Enterococci are a group of bacteria closely related to Staphylococcus species, but they are less virulent than SA. When the first VRE strains appeared in 1986, they spread rapidly through hospitals. Currently about 25 percent of enterococci isolated in U.S. hospitals are VRE. Scientists are especially concerned about VRE because these bacteria could potentially transfer the genes that make them resistant to vancomycin to other species of bacteria. Because of their close relationship, it is highly likely that vancomycin-resistance genes will spread from VRE to SA. Laboratory experiments have already confirmed this possibility.
As of 1999, there have been several cases of Staphylococcus aureus (SA) bacterial infections with intermediate resistance to the antibiotic vancomycin reported. The first case was reported in 1996 in Japan, when vancomycin failed to cure a four-month-old boy who became infected with SA after heart surgery. Despite 29 days of vancomycin therapy, the infection persisted. Although doctors finally stopped the infection using a combination of different antibiotics, they understood that a barrier had been crossed. One researcher underscored the urgency of the situation: "S. aureus, a major cause of hospital-acquired infections, has thus moved one step closer to becoming an unstoppable killer."
Since that time, three independent cases of SA with intermediate resistance to vancomycin have occurred in the United States: in Michigan, New York, and New Jersey. In these patients, doctors resorted to alternative antibiotics. Although they eliminated the infection in two of the patients, all the patients eventually died. (All of these patients were quite ill, so the infection might not have been the critical factor in their deaths.) Individual cases of SA with intermediate resistance have also cropped up in France and Hong Kong.
There have been only a handful of confirmed cases of Staphylococcus aureus (SA) with intermediate resistance to the antibiotic vancomycin. But researchers fear it is only a matter of time until strains of SA that are fully resistant to vancomycin (vancomycin-resistant SA, or VRSA) appear. VRSA will probably appear first in developed countries with the highest rates of vancomycin use, such as the United States.
Although there is no way to predict exactly when VRSA will appear or how rapidly it will spread, researchers can make reasonable estimates using a parallel case: the evolution of vancomycin-resistant enterococci (VRE). Enterococci are harmful bacteria closely related to staphylococci. Until the late 1980s, most enterococci were susceptible to vancomycin. The first case of VRE was reported in 1986 in Europe and then another in 1988 in the United States. Then, between 1989 and 1993, the number of VRE cases in hospital patients increased 20-fold. In New York City in 1993, 97 percent of clinical labs had found at least one strain of VRE. By 1994, 61 percent of hospitals nationwide had reported cases of VRE.
In 1995, the Centers for Disease Control and Prevention (CDC) published recommendations for use of the antibiotic vancomycin use in order to prevent the rapid spread of vancomycin resistance among bacteria. It emphasized the importance of wise use of vancomycin, continuing education for health care providers on prevention and control, and active screening and microbiological testing for resistant strains. The CDC recommends that vancomycin use be restricted to
Research continues along several lines to develop new therapies to cure infections that are caused by emerging Staphylococcus aureus bacteria that are resistant to the antibiotic vancomycin (called VRSA). Some researchers hope to improve the effectiveness of vancomycin by modifying its structure. One promising experiment showed that a subpart of the vancomycin molecule killed bacteria 10 times better than the whole molecule does. Other modifications to vancomycin may produce additional, effective antimicrobial drugs.
Another promising therapy uses synthetic peptides (short protein molecules) to block the release of toxins produced by Staphylococcus aureus (SA). One of the reasons that SA is so virulent is that it produces potent toxins. If the release of the toxins is prevented, much of the damage caused by SA is also prevented. The peptides bind to a receptor on the surface of the SA bacterium that controls the release of toxins. In preliminary tests, researchers have used synthetic peptides to reduce toxin release, curing mice infected with SA. Even though the peptides do not kill the bacteria, by preventing the damage caused by SA they could give patients' immune systems enough of an edge to knock out the infection. Research is needed to bring such a therapy to reality.
Other research studies may lead to the development of effective vaccines against SA or the toxins it produces. Scientists are currently testing yet another strategy. To slow the growth of virulent strains of SA, they infect patients with a non-disease-causing strain of SA. The hope is that the non-disease-causing strain will crowd out the virulent strain.
People at the greatest risk from infections caused by emerging Staphylococcus aureus that are resistant to the antibiotic vancomycin (called VRSA) are the same as those at risk from the usual Staphylococcus aureus (SA) bacteria: people who have weak immune systems due to injury, illness, or age (either very young or very old). At particular risk will be hospital patients, because their health is already compromised and they are more likely to encounter VRSA in hospitals. Because of the increased risk, a VRSA epidemic might discourage people from having elective surgeries and make nonelective surgery more risky.
Vancomycin is a naturally occurring compound, derived from a fungus. It is also an antibiotic-of-last-resort: Vancomycin is the only drug effective against infections caused by strains of Staphylococcus aureus (SA) that are resistant to all of the other drugs that previously cured SA infections.
Scientists do not know precisely how vancomycin kills bacteria. They hypothesize that it interferes with cell wall formation. A bacterium without an intact cell wall is likely to rupture during growth and cell division; thus, any drug that prevents or disturbs cell wall formation will kill the bacterium.
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