The two recognized species of staphylococci are S. aureus and S. epidermidis. Staphylococci are called coagulase positive when they are capable of clotting plasma and coagulase negative when the plasma clumps them. Coagulase-positive staphylococci are more virulent or pathogenic than coagulase-negative staphylococci. S. aureus is hemolytic, parasitic, pathogenic, and coagulase positive. S. epidermidis is parasitic, less pathogenic, and coagulase negative. S. aureus is a long-recognized cause of surgical site infections. More recently, S. epidermidis has been implicated in infections of prosthetic devices and indwelling medical devices (CDC, 2008a; Geipl 2009; Widerstrom et al, 2012). The skin surface is the most common site of S. epidermidis. Approximately 30% to 70% of individuals carry staphylococci on their skin. This can lead to contamination of clothing and dispersal of the microorganisms. For no known reason individuals who are skin carriers of staphylococci differ in the rate at which they shed the microorganisms. There is no obvious difference in hygiene and skin condition between light and heavy shedders, and no other contributing factor is apparent. Heavy shedders seem to be in normal good health.

S. aureus infections in hospitals can lead to prolonged hospital stays and may result in death. S. aureus is a medically important human pathogen that is found in the nares of approximately one third of the population (Pynnonen et al, 2011). Human nasal and throat cavities are the most important reservoirs that continually replenish the external environment. Among perioperative personnel, S. aureus has been found most commonly in the respiratory passages. The potential for patient infection increases greatly as the personnel carrier rate increases. Nasal carriers also may be skin carriers. Carriers usually harbor either coagulase-positive (pathogenic) or coagulase-negative (nonpathogenic) staphylococci; seldom are there both types, and rarely more than one strain is identified. Because an individual may be a carrier of staphylococci one day and a noncarrier the next, frequent swab testing of the nose as an infection control measure is impractical. Staphylococci survive for long periods in the air, dust, debris, bedding, and clothing. Pathogenic staphylococci grow in the sweat, urine, and tissue and on the human skin. They are more difficult to destroy than many other non–spore-forming organisms. Cleanliness of the environment; proper handling, and, when appropriate, sterilization of linens and equipment; and adherence to adequate hand hygiene practices are important controls to prevent transmission of infection (AORN, 2013a).

Enterococci are gram-positive organisms that are found in the normal flora of the gastrointestinal and female genital tracts. These organisms are responsible for many serious healthcare-associated infections, including surgical site infections, bacterial endocarditis, septicemia, and urinary tract infections (UTIs). Enterococci also have been implicated in polymicrobial wound infections (CDC, 2007a; Scheithauer et al, 2012). Enterococcal infections are most often healthcare associated and seen in patients with comorbid conditions.

Group A streptococci account for most streptococcal infections in humans. Known as the flesh-eating bacteria because of their ability to cause necrotizing fasciitis, group A streptococci are of concern because of the sporadic and deadly outbreaks of community-acquired and healthcare-associated infection (CDC, 2006a; Ramirez et al, 2011). An example is Streptococcus pyogenes, which is responsible for most soft tissue infections, otitis media, pharyngitis, impetigo, septicemia, and surgical site infections. Virulent streptococci are more serious invaders than staphylococci. Streptococci tend to involve wide areas of tissue and cause necrosis without localization. Streptococci are usually sensitive to penicillin, whereas staphylococci may not be. Streptococci also occur in mixed infections with other pathogens.

In surgical wounds, streptococci can be introduced into the incision and spread via the lymph vessels and nodes. This distribution can result in inflammation and cellulitis. Streptococcal transmission occurs by droplet transmission and by contamination of the environment. Inhalation of infectious droplets expelled from the nose and mouth of an infected individual is considered direct contact. Indirect contact occurs when infected air and dust from the environment enter a susceptible host. Group A streptococcus can be carried in the nasal passages, anus, or vagina. The upper respiratory tract is not a significant reservoir for microorganisms that cause surgical site infections except in the presence of an acute upper respiratory tract infection. In several randomized controlled studies, it was found that surgical wound infection rates are unaffected by the use or nonuse of surgical masks by noninfected individuals during the operative procedure. It is not always possible to know who might be infected, and the use of masks during operative procedures continues to be strongly recommended in the prevention of SSIs. Most bacteria in the operating room (OR) environment are shed from the skin of perioperative personnel (AORN, 2013b).

The clostridia bacteria are spore-forming, anaerobic, gram-positive bacilli that produce virulent toxins. Clostridium difficile is a bacterium in the Clostridium genus, which also includes C. perfringens (gas gangrene), C. tetani (tetanus), and C. botulinum (botulism). C. difficile is an anaerobic, gram-positive, spore-forming bacillus. C. difficile is an overgrowth in the colon that can manifest symptoms of diarrhea, colitis, toxic megacolon, dehydration, colonic perforation, and death. The overgrowth of C. difficile in the colon usually results from alterations in the normal flora of the colon that are associated with the use of antibiotics (CDC, 2006a; Gould et al, 2008). For this organism to cause disease, C. difficile must already be in the GI system. Subsequently, there must be a change in the normal flora of the colon to allow the organism to grow and produce toxins. The two toxins produced are toxin A, which is an enterotoxin causing excretion of large amounts of fluid from the bowel, and toxin B, which is cytotoxic. Toxin B attacks and disintegrates cells of the intestines. Additionally, C. difficile produces tissue-degrading enzymes, which produce an inflammatory response within the colon that can result in a spectrum of disease entities.

In its spore form, C. difficile can withstand drying and heat and may be resistant to many disinfectants. The spores can survive up to 5 months in the environment. C. difficile can be transmitted between individuals and by touching objects contaminated with the organism. In the healthcare environment, C. difficile has been cultured in rooms of infected individuals 40 days after discharge. C. difficile also has been cultured from healthcare workers’ shoes, fingernails, fingertips, and the underside of rings (Mitchum, 2009).

Several interventions can assist in the prevention of C. difficile transmission in the healthcare environment, including following Contact Precautions, handwashing with antimicrobial soap and water, using personal protective equipment (PPE), cleaning and disinfecting all surfaces and equipment, and cleaning and disinfecting reusable devices in the perioperative suite. The use of disposable equipment only is recommended for infected patients (CDC, 2010a). Additionally, clinical practice guidelines from the Society for Healthcare Epidemiology of America (SHEA) and the Infectious Diseases Society of America (IDSA) recommend that in a setting in which there is an outbreak or an increased rate of C. difficile infection to instruct visitors and healthcare workers caring for patients who are infected with C. difficile to wash their hands with soap, or antimicrobial soap and water. Further, they recommend that the frequency and duration of antimicrobial therapy be minimized and to implement an antimicrobial stewardship program (Cohen et al, 2010).

M. tuberculosis is a non–spore-forming, nonmotile, aerobic bacillus. These bacilli can infect almost any tissue—skin, bones, kidney, lymph nodes, intestinal tract, and fallopian tubes—and cause tuberculosis (TB). Tubercle bacilli spread in the host through the lymphatic channels and bloodstream and by way of the alveoli and GI tract. Tuberculosis is responsible for more than 3 million deaths a year and is the most opportunistic infection associated with human immunodeficiency virus (HIV) (Neil, 2008).

Tubercle bacilli are transmitted directly by means of discharge from the respiratory tract (e.g., by inhalation of droplets expelled during coughing or kissing) and, less frequently, through the digestive tract. M. tuberculosis is carried via airborne droplet nuclei when infected people sneeze, cough, or speak. These nuclei particles are less than 5 micrometers in size and contain up to three bacteria, allowing them to be kept airborne for a prolonged period (CDC, 2006a). Infection occurs when individuals inhale these infected droplet nuclei. The droplet nuclei travel through the nasal passages, upper respiratory tract, and bronchi to reach the lung alveoli, where they are engulfed by macrophages and spread throughout the body. Symptoms of TB are dependent on the part of the body infected, but may be vague at the onset and include fever, fatigue, loss of appetite, cough, fever, and night sweats.

Generally 2 to 10 weeks after initial infection, an immune response limits additional multiplication and spread of the bacilli. Some of the bacilli can remain dormant for many years, however, a condition referred to as latent tuberculosis infection. Individuals with latent TB usually have positive purified protein derivative (PPD) results, but they exhibit none of the symptoms of active TB and are considered noninfectious. The probability that a person who is exposed to M. tuberculosis will become infected depends on the concentration of infectious droplet nuclei and the duration of exposure. When infected, an individual has approximately a 10% risk of developing active TB in his or her lifetime. The risk is greatest during the first 2 years after initial exposure. In individuals with compromised immune systems, there is a higher risk that latent TB will progress into active TB (CDC, 2006a). Latent TB is treated with isoniazid or rifampin. Active TB is treated with a combination of medications (e.g., isoniazid, rifampin, ethambutol, pyrazinamide) (Neil, 2008).

The first antibiotics, sulfonamides, were introduced in 1935 to treat staphylococcal and streptococcal infections. Penicillin was introduced in the 1940s during World War II, followed by the discovery of streptomycin in the mid- to late 1940s. Although the introduction of these medications was viewed as miraculous and did save many lives, in the mid-1940s strains of previously susceptible microorganisms began showing resistance to some of these medications. During the 1960s, cephalosporin and semisynthetic penicillins were developed, and it was believed that the problem of healthcare-associated infections was solved. Many gram-negative bacteria were found to be susceptible to these new drugs. By the late 1970s, however, strains of S. aureus resistant to penicillin, methicillin, cephalosporins, aminoglycosides, clindamycin, erythromycin, and other antibiotics were isolated in hospital outbreaks of infection. This situation led to the development of new antibiotics, including carbapenems, cephamycins, and fluoroquinolones. These broad-spectrum antimicrobials were bactericidal at low concentrations and led to a false sense of euphoria during the 1980s, when it was believed that, at last, resistance to these antimicrobials would be impossible (Sandlin, 2008).

In the 1990s it became evident that the potential for resistance to any and all antimicrobials existed as healthcare-associated outbreaks of multidrug-resistant tuberculosis (MDR-TB) occurred. Significant outbreaks of methicillin-resistant Staphylococcus aureus (MRSA) (Surgical Pharmacology) and vancomycin-resistant Enterococcus (VRE) also occurred in the 1990s. More recently Klebsiella, a gram-negative bacteria associated with surgical site infection, has shown resistance to the carbapenems (CDC, 2010b). In some cases, organisms seemed to acquire resistance almost immediately on exposure to the particular antibiotic. As fewer new antimicrobial drugs are being developed by the pharmaceutical industry, many consider the 1990s to be the beginning of the postantibiotic era (Sandlin, 2008) (see Surgical Pharmacology).

Similar to their unwilling human hosts, pathogenic bacteria have an instinct to survive. When faced with an antimicrobial attack, they assemble their defensive resources. These microorganisms have the remarkable capability to incapacitate the threatening antibiotic and to mutate and outwit the most lethal clinical weapons. Although carrying only a single chromosome, bacteria by nature have extra minichromosomes called plasmids. These plasmids are hearty, and some may survive even the most aggressive antibiotic attack. Surviving plasmids are resistant and reproduce in kind, creating dominant organisms within the host. In addition, incompletely or ineffectively treated infections create the potential for reinfection with resistant organisms (CDC, 2006a).

Microbial resistance can be divided into three categories: (1) presence of a naturally resistant strain of an organism before any drugs are administered, (2) acquisition of a drug-resistant strain from an external source, and (3) drug resistance from treatment-related causes. Occurrence of naturally resistant strains of organisms without any exposure to drugs can occur by intrinsic resistance, genetic mutation, or transfer of genetic material. Some microorganisms possess genes that make them resistant to an antibiotic. These genes may always be present in the microorganism but remain in an inactive stage until challenged by an antibiotic. Genetic mutation can occur spontaneously in the course of rapid multiplication of the microbe. These antibiotic-resistant mutants reproduce within the host. New genetic material also can be transferred into bacteria by means of free DNA that contains resistant genes (CDC, 2006a).

Introduction of drug-resistant microorganisms can occur through a person or an inanimate object. Bacteria become mobile and accessible to humans on the hands or clothing of care providers, through instruments and procedures, or through food. Resistant microorganisms may travel from distant parts of the world by means of infected travelers. Surgical instruments that have been ineffectively cleaned and processed can contribute to the spread of resistant organisms. Use of antibiotics in agriculture and in animal feed products also has contributed to the development of resistant organisms. When the food is ingested, resistant genes may be spread to humans (CDC, 2006a).

Drug resistance from treatment-related causes is often the result of misuse (e.g., incorrect use, overuse, or underuse) of antibiotics. It is believed that 50% of all antibiotic use in the United States can be characterized by misuse in one form or another, and efforts to reduce surgical site infections include appropriate prophylactic antibiotic use in surgical patients (Evidence for Practice). It is estimated that half of all antibiotic prescriptions written are not warranted. During antibiotic therapy, the patient may have had a few resistant organisms. By natural selection, as the susceptible organisms are killed, the resistant organisms multiply and become predominant. Inadequate drug therapy may contribute to the phenomenon and may be the fault of the patient, the provider, or both. Failure to perform sensitivity testing along with inappropriate dosing can contribute to resistance. If the patient is noncompliant with the prescribed regimen or discontinues the drug prematurely, he or she may also be contributing to drug resistance (CDC, 2012a).

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