 cases a year given by the Department of Health is a 'gross underestimate'. A large district general hospital alone should see about five cases each year. 'Our experience is that the harder you look for this disease, the more cases you find.'

Mr Seal's point is not that the microbe is becoming more virulent - historically it has always been dangerous to some people at some times - but that the shock which greeted the coverage of necrotic cases this week was not entirely the result of public ignorance. The Department of Health itself did not know, but should have known, what the real frequency of infections was.

Compounding the professional worries last week was the latest act of official economy. With characteristically unhappy timing, the Department chose last Monday to announce sweeping cuts to the Public Health Laboratory Service, which monitors the spread not only of this bacterium but of Aids, salmonella and legionnaires' disease. Forty-five of the 371 scientific jobs will be lost and pounds 10m - about one-fifth of the budget - will be cut by 1997.

The scientists who will lose their jobs are responsible for checking specimens from all over the country to provide hospitals and doctors with back-up and to support research into new techniques for dealing with disease. They helped Britain develop a strategy for combatting Aids by approving HIV testing kits and being among the first scientists in the West to urge the promotion of safe sex.

Graham White, the Manufacturing Science and Finance representative for the Colindale staff, says the cuts come at a time when the public wants more resources put into such work, and not less. He believes that last week's alarm was a reflection of this. 'What the fuss shows is a general unease. TB is making a comeback. We have Aids, legionella and organisms changing in response to anti-biotics. Meanwhile, our central mechanism for tracking and dealing with communicable diseases is being cut back. This may be dangerous in the long term. The public is right to be a little worried.'

IF SUCH concerns underlay what happened last week, they were deep beneath the surface. What impressed the public most forcefully were the consequences of a particularly horrible disease. Although Hippocrates may have seen it, the foundation of modern knowledge of necrotising fasciitis was laid by an American surgeon, Frank Meleney, who came across many cases while working in a missionary hospital in Peking in 1924. His writings on haemolytic streptococcal gangrene are still studied by medical students today.

'Sometimes the (initial) injury is so slight that it appears to be a spontaneous infection,' he said. 'But in general there is a history of superficial injury of the skin, a scratch, a cut, or a hypodermic injection.'

As the bacteria penetrate tissue layers under the skin, the flesh becomes inflamed. The redness spreads rapidly during the first two days, there is usually 'a marked lassitude' on the part of the patient. 'He becomes indifferent to his surroundings and has a total lack of appreciation of the severity of his illness.'

The techniques used today for treating the illness are in essence those developed by Meleney. He recommended a long 'radical' incision along the length of the affected tissue to relieve the pressure caused by the suppurating fluid beneath, and the opening of the wound for the removal of the tissue killed by the toxins of the bacteria. The only significant difference between the 1920s and the 1990s is that now doctors can use antibiotics to attack the bacterium.

Modern victims of the bacterium would recognise Meleney's descriptions of the disease and the painful treatment. For Roseanne Millar, 41, a nurse from Bonnybridge, Stirlingshire, the attack began with severe pains around the pelvis. The next day bruising spread over her stomach and part of a leg. She went into hospital and surgeons worked feverishly to contain the spread of the bacterium. She woke up to find her stomach cut open.

'It was left open for 10 days,' she told a reporter. 'The nurses had to wash the wound twice a day with a bleach-like solution. The pain was unbelievable. Those days were the worst of my life.'

Ms Millar survived. Others have not been so lucky. Terry Bowden, 39, of Beckenham Hill, Kent, made breakfast for his four children on a Sunday morning and was dead 36 hours later. His wife, Christine, said: 'He suddenly started complaining his leg was hurting him and then it swelled up. It got hold him of so fast. He was in a terrible state within hours.

'It was such a surprise to Terry because he was never ill. He was the sort of bloke who never had to take time off work for sickness. In the end I don't think he really knew who I was. He was just staring at me, looking really frightened.' Mr Bowden's death would have remained a private tragedy were it not for the explosion of interest in the cluster of cases around Gloucester.

The alleged epidemic there began when two people were infected, taken to Stroud General Hospital in February and successfully treated. A third, David Somerville, from a village near Stroud, collapsed in March and had a leg amputated. Then three people living within a 25-mile radius of Gloucester died. A woman pensioner collapsed on a train. A man already in the Gloucestershire Royal Infirmary was infected and died in April; and the bacterium contributed to the death of a woman in her sixties from the Forest of Dean.

When a travel agent from Stroud collapsed two weeks ago, the media bandwagon began rolling. All over the country, journalists looked for, and found, other killer-bug victims. Fears of an epidemic seemed eminently reasonable.

But the fears have been crushed by the scientists who investigated the Gloucestershire cluster. They have found nothing but a series of wretchedly unhappy coincidences.

The streptococcus bacterium, like all bacteria, lives in the nutrient-rich fluid that bathes the body's tissues, consuming the nutrients the body provides. It does not actually eat flesh, but produces substances that can dissolve away fatty tissue beneath the skin and between the muscles. Death or crippling injury is caused by different sub-types of the streptococcus microbe - called the M-types.

Robert George, at Colindale, was one of the team which identified the strains that infected the Gloucestershire patients. It found that many were infected with different M-types. From this he concluded that the cluster was a statistical freak - a series of coincidences - but not the start of a plague. If the microbe had spread from one person to another they would all have been infected with the same M-type. Stroud, Gloucestershire and Britain were not threatened by an epidemic.

THE PICTURE this suggests, of neutral, detached experts able to knock down scare stories with authority, is comforting and largely fair. But the scientists are the first to admit that they do not really understand how forms of the streptococcus bacteria can suddenly kill.

There are many intangibles. 'It needs to be in the right patient at the right time - if I can put it like that - to go crazy,' said Dr George. 'Some patients have other illnesses. They may be debilitated and are consequently more likely to have devastating infection than others. It also depends to some extent on the route of access of the micro-organism to the deep tissue. Some of these cases may follow injuries. It doesn't eat its way in; it has to have a route into the deep tissue.'

Dr Begg said the danger of one person infecting another was tiny. 'Clearly that risk is extremely remote because there are so few cases. The fact that 10 per cent of the population carries the bacteria in the throat, and yet only a handful gets seriously ill, shows this.'

But again there are variables. Exceptional though they may be, rare instances of the bacterium being passed on have been discovered - in one recent case reported in the medical literature, a woman with bed sores passed on the bacterial condition to a doctor and nurse and 10 other hospital patients.

Henry Taylor, the former vicar of Crook in Co. Durham, believes there is no reason to panic, but there is reason to be worried. He became a reluctant lay expert on the bacterium two years ago. He was woken at 5am by the sound of his young daughter crying in her cot. He cuddled her, and went back towards his bed. Suddenly he vommited and found himself close to collapse. Fortunately, a friend, who happened to be a trained nurse, came to the house in the morning to take his children to school.

She took one look at the vicar and called the ambulance. By the time he got to hospital, both his lungs had collapsed, his kidneys had failed, his blood pressure was undetectable and he was in a deep coma.

He was infected with Streptococcus B, a biological cousin of the group A Gloucestershire bacterium. It caused blood clots. He lost both legs beneath the knee, all his fingers and a large part of one hand. Out of hospital and at home with his wife and five children, he now looks on the public discovery of the illness that all but destroyed him with experienced eyes.

'No I don't think the public reaction is completely wrong,' he said. 'It's fair enough. No one has the faintest idea why this thing happened to me. It's perfectly reasonable to be extremely frightened.'

(Photographs omitted)