to the first ward to be a virtual death sentence. Both wards were equally crowded, with three patients sharing each bed and the sick mixed indiscriminately with the well. Both wards contained women of similar socioeconomic status. The only difference between the two clinics was that the first clinic was used for teaching medical students, who also were dissecting cadavers in between delivering babies, and the second was used for teaching midwives, who were not exposed to potential disease-carrying cadavers.
Semmelweis deduced that the medical students were transmitting childbed fever (which we now know is caused most frequently by the bacterium Streptococcus pyogenes) to their patients because they failed to cleanse their hands properly. In 1846, he instituted a policy requiring that all midwives and medical students wash their hands with a chlorinated lime solution before examining patients. The mortality rate in both wards promptly dropped to 1% (red box in figure). Unfortunately, Semmelweis’ colleagues and detractors did not believe him and refused to follow his recommendations. His discovery remained controversial for many years, and it was only in the early 1900s that handwashing was universally accepted as an essential medical practice.
Today, proper disinfection of hands is one of the most basic and firmly entrenched of clinical procedures, especially for surgeons. Nonetheless, the advent of antibiotics and the consequent decrease in deaths due to hospital-acquired infections has led some surgeons to neglect this important practice. More recently, a surgeon in a large northeastern U.S. hospital, who started bypassing the rigorous surgical scrub procedure because he was troubled by dermatitis on his hands, provided a particularly dramatic example of this. The surgeon trusted the two pairs of surgical gloves, which were commonly worn during operations. But tiny holes in gloves can be made by contact with sharp objects or bone fragments. Also, the surgeon was using mineral oil to ease the irritation to his hands, and mineral oil undermines the integrity of surgical gloves. During the course of his duties, this physician managed to contaminate heart valve implants in a number of patients with Staphylococcus epidermidis before he was identified as the source of the outbreak.
S. epidermidis is commonly found as part of the resident microbiota of the skin, where it is not normally pathogenic, but it can cause infections if introduced into the body through wounds. Infections of heart valve implants usually cannot be treated effectively with a simple course of antibiotics, not only because of the high resistance level of S. epidermidis strains, but also because of the formation of bacterial biofilms that are more resistant than individual bacteria to antibiotics. Thus, the patients with the infected valves had to endure a second operation to remove and replace the infected valves, not to mention additional damage to the heart due to the infection.
As is evident from the date on the reference cited at the end of this box, this case occurred in the 1980s. Does this mean that such cases have ceased to occur? Not at all! This case was used because it is a classic example of the handwashing problem, but there have been many other cases since. The difference between the 1980s and the 21st century is that the surgeon in this case would probably have been identified today before he infected so many people because infectious disease surveillance systems in hospitals have improved dramatically. But the attitude and behavior that sparked this episode do still sometimes occur in hospitals.
The silver lining in this particularly black cloud is that accountants for health insurance agencies have figured out how much the lack of handwashing and improper use of gloves are costing them, and they are mounting increasingly vigorous campaigns in favor of handwashing and against health care workers who ignore these simple but effective precautions. In fact, relatives of hospital patients are being urged to question unhygienic practices they witness. The lawyers are circling. Together these trends will continue to increase the safety of hospitals.
Sources:
Semmelweis I. 1983. Etiology, Concept and Prophylaxis of Childbed Fever. Series: History of Science and Medicine (Book 2). (Codell Carter K, translator.) University of Wisconsin Press, Madison, WI.
Carter KC, Carter B. 2005. Childbed Fever: A Scientific Biography of Ignaz Semmelweis. Transaction Publishers, Piscataway, NJ.
Boyce JM, Potter-Bynoe G, Opal SM, Dziobek L, Medeiros AA. 1990. A common-source outbreak of Staphylococcus epidermidis infections among patients undergoing cardiac surgery. J Infect Dis 161:493–499 .[PubMed][CrossRef]
To make matters worse, an alarming number of recent infectious outbreaks have been attributed to hospital-acquired pathogens (such as Klebsiella pneumoniae, Pseudomonas aeruginosa, Candida albicans, methicillin-resistant Staphylococcus aureus (MRSA), and Serratia marcescens) that also are resistant to multiple antibiotics. We will cover this serious problem in much more detail in chapters 15 and 16, when we discuss the topics of antimicrobial compounds and how bacteria become resistant to antibiotics.
Defenses of the Skin
Bacteria are unable to penetrate intact skin unaided. That is why skin infections are usually associated with breaches of skin caused by wounds, burns, or insect bites (Table 2-4). See Box 2-1 for a few examples of infections that changed the course of history due to the dire consequences of breaches in barrier defenses resulting from wounds.
Table 2-4. Some consequences of breaching barrier defenses
Why is intact skin such an effective barrier to bacterial invasion? A number of characteristics combine to make skin inhospitable to bacterial growth, as well as difficult to penetrate (Figure 2-1). The epidermis consists of stratified squamous cells, most of which are keratinocytes. Keratinocytes produce the protein keratin, which is not readily degraded by most microorganisms. As cells from the dermis are pushed outward into the epidermal region, they produce copious amounts of keratin and then die. This layer of dead keratinized cells forms the surface of skin. The dead cells of the epidermis are continuously shed (desquamation). Thus, any bacteria that manage to bind to epidermal cells are constantly being removed from the body.
Skin is dry and slightly acidic (pH ∼5), two features that inhibit the growth of many pathogenic bacteria, which prefer a wet, neutral (pH ∼7) environment. Also, the temperature of skin (34 to 35°C) is lower than that of the body interior (37°C). Accordingly, bacteria that succeed in colonizing skin must be able to adapt to the very different internal environment of the body if they manage to reach underlying tissue. Interestingly, the causative agent of leprosy, Mycobacterium leprae, has an optimal growth temperature of 35°C, which may account for its predilection for the skin and mucosa of the upper respiratory tract.
Hair follicles, sebaceous (fat) glands, and sweat glands are composed of simple epithelial cells and offer sites for potential breaches in the skin that could be used by some bacteria to move past the skin surface. These sites are normally protected by peptidoglycan-degrading lysozyme (Figure 2-5) and by lipids that are toxic to many bacteria. However, some pathogenic bacteria are capable of infecting hair follicles or sweat glands, which is why skin infections such as boils (furuncles) and acne (pustules) are commonly centered at hair follicles.
Figure
