Figure 2-4. Skin infection with the commensal bacteria. Overgrowth of the commensal bacterium Propionibacterium acnes can lead to formation of a comedo that is open but plugged with air-oxidized sebum (blackhead) or closed by sebum-glued skin cells (whitehead). Inflammation of the comedo leads to acne (pimples).
Although most mucosal surfaces are protected by normal resident microbiota (exceptions being the uterus and upper female genital tract and the urinary tract), the species composition of the microbiota found at different parts of the body varies from one site to another. Nonetheless, all have in common the predominance of Gram-positive resident bacteria. Shifts in these populations can be pathological, as is seen from diseases such as periodontal disease and bacterial vaginosis. The large intestine (colon) harbors an abundant and rich assortment of normal microbiota, the majority (97%) of which are anaerobes or facultative anaerobes. Many of these bacteria use carbohydrates and fats that are not digested by the stomach or absorbed by the small intestine. In return, some resident microbes provide a beneficial function to the host by synthesizing and secreting vitamins (e.g., vitamin K, vitamin B12, and other B vitamins) and other nutrients that the intestine can absorb. Recent experimental evidence indicates that indigenous bacteria play a crucial inducive role in gut and immune development during early postnatal life. They stimulate development of certain tissues, in particular the caecum and Peyer’s patches, the latter of which stimulate production of cross-reactive antibodies that prevent infection by related bacteria that may be pathogens (more on this later).
Members of the skin microbiota normally do not cause human infections unless they are introduced into the body by abrasions, catheters, or surgery. Staphylococcus epidermidis, a common skin bacterium, has been implicated in postsurgical and catheter-related infections. (S. epidermidis was the bacterial villain in the surgeon-transmitted infections described in Box 2-1.) Relatively nonpathogenic bacteria like S. epidermidis would normally be rapidly killed by the defenses of the bloodstream, but if they can reach an area that is somewhat protected from host defenses, such as the plastic surface of a heart valve implant, they can grow into surface-attached biofilms and produce quite serious infections. Catheters can provide skin-associated bacteria with a conduit into the bloodstream, thus bypassing the defenses of the epidermis and dermis. Catheter-associated infections have become a serious enough problem in hospitals that catheter companies are developing plastic catheters that are impregnated with antibacterial compounds.
Box 2-1.
Notable Breaches in Host Defenses that Changed the Course of U.S. History
Four presidents of the United States were assassinated during their presidencies: Abraham Lincoln (16th president: 1861–1865), James A. Garfield (20th president: 1881), William McKinley, Jr. (25th president: 1897–1901), and John F. Kennedy (35th president: 1961–1963). Kennedy died shortly after being shot, Lincoln died about nine hours afterward, and McKinley survived for about a week before dying, whereas Garfield lasted for 11 weeks before succumbing. Lincoln and Kennedy clearly died from complications due to the damage from the bullets’ impact. In contrast, Garfield and McKinley did not die from the impact of the bullets that hit them, but instead they succumbed to the subsequent infections resulting from the wounds. In both cases, the lethal infections were caused by bacteria introduced by the physicians trying to remove the bullets lodged in their bodies.
In Garfield’s case, one bullet grazed his shoulder and another hit his back, barely missing his spine before lodging in his pancreas, where doctors could not find it. Garfield was shot on July 2, 1881, and although his condition fluctuated with apparent signs of recovery alternating with fevers from infection, his illness worsened over the summer. Blood poisoning (sepsis) eventually took hold, and pus-filled abscesses formed all over his body. He finally died from uncontrolled septicemia (bacteria in bloodstream) and a ruptured splenic aneurysm on September 19, 1881. Most historians and medical experts are convinced that Garfield might have lived had the physicians of his time believed in aseptic technique while probing for the bullet, instead of using unwashed fingers and instruments.
Twenty years later, on September 14, 1901, McKinley died from gangrene resulting from bullet wounds received on September 6. Again, one bullet grazed McKinley while the other entered his abdomen and could not be found. Initially, he seemed to be on the mend, but his condition deteriorated rapidly on September 13 and he died early the next day. Although medical practices and precautions against infections were much improved by 1901, autopsy revealed that the bullet had penetrated the stomach, colon, kidney, and peritoneum along its way. These breaches to the normal epithelial barriers introduced the contents from the stomach and colon into the body’s tissues and the bloodstream, leading to the subsequent sepsis and death.
Sources:
Leech M. 1959. In the Days of McKinley. Harper and Brothers, New York, NY.
Peskin A. 1978. Garfield: A Biography. The Kent State University Press, Kent, OH.
Surgical wound infections and catheter-associated infections caused by skin bacteria, especially S. epidermidis, have become an ever more prevalent problem due to the fact that many of these skin bacteria are now resistant to most available antibiotics. How has this happened? It is clear that at least some antibiotics are exuded in sweat. Also, ointments containing antibiotics are widely used in the treatment of skin conditions such as acne and rosacea (unnaturally red skin) over the course of months or years. Thus, it is not surprising that skin bacteria like S. epidermidis have become increasingly resistant to a variety of antibiotics. Moreover, growth of bacteria in biofilms increases any antibiotic resistance that already exists. Bacteria-containing biofilms will be discussed in a later chapter.
Since transient colonization with pathogens can occur and since even normally harmless skin bacteria can cause infections under certain conditions, handwashing and disinfection of hands adds yet another barrier to infection, and reduces transmission to other people with whom one may come into contact. In the mid-1800s, Ignaz Semmelweis first introduced the concept of handwashing and cleanliness in maternity wards (see Box 2-2). The low-tech, but very effective, protective barrier provided by handwashing and the frequent changing of gloves has probably been a key contributing factor toward the good safety record of research scientists. However, despite strong and convincing experimental data and persistent promotion of good hygiene policies by health care officials, compliance of health care workers with the recommended hygiene practices is still low, with rates of compliance sometimes lower than 50%. An added source of concern is the strong correlation between life-threatening nosocomial infections and the wearing of long or artificial fingernails, despite scrubbing practices. For example, from 1997 to 1998 the death of 16 babies in the neonatal ICU at a hospital in Oklahoma City was linked to a particular strain of P. aeruginosa found under the nails of three nurses.
Box 2-2.
Handwashing Past and Present: A Lesson in Learning and Forgetting
The idea that physicians and nurses should wash their hands before treating a new patient is actually not a recent innovation. Ignaz Semmelweis, the man credited with making handwashing a standard part of medical practice, lived and practiced medicine in the mid-1800s. Although he was not the first physician to make the connection between contaminated hands and the spread of disease by physicians to their patients, he was the first to prove that proper disinfection of hands could dramatically reduce hospital-acquired infections.
Semmelweis had noted that two maternity wards in the Vienna Lying-in Hospital had very different mortality rates. In one, the death rate due to puerperal “childbed” fever (a common cause of death in women of the period) was over 10%, whereas in the second ward it was less than 3%. This fact was well known to women entering the hospital, who considered
