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Chapter 27 Wound Infections

Infected Wound With Pus And Stitches

Figure 27.3 Surgical Wound Infection Due to Staphylococcus aureus

The stitches pull through the infected tissue, causing the wound to open.

Figure 27.3 Surgical Wound Infection Due to Staphylococcus aureus

The stitches pull through the infected tissue, causing the wound to open.

redness, and pain. If the infected area is extensive or if the infection has spread to the general circulation, fever is a prominent symptom. Wound infections by some strains produce the toxic shock syndrome, with high fever, muscle aches, and life-threatening shock, sometimes accompanied by a rash and diarrhea. ■ toxic shock syndrome, p. 641

Causative Agents

Staphylococci are Gram-positive cocci that arrange themselves in clusters (figure 27.4). They grow readily aerobically or anaer-obically and are salt tolerant, probably because they evolved on

Staph Infection Stitches

10 mm

Figure 27.4 Staphylococcus aureus in Pus The dark-colored dots are staphylococci; the red objects, leukocytes.

10 mm

Figure 27.4 Staphylococcus aureus in Pus The dark-colored dots are staphylococci; the red objects, leukocytes.

the skin where evaporation concentrates the salt in sweat. The most important species are S. aureus and S. epidermidis. Both species survive well in the environment, making it easy for them to transfer from one person to another.

Staphylococcus aureus One of the most useful identifying characteristics of S. aureus is that it produces coagulase. Despite its -ase ending, coagulase is not an enzyme. This protein product of S. aureus is largely extracellular, meaning it is released from the bacterium. It reacts with a substance in blood called prothrombin. The resulting complex, called staphylothrombin, causes blood to clot by converting fibrinogen to fibrin. Conclusive evidence is lacking that coagulase is a virulence factor for S. aureus. Some coagulase is tightly bound to the surface of the bacteria, however, and coats their surface with fibrin upon contact with blood. Fibrin-coated staphylococci resist phagocytosis.

Generally, S. aureus also possesses clumping factor, often called "slide coagulase," because it causes a suspension of the bacteria to clump together when mixed with a drop of blood plasma on a microscope slide. The clumping is caused by a cell-fixed protein that attaches specifically to fibrinogen in the plasma. Clumping factor protein is a virulence factor for S. aureus because it attaches to fibrinogen and fibrin present in wounds, thus aiding colonization of wound surfaces. Plastic devices, such as intravenous catheters and heart valves, become coated with fibrinogen shortly after insertion, thus making them, too, a target for colonization. The gene for clumping factor is distinct from the one controlling coagulase.

Other virulence factors possessed by S. aureus that aid colonization of wounds include binding proteins for fibronectin, fibrin, fibrinogen, and collagen. Protein A, another component of the bacterial surface, also aids virulence. It binds IgG by the Fc portion of the immunoglobulin molecule. Thus, not only does protein A compete with the Fc receptors of phagocytes for antibody molecules, it also coats staphylococci with host protein and therefore hides them from phagocytes and the cells responsible for immunity. Most strains of S. aureus also produce a-toxin, which kills cells by attaching to specific receptors on host cell membranes and making holes in them. A relatively small percentage of S. aureus strains produce one or more additional toxins. ■ IgG, p. 400 ■ Fc region, p. 398

Table 27.1 summarizes properties of S. aureus that contribute to its virulence. The bacterium also produces a variety of extracellular enzymes that probably do not contribute directly to virulence but supply it with nutrients by degrading blood cells and components of damaged tissue. ■ Staphylococcus aureus, p. 537

Staphylococcus epidermidis Most strains of S. epidermidis have little or no invasive ability for normal people. They commonly cause small abscesses of little consequence around the stitches used in surgery. Most strains bind fibronectin, however, and can therefore colonize the plastic intravenous catheters, heart valves, and other devices employed in modern medicine. Following adherence, the bacteria may produce a kind of slime or glycocalyx that cements the growing colony to the plastic in a biofilm, protecting it from attack by phagocytes and other host defense mechanisms, and antibacterial medications. ■ glycocalyx, p. 63 ■ biofilm, p. 104

27.2 Common Bacterial Wound Infections

Table 27.1 Properties of Staphylococcus aureus Implicated in Its Virulence

Virulence Factor

Action Site

Action

Clumping factor

Bacterial surface

Attaches bacterium to fibrin, fibrinogen, plastic devices

Fibronectin-binding protein

Bacterial surface

Attaches bacterium to acellular tissue substance, endothelium, epithelium, clots, indwelling plastic devices

Protein A

Bacterial surface, extracellular

Competes with Fc receptors of phagocytes; coats bacterium with host's immunoglobulin

a-toxin

Extracellular

Makes holes in host cell membranes

Leukocidin

Extracellular

Kills neutrophils or causes them to release their enzymes

Enterotoxins

Extracellular

Superantigens. If systemic, cause toxic shock; cause food poisoning if ingested

Toxic shock syndrome toxin-1

Extracellular

A superantigen. If systemic, causes toxic shock

Pathogenesis

Staphylococcus aureus Many years ago, it was shown that it takes more than 100,000 staphylococci injected into the skin to produce a small abscess. When injected along with a suture, however, only about 100 S. aureus are required to produce the same lesion. These studies, which used students as guinea pigs, dramatized the effect of foreign material in the pathogenesis of staphylococcal infections.

Studies cloning the genes controlling suspected staphylococcal virulence factors and then deleting or reinserting the genes have indicated that multiple virulence factors act together to produce the usual wound infection. Clumping factor and the other binding proteins attach the organisms to clots and tissue components, fostering colonization. Clumping factor, coagulase, and protein A serve to coat the organisms with host proteins, giving them a disguise that hides them from attack by phagocytes and the immune system. This may explain why immunity to staphylococcal infection is generally weak or non-existent. Some protein A is released from the bacterial surface and reacts with circulating immunoglobulin. The resulting complexes activate complement and probably contribute to the intense inflammatory response and accumulation of pus. Colonization of plastics and other foreign materials occurs because they quickly become coated with fibrinogen and fibronectin to which the staphylococci attach. Systemic spread of wound infections can lead to abscesses in other tissues, such as the heart and joints. Staphylococcal toxins that enter the circulation act as superantigens, causing the widespread release of cytokines, thereby producing toxic shock. ■ superantigens, p. 474 ■ cytokines, p. 379 ■ complement, p. 381

Staphylococcus epidermidis Wound infections by S. epidermidis in healthy people are frequently cleared by host defenses alone. Organisms come loose from biofilms on indwelling plastic catheters and are carried by the bloodstream to the heart and other tissues. This can result in subacute bacterial endocarditis or multiple tissue abscesses in people with impaired host defenses as from cancer, diabetes mellitus, or other causes. ■ bacterial endocarditis, p. 718

Epidemiology

The epidemiology of S. aureus is discussed in the chapter on skin infections. Various studies have shown that in the case of surgical wound infections, nasal carriers have a two to seven times greater risk of infection than do those who are not nasal carriers. From 30% to 100% of the infections in different studies are due to a patient's own staphylococcus strain. Advanced age, poor general health, immunosuppression, prolonged preoperative hospital stay, and infection at a site other than the site of surgery increase the risk of infection. ■ S. aureus, epidemiology, p. 538

Prevention and Treatment

Cleansing and removal of dirt and devitalized tissue from accidental wounds minimizes the chance of infection, as does prompt closure of clean wounds by sutures. Trying to eliminate the nasal carrier state with antistaphylococcal medications is occasionally successful. Infections in surgical wounds can be reduced by half by administering an effective antistaphylococcal medication immediately before surgery. For unknown reasons, the infection rate is actually increased if the medication is given more than 3 hours before or 2 hours after the surgical incision.

Treatment of staphylococcal infections has been problematic because of the development of resistance to antibacterial medications. When penicillin was first introduced, more than 95% of the strains of S. aureus were susceptible to it. These strains soon largely disappeared with the widespread use of the antibiotic. The remaining strains are resistant by virtue of plasmid-encoded ^-lactamase. Treatment of these strains became much easier with the development of penicillins and cephalosporins resistant to ^-lactamase. Soon thereafter, however, strains of S. aureus, referred to as MRSAs, methicillin-resistant Staphylococcus aureus, appeared that were resistant because of modified penicillin-binding proteins. In the United States, these strains were reliably

696 Chapter 27 Wound Infections treated with the antibiotic vancomycin until 1997, when the first vancomycin resistant strain was identified. Since MRSAs have R plasmids, making them resistant to most anti-staphylococcal medications, the appearance of vancomycin-resistance is an alarming development. In late 1999, a new medication active against vancomycin-resistant bacteria, marketed under the trade name Synercid, became available. This new medication is a combination of two substances that act synergistically to block bacterial protein synthesis. In 2000, linezolid (trade name Zyvox) was introduced representing a new class of antibacterials, the oxazolidinones. It is hoped that other new medications will be developed to keep pace with the growth of resistance, but this will depend on how intelligent human beings are in avoiding overuse of these valuable substances. ■ b-lactamase, p. 512 ■ antibacterial resistance, p. 521

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