In 1790 the Home Fleet of the Royal Navy was ravaged by an outbreak of what was known as 'malignant ulcer'. Sometimes it began with a small skin pimple but more often it followed a bruise, burn or scald. It progressed rapidly, eating the flesh away, causing agonising pain. Within a day or two the whole lower leg bone would be exposed, or all the bones of the hand. Amputation was the only treatment and the death rate was high.

In one memorable case described by Thomas Trotter, a naval physician in Portsmouth, in his book Medicina Nautica, the infection started in a sailor's penis which turned gangrenous and dropped off. Then his scrotum was 'eaten' away, leaving the testicles exposed. Thankfully, the man died.

Dr Trotter, who had seen all manner of horrible infections, wounds and ulcers contracted by sailors in different parts of the world, wrote that he had never seen a disease so terrifying. He could find nothing about it in his medical textbooks and assumed that it was a new condition. Medical historians now believe that Dr Trotter was describing an outbreak of necrotising fasciitis, a gangrene-like condition caused by Group A beta-haemolytic streptococcus, the bacterium which this week achieved superstardom as the 'flesh-eating killer bug'.

What began as an unusual cluster of seven cases in Gloucestershire, first reported in the Independent on 6 May, had by the end of this week escalated into a worldwide health alert and a media feeding frenzy.

Henry Taylor, a 46-year-old vicar from County Durham, lost both his legs below the knee and all his fingers after contracting the infection from his wife, who had a sore throat. Stephen Smith, 25, from London, underwent three operations to remove the grey and black gangrenous tissue from his buttocks, abdomen and back. 'Every time I went to see him it as if there was a little bit less of him there,' his mother said. Ralph Antrum, a consultant at Bradford Royal Infirmary, described how the bacterium 'digested the back muscles' of one young woman.

The most heart-rending case was that of a young mother from Surrey, Beverley Biggar, who developed symptoms shortly after giving birth to her first child, Charlie, by Caesarean section. Emergency surgery and intensive antibiotic therapy cured her, and she was transferred to Queen Mary's Hospital, Roehampton, for plastic surgery on her wounds. She died suddenly on the day before her discharge.

The appetite of both the media and the public for these tragic stories was huge. Attention shifted away from the Gloucester cluster - the genuine news story - as local newspapers busied themselves finding home-grown victims. Cases of necrotising fasciitis linked to strep A infection rose beyond the figure of 10 or fewer cases which government scientists assured people was the expected number in one year. The unofficial death toll climbed steadily too; from three at the beginning of the week, to six, then nine, then to 15 deaths by yesterday.

Dr Norman Begg, deputy director of the Public Health Laboratory Service's Communicable Disease Surveillance Centre at Colindale, north London, attempted to reassure people. There was, he admitted, an unusual cluster of cases in Gloucester, but analysis showed they involved five unrelated strains of the bacterium - probably a chance occurrence. 'There is no need for panic. Patients that do develop this condition do become very ill and GPs are not going to mis-diagnose them and fail to send them to hospital,' Dr Begg said. The PHLS had set up a 'crisis' management team to collect data on all the cases being reported.

His words fell on deaf ears. After the Prime Minister intervened, Dr Kenneth Calman, the chief medical officer, stepped in. 'Everything that can be done is being done to investigate the so-called 'killer-bug' infection,' he said. There was no evidence of any increase in the normal incidence of strep A infections, and no firm evidence that all cases reported in the media were necrotising fasciitis due to the microbe.

Internationally, the media had been unable to resist a microbe that 'liquefied' fat, skin and muscle at the rate of three inches an hour and could kill in 24 hours. 'Is it true that you Brits have been overrun by a flesh-eating super-bug?' asked WOAI radio in San Antonio, Texas.

Health scares are far from rare: 'listeria' hysteria, salmonella in eggs and periodic outbreaks of legionnaire's disease as well as that hardy perennial, 'mad cow disease', have filled pages of newsprint in the last decade. But this was different. True, the infection had devastating effects which caught the imagination, but something else was at work, says Dr Irvine Loudon, a medical historian and retired GP from Oxford. The stories had hit a nerve in a population made complacent by more than 50 years of antibiotic therapy and medical mastery of infectious disease.

Most of us are still largely untouched by Aids and see the re-emergence of tuberculosis as an interesting but unworrying anomaly. We are only a little disturbed by the rise of drug-resistant microbes, the return of cholera in Latin America and diphtheria in Russia. Many of us are, for the first time, seeing the most horrific manifestations of infectious disease. And an almost harmless throat bug was to blame?

Group A streptococci are common bacteria, causing a range of minor illnesses - sore throats and skin infections - which are quickly dealt with by antibiotic treatment. Up to 8 per cent of people are carriers, with the bacterium living harmlessly in their throat and nasal passages. Occasionally a strep A infection can progress to a serious systemic illness, including blood poisoning, usually in the elderly or sick. About 550 cases occur in England and Wales each year.

Even more rarely, streptococcus A causes necrotising fasciitis - about 20 per cent of all cases. The only treatment is disfiguring surgery and intensive antibiotic therapy. As more cases emerged this week it appeared that there was no way of protecting yourself. People who had surgery were at greater risk - but the healthy were vulnerable too. Surgeries were inundated. What was going on? Had the bacterium mutated into a more virulent form which was, like some malignant sci-fi creation, out of control? Perhaps the microbe had become infected with a virus which 'switched on' lethal genes? Or were all these cases, as the authorities insisted, within normal limits?

In reality, the authorities did not know what the normal limits were - but refused to admit it. Neither severe streptococcal A disease nor necrotising fasciitis are notifiable diseases, and what figures the PHLS has are the result of voluntary reporting by motivated doctors.

What the 'media hype' has probably done is to reveal the real number of cases that occur. Towards the end of the week the PHLS was saying that the figure of 10 or fewer cases was intended only to give a 'handle' on the situation. 'We know that we aren't talking about hundreds or thousands of cases,' a spokeswoman said.

The PHLS crisis team has now confirmed a total of 15 cases of necrotising fasciitis linked with strep A in the first five months of the year - an increase of at least 50 per cent on its expected annual total. The figures included four of the seven cases in the Gloucester cluster, which is now expected to be no more than a statistical blip. Is that the end of the story?

In a week of dramatic and emotive statements, a comment by Hugh Pennington, professor of bacteriology at Aberdeen University and a leading authority on streptococcal infections, passed almost unnoticed. It was, perhaps, the most chilling of all. 'Perhaps we should be improving our surveillance and maybe give these (strep A) infections a higher priority in the future,' he said.

Eighteen months ago Professor Pennington started collecting and analysing the genetic make-up of different strep A strains. He was concerned that a 'hot new' strain would arrive here from the US, where the bacterium was associated with a rise in cases of toxic shock syndrome.

Although Bob Howard, of the American Center for Disease Control in Atlanta, Georgia, says they are not experiencing anything out of the usual, some other British microbiologists share Professor Pennington's concern. Michael Barnham, a streptococcal specialist at Harrogate General Hospital, says there has been a marked increase in dangerous strains of the bacterium in Western countries in the past decade.

The streptococcus bacterium was not discovered until the 1870s but throughout the 18th and 19th centuries it claimed thousands of lives. A century ago 35,000 people died from scarlet fever in England and Wales annually; 3,000 from puerperal (childbirth) fever - one in three women died in bad years - and 3,000 from erysipelas (an itchy rash, usually on the face). All were caused by strep A. Then there was gangrenous erysipelas, similar to Dr Trotter's malignant ulcers, and the much-feared hospital gangrene, probably streptococcal in origin.

Towards the end of the 19th century the virulence of the bacterium appeared to wane. No one knows why - probably an evolutionary change which favoured a less virulent strain over a more virulent one. Fewer people were dying from strep A. There was then another steep decline in virulence between 1940 and the 1950s.

Professor Pennington is reluctant to be drawn but says his data so far provides a 'whiff of evidence' that strep A is regaining some of its old virulence. Dr Loudon agrees: 'I have often written that it is by no means unlikely that a highly virulent strain would re-emerge. It is too soon to say that it has, but it will be interesting to see what happens in the rest of the year.' Strep A infections tend to occur more frequently in the first half of the year, he said. 'We may not see any more but then again . . . when I was researching a book, Death in Childbirth, in the late 1980s I could not find a microbiologist who was interested in strep A. That certainly isn't the case now.'

(Photographs omitted)