One VISA patient dies, and the other recovers
One VISA patient dies, and the other recovers
No new cases after sudden appearance of first two
A Camden, NJ, patient who was the second documented case in the United States of infection with vancomycin intermediate-resistant Staphylococcus aureus (VISA) has died of underlying medical conditions, Hospital Infection Control has learned. The other U.S. VISA patient, reported in Michigan, has recovered after successful treatment with antibiotics that were still effective against the emerging pathogen, which was first reported in Japan.1-3
The first two U.S. cases were reported within a month of each other last year by the Centers for Disease Control and Prevention. (See Hospital Infection Control, October, 1997, pp. 145-152.) VISA infection in a peritoneal dialysis patient in Michigan was followed by confirmation of a second VISA case in the New Jersey patient, who had a bloodstream infection. While little can be surmised about the anticipated mortality rate of future VISA cases based on the first two, the New Jersey patient’s death was attributed to underlying conditions rather than the VISA infection, says William Jarvis, MD, acting director of the CDC hospital infections program.
"[VISA] certainly did not kill either of these patients," he says.
According to the CDC report on the New Jersey case, in August 1997 a VISA-associated bloodstream infection was diagnosed in a patient who had long-term methicillin-resistant S. aureus (MRSA) colonization and repeated MRSA infections since February. The patient was not receiving chronic dialysis like the first U.S. case, but had undergone a similar pattern of intermittent exposure to vancomycin. In addition, the patient had vancomycin-resistant enterococci (VRE) colonization. From March to August of 1997, the patient was treated with multiple courses of vancomycin for repeated MRSA bloodstream infections. Neither the subsequent treatment or detailed clinical course of the patient have been reported, but the infecting VISA strain was susceptible to several other drugs.
No investigational drugs used
Likewise, the Michigan patient who recovered was infected with a strain of VISA that was susceptible to rifampin, chloramphenicol, trimethoprim-sulfamethoxazole, and tetracycline. The specific regimen used to clear the infection has not been reported, but Jarvis notes that no investigational drugs were used.
"Basically, they used a variety of combination of antibiotics, none of them of being investigational, that the strain was sensitive to," he says.
Though few additional details were being released, Jarvis reports that no VISA transmission was found in contacts of either patient, despite "literally hundreds" of cultures on health care workers and community contacts. The lack of transmission may be reflective of the site of infection, he notes.
"These patients were somewhat different than one would expect for staph transmission," he says. "Both of them really had infections of their catheters and/or peritonitis. They really had an internal site that was the source of this. Neither of them had either hand carriage or nasal carriage of the organism. If you were going to get dissemination that’s what you would expect."
The lack of subsequent transmission also indicates that contact precautions for MRSA while the patients were hospitalized were effective, suggesting that future VISA cases can be controlled by infection precautions.
"We’re hopeful that that’s the case," Jarvis says. "With [only two cases] it’s hard to say much of anything, particularly when these patients did not have external site colonization. At least in these two patients we are encouraged that the infection control practices that were implemented seemed to have worked."
Both U.S. cases involved MRSA infections that developed an intermediate resistance after prolonged exposure to vancomycin. The emerging VISA strain in each case had a minimum inhibitory concentration (MIC) of 8 the same level of reduced vancomycin susceptibility in the first reported VISA patient in Japan. Neither the strain genotypes nor the mechanisms of resistance have been reported in the U.S. cases, but the first case in Japan involved a strain with thicker cell walls that reduced its susceptibility to vancomycin. All three strains are thought to have evolved independently, indicating more cases may follow in other patients being treated under similar conditions.
"We have had no further episodes of VISA or [vancomycin] resistance that we have confirmed," Jarvis tells HIC. "Who would have guessed that these two would have occurred so close in time to one another? We kind of expected we would see more, but so far we have not confirmed it."
Where is expected reaction?
One suspected VISA case investigated at Vanderbilt University Medical Center turned out to be a vancomycin-susceptible staph strain, reports William Schaffner, MD, infectious disease professor and chairman of the department of preventive medicine at the university. Regardless, there is some sense that the emergence of VISA in Japan and the United States has not greatly stirred the medical community to action, he adds.
"Our infection control nurses are disappointed," he says. "They really hoped that these reports and the wide publicity attendant to them would galvanize the physician community here concerning the need to institute much more rigorous antibiotic controls and infection control practices. I was always more pessimistic about that. As they say in show business, the story didn’t have legs.’ It’s a flash on the scene, people note it, and then the average doctor is [again] preoccupied with the thousand-and-three other concerns they have about all of their patients."
References
1. Centers for Disease Control and Prevention. Staphylococcus aureus with reduced susceptibility to Vancomycin United States, 1997. MMWR 1997; 46:765-766.
2. Centers for Disease Control and Prevention. Update: Staphylococcus aureus with reduced susceptibility to vancomycin United States, 1997. MMWR 1997; 46:813-814.
3. Centers for Disease Control and Prevention. Reduced susceptibility of Staphylococcus aureus to vancomycin Japan, 1996. MMWR 1997; 46:624-626.
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