Culture and Sensitivity of Infected Chronic Wounds

LETTERS TO THE EDITOR Culture and Sensitivity of Infected Chronic Wounds To the Editor: “Preventing antimicrobial-resistant bacterial infections among older adults in long-term care facilities” contains an incredible amount of useful information, including a statement that surface cultures from infected wounds are not recommended because of the high likelihood of contamination.1 Given the high prevalence of methicillin-resistant Staphylococcus aureus (MRSA) skin infections in some facilities, I believe that clinicians need additional practical guidance to get below the “surface” to obtain culture and sensitivity of chronic wounds if they become acutely infected and antibiotic therapy is indicated. Chronic wounds are risk factors for the presence of resistant pathogens, including MRSA, quinolone-resistant Pseudomonas aeruginosa, Escherichia coli, and other gram-negative enteric rods.2– 6 Chronic wounds are like a Petrie dish filled with a succulent nutritious culture media able to sustain the growth of pathogens inoculated onto the surface. Therefore, caregivers should routinely use gloves for contact and sanitize their hands between residents to avoid transmission. All chronic wounds are colonized by bacteria, so that the finding of a potential pathogen alone is not an indication for antibiotic therapy. In general, a clinician should only obtain a culture if a wound appears to be infected on the basis of clinical findings and the clinician has decided to administer antibiotic therapy. The results of a semiquantitative swab culture alone are not adequate criteria for dianosing infection or initiating antibiotic therapy. Minimum clinical criteria for the initiation of antibiotics and obtaining a culture for soft tissue infections have been developed by consensus for residents of long-term care facilities. Criteria include new or increasing purulent drainage, or at least 2 of the following: temperature ⬎100°F, redness, tenderness, warmth, or swelling that is new or increasing.7 Local indications of even greater severity include ecchymosis, bullae, crepitation, anesthesia, pain out of proportion to objective findings, exposed bone, or a fetid odor that suggests the presence of anaerobes.3 A green exudate suggests Pseudomonas. The finding of MRSA and/or P aeruginosa as predominant organisms is of special interest even in the case of severe synergistic infections, given the fact that these aerobic bacteria along with beta-hemolytic Streptococci may consume oxygen and produce metabolic by-products that facilitate the development of a severe “synergistic” infection with anaerobes.4 All residents with infected wounds should be assessed for the presence of systemic toxicity and the need for debridement and hospitalization. Adequate debridement might require aggressive drainage and resection of ischemic and necrotic tissue, or in some cases, may simply require removal of superficial exudate. The latter is often the case in the presence of a simple cellulitis that may be treated in the nursing home.8 LETTERS TO THE EDITOR

Unfortunately, infected wounds may be sampled through a superficial necrotic exudate containing different bacteria from those present in deeper infected tissue. Some clinicians, therefore, consider culture and sensitivity specimens obtained by swab to be of limited or no value, especially if performed by nursing staff. The potential existence of antibiotic-resistant pathogens as a cause of wound infections, however, creates a significant dilemma for the practicing physician skeptical of the value of such wound cultures. An expert panel has made recommendations regarding key decision points in the management of skin and soft tissue infections that might be useful.3 The panel recommended, “obtaining specimens from infected wounds for gram stain, smear and culture is almost always useful, especially if there is reason to believe that the pathogen is MRSA. The lower the prevalence of resistant strains, the less the need for culture.” The panel recommend collection of a tissue sample obtained by curette after debridement by a practitioner.3,8 The panel recommendations in turn referenced a comprehensive review of wound microbiology comparing various sampling techniques. The review concluded that a correlation has been demonstrated between semiquantitative swab data and quantitative biopsy data and “if the wound is clinically infected, the surface swab sample can provide useful data regarding the presence of potential pathogens”.4 In one small study (n ⫽ 29) of “deep tissue biopsy versus superficial swab culture of life-threatening diabetic foot infections,” “swabbing and deep tissue cultures appeared to be equally reliable” for choosing initial antibiotic treatment. However, superficial swabbing was performed after surgical debridement, scrubbing, and cleaning with sterile gauze soaked in sterile saline.9 This underscores the need to remove devitalized tissue and superficial exudate prior to obtaining a specimen. The following comments apply to acutely infected chronic wounds if therapy in the nursing home is elected. Currently, many facilities employ nursing or physical therapy staff with special certification and interest in wound care. These staff should receive in-service instruction regarding simple mechanical debridement (saline-soaked gauze and irrigation), specimen collection, and handling, including transport media. There may be times, especially in the presence of simple cellulitis without systemic toxicity, when adequate debridement can be accomplished by nursing staff and the search for resistant organisms may/must be based on a swab rubbed on the base of the wound following thorough removal of superficial exudate. I believe that this procedure provides useful information that may facilitate appropriate antibiotic therapy if MRSA or a quinolone-resistant P aeruginosa is cultured as a predominant organism. Paul J. Drinka, MD, CMD Medical Director Wisconsin Veterans Home King, Wisconsin LETTERS TO THE EDITOR 421

REFERENCES 1. Richards C Jr. Preventing antimicrobial-resistant bacterial infections among older adults in long-term care facilities. J Am Med Dir Asoc 2005;6:144 –151. 2. Safdar N, Maki DG. The commonality of risk factors for nosocomial colonization and infection with antimicrobial-resistant Staphylococcus aureus, Enterococcus, Gram-negative Bacilli, Clostridium difficile, and Candida. Ann Intern Med 2002;136:834 – 844. 3. Eron LJ, Lipsky BA, Low DE, Nathwani D, Tice AD, Volturo GA. Managing skin and soft tissue infections: Expert panel recommendations on key decision points. J Antimicrobial Chemother 2003;52(Suppl S1):i3–i17. 4. Bowler PG, Duerden BI, Armstrong DG. Clinical microbiology review: Wound microbiology and associated approaches to wound management. Clin Microbiol Rev 2001;14:244 –269. 5. Siegel J, Strausbaugh L, Jackson M, Rhinehart E, Chiarello LA. Draft Guideline for Isolation Precautions: Preventing transmission of infectious agents in healthcare settings. Recommendations of the Healthcare Infection Control Practices Advisory Committee (HICPAC). Centers for Disease Control and Prevention/Society for Healthcare Epidemiology of America, 2004. Available at: http://www.cdc.gov/ ncidod/hip/isoguide.htm. Accessed August 11, 2004. 6. Viray M, Linkin D, Maslow JN, et al. Longitudinal trends in antimicrobial susceptibilities across long-term care facilities: Emergence of fluoroquinolone resistance. Infect Control Hosp Epidemiol 2005;26:56 – 62. 7. Loeb M, Bentley DW, Bradley S, et al. Development of minimum criteria for the initiation of antibiotics in residents of long-term care facilities: Results of a consensus conference. Infect Control Hosp Epidemiol 2001; 22:120 –124. 8. Lipsky BA, Pecoraro RE, Larson SA, Hanley ME, Ahroni JH. Outpatient management of uncomplicated lower-extremity infections in diabetic patients. Arch Intern Med 1990;150:790 –797. 9. Pellizzer G, Strazzabosco M, Presi S, et al. Deep tissue biopsy vs superficial swab culture monitoring in the microbiological assessment of limb-threatening diabetic foot infection. Diabet Med 2001;18:822– 827.

DOI: 10.1016/j.jamda.2005.06.006

Misleading Cases To the Editor: The report by Gnanadesigan et al1 illustrates how an incomplete understanding of “serotonin syndrome” can confuse the interpretation and understanding of case reports, which are inherently unreliable anyway. The complex topic of serotonin toxicity (ST), which is a better term than serotonin syndrome, needs more than a brief review, as discussed in this author’s comments on Ener et al.2 There are various recent original research papers and reviews that a systematic literature search would have revealed, and it would have been helpful for these authors to include them in their considerations.3–12 Typifying the paper by Radomski et al.13 as a “prospective case series” is inaccurate. It is, like Sternbach’s,14 a review of the disparate published case reports. It would have been more helpful for your readers, as well as more appropriate, to discuss the Human Area Toxicology Service data from Professor Whyte’s group which is more recent higher quality data, from a large prospective case series. Whyte and Gillman have developed the evidence and the concept of ST as a spectrum of serotonin-related side effects progressing to toxicity. ST is a form of poisoning or toxicity, whose features have been clearly defined5,12: 422 LETTERS TO THE EDITOR

(1) Neuromuscular hyperactivity: tremor, clonus, myoclonus, hyperreflexia, and (in the advanced stage) hypertonia/pyramidal rigidity (2) Altered mental status: agitation, excitement, and (in the advanced stage) confusion (3) Autonomic hyperactivity: diaphoresis, fever, mydriasis, tachycardia, and tachypnoea To think in terms of “criteria” for a “diagnosis” of serotonin syndrome is misleading; rather, the question is, what drugs are capable of causing what degrees of side effects and toxicity, and what are the key signs that indicate impending toxicity. These questions have already been usefully addressed by Whyte’s work and Gillman’s reviews. Those drugs capable of elevating serotonin sufficiently to cause serious side effects, or toxicity, have been well defined.15 If brain serotonin levels are sufficiently elevated, and this requires particular drugs and combinations, viz monoamine oxidase inhibitors (MAOIs) plus serotonin reuptake inhibitors (SRIs) or MAOIs plus serotonin releasers (ie, 3,4-methylenedioxymethamphetamine [MDMA] or amphetamine), then it is possible that patients will exhibit severe symptoms and signs of ST. The relative risk of serotonergic side effects or ST with different drugs and combinations has been evaluated in detail12 and recent papers from Whyte’s group add substance to that estimate of risk,3–5 for a detailed analysis see also: www.psychotropical.com/SerotoninToxicity.doc. Of the cases described, all very aged, A and B show nothing more than typical and well-documented serotonergic side effects (but not elevated temperature) that are accounted for by therapeutic doses of the serotonergic antidepressants they were taking; C and D show no specific serotonergic features at all. It is well established that selective SRIs (SSRIs) alone produce such symptoms, both in therapeutic doses, in susceptible patients like the aged, or those with organic brain disease, and extensively even after “small” overdoses. To posit the involvement of oxycodone, which has no known serotonergic effects, has insufficient theoretical or evidential basis and is unsound science. This author has recently reviewed the possible serotonergic properties of opioid analgesics15; that paper would not have been available to these authors. Doubt remains about the mechanisms of the serotonergic effect that some opioids have. Morphine, codeine, oxycodone, and buprenorphine have no SRI activity16 and can be safely administered in conjunction with MAOIs. The weak SRI activity of drugs like tramadol and pethidine, in assays, may not account for the reported interactions with MAOIs; these have been extensively reviewed and discussed elsewhere.12,15 The possibility remains that some opioid analgesics act as serotonin releasers (like MDMA). This would account for their fatal ST interactions with MAOIs. However, this releaser mechanism is blocked by SRIs (because reuptake is a prerequisite for release), which will therefore lessen the clinical effects of drugs acting via this mechanism.17 Releaser actions therefore could not account for any serotonergic interaction between SRIs and opioids. On the other hand, if opioids were acting as SRIs then, because their potency is 1000 times less than SSRIs like JAMDA – November/December 2005