COLUMN ONE : ‘Killer Bug’ Perfect for Prime Time : What tabloids call ‘flesh-eating bacteria’ is a rare but virulent form of germ that causes strep throat. After years of dormancy, its return has stumped doctors and fueled fear, fascination.

Before the nightly news showed gruesome photos of human limbs devoured, before drive-time deejays yukked up the dreaded “flesh-eating bacteria,” before British tabloids screamed, “Killer Bug Ate My Face,” and people fretted over an epidemic that does not exist, there was Luis.

This little boy, then 4, arrived at the emergency room of Childrens Hospital Los Angeles 18 months ago. He had a bad case of chickenpox, and his parents said his hip hurt. The doctors knew immediately that it was far more serious.

The child, whose real name has been kept confidential, was in shock when he entered the intensive care unit. His kidneys were failing, his blood pressure was erratic. Clots were forming in his arteries. Worse, he had a ghoulish case of gangrene. His legs, swollen and purple, were withering away.

“He was perilously close to death,” says Dr. Larry Ross, an infectious disease specialist at Childrens. Luis survived--”It’s miraculous,” Ross says--but today is in a wheelchair. Both legs were amputated below the knees.

What Luis had was devastating. But it was rare, and it is certainly not new.

His ailment was the same one that has gripped the public consciousness--and imagination--in recent weeks: infection with a deadly, fast-acting strain of a common and ordinarily benign germ, Group A streptococcus.

Most Group A infections cause nothing more than strep throat. But Luis had a rare, aggressive form that entered his body through a chickenpox sore and released lethal toxins that caused “necrotizing fasciitis”--literally, death of the fascia, the tissue that binds skin to muscle.

Over the last five years, scientists have tracked the spotty reemergence of similar, highly virulent strains of Group A strep. These strains had been dormant for half a century or more, and were nearly nonexistent in the late 1970s and early 1980s. But since recent reports of the disease appeared in Great Britain, the tabloids have had a field day with “the flesh-eating bacteria.”

The catchy phrase--if technically inaccurate--has catapulted Group A strep from scientific curiosity to disease lore. It now holds a place on a list of mysterious health threats that seem to come out of nowhere, whipping up fear and then quickly fading from the spotlight: Legionnaire’s disease, Lyme disease, E. coli, hantavirus.

In fact, Group A strep has made this list before. Four years ago, it killed Jim Henson, the creator of the Muppets. A spate of frightening news stories followed. “A Mean Strain of Strep,” trumpeted Newsweek. “Bad News Bacteria,” announced the highly regarded journal Science, in a report picked up by media outlets nationwide.

Killer germs are perfect for prime time. They are invisible, uncontrollable and, in the case of Group A strep, can invade the body in an unnervingly simple manner: through a cut or scrape.

“This is one of the eternal fascinations of people, like horror movies,” says Jim Whorton, a professor of medical history at the University of Washington. “It’s something we’re terrified of, but we just can’t help peeking.”

Whorton says that ever since the germ theory--that said small, invisible organisms could cause disease--was proved in the 1880s, people have spied germs lurking behind every corner. Even scientists “began finding germ causes for everything.”

There were at least a dozen reports in the late 1800s of the discovery of “the germ of beriberi”--a disease that was later found to be caused by a deficiency of Vitamin B1. Before the bacterium that causes syphilis was discovered, people were convinced they could catch the disease without having sexual contact--from sharing utensils, touching doorknobs, even breathing the same air as someone who was infected.

“If the British tabloids had been around in the early 20th Century,” Whorton says, “we would have seen very similar stories about syphilis. It would have been portrayed as a menace that was overrunning society.”

But Dr. Michael Wilkes, a professor of medicine at UCLA, sees more than media hype at work. True tales of grisly diseases, he says, put the lie to a uniquely American belief.

“For decades, and maybe even half a century,” he says, “the American medical machine has tried, to a great extent, to put a myth over the public that everything is within our ability to control, that we have medicine and we have technology and we have surgery to deal with the common ills of humans.

“It’s these sorts of episodes that pop their head up on a regular basis, that remind the public how terribly vulnerable we all are, and how medicine is really very much an art, not a science.”

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Reports of the “flesh-eating bacteria” have been nothing short of horrific. The fast-moving infections do respond well to antibiotics if treated immediately, but symptoms are often difficult to recognize at first. Of those afflicted with aggressive strains of Group A strep, 30% to 50% die. Some strains spawn necrotizing fasciitis--the “flesh-eating” gangrene that Luis suffered. Others cause myositis, which eats away at muscle. Others cause severe damage to organs, such as kidneys and lungs.

Equally frightening are suggestions that the disease occurs in clusters: In Los Angeles and Orange counties, 28 children who had chickenpox this winter also became infected with severe strains of strep--although not the “flesh-eating” kind--and five died.

In Connecticut, Norwalk Hospital admitted a man and a woman--unrelated to one another--during the same week in May. The man was in critical condition until Tuesday, when his status was upgraded to serious. The woman was discharged last Thursday.

In Gloucestershire, England, a cluster of seven cases was reported, and health officials say the lethal organisms have caused more than a dozen deaths in their country this year.

While the public thirsts for explanations, scientists can offer few. Many questions--such as why toxic streptococcus infections appear to be on the rise and how bacteria can be transformed from tame to ferocious--lack answers.

“The truth is that we have an incomplete explanation for it at this point in time,” says Dr. Edward Kaplan of the University of Minnesota, who runs a World Health Organization laboratory responsible for tracking the strep germ. Still, Kaplan is angry at what he views as overwrought media coverage of the Group A threat.

“This is not anything that danced in out of the blue,” he says. “If I lived in your part of the country, I would be much more worried about an earthquake than I would about getting a flesh-eating bacteria.”

Statistics are also incomplete on how frequently these toxic strains infect people. Only 22 states require doctors to report Group A strep infections to health officials, although the current furor has caused an upsurge in reporting. The federal Centers for Disease Control and Prevention estimates that in 1990, the last year in which it gathered figures, there were 10,000 to 15,000 severe cases of Group A strep in the United States, resulting in 2,000 to 3,000 deaths. Of those, 500 to 1,500 included necrotizing fasciitis.

Although the incidence is up from the early 1980s, the numbers are minuscule compared to the many thousands of routine strep infections each year. The organism is so common it has been called “an occupational disease of schoolchildren.” Experts estimate that 10% to 15% of all pupils are infected at any given time.

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Although they are rare, severe Group A strep infections are not to be dismissed, as those who have been afflicted can attest.

Pat Scott nearly succumbed to one of these germs three years ago. Her face was eaten away by the disease. After 33 plastic surgery operations, the 57-year-old El Cajon woman still is not whole. Because her reconstructed eyelids do not close perfectly, she must wear a mask to sleep. Every hour, she puts saline drops in her eyes so they do not dry out.

“I lost my forehead. I have no eyebrows. I lost both sides of my face, part of my nose, my eyelids,” she said. “The only part of my face that is still really me is under my nose and my lips. The rest of it has been grafted.”

She was stricken in 1991, after she tripped and hit her head on a bar stool. The wound was not much bigger than the head of a pin. She says she was given antibiotics, although the first of two surgeons who cared for her, Dr. Randal Vecchione, says it is unclear whether Scott took the drugs as required.

Vecchione says Scott was infected not only with Group A strep, but with three other organisms that combined to create “an anatomical nightmare.” When he met her, 10 days after her injury, the surgeon cut away the patient’s face to save her life. Had he not done so, he said, the infection would have marched on, killing her.

“The most maligning thing that can be done to any individual is to remove her face,” the surgeon said. “And that’s what she was, the faceless woman.”

Scott will probably undergo another dozen reconstructive operations, according to her current surgeon, Dr. Leonard Glass of UC San Diego. But she will always need special hair treatments and makeup to appear normal. “Functionally, I think she’s going to be fine, eventually,” Glass said. “Appearance-wise, I think she’s going to be good enough. . . . She’s always going to be terribly scarred and deformed.”

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In the earlier part of this century, before the advent of antibiotics, such aggressive streptococcal infections were a serious problem. Often they led to severe cases of rheumatic fever and scarlet fever. But around World War II, says Kaplan of the University of Minnesota, the cases began to drop.

Some have attributed the downturn to the arrival of antibiotics, but Kaplan says the decline actually began before then.

By the 1970s and early 1980s, deadly Group A strep infections were extremely uncommon.

In the mid-1980s, the tide began to turn. In 1989, along with Dr. Dennis L. Stevens of the University of Washington, Kaplan co-authored a landmark article in the New England Journal of Medicine on the rise of highly toxic Group A infections.

The article described 20 patients from the Rocky Mountain region, all infected between 1986 and 1988. Eleven suffered from necrotizing fasciitis; six died.

Viewed over the long term, the upturn in severe Group A strep infections is not surprising. Students of medical history know that diseases from smallpox to tuberculosis wax and wane with the times. Dr. Jay Wenger of the CDC says: “Infectious diseases tend to be a little bit cyclical.”

Over the past several years, scientists have devoted a lot of attention to understanding these “emerging infections,” as they are called. Sometimes, there is an explanation for cycles of disease, or for the appearance of a microorganism that appears to be new but in fact may not be.

Lyme disease--a fatiguing condition that can cause neurological symptoms and pain and swelling in joints--became prevalent in New England when developers began building suburban subdivisions in wooded areas inhabited by deer. Ticks that had bitten infected deer began biting people as well, passing on the disease.

Sometimes, one disease can lead to another. The spread of AIDS has created an immune-suppressed population that is vulnerable to tuberculosis. The recent upswing in TB has also been attributed, in part, to the phenomenon of drug resistance, in which new strains crop up to outsmart old antibiotics.

Still other diseases, like hantavirus--which captured public attention last year when a new strain, carried by rodent droppings, caused more than 30 deaths--have existed for a long time before being recognized and named. And sometimes old illnesses re-emerge when “herd immunity” no longer exists; a measles outbreak occurred in Los Angeles County several years ago because many children were not vaccinated.

These explanations, however, fail to account for the increase in toxic strains of Group A strep.

“None of the usual reasons seem to apply,” says Dr. Michael Dube, an infectious disease specialist at USC. “Streptococcus sort of has a mind of its own.”

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At the University of Minnesota, Kaplan is trying to gain a greater understanding of that “mind.” He has been able to type about 80 varieties of Group A strep, distinguished by subtle genetic differences. But much more needs to be learned, he says, including how many types are especially virulent and what makes them so.

Kaplan theorizes that the reemergence of deadly strep strains has to do more with a change in the bacterium itself than with any outside force.

He believes the strep germ may have become infected with a virus that inserts new genetic material into the organism, causing it to manufacture toxins. Once inside the body, the streptococcus bacteria multiply quickly, producing the toxins, which are then secreted.

If patients receive antibiotics within about three days of infection, the drugs can generally head off release of the toxins. But once the poisons are released, it is difficult to stop them. Often, the only cure is to cut out infected tissue or muscle.

“It’s the toxin that causes the damage, not the bug itself,” Kaplan says. The toxin “starts a cascade of abnormal physiological events, causing damage to the liver, kidneys and lungs and so on. And then you can see how you’re off to the races.”

Why one person becomes infected and another does not remains unclear. So is why some people get strep throat and others do not. Some may have heartier immune systems and resist infection. Others may be susceptible because of poor nutrition or underlying diseases.

As for the big question--Is this contagious?--Kaplan says:

“There is evidence that these strains can spread. Streptococcal infections have been known to be contagious for years. Does that mean everybody should go in the house and lock the door? No, not yet.”

How Deadly Bacteria Spread

The so-called “flesh-eating bacteria” is a highly virulent form of an ordinarily innocuous germ, Group A streptococcus. Scientists theorize that virulent Group A strains occur when bacteria mutate to produce toxins. These toxins can cause a range of lethal symptoms, including necrotizing fasciitis, a condition in which tissue is rapidly destroyed.

HOW THE BACTERIA KILL:

1) Bacteria enter the body through a break in skin, including chicken pox lesions, or sore throat.

2) Bacteria multiply, producing toxins that spread in skin and fatty tissues.

3) Toxins introduced into the bloodstream spread to other parts of the body, including organs such as the kidneys and lungs.

4) Toxins can also cause necrotizing fasciitis, cutting off circulation in the affected area, depriving tissue of oxygen and destroying the tissue.

THE FIRST 72 HOURS: Symptoms can include a sudden rash, a spreading infection, swollen lymph nodes or a rise in fever. At this stage, antibiotics can stop the bacteria, preventing release of the deadly toxins.

UNTREATED SYMPTOMS: Without treatment, the possibility of heading off the disease decreases. In some individuals the disease can become dangerous in a matter of two or three days; others longer. Once toxins are released, surgery may be required to remove necrotic tissue. The disease kills 30% to 50% of those afflicted.

OCCURENCES: Infections with aggressive Group A strep are rare. Recent cases have been reported in California, Colorado, Connecticut, Florida, Michigan and New York.

Sources: Dr. Michael Dube, County-USC Medical Center, Dr. Edward Kaplan University of Minnesota.

Researched by DAVID F. MONTESINO / Los Angeles Times