Dr. Thomas Vescio was reading lab reports in his office at Evanston Hospital early on the morning of Thursday, August 2, when he received an urgent call from the intensive care unit. A woman who’d delivered her first baby by cesarean section two days earlier had developed a high fever Wednesday night, along with pain in her belly. She’d been prescribed a broad-spectrum antibiotic, one effective against a wide range of infections, but she showed no improvement. Then, within hours, her blood pressure dropped sharply and her heart began beating erratically. Her breathing became difficult as her lungs began to stop absorbing oxygen, and her kidneys started to shut down.
The woman became very sick very fast and Vescio, the hospital’s head of infection control, had an idea why. “When they were telling me over the phone about it,” he says, “before I had even seen the patient, I was afraid that this was the start of an outbreak.”
He suspected an invasive Group A streptococcal (GAS) infection. The bacteria is a common one–the same that causes strep throat–but less commonly it can get under the skin or into the lungs or blood. When it does it’s fast and deadly, manifesting in illnesses like meningitis, streptococcal toxic shock syndrome (STSS), and necrotizing fasciitis–otherwise known as the flesh-eating disease.
When Vescio visited her bedside, the woman was incoherent and couldn’t describe her symptoms. The first thing he noticed was that her face was flushed and her whole body covered by rash, like a sunburn. But she had been admitted to the hospital 11 days earlier–for an obstetric problem, says Vescio–so he knew that wasn’t possible. Whatever made her sick had come from inside the hospital–from a visitor or a member of the hospital staff. All signs said the woman was headed for toxic shock, and probably wouldn’t survive another 24 hours without treatment. He needed to diagnose the problem fast.
The long horizontal abdominal incision is the most obvious point of infection in a postcesarean mother. To Vescio, the woman’s looked healthy, showing no inflammation and exuding no pus. In fact, that’s consistent with toxic shock, when bacteria produce toxins that kill the white blood cells that produce those symptoms. A surgical resident removed a few staples from the corner of her incision so Vescio could get a closer look. “The fluid that was inside there was clearly abnormal,” he says. “If you open a normal wound, it should bleed and the blood should be red. Her blood was brown and it didn’t clot the way it should.” He swabbed the inside of the wound and prepared a slide, rushing it to the hospital’s microbiology lab. Within 15 minutes his fears were confirmed. “We saw tons of bacteria classic for GAS.”
Vescio worried that the woman couldn’t be saved, but for the time being her fate was out of his hands. A surgeon was already at her bedside examining her wound and observed that the bacteria’s toxins were destroying her subcutaneous tissue and fat. The woman had necrotizing fasciitis, and the only way to treat it was to cut the diseased tissue out of her body, a procedure called a debridement. She was immediately taken into the operating room and placed on a ventilator. Her baby, who had already been given antibiotics, was isolated for 24 hours and monitored for signs of infection.
But with the threat of an outbreak, Vescio couldn’t sit idly by. “Most [disease] clusters you define as three or more cases,” he says. “With GAS I don’t think anyone would wait until you hit three cases. In my opinion if you see one case you gotta get going on it because it moves so rapidly. And people die very quickly.” Vescio began searching the hospital for the source of the bacteria.
Evanston Hospital is a 420-bed Northwestern University teaching facility, one of three North Shore hospitals in the heavily endowed, not-for-profit Evanston Northwestern Healthcare system. In 2001, 3,751 babies were delivered at Evanston, one of ten facilities statewide that offer intensive care to high-risk mothers and newborns.
Infections, disease clusters, and epidemics occur in hospitals all the time. That’s why they staff epidemiologists like Vescio. But outbreaks of invasive Group A streptococci are uncommon occurrences inside a modern one such as Evanston. When one does occur–in geriatric wards or burn units, for example–it’s usually spread via physical contact between health-care workers and patients. In the aftermath, the Illinois Department of Public Health and other regulatory bodies investigate, and the hospital better have a good explanation of why it happened and what it’ll do to prevent it in the future.
But while isolated invasive GAS infections after surgery do occur, epidemics of postpartum or postsurgical necrotizing fasciitis are extremely rare. In the handful of reports published on them in the medical literature over the past 37 years, nobody has been able to offer a solid explanation for how Group A strep is spread in the sterile environment of the operating room.
Epidemics weren’t always rare. The streptococcus is an ancient organism, and though it wasn’t identified until 1874, references to one of its deadlier manifestations go back as far as Hippocrates. Puerperal, or childbed, fever is a bacterial infection of the uterus that confounded doctors and decimated birthing wards for centuries. Prior to the late 1800s, delivering a child in even the best hospitals was a risky bet.
GAS is the microbe that launched modern infection control. In 1843, Oliver Wendell Holmes–better known as a man of letters–published a controversial paper proving the contagiousness of childbed fever. Four years later a Hungarian obstetrician named Ignaz Semmelweis, working in the world-renowned Vienna Lying-in Hospital, discovered how it was spread.
At Vienna, laboring mothers were divided between two wards, one attended by the hospital’s medical students and the other by midwives. The mortality rate among the students’ patients so far outstripped that of the midwives’ that women frequently opted to give birth on the street if they weren’t admitted to the midwives’ ward. After careful study of the two groups, Semmelweis observed that the students regularly examined and treated their patients with hands fouled from dissecting cadavers. He subsequently ordered all students and physicians to wash their hands with a chlorine solution before examining patients, and the outbreaks declined dramatically.
For a variety of reasons, Semmelweis’s doctrine was misunderstood and ridiculed for years, and women continued to die by the thousands. It wasn’t until the latter part of that century that he was vindicated by the work of surgeon Joseph Lister and bacteriologist Louis Pasteur. By then he was dead–from a self-inflicted strep infection by some accounts. Says one biographer, he was “a martyr to the world’s stupidity.”
Hospital-acquired, or nosocomial, invasive GAS epidemics continued to occur but with decreasing frequency as hospitals improved antiseptic techniques and more was learned about the organism and how to fight it. Certain types of community-acquired invasive GAS infections decreased also.
During the Civil War, illnesses like necrotizing fasciitis killed almost as many soldiers as did bullets and bayonets. But in 1999, of the 9,400 cases of invasive GAS reported to the Centers for Disease Control, only 600 were necrotizing fasciitis and 300 STSS. That’s compared to ten million yearly cases of noninvasive GAS, like strep throat or impetigo. At any given time it is estimated that one in five asymptomatic people are carrying the bacteria in their throats or noses or on their skin.
Because of its rarity, and in spite of the media attention it receives, an invasive infection like necrotizing fasciitis is easily misdiagnosed. Frequently the point at which the bacteria invades the body is a barely noticed scratch or bruise. Later an infected person may complain of flulike symptoms: fever, sore throat, nausea, diarrhea, chills, or aches. Disproportionate soreness may be felt around the wound. If the patient reports to an emergency room he or she might be sent home with orders to take aspirin and rest. Meanwhile, the bacteria are rapidly multiplying along the fascia, the deep layers of skin and fatty tissue that separate the upper layers from the muscles. They produce enzymes that destroy tissue cells and stop clotting. As the necrosis spreads, the blood vessels that irrigate the fascia are destroyed, preventing blood, oxygen, and antibiotics from reaching the infected area.
Within hours the pain increases, becoming intolerable, and the wound might become swollen and hot, turning blotchy red, purple, and black. The rash spreads, sometimes inches within hours. Large blisters rise up, or the skin may pock like a citrus peel, often breaking open and leaking a thin fluid called “dishwater pus.” The patient becomes delirious as blood pressure drops, heart rate increases, breathing becomes labored, and organs begin to fail.
Estimates of the mortality rate of patients with necrotizing fasciitis–which can also be caused by other bacteria–vary from 25 to 80 percent. If the patient goes into toxic shock, as Vescio’s did, it is around 50 percent. Survivors face a long and difficult recovery, negotiating secondary infections, extended wound care, painful scarring or amputations, physical therapy, plastic surgery, and emotional trauma.
Most researchers agree that we are currently experiencing an increase in invasive GAS infections, despite their relative rarity. “Group A strep has a tendency to increase and decrease virulence factors sort of willy-nilly over time,” says Dennis Stevens, a researcher and chief of infectious diseases at the Veterans Affairs Medical Center in Boise, Idaho. “So that explains why at different periods over the last 200 years there’ve been epidemics of pharyngitis, impetigo, rheumatic fever, scarlet fever. And now we’re seeing an increased incidence of invasive Group A strep infections…the adaptability of the organism seems to be infinite.”
But he agrees that transmission of invasive GAS to a group of postsurgical patients is a mysterious, inexplicable anomaly. Yet it’s one that every student of infectious disease has read about.
As a second-year resident in 1994, Vescio became interested in infectious diseases after Francis Cook, now head of Evanston’s division of infectious diseases, treated a case of invasive Group A strep. “It was a young woman who had a scab on her hand from a firecracker three weeks earlier,” recalls Vescio. “She came in and the emergency room missed the diagnosis. And when Cook had seen her in the ICU he recognized that it was toxic shock and she went into the operating room. He had nailed the diagnosis right away and actually saved this lady’s life. I was really kind of impressed how you could make a big intervention in infectious disease.” Vescio decided to specialize, pursuing a fellowship in the field at Loyola before returning to Evanston in 1999.
Nowadays Vescio is most interested in HIV, but as a student he had heard of the handful of reports written on surgical-wound outbreaks of invasive GAS in the medical literature. Because of the high mortality rate of such cases and the speed at which they can develop into outbreaks, they tend to be cited in textbooks. “In infectious disease, when you’re in training,” says Vescio, “you learned that one case of Group A strep is reason for concern.” But few doctors have ever had to manage an outbreak, something Vescio discovered on August 2 when he called some of his older colleagues for advice.
While his patient was in surgery he searched the published literature on medical databases. He dug up only 15 relevant journal articles, dating back to 1965, which all indicated that postsurgical-wound GAS outbreaks began in the operating room. These were each traced back to a single hospital worker–all but one of whom showed no signs of illness.
Sometimes the carrier was discovered to be a surgeon or obstetrician. But often it turned out to be someone who had little or no physical contact with the patient, such as an anesthesiologist, circulating nurse, or technician. That’s peculiar because the Group A streptococcus is not airborne, and is usually transmitted through hand contact or respiratory droplets from coughing or sneezing. Stranger still, the carriers were frequently not colonized by the bacteria in the nose or throat, where they are commonly found, but more often in the vagina or rectum. Because these sites are so unusual, the carriers of these outbreaks went undiscovered–sometimes for months–and some of them infected many patients.
Vescio ordered a list made of everyone present in the operating room during his patient’s operation, including her husband. The three nurse epidemiologists on his staff also contacted members of the woman’s family who had visited. That afternoon they began culturing the group, which numbered around a dozen.
Each person was interviewed and Vescio’s team took throat, rectal, and vaginal cultures. Any skin lesions were also cultured. The group members were asked if they had recently experienced any fevers, sore throats, or rashes, or if family members had shown signs or symptoms of infection. The answers gave no clues.
It would take several days for the cultures to incubate and show signs of bacterial growth, so the infection control department began watching the hospital’s patients. Though the hospital’s lab workers are required to report evidence of Group A strep in any patient, Vescio reminded them to be on the lookout for it. “We generated a list of all patients that we thought might potentially be at risk and kept a real close surveillance on them,” he says. “One person talked to the operating room manager to get the names of all the patients that were operated on. We were just looking for anyone that developed a fever or a rash. I would call the nurse manager and get verbal reports from her. She would go around and make sure everyone was OK.”
While the only way to positively identify the chains of spherical Group A streptococci is to observe them under a microscope, necrotizing fasciitis is best diagnosed by an exploration of the wound, either in the operating room or at the bedside. A surgeon probes the infected tissue with a finger or scalpel and if no resistance is met between the lower layers of skin and the fascia, the flesh is as good as dead. It’s hard to miss by peering under the skin. The normally glistening fascia takes on a green, gray, or black hue, and if the infection has gone deeper, the underlying muscle will also be discolored and won’t bleed or contract when prodded. At a certain point the patient will feel no pain in the area since the bacteria will have destroyed the nerves as well.
While major surgery isn’t normally advisable for an unstable patient like Vescio’s, one with necrotizing fasciitis won’t survive without a debridement. Antibiotics and other treatments effective against the bacteria won’t rid the body of the toxins it has already produced. And they can’t stop tissue death from spreading to different parts of the body.
Vescio’s patient was lucky in this respect. Necrosis hadn’t spread far beyond her wound and the surgeon was able to complete the operation through the original cesarean incision, removing relatively little dead tissue. What’s more, it hadn’t reached her uterus.
But she wasn’t out of the woods. Necrotizing fasciitis patients require a second exploration to check the thoroughness of the first. If the surgeon finds more dead tissue on the second look, a third must be scheduled, and so on.
The first thing Vescio did after her surgery was change her antibiotics. When she was first transferred to the ICU she had been placed on a cocktail of three drugs. Vescio dropped two of them and, because she was allergic to penicillin, placed her on clindamycin, which is specifically effective against strep infection. He also treated her with intravenous immunoglobulin (IVIG), an experimental treatment for toxic shock that consists of blood plasma blended from many donors. It’s thought that immunoglobulin, because it’s drawn from a wide variety of people, will contain some natural antibodies that neutralize the toxins produced by the bacteria.
Vescio returned to the woman’s bedside many times over the next 48 hours. Gradually her blood pressure returned to normal, her organs revived, and she began to breathe comfortably. On Friday, after her second surgery revealed only a minimal amount of necrosis, she was removed from the ventilator, but remained in the ICU.
In a way, says Vescio, the woman was much like one of Ignaz Semmelweis’s puerperal fever patients, in that her blood was more afflicted than her soft tissues. The next patient to be infected was different.
Thursday and Friday, as Vescio’s infection control team monitored patients in the hospital, they became aware of a few that seemed more at risk than others for developing an infection. Vescio says there were two patients who developed fevers at the time, but neither illness clearly matched the rapid onset of a Group A strep infection.
But around six on Friday evening, Vescio and a partner were called to the bedside of a different patient. She’d been admitted to the hospital on Tuesday afternoon, and delivered her first child in an uneventful cesarean section just a few hours after the woman who’d initially taken ill delivered her baby. Like that woman, she developed a fever on Wednesday, though much earlier in the day. At the time it was thought that she had a common uterine infection and she was given a broad-spectrum antibiotic cocktail that included clindamycin. Her fever went down and she spent Thursday enjoying her newborn.
She was doing so well that she was scheduled to be discharged on Friday, until she developed a tender rash on the flanks of her back. Still, she was feeling fine and it was suspected that she was allergic to the detergent used on her bed linens, since she’d experienced a similar reaction in the past. “They’d asked us to come by and take a look at her just to be on the safe side,” says Vescio. He had some concern that the rash was a sign of GAS, but he was dissuaded by her lack of other symptoms. “Her blood pressure was normal. Her vital signs were normal and she was actually feeling good. She didn’t have severe pain. As a matter of fact, when I first met her she was walking in the hallways with her husband and sat down in bed and started to eat her dinner. I thought to myself, ‘This lady doesn’t have necrotizing fasciitis. She looks too healthy.'”
Vescio suspected she might have a superficial skin infection such as cellulitis–for which, in its early stages, necrotizing fasciitis is often mistaken. He ordered a white blood cell count. It was highly elevated, indicating that she was fighting off something. But he didn’t believe that her apparently healthy incision was infected because her rash was so far from it.
He canceled her discharge and put her on penicillin, and she was given a CT scan, which can often detect the presence of the inflammation and accumulated fluids that sometimes accompany a soft tissue infection. The results were inconclusive. She was moved from the women’s hospital to a general medical floor to be watched closely overnight. If her symptoms progressed she’d have to go into surgery immediately.
Vescio also noticed, with some concern, that she was breast-feeding her child. “The baby was lying on her belly, right by her wound. So my thought was that this baby could probably very easily become infected. I didn’t want to take a chance.” He prescribed antibiotics for the newborn and placed it in 24-hour isolation.
Overnight the woman developed more pain, and while her incision remained normal her rash began to spread from her back to her abdomen. Vescio says he didn’t bother to swab her wound to look for GAS. She was going into the operating room either way. A surgeon confirmed the diagnosis: she had necrotizing fasciitis, and it was much more advanced than the first woman’s.
The disease had spread to parts of her body wholly removed from her surgical wound, and the surgeon was forced to make additional incisions five to ten inches long down her flanks to her thighs. Generally, during a debridement the surgeon uses forceps, scalpels, and scissors to carefully work outward from the middle of the necrotic area, excising it in thin parallel layers until reaching healthy pink, bleeding tissue. The wound is irrigated, packed with sterile gauze, and left open, so it can be checked regularly. The second woman required a much greater degree of debridement through her incisions and her surgical wound.
After surgery, Vescio adjusted her antibiotics, adding IVIG treatment. He now had two patients for comparison. Though their infections developed differently, the two women shared some important similarities that could help pin down the carrier. For one, they’d undergone their cesareans in adjacent operating rooms. They’d also shared the same surgical team.
While the second woman was in surgery Vescio ordered a comprehensive list made of everyone who’d given birth in the hospital 24 hours before and after Wednesday. Calls were placed to those patients’ physicians, asking them to check on those who had already been discharged.
Now he was certain that the carrier had to have worked on the first woman’s surgical team. But as an extra precaution he ordered a second round of cultures, this time including the second woman’s family members and a few hospital staff workers not present for the first surgery. “As things went on we cultured other individuals who were in the area at the time, just to make sure we didn’t miss anything.” This would allow for the possibility of a second carrier, and would confirm the results of the first round.
But Vescio wouldn’t have to wait out another incubation period for an answer. On Sunday the microbiology lab reported that one of the cultures taken from the first round grew Group A streptococci. The carrier had been identified.
Vescio has been careful not to reveal the identities of the two women or the carrier of the bacteria that infected them. When discussing the outbreak he refers to the carrier without using gender-specific pronouns. He will say that prior to the first woman’s infection, the surgical team member was working full-time and was busy. “The carrier was involved in other cases and those other individuals did fine. They didn’t develop any kind of infection. Why that is I don’t know.” It is possible that others were exposed but possess some kind of immunity to the bacteria. Over the weekend, before the cultures incubated, Vescio says, the carrier participated in one surgery.
When the carrier’s rectal culture grew the bacteria, the individual was given antibiotics and sent home. “There have been cases published whereby the actual carrier was the spouse or the child at home,” says Vescio. “And so the health-care worker had picked it up from them and took it to work. There was one case where they treated the health-care worker who at some point reacquired the colonization and spread the bacteria again. That’s why we felt it was important to take it to the home and make sure that everyone at home, if they were a carrier, got treated.” That week the carrier’s spouse and child were cultured and were found to have the bacteria in their gastrointestinal tracts, though they too showed no signs of illness. They were also given antibiotics.
Ten days after starting antibiotic treatment the Evanston carrier was recultured, pronounced GAS free, and cleared to return to work. The hospital also compared the DNA of the carrier’s bacteria with those of the mothers’, and as expected, they made a match. The second round of cultures did not reveal a second carrier and no other patients developed infections.
Both babies emerged from isolation without developing infections. And both mothers recovered, albeit slowly. The first, who’d suffered little necrosis but had gone into toxic shock, remained in the ICU for a week after her surgery. “I was really nervous that she was going to die regardless of what we did,” says Vescio. “For the first two days I didn’t think she was going to survive. I would say probably four or five days after we started therapy I was convinced she was gonna do OK.”
Vescio had no doubt the second mother, who did not suffer toxic shock, would survive, but her recovery would be more difficult. He theorizes that because she was placed on antibiotics earlier in the day than the first mother, the progression of her illness was modified, disguising the early and often misunderstood symptoms of necrotizing fasciitis–the very ones he was looking for.
Overall, Vescio says, both women were lucky. Each survived an infection known for its high mortality rate, their babies remained healthy, and their surgeons were able to stop the infection before it destroyed their reproductive organs.
The hospital was also fortunate. Because the outbreak was limited to only two patients, Vescio believes that the source couldn’t have been carrying the bacteria very long before it was discovered. In the previously published reports on the phenomenon, a total of 136 patients were infected. In one case the bacteria infected 20 people.
But the articles don’t answer all the questions. Why were support personnel and anesthesiologists so often found to be the carriers when they were not likely to have much physical contact with patients? One report identified a carrier as a technician who periodically entered the OR between operations but was never present during surgeries. She had been colonized on eczema lesions on her scalp that were missed by investigators the first four times she was cultured.
Still more perplexing, while two carriers were colonized on skin lesions, a few others in the throat, and two in the vagina, the rest were found to be carrying the bacteria only in the gastrointestinal tract (one of the vaginal carriers was also colonized in the GI tract).
So how does a nonairborne bacteria like Group A streptococcus make its way from someone’s colon through a pair of surgical scrubs and into a couple of otherwise sterile cesarean incisions? That’s what the Illinois Department of Public Health and a roomful of reporters wanted to know.
Both women spent the better part of August recovering in the hospital and were discharged right around the time the press discovered there had been an outbreak of the “flesh-eating bacteria.” On the day of the first mother’s diagnosis the hospital informed the Evanston health department of the potential for an outbreak. “We reported it actually even before we confirmed it,” says Vescio. “I just felt ethically it was something we should do even if we were jumping the gun.” But jurisdiction belonged to the state Department of Public Health, which also received an anonymous complaint about the outbreak. IDPH wants to know about any cases of invasive Group A strep, whether nosocomial or community acquired. It also investigates hospital outbreaks, and an inspector visited Evanston on August 22.
The hospital conducted its own investigation and submitted its own report to IDPH. “We looked at every member of the operating-room team for both C-sections,” says Vescio. “And we looked at what they do in the operating room, and did they follow the procedures? We scrutinized everything, and no procedure was breached. The literature in these cases–same thing. In none of those cases did anyone find something that was done improperly.”
On August 26, IDPH announced the outbreak to the press and the impending report on its probe. The hospital scheduled a press conference for the following afternoon to announce the results of their investigation. Vescio says he’d been interviewed by the press before, but he underestimated the ardor of reporters hot on the trail of the flesh-eating bacteria. “That wasn’t fun,” he says. “It felt like I was being deposed by a bunch of attorneys.”
In the hospital’s auditorium, he outlined some hypotheses in the literature, suggesting that the bacteria can become airborne in the OR. In a few outbreaks epidemiologists put rectal carriers in rooms distributed with petri dishes, and instructed them to move around and exercise. The plates grew GAS. The authors of those studies guessed that gastrointestinal carriers somehow became colonized on parts of the skin, and the bacteria hitched a ride into the air on exfoliated skin cells disturbed by physical activity. Because of the high virulence of GAS only a small number of the organisms would need to escape the operating room ventilation systems to cause infection in an open wound. Though none of the gastrointestinal carriers showed symptoms of strep infection, a few had hemorrhoids, and one was going through a bout of diarrhea. Vescio says the Evanston carrier was totally free of these conditions.
Vescio supposed the bacteria made its way from the carrier into the wounds via this unusual airborne route. Still, it was just a theory. “I said, ‘But no one really knows for sure,'” he recalls. “No one’s ever done a double-blinded, randomized, controlled trial.”
One reporter had his own hypothesis. “He said, ‘Is it possible that people spread it by passing gas?’ I said, ‘Who knows? Anything is possible.’ And that was my mistake, because they put that on the news. They said, ‘Doctors think that this person passed gas.'” Channel Five ran with the gas angle (as did this paper in Chuck Shepherd’s News of the Weird column one month later). “I had that idiot Mancow in the Morning trying to page me,” says Vescio. The rumor persisted among rank-and-file Evanston Hospital employees for months, and even an IDPH spokesman said he’d heard from one of the state’s own epidemiologists that it was possible.
“That night it seemed like it was a big joke,” says Vescio. “And when people realized the severity of these infections and that two women almost died they took it more seriously.” Most news outlets were more circumspect, but the story went worldwide on CNN and over the next few weeks he fielded calls from doctors as far afield as Australia looking for advice on their own GAS cases.
Flesh-eating bacteria became pathogenic celebrities in the early 90s, and since then the media have been guilty of some outrageous excesses in reporting on them, from blaming the infection on Costa Rican bananas to running screaming headlines like “The Flesh Eating Bug Ate My Face!” But the question of flesh-eating flatus didn’t originate on the evening news. Mention of it can be found as far back as the March 1977 issue of the Journal of Pediatrics, in an article coauthored by Donald A. Goldmann of Harvard Medical School–one of the published reports Vescio dug up. Goldmann anecdotally mentioned the possibility of streptococcal “aerosolization by flatus” in postoperative cases. The hypothesis has resurfaced at least twice since then–in a 1990 article in Infection Control and Hospital Epidemiology, which cites five previous articles to support the theory, none of which actually mention it, and again in a textbook chapter coauthored by Goldmann in 1998.
So where did Goldmann get his information?
“Good question,” he writes in an E-mail. “Whenever I cite the possibility of flatus, I think back to a study I heard about more than 20 years ago where this was actually tested. Problem is that I can’t find the original reference. So I guess one would have to test it again to be sure.” Goldmann doubts the theory that GAS is exfoliated into the air along with skin cells because “colonization in these carriers tends to be pretty confined to the rectum.”
“I think somebody’s got a flair for the dramatic,” says Dennis Stevens, who may have been responsible for whetting the popular media’s appetite for necrotizing fasciitis after he published a 1989 article in the New England Journal of Medicine with the less-than-snappy title “Reappearance of scarlet fever toxin A among streptococci in the Rocky Mountain West: Severe Group A streptococcal infections associated with a toxic shock-like syndrome.”
Stevens is unimpressed with reports of gastrointestinal carriage. When GAS is found in the rectum or vagina, he says, “I think it’s a fluke. It’s a mistake. It’s an accident.” The disparity in the literature between nose and throat carriers and vaginal and rectal carriers, he says, can be chalked up to underreporting–no one wants to write about boring old nasopharyngeal carriers. Publishing a report on a rectal carrier “is more interesting and dramatic. It takes some real sleuthing and a lot of real hard work to do that kind of epidemiology. Ninety-nine-point-nine percent of the time it is found on the skin or in the throat.”
Vescio agrees that surgical-site GAS infection occurs more than doctors report on it. “It’s not the kind of thing hospitals want to get out,” he says. Testimonials from at least a dozen survivors of postsurgical necrotizing fasciitis appear on the National Necrotizing Fasciitis Foundation’s Web site, suggesting it happens more often than it hits the headlines.
Maybe not all hospitals are as forthcoming as Evanston. Jennifer Young is filing a lawsuit against the Georgia hospital where she developed necrotizing fasciitis after delivering her daughter by cesarean section. She says doctors there would not tell her what she had, and tried to prevent her from reading her own pathology report.
Last month, attorney Terrence Lavin won $6.5 million for the family of a woman who died from the disease after tubal ligation surgery in 1998 at Northwestern Memorial Hospital. He sued the woman’s doctors, and the hospital settled out of court last year. He’s learned that getting the results of epidemiological investigations is pretty much a lost cause. “I so seldom have ever gotten anything meaningful that half the time I don’t even follow up on it anymore,” says Lavin, who’s handled two previous necrotizing fasciitis malpractice cases. “What the doctors and hospitals have done is set up a system of secrecy that allows them to sweep almost all of the results of their investigations under the rug.”
For its forthrightness, Evanston Hospital paid a price in publicity. The IDPH did not release the results of its survey until mid-December, leaving the question of the bacteria’s transmission hanging for months. First, the report had to be vetted by the Centers for Medicaid and Medicare Services (CMMS), the agency that oversees federal funding of hospitals. When it was finally released to the media, it still didn’t provide an answer, but stated that the hospital “failed to develop and implement a corrective action plan that would prevent the further spread of infectious disease. This was evidenced by the lack of additional control measures related to the assessment and observation of hand washing technique and compliance, possible breaks in surgical technique, and adequacy of the terminal cleaning process.”
“It probably could have been said clearer,” says IDPH spokesman Tom Schafer. “The bottom line is if everything was done perfectly, there wouldn’t have been two women who came down with necrotizing fasciitis. Now, how that happened nobody knows. And there’s nothing we can prove on how that happened. But something went wrong. It shouldn’t happen.”
Vescio thinks IDPH didn’t give Evanston a fair shake, and in the hospital’s defense he’s willing to reveal more about the carrier. “What they expect is, that if something like this happens, they want to know how you are going to do things differently in the future to prevent it. And at the time I told them that this can’t be predicted or stopped. No one has to do anything wrong for this to happen. It’s bad luck. So I told them, ‘How can we say we’re gonna do anything different in the future?’ They didn’t find anything wrong and still they come out and say people should wash their hands better. Well, that’s a given. Everyone should wash their hands. But as a matter of fact, the individual that was the carrier didn’t have contact with these two women. So to say that hand washing was the key is ludicrous and shows a complete misunderstanding on the part of the investigators. I mean, there are some cases where the carrier wasn’t even in the room.”
Vescio says that an independent infectious disease consultant brought in by the hospital to examine the case reached the same conclusions that the hospital’s quality control department did. And in November, the Joint Commission on Accreditation of Healthcare Organizations, the independent body that evaluates safety and quality of care in hospitals, accepted Evanston’s analysis of the outbreak.
IDPH and CMMS didn’t penalize Evanston, but required it to submit a prevention plan and progress reports over the next six months. “We’ve taken it upon ourselves to actually go into the operating room and stand in the corner and observe everything” at random, says Vescio. “I think that it’s something that’s probably overkill, but that’s what the state has asked us to do and we’ll comply with that.” Seminars were also held for medical staff reviewing sterile technique and precautions.
The publicity wasn’t all so ambiguous. Vescio proudly points to a laudatory article in a trade publication called Inside the Joint Commission that quotes an “insider” stating, “this organization did what it was supposed to do. They investigated it and went above and beyond the call of duty.”
The important thing, Vescio stresses, is that the women survived and are healthy. So is the carrier, who is being recultured every three to four months for a year to check for recolonization. So far, the cultures have remained clean. “Let’s face it,” says Vescio. “Not every patient has a positive outcome and there are a lot of things that happen that you can’t affect. Or you think, ‘Oh jeez, if I had done it a different way’ or ‘If I would have thought of this earlier maybe there would have been a better outcome.’ That, I think, happens to every doctor. At least with this case, I really honestly look back and I’m pretty happy with the way we managed things. I think, ‘Thank God I opened that wound. Thank God we screened everyone.’ If we hadn’t, maybe we wouldn’t have caught the carrier. Maybe there would have been ten cases. Maybe someone would have died from it. I’m happy that for whatever reason, we were able to find out a way to do the right things.”
Sometime within the next three months he plans to add a published article on the outbreak to the 15 already out there. “You generally don’t like to wait too long, because the interest kind of wanes,” he says. “This being in the news, there are a lot of people interested.”
Art accompanying story in printed newspaper (not available in this archive): photos/J.B. Spector.