The epidemiology of contact transmission: beyond Semmelweis.

In his article on the transmission of nosocomial infections, published in the Proceedings of the Third Decennial International Conference on Nosocomial Infections, sponsored by the Centers for Disease Control and Prevention (CDC) in 1991, Robert Weinstein placed hospital personnel in the center of the maelstrom of nosocomial transmission (Figure).1 He estimated that hospital personnel were responsible for approximately 20% to 40% of the nosocomial spread of pathogens from patient to patient through contact transmission. The conventional wisdom is that, during direct contact, the hands of personnel pick up exogenous organisms that are then deposited onto medical devices or wounds to cause infection. This mechanism of spread of infection is precisely what Semmelweis hypothesized when he observed the spread of puerperal sepsis. Since the Fourth Decennial Conference on Nosocomial Infections will be held shortly in Atlanta, Georgia, it is fair to ask whether we have learned anything new about contact transmission since the last decennial conference. How far beyond Semmelweis have we gone? Semmelweis correctly postulated that the hands carried a potentially deadly agent, but he did not know that it was a microbiological agent. We now know that our hands are an ecosystem comprised of permanent or resident flora and transient flora.2,3 The permanent florae consist of proprionibacteria, corynebacteria, micrococci and other staphylococcal species, including Staphylococcus epidermidis, Staphylococcus hominis, Staphylococcus capitis, all residing in stratum corneal layer, feeding on lipids and cellular debris. Permanent florae are viewed as “good” florae, as they rarely lead to disease; and, by their production of lipids and bacteriocins, permanent florae act to resist colonization by other microorganisms that potentially are more pathogenic. Transient florae do not normally reside on the skin, but are picked up during direct contact with patients or contaminated fomites. Unless they are eradicated through hand washing, they can be passed on or shed onto wounds, where, because of their pathogenic potential, they can lead to infection. What do we know about the epidemiology of hand contamination, since this is the critical first step in the process of cross-infection? Are certain patient-care activities more prone to result in hand contamination? Is there a critical inoculum that is more likely to lead to infection versus colonization? During the 1970s, the Fulkerson scale was developed and used to rank nursing activities according to their potential for hand contamination.4 Activities, ranked from 1 to 7, ranged from contact with cleaned or washed materials down to contact with objects in contact with patient secretions. These were considered “clean” activities. “Dirty” activities included contact with uninfected patient secretions, infected secretions or excretions, materials contaminated with secretions or excretions, or the infected sites themselves. The purpose of the Fulkerson scale was to identify nursing activities that require hand washing. The presumption was that dirtier activities led to higher rates of cross-infection, but this has never been shown. Recently, Pittet and coworkers published studies that add to and further refine our knowledge of hand contamination.5,6 Pittet and coworkers reconfirmed that the type of patient contact activity was important in determining the degree of hand contamination. In their study, respiratory care qualitatively resulted in a greater degree of hand contamination than handling of body fluid secretions (uninfected), which in turn posed a greater risk of contamination than skin contact. They also were able to demonstrate