O’Brien TF. The global epidemic nature of antimicrobial resistance and the need to monitor and manage it locally. Clin Infect Dis 1997; 24(suppl 1):S2-S8.

Infection control measures such as hand washing and barrier precautions have long been known to protect patients from infection, but they may also work on a genetic level to hamper the proliferation of antibiotic-resistant bacteria, the author reports. Infection control practices "physically interrupt" bacterial populations and delay or prevent the dissemination of genes that allow antibiotic resistance, he observes in this overview article.

"Although these practices were initially intended to prevent infection, they also tend to disconnect networks of bacterial populations between patients and between patients and care givers, thus impeding the delivery of resistance genes to whatever bacteria are still causing infections," he reports.

The importance of host-to-host transmission of resistant strains makes infection control skills central to the management of resistance. These skills may be strengthened by establishing, targeting, and providing quality assurance for infection control procedures. In addition, skilled clinical use of antimicrobials is essential in retarding the spread of resistance and in treating patients infected with resistant bacteria.

An antimicrobial agent may be used for years before a gene expressing resistance to it emerges in a strain of bacteria somewhere. Progeny of that strain, or of others to which the gene is transferred, may then disseminate through global networks of bacterial populations on people or animals. Thus, the chances are low that a resistant gene in an isolate from a patient actually emerged in the bacterial populations of that patient.

"It is more likely to have emerged in the antimicrobial-treated bacterial populations of some other host, perhaps on another continent years earlier, and to have been conveyed ultimately to the patient through networks of such populations," the author concludes. "Retarding dissemination of emerged genes thus appears to be the major way to reduce rates of resistance."

Hoiby N, Jarlov JO, Kemp, M, et al. Excretion of ciprofloxacin in sweat and multiresistant Staphylococcus epidermidis. Lancet 1997; 349:167-169.

The rapid development of resistance to ciprofloxacin due to excretion of the drug into the sweat glands might be involved in the development of multiresistant Staphylococcus epidermidis and possibly other skin bacteria in hospitals, the authors report.

They assessed whether S. epidermidis isolated from the axilla and nasal flora of healthy people could develop resistance to ciprofloxacin after a one-week course of ciprofloxacin.

The concentration of ciprofloxacin in sweat was measured in seven volunteers after oral administration of 750 mg ciprofloxacin twice daily for a week, and the development of resistance in S. epidermidis from axilla and nostrils was monitored for two months after the treatment. Genotyping of S. epidermidis was done by restriction fragment length polymorphism.

The results show that the sensitive S. epidermidis strains present in all individuals investigated were replaced surprisingly rapidly in the axilla by intermediate-resistant and highly resistant strains. The resistant strains appeared much slower in the nostrils, probably because of secondary colonization with the resistant strains from the axilla. The axilla rather than the nostrils, therefore, seem to be the preferable area for early detection of resistant S. epidermidis in the skin.

"In view of the resistance problems in staphylococci and other permanent or transient bacteria of the skin flora which cause infections in human beings, it is surprising that little attention has been given to excretion of antibiotics in sweat," the authors conclude. ". . . Our findings suggest that excretion of antibiotics in sweat might explain the development of resistance by S. epidermidis in the human skin, which are among the most important causes of nosocomial and foreign-body-related infections. A question remains about whether any of the other currently used groups of antibiotics are excreted in sweat."

VandenBergh M, Kluytmans J, van Hout B, et al. Cost-effectiveness of perioperative mupirocin nasal ointment in cardiothoracic surgery. Infect Control Hosp Epidemiol 1996; 17:786-792.

Surgical site infections (SSIs) in patients undergoing cardiothoracic surgery are associated with a substantial increase in postoperative costs. Provided that perioperative mupirocin reduces the SSI rate, the measure will be highly cost-effective in most centers providing cardiothoracic surgical services, the authors conclude.

The effectiveness of mupirocin has not been established definitively and awaits the results of a double-blind, placebo-controlled, randomized trial, they noted. However, even with an effectiveness of only 1%, their sensitivity analysis revealed that perioperative administration of nasal mupirocin would be a cost-effective measure.

They studied perioperative nasal application of mupirocin calcium ointment started on the day before surgery, then continued for five days at twice-daily doses. Postoperative costs increased significantly in patients with an SSI, with mean SSI-attributable costs estimated at $16,878. The incidence of SSIs was 7.3% in a control group and 2.8% in an intervention group, with mupirocin effectiveness calculated at 62%. The costs of mupirocin were $11 per patient. Thus, the savings per SSI prevented were $1,633.

"Therefore, provided that perioperative mupirocin reduces the SSI rate, we conclude that this measure will be highly cost-effective in most groups of patients undergoing cardiothoracic surgery," they conclude. "Restricting perioperative use of nasal mupirocin to nasal carriers of Staphylococcus aureus has negligible effect on the cost-effectiveness and therefore may be the best prophylactic strategy that will be both cost-effective and will prevent the emergence of mupirocin resistance among S. aureus."