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Toxic staph strain may be emerging
Patients die rapidly with incredibly high fevers
The recently reported rapid deaths of two patients infected with a new highly toxic staph strain suggests the deadly pathogen is emerging in the community and certainly will pose a threat to hospitals, a researcher tells Hospital Infection Control & Prevention.
"This is clearly newly emergent," says Patrick M. Schlievert, PhD, a Staphylococcus aureus researcher at the University of Minnesota Medical School in Minneapolis. "I have tested 6,000 Staph aureus strains, and none of them came from patients with this kind of an illness. I think it is just going to continue to spread. There is no question in my mind that this really severe syndrome is going to be continually increasing. The organism has almost certainly got a foothold and it is spreading around."'
Schlievert and colleagues reported two cases of extreme pyrexia associated with S. aureus infection that they believe represents a new syndrome most likely related to changes in pyrogenic toxin superantigens.1 Both causative organisms in the fatal infections produced a deletion mutant form of toxic shock syndrome toxin-1 (TST1) and variant enterotoxin C.
"This variant of TST1 is getting into the central nervous system, affecting the hypothalamus, causing this massive fever that is basically what is killing the person," he hypothesizes. "They have the profile of a community-acquired organism, but you can imagine when these people come into a hospital, they could easily spread this."
Both patients had documented temperatures of 108°F and unexpectedly rapid deaths. "It is really, really unusual for anybody with a staph infection to get 108-plus fever," Schlievert tells HIC. "That is just unheard of. What we found associated with this was a variant form of toxic shock syndrome toxin. I do think the organism has changed. We are trying to figure out what is going on with it, but as with any Staph aureus, the potential for spread is enormous."
In both cases, the staph strain was a USA300, which is widely circulating as a community problem and increasingly spreading in hospitals. However, one infection was methicillin-resistant, and the other was methicillin-susceptible. The "deletion mutant" toxic trait could be transferred to other staph strains in much the same way that elements of drug resistance and other genetic traits move between and among bacterial species, he explains. "These are variable genetic traits that are moving around, there is no question about it," Schlievert says." The toxins are on a pathogenity island — an island of virulence — that is transferable. It is a mobile DNA element."
While certainly of major concern, it is too early to conclude that this toxic staph strain will widely emerge, cautions William Schaffner, MD, chairman of the department of preventive medicine at Vanderbilt University Medical Center in Nashville, TN.
"It's an extraordinary clinical syndrome, and [the researchers] provide a molecular reason for the profound illness in these two patients," he says. "However, there is no evidence yet that it is spreading around. We certainly ought to be on the alert for it, look for patients that have this syndrome, collect the organisms, and send them in for testing. But the question remains: Is it spreading? We don't know the answer to that. It might be, and that's kind of a frightening prospect, but I'm not ready to say yet that [it is going to broadly emerge]."
Clinical and epidemiological highlights of the two fatal infections include:
• Patient 1 was a previously healthy 39-year-old woman who presented to an outside hospital with back, hip, and abdominal pain, which had been gradually worsening over the prior week. Fever, nausea, and vomiting had begun in the 24-48 h before presentation. Upon questioning, the patient and family related a history of a recent fall and heavy use of ibuprofen for pain. Her temperature was 37°C (98.2°F), her pulse was 120 beats/min, her respiration rate was 20 breaths/min, her systolic blood pressure was 135 mm Hg, and her oxygen saturation was 99% on room air. The patient was admitted to the intensive care unit, and she began receiving intravenous fluids, vancomycin, and ceftriaxone.
The patient remained hemodynamically stable except for some sinus tachycardia, which was treated with intravenous metoprolol. Her oxygen requirements increased, and she required intubation and mechanical ventilation 11 h after admission. Her temperature increased steadily after hospital admission. Despite having received acetaminophen, methylprednisolone, and application of a cooling blanket, her temperature increased to 41°C (106.5°F), determined rectally, 13 hours after admission. Because she received succinylcholine during intubation earlier in the day, dantrolene was administered without effect. Subsequently, she became completely obtunded, and her systolic blood pressure rapidly decreased to 90 mm Hg and then to 60 mm Hg. The cardiac resuscitation team was called, and unsuccessful resuscitative measures were undertaken. A peak temperature of 42.2°C (108°F) was recorded prior to death, which occurred 14 h after admission. The patient's peak temperature may have been higher but was not recorded. Two blood cultures revealed methicillin-resistant S. aureus with intermediate susceptibility to fluoroquinolones and resistance to erythromycin.
• Patient 2 was a 68-year-old man who presented to the emergency department with shortness of breath, which had been worsening over the prior 48 h. He had an extensive history of tobacco use but had quit seven years previously. He had received a diagnosis of chronic obstructive pulmonary disease (COPD) and was using inhalers. His temperature was 37.8°C (100°F), his pulse was 154 beats/min, his respiration rate was 45 breaths/min, his systolic blood pressure was 162 mm Hg, and he had initial oxygen saturation of 89% on room air. He appeared dyspneic and had intermittent wheezing, with rales and decreased breath sounds in the left lower lung fields. Tests for influenza A and B antigens yielded negative results. Initial chest radiography revealed extensive infiltrates in the left lower lobe. CT angiography revealed extensive infiltrates involving the entire left lung, but no pulmonary emboli. Levofloxacin, vancomycin, and methylprednisolone were administered.
The patient was then admitted to the intensive care unit with a diagnosis of severe community-acquired pneumonia and COPD exacerbation. Shortly after admission, he required intubation and mechanical ventilation. He developed hypotension, which initially responded to norepinephrine and intravenous fluids. Treatment with vancomycin and levofloxacin was discontinued, and linezolid, ceftriaxone, and drotrecogin were commenced. His hypotension progressively worsened. Vasopression and, subsequently, phenylephrine were added. Despite continuation of methylprednisolone treatment, administration of acetaminophen, and application of a cooling blanket, the patient's temperature increased to 40°C (104°F), peaking at 42.3°C (108.3°F), determined rectally, 19 h after admission. Shortly thereafter, he became acutely hypotensive, with pulseless electrical activity, and the cardiac resuscitation team was called. Resuscitative efforts were initially successful. However, the patient again became hypotensive, and despite maximal vasopressor support, further resuscitative efforts were unsuccessful; the patient died 20 h after hospital admission. Tracheal aspirate culture yielded heavy growth of methicillin-susceptible S. aureus, with intermediate susceptibility to fluoroquinolones; whereas, the results of cultures of blood samples obtained at the time of admission remained negative.