by N. Seppa
The following article is located at: http://www.sciencenews.org/sn_arc97/6_7_97/ref1.htm
Not long ago, to demonstrate how staphylococcus bacteria invade the body, instructors would have medical students roll up their sleeves and smear the microbes on their forearms. The instructors then pricked the skin. Within days, the students developed infections -- which the instructors treated with antibiotics. Point made.
They don't do that anymore.
Like other bacteria, some staph strains are showing resistance to many antibiotics. Indeed, concerned scientists have kept an uneasy vigil, watching for a microbe that would repel all drugs.
Now, a strain of staphylococcus infecting a 4-month-old Japanese boy has withstood a pharmaceutical onslaught from vancomycin, physicians' lone remaining surefire drug against the bacterium. The microbe, a strain of Staphylococcus aureus, had already acquired resistance to every other antibiotic.
The unsettling news that vancomycin had failed after 29 days of treatment has the federal Centers for Disease Control and Prevention (CDC) in Atlanta scrambling to warn U.S. hospitals to redouble their vigilance against the spread of staphylococcus.
The report has also sent a shudder through the research community, which some scientists claim has become complacent about resistant microbes.
At worst, the S. aureus could signal the rise of a microbe that no drug on the U.S. market can handle.
The CDC terms the Japanese infection "intermediate resistance" -- somewhat short of full resistance, a medical red alert. Nonetheless, scientists consider the case ominous. S. aureus is a potentially lethal staph that occurs naturally in humans, residing on the skin and along the mucous membranes. This opportunistic microbe typically needs a break in the skin to invade the body. It can form an abscess at that spot or travel in the bloodstream to infect kidneys, bones, or other tissues.
Vancomycin routinely stops it and probably still will for a time, says Stuart Levy, director of the Center for Adaptation Genetics and Drug Resistance at Tufts University School of Medicine in Boston. However, Levy and others expect the resistant strain to spread.
"Bacteria do not sit around," he says. "They are moving targets."
The fact that this strain was found in only one individual "doesn't make any difference," says Anthony S. Fauci, director of the National Institute of Allergy and Infectious Diseases. "It's not a question of whether it's going to happen here, it's a question of when."
Despite a recent research push, the U.S. pharmaceutical industry could be caught flat-footed. Work on new antibiotics slowed in the 1980s and early 1990s. It can take a decade to bring a new antibiotic to market (SN: 5/17/97, p. 310).
"We have a few drugs in the pipeline that appear effective against vancomycin-resistant microbes," Fauci says. "But they are only in the development stage."
The staphylococcus group of bacteria is especially hardy and difficult to wipe out with normal precautions. Hospitals fight a running battle against the microbes, which can withstand hot water and some disinfectants, says Gail H. Cassell, a microbiologist at the University of Alabama at Birmingham.
Scientists have worried that staph would gain resistance by swapping genes with other bacteria. Of the enterococci, less virulent bacteria that inhabit the intestines but seldom cause problems in healthy people, as many as one in four strains has proved resistant to vancomycin, report researchers at the University of Pennsylvania Medical Center in Philadelphia in the Feb. 19 Journal of the American Chemical Society.
Instead of swapping genes, S. aureus has apparently become resistant by mutating its own genes, Levy says. Exactly how S. aureus did so remains unknown.
Thus far, the story in Japan has a happy ending. Doctors gave the boy a combination of other drugs -- including some that aren't commercially available in the United States -- and he warded off the infection. Japanese officials are withholding details, awaiting publication of a report on the case in the July Journal of Antimicrobial Chemotherapy.
Loll, P., et al. 1997. Simultaneous recognition of a carboxylate-containing ligand and an intramolecular surrogate ligand in the crystal structure of an asymmetric vancomycin dimer. Journal of the American Chemical Society 119(Feb. 19):1516.
Seachrist, L. 1996. Infections making a deadly comeback. Science News 149(Jan. 20):38.
Smaglik, P. 1997. Proliferation of pills. Science News 151(May 17):310.
Gail Cassell
Department of Microbiology
University of Alabama–Birmingham
Birmingham, AL 35294-0113
Anthony Fauci
National Institute of Allergy and Infectious Disease
National Institutes of Health
Bethesda, MD 20892-2520
Stuart Levy
Center for Adaptations, Genetics and Drug Resistance
Tufts University School of Medicine
Boston, MA 02111