Antibiotics and Resistance

Vancomycin intermediate 5. aureus, first isolated in Japan in May 1996, then subsequently in the eastern United States (2,3), may be an example of transfer of exogenous genetic material. Transfer of vancomycin resistance from vancomycin-resistant enterococci (VRE) to S. aureus has been demonstrated in the laboratory (4,5). Because S. aureus is a leading cause of nosocomial pneumonia, 37.5% of which have become methicillin resistant (6), the threat of an increasing prevalence of VISA and the eventual appearance of vancomycin-resistant 5. aureus (VRSA) have sobering implications. Detection of VISA will ensure proper isolation to prevent nosocomial spread and initiate appropriate, albeit less than optimal, therapy. 

Of more clinical significance are the producers of ESBLs, which result 

Marcel Dekker, Inc. 270 Madison Avenue, New York, New York 10016 

The ability to detect ESBLs has clinical relevance because it will have an impact on antibiotic therapy. Producers of ESBLs are suspected when susceptibility testing indicates resistance to ceftazidime (but may be paradoxically susceptible to ceftriaxone and cefotaxime by the minimal inhibitory concentration [MIC] or disc diffusion) and susceptible to the cephamycins (11). More recently, a breakpoint of 2 ig/mL to cefpodoxime has been suggested as a standard. Another method of detection is the use of the E-test strip with a gradient of ceftazidime on one side and ceftazidime in combination with clavu-lanate on the other. The ESBLs are thought to be present when enhancement of inhibition is demonstrated. Table 2 highlights some of the more common resistance mechanisms for antimicrobial agents used commonly in the treatment of nosocomial pneumonia. 

---

Resistance may increase in biomembrane reactors due to the enrichment of antibiotics and resistant bacteria. 

---