Environmental Contamination with Staphylococcus aureus and Outbreaks: The Cause or the Effect?

Abstract

Determining whether antibiotic-resistant nosocomial bacteria arise from a common source remains a constant problem for the hospital epidemiologist, particularly in view of the recent emergence of bacterial strains resistant to expanded-spectrum antibiotics such as ceftazidime, imipenam, and mupirocin. The article in this issue by Layton et all describes an outbreak of mupirocin-resistant Staphylococcus aureus thought to disseminate from an environmental source. The epidemiology of infections caused by S aureus was well described in studies completed during the 1950s and 1960s, when staphylococci were the predominant nosocomial pathogens. Outbreak strains often were identified through the use of phage typing and antibiograms and thus were discriminated from endemic colonizing isolates. A new phage type, or the sudden appearance of a new antibiotic-resistant strain, was sufficiently unusual to permit such discrimination. The source of staphylococcal strains causing nosocomial outbreaks was often the primary concern of the epidemiologists. Extensive analysis using casecontrol studies and surveillance cultures of patients, personnel, and environmental surfaces led investigators to conclude that environmental surfaces were not an important source of S aureus. One editor cautioned, Care should be taken to avoid the too facile assumptions that an article carrying staphylococci is necessarily implicated in staphylococcal cross infections.2 Outbreak strains actually were shown to spread from patient to patient by transient carriage of S aureus on the hands of hospital personnel.3 The sudden appearance of mupirocin-resistant S aureus among patient isolates from a dermatology ward prompted a surveillance study by Layton et al.1 Strains obtained from patients and environmental surfaces were compared using pulsed-field gel electrophoresis (PFGE). The method chosen to compare strains isolated in this epidemic has been shown by other investigators to accurately discriminate among staphylococcal clones.4-6 In the present study, a predominant clone of S aureus resistant to mupirocin was identified by finding a single PFGE pattern. Strains of the same clone also were found on a blood pressure cuff and a shower stall during a single sweep of environmental surfaces. No S aureus isolates were recovered from the hands of sampled personnel. These data contrast with the findings of previous studies. For example, Venezia et al, in a study of a similar S aureus outbreak, found the epidemic strain on the hands of one nurse but not on environmental surfaces.' What do we make of two studies that investigated a similar phenomenon in a similar patient population, yet implicated different sources for antibiotic-resistant S aureus? These studies may reflect accurately different circumstances. On the other hand, this apparent contradiction may exist because of insufficient surveillance. In the present study of mupirocin-resistant S aureus, the use of PFGE unequivocally established the similarity of the predominant patient strain to the environmental isolates. However, we cannot determine if the environment was the source of isolates subsequently colonizing patients or if person-to-person spread was the major route of dissemination, with the environment as an innocent bystander. A single sampling of the environment and a single sampling of personnel hands were performed.