Enterobacter cloacae: Bacteremia, Epidemiology, and Antibiotic Resistance

Abstract

From the clinical viewpoint, Enterobacter cloacae and Enterobacter aerogenes are the two most important species of the genus Enterobacter. E. cloacae lacks lysine and arginine decarboxylases, whereas E. aerogenes has these enzymes. Enterobacter currently accounts for 40%–12% of all cases of gram-negative bacteremia although it is not a cause of bacteremia at some hospitals. This study showed that E. cloacae has been endemic at a medical center hospital for at least five years and caused 4.5% of all cases of bacteremia in 1978. In May 1977 and July 1979 outbreaks of bacteremia due to E. cloacae occurred in the burn ward of the hospital. Most infected patients had multiple sites (urine, wound, and sputum) colonized before bacteremia occurred. No environmental or personnel sources of E. cloacae in the burn ward were discovered. Isolates of E. cloacae from the second outbreak were resistant to tobramycin, amikacin, and silver nitrate. The plasmid content of these strains differed from those of the first outbreak. For a five-year period, most strains of E. cloacae were resistant to cephalothin and ampicillin; however, resistance to aminoglycosides was rare. A literature review disclosed that E. cloacae has become prominent in burn units, but that it also has caused serious infections in nonburned patients. E. cloacae tends to contaminate various medicinal, iv, and other hospital products. Therefore, bacteremia due to E. cloacae, should prompt an investigation of exposures to potentially contaminated materials, especially those introduced into the bloodstream. Therapy of E. cloacae infections remains problematic and is complicated by the emergence of multiresistant strains. Aminoglycosides are the most active agents against E. cloacae, but new agents such as cefotaxime, cefaperazone, moxalactam, and thienamycin are active and eventually may be valuable in single-drug therapy of infection due to E. cloacae.