Antibiotic Resistant Infections : Part 3

by Food and Drug Administration (FDA)

(Page 3 of 3)

Targeting TB

Stephen Weis and colleagues at the University of North Texas Health Science Center in Fort Worth reported in the April 28, 1994, New England Journal of Medicine on research they conducted in Tarrant County, Texas, that vividly illustrates how helping patients to take the full course of their medication can actually lower resistance rates. The subject — tuberculosis.

TB is an infection that has experienced spectacular ups and downs. Drugs were developed to treat it, complacency set in that it was beaten, and the disease resurged because patients stopped their medication too soon and infected others. Today, one in seven new TB cases is resistant to the two drugs most commonly used to treat it (isoniazid and rifampin), and 5 percent of these patients die.

In the Texas study, 407 patients from 1980 to 1986 were allowed to take their medication on their own. From 1986 until the end of 1992, 581 patients were closely followed, with nurses observing them take their pills. By the end of the study, the relapse rate — which reflects antibiotic resistance — fell from 20.9 to 5.5 percent. This trend is especially significant, the researchers note, because it occurred as risk factors for spreading TB — including AIDS, intravenous drug use, and homelessness — were increasing. The conclusion: Resistance can be slowed if patients take medications correctly.

Narrowing the Spectrum

Appropriate prescribing also means that physicians use "narrow spectrum" antibiotics — those that target only a few bacterial types — whenever possible, so that resistances can be restricted. The only national survey of antibiotic prescribing practices of office physicians, conducted by the National Center for Health Statistics, finds that the number of prescriptions has not risen appreciably from 1980 to 1992, but there has been a shift to using costlier, broader spectrum agents. This prescribing trend heightens the resistance problem, write McCaig and Hughes, because more diverse bacteria are being exposed to antibiotics.

One way FDA can help physicians choose narrower spectrum antibiotics is to ensure that labeling keeps up with evolving bacterial resistances. Blum hopes that the surveillance information on emerging antibiotic resistances from CDC will enable FDA to require that product labels be updated with the most current surveillance information.

Many of us have come to take antibiotics for granted. A child develops strep throat or an ear infection, and soon a bottle of "pink medicine" makes everything better. An adult suffers a sinus headache, and antibiotic pills quickly control it. But infections can and do still kill. Because of a complex combination of factors, serious infections may be on the rise. While awaiting the next "wonder drug," we must appreciate, and use correctly, the ones that we already have.

Big Difference

If this bacterium could be shown four times bigger, it would be the right relative size to the virus beneath it. (Both are microscopic and are shown many times larger than life.)

Although bacteria are single-celled organisms, viruses are far simpler, consisting of one type of biochemical (a nucleic acid, such as DNA or RNA) wrapped in another (protein). Most biologists do not consider viruses to be living things, but instead, infectious particles. Antibiotic drugs attack bacteria, not viruses.

The Greatest Fear — Vancomycin Resistance

When microbes began resisting penicillin, medical researchers fought back with chemical cousins, such as methicillin and oxacillin. By 1953, the antibiotic armamentarium included chloramphenicol, neomycin, terramycin, tetracycline, and cephalosporins. But today, researchers fear that we may be nearing an end to the seemingly endless flow of antimicrobial drugs.

At the center of current concern is the antibiotic vancomycin, which for many infections is literally the drug of "last resort," says Michael Blum, M.D., medical officer in FDA's division of anti-infective drug products. Some hospital-acquired staph infections are resistant to all antibiotics except vancomycin.

Now vancomycin resistance has turned up in another common hospital bug, enterococcus. And since bacteria swap resistance genes like teenagers swap T-shirts, it is only a matter of time, many microbiologists believe, until vancomycin-resistant staph infections appear. "Staph aureus may pick up vancomycin resistance from enterococci, which are found in the normal human gut," says Madden. And the speed with which vancomycin resistance has spread through enterococci has prompted researchers to use the word "crisis" when discussing the possibility of vancomycin-resistant staph.

Vancomycin-resistant enterococci were first reported in England and France in 1987, and appeared in one New York City hospital in 1989. By 1991, 38 hospitals in the United States reported the bug. By 1993, 14 percent of patients with enterococcus in intensive-care units in some hospitals had vancomycin-resistant strains, a 20-fold increase from 1987. A frightening report came in 1992, when a British researcher observed a transfer of a vancomycin-resistant gene from enterococcus to Staph aureus in the laboratory. Alarmed, the researcher immediately destroyed the bacteria.

About the Author

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FDA is A United States government body that oversees medical devices, including contact lenses, intraocular lenses, excimer lasers and eyedrops. In the US, these products must be approved by the FDA before they can be marketed.