When dealing with pressure sores, there is no definitive way of making a diagnosis of osteomyelitis short of a biopsy of the involved bone1. In fact, only about a third of stage IV pressure ulcers (those extending to the bone) may be associated with osteomyelitis2. In a study of pressure sores related to spinal cord injury or cerebrovascular accident, the clinical judgement of physicians with respect to the presence of osteomyelitis was accurate in only 56% of patients. Only 3 of 21 patients with exposed bone had a diagnosis of osteomyelitis confirmed on biopsy3.
The “Probe to the Bone” bedside procedure has been studied primarily in diabetic foot infections with a recent systematic review reporting pooled sensitivity and specificity of 0.87 (95% confidence interval [CI], .75-.93) and 0.83 (95% CI, .65-.93), respectively4. Its performance in non-diabetic patients or those without a foot infection needs further study.
So in our patient, we should not assume a diagnosis of osteomyelitis; a bone biopsy is necessary for a definitive diagnosis.
- Larson DL, Gilstrap J, Simonelic K, et al. Is there a simple, definitive, and cost-effective way to diagnose osteomyelitis in the pressure ulcer patient? Plast Reconstr Surg 2011; 127:67
- Bodavula P, Liang SY, Wu J et al. Pressure ulcer-related pelvic osteomyelitis: a neglected disease? Open Forum Infect Dis 2015. DOI:10.1093/ofid/ofv112.
- Darouiche RO, Landon GC, Klima M et al. Osteomyelitis associated with pressure sores. Arch Intern Med 1994;154:753-58.
- Lam K, van Asten SA, Nguyen T, et al. Diagnostic accuracy of probe to bone to detect osteomyelitis in the diabetic foot: a systematic review. Clin Infect Dis 2016;63:944-8.
Clindamycin is active in-vitro against many strains of SA and is indicated in the treatment of SA mild-to-moderate skin and soft tissue infections (SSTIs), including some methicillin-resistant strains 1,2. However, evidence for its use as monotherapy against SA infections in other body sites is limited or lacking. For example, in adults with pneumonia, efficacy of clindamycin is based solely on case series that excluded monotherapy3. For bone and joint infections, clindamycin has limited evidence of efficacy in adults, and is not recommended in the treatment of endovascular or central nervous system infections2.
Emergence of resistance to clindamycin in previously susceptible SA isolates may also occur during therapy conferred by erythromycin resistance methylase (erm) gene which is typically screened for by the “D-zone” test2 (Figure). Increasing resistance of SA to clindamycin has led to recommendation against its empiric use for severe or complicated SSTIs (e.g. large abscess or deep infections)4.
Fig. The “E” disk (on left) contains erythromycin; “CC” disk (on right) contains clindamycin. The test detects inducible clindamycin resistance in erythromycin-resistant , clindamycin- susceptible isolates (http://www.cdc.gov/groupbstrep/images/lab-positivegbs-lg.jpg).
- Miller LG, Daum RS, Creech CB, Young D, Downing MD, Eells SJ, Pettibone S, Hoagland RJ, Chambers HF. Clindamycin versus trimethoprim–sulfamethoxazole for uncomplicated skin infections. N Engl J Med 2015;372:1093-103.
- Liu C, Bayer A, Cosgrove SE, Daum RS, Fridkin SK, Gorwitz RJ, Kaplan SL, Karchmer AW, Levine DP, Murray BE, Rybak MJ. Clinical practice guidelines by the Infectious Diseases Society of America for the treatment of methicillin-resistant Staphylococcus aureus infections in adults and children. Clin Infect Dis 2011;52:e18-55.
- Lobo LJ, Reed KD, Wunderink RG. Expanded clinical presentation of community-acquired methicillin-resistant Staphylococcus aureus pneumonia. Chest 2010; 138:130-6.
- VanEperen AS, Segreti J. Empirical therapy in Methicillin-resistant Staphylococcus Aureus infections: An Up-To-Date approach. J Infect Chemother 2016;22:351-9.
Contributed by Nathan T. Georgette, 4th year, Harvard Medical School student
The short answer is “No”! The myth that diabetics with acute bacterial skin and skin structure infections should be routinely placed on antibiotics against gram-positives as well as gram-negatives and/or anaerobes probably originates from the extrapolation of data revolving around the frequent polymicrobial nature of diabetic foot infections. These infections often originate from chronic ulcers and are complicated by deep tissue infection or gangrene (1), which is often not the case in our diabetic patients with cellulitis alone.
In a recent study of the microbiology of cellulitis or cutaneous abscess in hospitalized patients, Staphylococcus and Streptococcus sp. accounted for 90% of cultured organisms in diabetic patients, not significantly different than that of non-diabetics (1). This finding also supports national guidelines which do not recommend routine use of broader spectrum antibiotics in diabetics with cellulitis or cutaneous abscess (2). This may be a good area to include in our antibiotic stewardship practices.
1. Jenkins TC, Knepper BC, Moore SJ, et al. Comparison of the microbiology and antibiotic treatment among diabetic and nondiabetic patients hospitalized for cellulitis or cutaneous abscess. J Hosp Med 2014;9:788-794.
2. Stevens DL, Bisno AL, Chambers HF, et al. Practice guidelines for the diagnosis and management of skin and soft tissue infections. Clin Infect Dis 2014;59:e10-e52.
The reported rates of MRSA colonization in patients with community-associated MRSA SSTI have been surprisingly low, ranging from 7% to 41% (55% among hospitalized patients) (1), making it difficult to exclude MRSA as a causative pathogen based on a negative screening test alone. The concordance between what grows from the nares and what is isolated from the SSTI site is also far from ideal. Among patients with methicillin-sensitive S. aureus (MSSA) SSTI , 12% may be colonized with MRSA and of those with MRSA SSTI, 32% may be colonized with MSSA (1). In the absence of a reliable screening test to help us select an empiric antibiotic regimen in patients with SSTI, we should pay special attention to the clinical features of the SSTI. Empiric MRSA antibiotic coverage should be considered for patients with purulent SSTIs, deep tissue infections, or those with systemic toxicity( 2), irrespective of colonization status.
1. Ellis MW, Schlett CD, Millar EV, et al. Prevalence of nasal colonization and strain concordance in patients with community-associated Staphylococcus aureus skin and soft tissue infections. Infect Control Hosp Epidemiol 2014;35:1251-6.
2. Liu C, Bayer A, Cosgrove SE, et al. Clinical practice guidelines by the Infectious Diseases Society of America for the treatment of methicillin-resistant Staphylococcus aureus infections in adults and children. Clin Infect Dis 2011;52:e18-55.2.
β-hemolytic streptococci (BHS) are usually considered the primary cause of non-purulent cellulitis (e.g. without abscesses, or infections involving deep soft tissues, wounds, or ulcer) even in the MRSA era. In a prospective study of patients admitted to the hospital for “diffuse, non-culturable “(i.e. many of our patients), most had serological evidence of acute BHS, and >95% responded to a β-lactam antibiotic treatment (1) . The current Infectious Diseases Society of America guidelines do not endorse empiric coverage of MRSA for non-purulent cellulitis, unless there is systemic toxicity or poor response to β-lactam monotherapy (2). More specifically, the guidelines recommend a β-lactam antibiotic for treatment of non-purulent cellulitis in hospitalized patients with modification to MRSA coverage if no clinical response. One advantage to β-lactam monotherapy is the ease of switch to an equivalent oral antibiotic (e.g. cephalexin) when transitioning from parenteral antibiotic therapy.
1. Jeng A, Beheshti M, Li J, et al. The role of beta-hemolytic streptococci in causing diffuse nonculturable cellulitis: a prospective investigation. Medicine (Baltimore) 2010;89:217-26.
2. Liu C, Bayer A, Cosgrove SE, et al. Clinical practice guidelines by the Infectious Diseases Society of America for the treatment of methicillin-resistant Staphylococcus aureus infections in adults and children. Clin Infect Dis 2011;52:e18-55.