Dr. Bonham is Associate Professor and Director, Wound Care Education Program, Medical University of South Carolina, College of Nursing, Charleston, South Carolina.
The author discloses that she has no significant financial interests in any product or class of products discussed directly or indirectly in this activity, including research support.
Address correspondence to Phyllis A. Bonham, PhD, MSN, RN, CWOCN, DPNAP, Associate Professor and Director, Wound Care Education Program, Medical University of South Carolina, College of Nursing, 99 Jonathan Lucas Street, MSC 160, Charleston, SC 29425; e-mail: email@example.com.
Photo of a Wound Infected with Methicillin-Resistant Staphylococcus aureus.© 2009 iStockphoto LP/Jodi Jacobson
Chronic wounds are a significant and common cause of morbidity and mortality worldwide that in the presence of infection can lead to sepsis, limb loss, increased hospital stays, increased costs, and increased mortality (Cutting & White, 2004). The cumulative effects of aging alter skin integrity and impair the skin’s immune function, resulting in delayed wound healing and an increased risk of infection for older adults. Therefore, early diagnosis and treatment to prevent progression of infection and tissue loss is vitally important. This article will discuss the definition of infection, the clinical indicators of wound infection, the appropriate time and how to culture, and treating infection with topical and systemic antibiotic agents.
What Is Infection?
Infection is described as a continuum from contamination, colonization, critical colonization, to infection (Landis, 2008; Sibbald, Woo, & Ayello, 2009). It is important to recognize that all open wounds are contaminated with nonreplicating organisms on the surface of the wound that are ordinarily cleared by the host (Landis, 2008; Sibbald et al., 2009). As the bacterial burden increases, colonization occurs when organisms replicate, increase in number, and adhere to the wound bed without causing harm or injury to the host (Landis, 2008; Sibbald et al., 2009). When replicating organisms—present in the wound bed—cause changes that trigger the body’s immune response locally at the wound site but not systemically, critical colonization has occurred, which may begin to delay wound healing (Landis, 2008; Sibbald et al., 2009). If this process is unimpeded, the organisms in the wound and surrounding soft tissue can further increase and cause a host response resulting in nonhealing or deterioration and breakdown of the wound (Landis, 2008; Sibbald et al., 2009).
Infection occurs in wound tissue and not on the surface of the wound (Stotts, 2007). Infection is often described quantitatively as a bacterial burden of greater than 105 colony forming units (CFU) per gram of tissue (Stotts, 2007). This definition as the defining criteria for infection is limited due to the complexity and adaptability of bacteria in chronic wounds and because some organisms such as beta-hemolytic streptococci impair wound healing at less than 105 CFU per gram of tissue (Bowler, 2003). According to Kravitz (2006), the definition of infection should be the presence of bacteria in any quantity sufficient to prevent the wound from healing because immuno-suppression and other factors can impair host resistance, and a bacterial count of 105 CFU per gram of tissue alone does not account for these other variables.
Clinical Indicators of Wound Infection
Early manifestations of infection can be silent, without the obvious visible symptoms such as abscess, cellulitis, purulence, increasing erythema, and foul odor that occur later (Cutting & White, 2004; Gardner, Frantz, & Doebbling, 2001). Subtle signs of infection such as delayed or absent healing, wound breakdown, erythema, discolored or friable granulation tissue, unexpected or increased pain or tenderness, pocketing at the base of the wound, bridging of the epithelium or soft tissue, heat, and abnormal smell warrant investigation, but are often ignored (Cutting & White, 2004, 2005). Some wounds, such as arterial wounds, might exhibit only a faint halo of erythema around the wound as an indication of infection (Cutting & White, 2005). Studies have indicated that for chronic wounds, increasing pain, friable granulation tissue, wound breakdown, and foul odor have high validity compared with the classic signs of infection, such as pain, erythema, edema, heat, and purulence (Cutting & White, 2005; Gardner et al., 2001).
A complication of wound infection is osteomyelitis (i.e., bone infection), which is suspected if ulcers probe to the bone or the wound is not healing with or without signs of systemic infection (Bonham, 2001; Sibbald et al., 2009). Bone biopsy is the gold standard to diagnose osteomyelitis, but due to its invasiveness, noninvasive tests such as bone scans or magnetic resonance imaging, the latter of which is more reliable than bone scans and compares favorably to bone biopsy, are alternatives (Bonham, 2001; Stotts, 2007). Clinicians must be vigilant about osteomyelitis because it commonly requires long-term antibiotic therapy and might require surgical resection of the affected bone (Bonham, 2001; Stotts, 2007).
When and How to Culture?
The diagnosis of infection is first made clinically, and cultures should be taken only from wounds with overt or subtle clinical signs of infection (Bowler, 2003). Three methods are commonly used to culture wounds: tissue biopsy, needle aspiration, and swabs (Stotts, 2007). The gold standard for identifying wound infection is a quantitative culture of wound tissue from a tissue biopsy, and results are generally reported as the number of organisms per gram of tissue (Gardner et al., 2001; Stotts, 2007).
Although tissue biopsy is considered the gold standard to diagnose wound infection, it is not performed as commonly as swab cultures because of its invasiveness. Swab cultures are often used in clinical settings as a practical, cost-effective, and noninvasive technique that, in most cases, is adequate to identify the infecting organisms and determine sensitivity to guide antibiotic therapy (Bill et al., 2001; Bonham, 2009; Gardner et al., 2006; Ratliff & Rodeheaver, 2002). The technique described by Levine, Lindberg, Mason, and Pruitt (1976) is considered to be the most reliable and valid method for obtaining swab cultures and involves twirling the end of a sterile applicator on a 1-cm2 area of the open wound for 5 seconds with sufficient pressure to cause minimal bleeding in the underlying tissue (Bonham, 2009; Stotts, 2007).
On the basis of a comprehensive review of 19 studies and 22 expert opinion articles on swab cultures, Bonham (2009) reported the following steps were necessary for the swab culture to be accurate:
- Obtain specimens from clean, viable tissue and not exudate, pus, necrotic tissue, or eschar.
- Debride the wound prior to swabbing to remove surface debris, blood, or excess exudate.
- Use sufficient pressure on the swab to express fluid from the wound tissue.
- Use sterile supplies/technique.
- Use appropriate culture media (e.g., aerobic for superficial wounds, anaerobic for deep, undermined tracts).
- Label specimens properly (i.e., name, date, and time of sample; location of wound(s); specific site/source of the specimen; reason for the culture; relevant signs/symptoms; use of antibiotic agents; history of methicillin-resistant Staphylococcus aureus [MRSA] infections).
- Transport cultures in a timely manner (i.e., immediately or within 2 hours if not refrigerated).
- Request quantitative processing of the sample.
Treating Wound Infections
Prophylactic treatment of wounds with antibiotic agents is not recommended (Landis, 2008; Sibbald et al., 2009). However, a wound that is infected must be treated because it will not heal until the infection is eliminated. Decisions for choosing an antibiotic agent are based on the clinician’s assessment about the extent of the infection. Superficial tissue infection might be treated with topical agents, whereas deep tissue infection requires systemic antibiotic therapy (Landis, 2008).
Topical antimicrobial agents include antiseptic, antibiotic, and elemental antimicrobial agents. Expert opinion guides the use of topical antibiotic agents because guidelines with clear indications and duration of therapy are lacking (Landis, 2008). Antiseptic agents nonselectively kill or inhibit the growth of microorganisms on body surfaces. In the past they were used in attempts to disinfect wounds, which is no longer considered feasible or appropriate. Common antiseptic agents include acidic acid, alcohol, betadine, boric acid, chlorhexidine (PerioChip®), gentian violet, hexachlorophene (pHisoHex®), hydrogen peroxide, and hypochlorite (i.e., Dakin’s solution) (Stotts, 2007). In modern wound care, antiseptic use is discouraged because of the cellular toxicity of antiseptic agents, which exceeds their bactericidal effects (Stotts, 2007). Despite controversies about topical antiseptic agents, some health care providers continue to use these products; in such cases, their use should be restricted to a very limited time frame and with an explicit explanation of the indications and rationale for their use (Stotts, 2007).
Topical antibiotic agents are considered effective if the invading organisms are not resistant and if the infection is localized or superficial (Landis, 2008). Customarily used topical agents and their effectiveness against common infecting organism are outlined in Table 1. Indiscriminate use of topical agents should be avoided because unnecessary use of products such as mupirocin (Bactroban®), fusidic acid, or clindamycin (Cleocin®) increases the risk of MRSA developing high-level antibiotic resistance (Landis, 2008).
Table 1: Topical Antimicrobial Agents Effective Against Staphylococcus Aureus, Streptococcus, Pseudomonas, or Anaerobes
Other newer topical options are elemental antimicrobial products (e.g., cadexomer iodine, silver). Cadexomer iodine is a reformulation of iodine that absorbs bacteria while slowly releasing iodine (Stotts, 2007). At concentrations of up to 0.45%, cadexomer iodine has broad spectrum effectiveness against staphylococcus aureus, including MRSA, streptococci, pseudomonas, viruses, and fungi; is nontoxic to fibroblasts; and causes no structural damage to cells (Landis, 2008; Sibbald et al., 2009; Stotts, 2007).
Silver, long valued in wound care for its broad spectrum bacteriostatic properties, is now available in many formulations including creams and a sustained-release formulation that is incorporated into a variety of dressings such gels, pastes, calcium alginates, hydrofiber, and foams. When using silver dressings, if moisture is needed to activate ionized silver dressings or maintain a moist wound environment, sterile water is advised rather than saline because saline will precipitate silver chloride and inactivate the product (Stotts, 2007).
There is no current evidence of negative effects associated with elemental antimicrobial products. However, similar to the use of antibiotic agents, judicious use of elemental antimicrobial agents is recommended: limited to 2 to 4 weeks and based on individualized consideration of the wound and host (Stotts, 2007).
Systemic agents are recommended for infections that involve deep and surrounding wound tissue or have manifested systemically because topical agents are not able to penetrate into the deep tissue compartments (Sibbald et al., 2009). A topical agent might be used along with a systemic agent to eliminate bacteria on the surface and in superficial tissue where the perfusion may be less than adequate. Whether parenteral or oral antibiotic agents are superior remains unresolved. Commonly used systemic products and their effectiveness against common infecting organisms are outlined in Table 2.
Table 2: Systemic Antimicrobial Agents with Moderate to Excellent Effectiveness Against Staphylococcus Aureus, Streptococci, Pseudomonas, and Anaerobes
Due to antibiotic resistance of many organisms, culturing is preferable before antibiotic agents are started to determine the antimicrobial susceptibility (Armstrong & Lipsky, 2003). Because microbiological results are not immediately available in cases of wound infection, Landis (2008) recommended the following empirical approach to treat infections in chronic wounds according to whether the infection is mild, moderate, or severe. Mild infection is described as superficial, without signs of a systemic response or osteomyelitis, and ambulatory management is planned. Antibiotic agents recommended in this instance include one of the following for 2 weeks:
- Cephalexin (Keflex®) 500 mg orally four times per day.
- Clindamycin 300 to 450 mg orally three times per day.
- Amoxicillin/clavulanate (Augmentin®) 500/125 mg orally three times per day.
- Clindamycin 450 to 600 mg orally three times per day, plus ciprofloxacin (Cipro®) 500 mg orally twice per day.
- Moxifloxacin (Avelox®) 400 mg orally once per day, or linezolid (Zyvox®) (for MRSA) 600 mg orally twice per day.
For moderate infection with superficial to deep tissue involvement, a systemic response, no osteomyelitis, and either planned ambulatory or inpatient management, Landis (2008) advised treatment with one of these antibiotic agents for 2 to 4 weeks:
- Clindamycin 450 to 600 mg orally three times per day, plus ciprofloxacin 500 mg orally twice per day.
- Clindamycin 450 to 600 mg orally three times per day, plus ceftriaxone (Rocephin®) 1 g intravenous once per day.
- Vancomycin (for MRSA) 1 g intravenous twice per day.
- Linezolid (for MRSA) 600 mg intravenous twice per day.
According to Landis (2008), severe infections that require inpatient care and involve deep tissue with a systemic response, presence of osteomyelitis, or are limb/life threatening can be treated with one of the following intravenous/oral antibiotic agents:
- Clindamycin 450 to 600 mg orally three times per day, plus ceftriaxone 1 g intravenous once per day for 2 to 12 weeks.
- Piperacillin/tazobactam (Zosyn®) 4.5 g intravenous three times per day for 2 to 12 weeks.
- Clindamycin 450 to 600 mg orally three times per day, plus gentamicin 5 mg/kg intravenous once per day for 2 weeks.
- Imipenem (Primaxin®) 500 mg intravenous four times per day for 2 to 12 weeks.
- Meropenem (Merrem® I.V.) 1 g intravenous three times per day for 2 to 12 weeks.
- Vancomycin (for MRSA) 1 g intravenous twice per day for 2 to 4 weeks.
- Linezolid (for MRSA) 600 mg intravenous twice per day for 2 to 4 weeks.
For bone and joint involvement, prolonged oral therapy is required for 2 to 12 weeks after intravenous therapy is completed.
Gerontological nurse specialists often care for older patients with wounds who are at increased risk for infection. Therefore, early identification and treatment of infected wounds is essential in this vulnerable population. A diagnosis of wound infection is initially based on the clinical indicators of infection, and cultures are used to determine the infecting organisms and their drug sensitivity to guide antimicrobial therapy. Swab cultures performed using Levine et al.’s (1976) technique are noninvasive and cost-effective alternatives to invasive cultures. Clinicians have an array of topical and systemic products to treat wound infection on the basis of the infecting organism and its sensitivity to antimicrobial agents and whether the infection is localized/superficial or involves deep or surrounding tissue or bone.
- Armstrong, D.G. & Lipsky, B.A. (2003). Recognizing infections and taking appropriate cultures. Wounds, 5(Suppl.), 6–7.
- Bill, T., Ratliff, C., Donovan, A.M., Knox, L.K., Morgan, R.F. & Rodeheaver, G.T. (2001). Quantitative swab culture versus tissue biopsy: A comparison in chronic wounds. Ostomy/Wound Management, 47, 34–37.
- Bonham, P. (2001). A critical review of the literature. Part I: Diagnosing osteomyelitis in patients with diabetes and foot ulcers. Journal of Wound, Ostomy, and Continence Nursing, 28, 73–78.
- Bonham, P.A. (2009). Swab cultures for diagnosing wound infections: A literature review and clinical guideline. Journal of Wound, Ostomy, and Continence Nursing, 36, 389–395.
- Bowler, P.G. (2003). The 105 bacterial growth guideline: Reassessing its clinical relevance in wound healing. Ostomy/Wound Management, 49, 44–53.
- Cutting, K.F. & White, R. (2004). Defined and refined: Criteria for identifying wound infection revisited. British Journal of Community Nursing, 9(3), S6–S15.
- Cutting, K.F. & White, R.J. (2005). Criteria for identifying wound infection—Revisited. Ostomy/Wound Management, 51, 28–34.
- Gardner, S.E., Frantz, R.A. & Doebbling, B.N. (2001). The validity of the clinical signs and symptoms used to identify localized chronic wound infection. Wound Repair and Regeneration, 9, 178–186. doi:10.1046/j.1524-475x.2001.00178.x [CrossRef]
- Gardner, S.E., Frantz, R.A., Saltzman, C.L., Hillis, S.L., Park, H. & Scherubel, M. (2006). Diagnostic validity of three swab techniques for identifying chronic wound infection. Wound Repair and Regeneration, 14, 548–557. doi:10.1111/j.1743-6109.2006.00162.x [CrossRef]
- Kravitz, S. (2006). Infection: Are we defining it accurately?Advances in Skin and Wound Care, 19, 176. doi:10.1097/00129334-200605000-00001 [CrossRef]
- Landis, S.J. (2008). Chronic wound infection and antimicrobial use. Advances in Skin and Wound Care, 21, 531–540. doi:10.1097/01.ASW.0000323578.87700.a5 [CrossRef]
- Levine, N.S., Lindberg, R.B., Mason, A.D. Jr.. & Pruitt, B.A. Jr.. (1976). The quantitative swab culture and smear: A quick, simple method for determining the number of viable aerobic bacteria on open wounds. Journal of Trauma, 16, 89–94.
- Ratliff, C.R. & Rodeheaver, G.T. (2002). Correlation of semi-quantitative swab cultures to quantitative swab cultures from chronic wounds. Wounds, 14, 329–333.
- Sibbald, R.G., Woo, K.Y. & Ayello, E.A. (2009). Infection and inflammation. Ostomy/Wound Management, 55(Suppl.), 15–18.
- Stotts, N. (2007). Wound infection: Diagnosis and management. In Bryant, R.A. & Nix, D.P. (Eds.), Acute and chronic wounds: Current management concepts (3rd ed., pp. 161–175). St. Louis: Mosby.
Topical Antimicrobial Agents Effective Against Staphylococcus Aureus, Streptococcus, Pseudomonas, or Anaerobes
|Staphylococcus aureus and Streptococci||Staphylococcus aureus, Streptococci, and Pseudomonas||Anaerobes|
|Gentamicin sulfate||Gentamicin sulfate||Metronidazole (Metrogel®)|
|Mupiro cin (Bactroban®) 2%||Polymyxin B sulfate and bacitracin zinc||Polymyxin B sulfate and bacitracin zinc|
|Polymyxin B sulfate and bacitracin zinc (Polysporin®)||Polymyxin B sulfate, bacitracin zinc, and neomycin sulfate||Silver sulfadiazineb|
|Polymyxin B sulfate, bacitracin zinc, and neomycin sulfatea (Neosporin®)||Silver sulfadiazineb|
|Silver sulfadiazine (Silvadene®)b|
Systemic Antimicrobial Agents with Moderate to Excellent Effectiveness Against Staphylococcus Aureus, Streptococci, Pseudomonas, and Anaerobes
|Gram positives||Gram negatives||Anaerobes|
|Staphylococcus aureus, Streptococci||Pseudomonas|
|Amoxicillin/clavulanate (Augmentin®)||Metronidazole (Metrogel®)|