TheÂ skinÂ isÂ theÂ largestÂ organÂ ofÂ theÂ body,Â creating aÂ protectiveÂ barrierÂ toÂ preventÂ entryÂ ofÂ pathogenic particles.Â WhileÂ thisÂ physicalÂ barrierÂ servesÂ asÂ the firstÂ lineÂ ofÂ immunologicÂ defense,Â theÂ skinÂ also supports a complex microbial ecosystem comprised of a number of bacterial species, primarily the GrampositiveÂ Staphylococci, Micrococci,Â Corynebacteria, andÂ Propionibacteria,Â andÂ theÂ Gram-negative Acinetobacter (1, 2). These microbial species are referred to as commensal organisms because they can exist harmoniously and non-pathogenically on the skin so long as the integrity of the skin is maintained. These resident bacteriaÂ alsoÂ serveÂ toÂ protectÂ theirÂ hostÂ byÂ competingÂ outÂ other,Â more pathogenic bacteria through a number of methods (2). Any breach of this physical barrier could alter this relationship, allowing these commensal and other pathogenic bacteria to gain entry to and serve as pathogenic agents
withinÂ theÂ underlyingÂ tissue.Â SkinÂ damageÂ resultsÂ inÂ aÂ numberÂ ofÂ ways, including dermatologic irritations, burns, lacerations, abrasions, infection, blunt force trauma and surgery. All wounds have the potential to become infected. In large part the chances increase with anatomic site. The closer the wound is to the anatomic sites knownÂ toÂ serveÂ asÂ reservoirsÂ ofÂ bothÂ aerobicÂ andÂ anaerobicÂ bacteria, namely the respiratory and gastrointestinal tracts, the greater the chance of infection onset. The SENTRY Antimicrobial Surveillance Program has been recording information on and ranking pathogens isolated from skin and soft tissue infections (SSTIs) serious enough to require hospitalization. Within the United States the causative agents have been fairly static since this program was initiated, with Staphylococcus aureusaccounting for almost
50%Â ofÂ allÂ analyzedÂ casesÂ (3). AÂ summaryÂ ofÂ sevenÂ yearsÂ ofÂ analyses 1998-2004) ranks the leading ten pathogens detected in 5,837 cases of SSTIs (Table 1). A subsequent report compared molecular techniques with those of culture with regard to identifying pathogens associated with various wounds. They identified limitations associated with culturing methodologies that may skew the detection rates of some bacterial species, most notably the strict anaerobes, thus adversely affecting treatment regimens (4). In
this analysis, which used sequencing to identify pathogens within a number ofÂ samples,Â aÂ hostÂ ofÂ difficult-to-culture,Â bio-filmÂ associatedÂ anaerobic genera were identified from three different forms of skin ulcers (4, 5, 6). Medical Diagnostic Laboratories, L.L.C. (MDL) has developed a panel of testsÂ includingÂ theÂ mostÂ frequentlyÂ detectedÂ pathogensÂ associatedÂ with surgical site infections (SSIs) and SSTIs to aid physicians in the diagnosis and proper treatment of a host of wound types. Table 1. Incidence rates of pathogens isolated from SSTI and SSI within the United States as reported by the SENTRY Antimicrobial Surveillance ProgramÂ andÂ theÂ CDCâ€™sÂ GuidelinesÂ forÂ PreventionÂ ofÂ SurgicalÂ Site Infection. BothÂ reportsÂ summarizeÂ infectiousÂ ratesÂ overÂ aÂ sevenÂ yearÂ time frame. ND indicates â€œnot determinedâ€ in that study (3, 7). Skin and Soft Tissue Infections (SSTI) Panel Staging of Wounds WoundsÂ areÂ classifiedÂ accordingÂ toÂ theirÂ degreeÂ ofÂ severityÂ onÂ aÂ four point scale (8). Stage 1is typified by alteration in skin color, texture and temperature with no overt lesion present and does not involve the dermis. Stage 2describes instances whereby the epidermal and dermal layers of skin are breached as a result of a tear in the epidermal layer that can include infectionÂ andÂ tissueÂ necrosis;Â drainageÂ atÂ theÂ siteÂ isÂ notÂ anÂ uncommon characteristic. StageÂ 3 woundsÂ areÂ distinguishedÂ fromÂ StageÂ 2Â wounds based on the depth of the trauma. In these instances, the damage extends to,Â butÂ noÂ furtherÂ than,Â theÂ subcutaneousÂ fatÂ layerÂ ofÂ theÂ skin. StageÂ 4 wounds are by far the most serious, affecting both bone and muscle as well as supporting structures. Necrosis and drainage are extensive. Ulcers The term ulcer is ascribed to any slow healing, open sore on the surface ofÂ theÂ skinÂ orÂ mucousÂ membraneÂ thatÂ isÂ accompaniedÂ byÂ tissueÂ loss, disintegration and necrosis. Diabetic foot, venous and pressure ulcers are three common ulcer types routinely seen clinically.
Diabetic Foot Ulcers AccordingÂ toÂ theÂ 2011Â DiabetesÂ FactÂ SheetÂ publishedÂ byÂ the American Diabetes Association (9), there are currently 25.8 million Americans, 8.3%
ofÂ theÂ currentÂ population,Â sufferingÂ fromÂ DiabetesÂ Mellitus.Â WithinÂ this populationÂ approximatelyÂ 15%,Â orÂ 4Â millionÂ individuals,Â willÂ developÂ foot ulcers, 6% of which will require hospitalization for infection and complication (10). Statistical analysis of medical costs within the United States in 2007 report a total of $116 billion dollars in direct costs spent for the treatment of diabetes, with 33% ($38 billion) of this amount used specifically for the care and treatment of foot ulcers (11). These numbers are staggering when you
consider the number of newly diagnosed cases continues to rise. DiabeticÂ footÂ ulcersÂ are multifactorialÂ inÂ origin,Â theÂ resultÂ ofÂ aÂ hostÂ of biological issues brought about by uncontrolled blood sugar levels. First, diabetics are more prone to infection as a result of changes in their skin, leavingÂ itÂ dryÂ andÂ susceptibleÂ toÂ crackingÂ andÂ fissuring.Â DiabeticsÂ also experience atrophy of the small muscles of the foot leading to structural
deformity which results in increased amounts of pressure on the ball and heel of the foot leading to accelerated callous formation. The diabetic callous differs from that of the non-diabetic population in that they are often much thicker and more prone to cracking, infection and ulcer formation (Figure 1)Â (12).Â ThisÂ increasedÂ pressureÂ leadsÂ toÂ acceleratedÂ callousÂ formation which, if not properly attended, can readily become ulcers in the diabetic patient.Â CompoundingÂ mattersÂ areÂ twoÂ otherÂ anomaliesÂ associatedÂ with diabetes, sensory neuropathy and vascular disease. Diabetic neuropathy describesÂ theÂ sensoryÂ nerveÂ damageÂ thatÂ hindersÂ aÂ personâ€™sÂ abilityÂ to feel their extremities, allowing them to unknowingly continue on with their daily routines despite being injured. Poor circulation to the extremities as a result of narrowing and hardening of blood vessels complicates matters further by increasing the level of cell death and decreasing the numbers of immune mediators capable of trafficking to the affected areas. Ulcers detected early are highly treatable and curative as they are often infected withÂ aerobic,Â Gram-negativeÂ cocci. AsÂ theÂ infectionÂ progressesÂ andÂ the ulcer grows deeper, the infections predominantly become polymicrobial in natureÂ andÂ oftenÂ limbÂ threateningÂ (12).Â PromptÂ andÂ properÂ treatmentÂ is essentialÂ inÂ orderÂ toÂ saveÂ theÂ affectedÂ toe,Â footÂ orÂ legÂ fromÂ amputation. DespiteÂ physiciansâ€™Â bestÂ efforts,Â almostÂ 66,000Â lower-limbÂ amputations were performed in 2006 (9).
Detection in SSTIs
(N = 5,873)
Detection in SSI
(N = 17,671)
S. aureus 2,602 3,534
P. aeruginosa 648 1,414
Enterococcus species 542 2,121
E. coli 422 2,121
Enterobacter species 282 1,237
Klebsiella species 248 530
Streptococci 237 884
P. mirabilis 166 530
CoNS 161 2,474
Serratiaspecies 125 ND
Bacteroides fragilis ND 353
Other Gram Positive Aerobes ND 353
Medical Diagnostic Laboratories, L.L.C.
& Promp t nalizedÂ Â Perso
That’s Our Way
Pr essional o f
Compression of the affected area to minimize edema and swelling is the
primary form of treatment (16).
WhatÂ makesÂ theÂ skinÂ uniqueÂ isÂ itsÂ abilityÂ toÂ repairÂ itselfÂ andÂ recover fromÂ theseÂ variousÂ insults. TissueÂ repairÂ andÂ remodelingÂ isÂ aÂ multistep process that is orchestrated by a number of key cell types and factors working in concert with one another to seal-off the site in order to localize infection, decrease blood loss and initiate cellular replication to regenerate theÂ damagedÂ tissue.Â Typically,Â theseÂ eventsÂ occurÂ asÂ aÂ continuumÂ of overlapping stages, some lasting only a few hours and others potentially for several years. Initiation begins with the process of Hemostasis, typically not considered an actual stage in the process, then to Inflammation (early), transiting into the Proliferation Stage (intermediate) and culminating with Maturation (late) (Figure 3) (17).
FigureÂ 3.Â TheÂ stagesÂ andÂ durationÂ ofÂ theÂ woundÂ repairÂ process.
Adapted from (17). Pathogens Often Isolated from SSTIs and SSIs Pathogen association with various SSTI and SSI is often dictated by the anatomicÂ location;Â theÂ infectiousÂ agentÂ isÂ typicallyÂ consideredÂ normal flora within that region. For the first phase MDL has selected the following pathogenic agents for inclusion in the Skin and Soft Tissue Infection panel. BacteroidesÂ fragilis: BacteroidesÂ areÂ Gram-negative,Â anaerobicÂ bacilli
associated with a number of different types of infections that are typically polymicrobial in nature. Anatomic sites affected include the central nervous system, head, neck, chest, abdomen, pelvis, skin and soft tissue. Due to their fastidious growth requirements, Bacteroidesspecies are extremely hard to identify by culturing methodologies and, as a result, are believed to be under reported pathogenic agents (18). B. fragilis is considered normal flora of the gastrointestinal tract and is commonly associated with SSI of the abdomen and abscesses. E.Â coli:Â E.Â coli areÂ Gram-negative,Â facultative,Â rod-shapedÂ bacteria thatÂ naturallyÂ inhabitÂ theÂ gastrointestinalÂ tract.Â OutsideÂ theirÂ normal environment, E.Â coli canÂ causeÂ infection,Â particularlyÂ withinÂ theÂ urinary tract.Â TheyÂ areÂ alsoÂ associatedÂ withÂ skinÂ infectionsÂ inÂ regionsÂ inÂ close proximity to the rectum, particularly with incontinent individuals. Individuals undergoing surgical procedures associated with the gastrointestinal tract and lower regions of the spine are also at risk of contracting infection (19, 20, 21). Klebsiella species: Klebsiella speciesÂ areÂ Gram-negative,Â facultative rods that colonize the skin and gastrointestinal tract. These opportunistic pathogens are a leading cause of nosocomial infections second only to
E. coli, and account for 8% of all hospital-acquired infections (19, 21, 22). SuchÂ infectionsÂ typicallyÂ ariseÂ withinÂ theÂ respiratory,Â biliaryÂ andÂ urinary tracts as well as surgical sites. The ubiquitous nature of these bacteria, in combination with increased treatment with broad-spectrum antibiotics, has led to the development of resistant strains. Two species, K. pneumoniae and K. oxytoca, account for the majority of infections with K. pneumoniae
serving as an important cause of community-acquired pneumonia in the elderly and K. oxytocamore commonly associated with UTIs. Prevotella species: Prevotella speciesÂ areÂ Gram-negative,Â anaerobic bacilliÂ thatÂ colonizeÂ theÂ vaginalÂ andÂ oralÂ cavities.Â DependingÂ onÂ their anatomic location, these bacteria cause a wide-range of infections. Oral cavityÂ colonizationÂ isÂ associatedÂ withÂ sinusÂ andÂ periodontalÂ infections, Figure 1. An image of a diabetic foot ulcer that initiated from a thickened callous. (13)
Pressure Ulcers Pressure ulcers, also known as bed sores, typically arise as a result of
prolonged and persistent pressure applied to the skin, usually developing at bony areas like the hips, heels, elbows, shoulders, back and back of the head. Friction and shear forces also play parts in wound development as the skin is often pulled unnaturally either as the result of a caregiver repositioningÂ anÂ individualÂ byÂ draggingÂ themÂ acrossÂ aÂ surfaceÂ orÂ the repositioning of a mechanical bed that allows the individual to slide along
aÂ surfaceÂ (14,15).Â SoresÂ developÂ asÂ aÂ resultÂ ofÂ decreasedÂ bloodÂ flow o the compressed tissue, leading to increased cellular death and often develop quickly, making them difficult to manage. Those at greatest risk of developing pressure sores have limited mobility and are often unable to shift their position to alleviate the pressure; this includes those confined to a wheelchair or a bed (15). The incidence of developing such sores
increases with age, as the skin becomes more fragile, regenerates more slowly and sensory and mental perception begin to wane (15). Diabetics, as a result of their associated vascular issues, are also at greater risk of developing pressure sores. If not treated promptly and properly, serious complicationsÂ includingÂ cellulitis,Â bone/jointÂ infection,Â sepsisÂ andÂ even melanomaÂ canÂ occurÂ (15). AÂ jointÂ studyÂ performedÂ byÂ theÂ CentersÂ for Disease Control and Prevention (CDC) and National Center for Health
Statistics (NCHS) evaluated the incidence rate of pressure sores within nursing home facilities. Their study found 11% of 159,000 nursing home residentsÂ hadÂ pressureÂ soresÂ andÂ thatÂ halfÂ ofÂ themÂ wereÂ classifiedÂ as stage 2 sores on the Shea Pressure Sore Scale (14). Figure 2. Percentage of nursing home residents with pressure ulcers by stage. (CDC/NCHS National Nursing Home Survey). These values were reported for the year 2004 whereby approximately 159,000 (11%) of nursing home residents were reported to have some form of pressure ulcer. (14) Venous Stasis Ulcers Venous stasis ulcers arise as a result of the natural aging process. Bicuspid valvesÂ withinÂ legÂ veinsÂ beginÂ toÂ loseÂ theirÂ elasticity,Â allowingÂ bloodÂ to pool. Individuals with deep vein thrombosis and edema have a sedentary lifestyle or who are obese are at greater risk of developing these valvular
issues. The loss of valvular function leads to increased veinous pressure which puts more strain upon the affected valves, damaging them further, and elicits an immune response that affects tissues within these regions. 367Â Â SSTI Panel Antibiotic Resistance by Real-Time PCR [EnterococcusÂ faecalis,Â EscherichiaÂ coli, Group AÂ Streptococcus,Â GroupÂ BÂ Streptococcus, Klebsiella species, Proteus mirabilis, Pseudomonas aeruginosa, CommunityÂ AssociatedÂ MRSAÂ (CAMRSA):Â amoxicillin-clavulanicÂ acid,Â ampicillinÂ (for E. faecalis), cephalothin (cephalexin), clindamycin, doxycycline,Â trimethoprim-sulfamethoxazole, ciprofloxacin,Â cefepime,Â piperacillin-tazobactam,
imipenem, gentamicin] Benefits of this system include:
â€¢Â Real-Time PCR.
â€¢Â Simple and convenient sample collection.
â€¢Â No refrigeration is required before or after collection.
â€¢Â Specimen stable for up to five days.
â€¢Â Test additions are available up to 30 days after receipt of the specimen.
â€¢Â 24 – 48 hour turnaround time.
â€¢Â High diagnostic specificity and sensitivity.
â€¢Â One vial, multiple pathogens.
Antibiotic Treatment for Skin and Soft Tissue
Skin and soft tissue infections (SSTI), surgical site infections (SSI), and
wounds are a major issue of morbidity and mortality in the community and
healthcare system (reviewed in 33, 34, 35). Skin or our epidermal layer
provides us with a protective barrier between the microbial environment
andÂ ourÂ sub-dermalÂ tissue,Â organs,Â andÂ bloodÂ stream.Â WheneverÂ that
barrierÂ isÂ breachedÂ byÂ trauma,Â surgery,Â orÂ infectiousÂ abscess,Â aÂ strong
immuneÂ responseÂ isÂ triggeredÂ toÂ theÂ infectingÂ organism.Â SSTI,Â SSI,
andÂ woundÂ infectionsÂ canÂ beÂ causedÂ byÂ aÂ singleÂ bacteriumÂ orÂ canÂ be
polymicrobial depending on the site and length of time of the infection (33).
TheÂ initialÂ stagesÂ ofÂ theseÂ infectionsÂ usuallyÂ involveÂ theÂ Gram-positive
StaphylococcusÂ andÂ occasionallyÂ Streptococcus,Â especiallyÂ forÂ those
infections above the waist. The major cause and ever increasing in number
areÂ SSTIsÂ dueÂ toÂ methicillin-resistant StaphylococcusÂ aureus (MRSA),
which are resistant to the ÃŸ-lactam class of antibiotics (36). Other bacteria
in addition to Staphylococci and Streptococci can cause infections, such as
the facultative anaerobic Gram-negative rods Escherichia coli, Klebsiella
species, ProteusÂ mirabilis,Â andÂ PseudomonasÂ aeruginosa,Â orÂ Grampositive Enterococcus,Â especiallyÂ forÂ thoseÂ infectionsÂ belowÂ theÂ waist
although less frequently (33).The enterics, Pseudomonas, Enterococcus,
Gram-positive and Gram-negative anaerobic bacteria are usually present
in SSTIs and wounds, such as animal or human bites, lasting for weeks
or SSIs, especially those associated with the gut or OB/GYN surgeries
(33,34). Chronic wounds lasting weeks can be due to facultative anaerobic
bacteria such as Bacteriodes fragilis, Peptostreptococcus, and facultative
anaerobicÂ Gram-negativeÂ rodsÂ suchÂ as PseudomonasÂ aeruginosa and
Enterobacter species. DrainageÂ ofÂ theÂ abscessÂ isÂ recommendedÂ for
uncomplicated SSTI often associated with Staphylococcus. Topical, oral
(PO),Â intramuscularÂ (IM),Â andÂ intravenousÂ (IV)Â antibioticsÂ areÂ usedÂ to
treat these infections depending on the clinical presentation and severity
of the infections (Table 2) (36). Antibiotics suggested by the Infectious
Disease Society of America (IDSA, provider survey, and the Clinical and
LaboratoryÂ StandardsÂ InstituteÂ (CLSI)Â wereÂ selectedÂ forÂ thisÂ antibiotic
susceptibility assay (37). Other antibiotics recommended to treat MRSA
(non-community-associatedÂ MRSA)Â infectionsÂ includeÂ vancomycinÂ (IV),
linezolid (PO, IV), and daptomycin (IV). These antibiotics are not included
in the antibiotic susceptibility panel due to very low levels of resistance.
peritonsillar abscess and pneumonia, while those colonizing the GI tract
haveÂ beenÂ isolatedÂ fromÂ casesÂ ofÂ peritonitis,Â intra-abdominalÂ abscess,
postoperative wound infections, pelvic inflammatory disease, vulvovaginal
and perianal infections. Infections of the soft tissue include gangrene and
necrotizing fasciitis (23).
ProteusÂ mirabilis: Proteus speciesÂ areÂ aÂ Gram-negative,Â facultative
bacilliÂ thatÂ colonizeÂ theÂ gastrointestinalÂ tractÂ andÂ areÂ aÂ sourceÂ of
nosocomial infection within hospitals and long-term care facilities (19, 24).
Usually associated with UTI, Proteus mirabilishas also been isolated from
abscesses, SSI, decubitus ulcers and burns (24).
PseudomonasÂ aeruginosa:Â PseudomonasÂ aeruginosa isÂ aÂ GramnegativeÂ bacillusÂ associatedÂ withÂ aÂ numberÂ ofÂ differentÂ opportunistic
infectionsÂ andÂ isÂ particularlyÂ problematicÂ forÂ ventilatedÂ patients,Â burn
patients and those with chronic debilities (19, 21, 26). Infections of the skin
include those affecting the feet and toenails (tinea), hot tub/swimming pool
infections (folliculitis) and burn wound sepsis (27). Recently, the ability of
P. aeruginosato form bio-films has been postulated as a mechanism for
long standing wounds that will not heal. (28).
StreptococcusÂ pyogenes (GAS): GASÂ isÂ aÂ Gram-negative,Â coccus
that resides harmlessly on the skin as a commensal until the protective
skin barrier is breeched and it becomes pathogenic. GAS is a causative
factor,Â alongÂ with StaphylococcusÂ aureus,Â forÂ impetigo.Â WhileÂ impetigo
itselfÂ isÂ notÂ life-threatening,Â itÂ canÂ leadÂ toÂ moreÂ seriousÂ complictions,
includingÂ cellulitisÂ andÂ MRSAÂ affectingÂ theÂ skinÂ andÂ poststreptococcal
glomurelonephritis affecting the kidney (29).
Streptococcus agalactiae(GBS): GBS is a Gram-positive coccus that
causesÂ aÂ numberÂ ofÂ seriousÂ infectionsÂ inÂ bothÂ pregnantÂ womenÂ and
adults with underlying health issues, like diabetes mellitus, heart disease
and malignancy. Aside from its role in neonatal sepsis, GBS has been
associatedÂ withÂ infectionsÂ withinÂ theÂ over-seventyÂ yearsÂ ofÂ ageÂ group,
particularly the bedridden and those afflicted with congestive heart failure,
where UTI, pneumonia and soft tissue infections are the most frequent
manifestationsÂ (19,Â 21,Â 30).Â Streptococci,Â alongÂ withÂ Staphylococci,
areÂ theÂ leadingÂ causativeÂ agentsÂ associatedÂ withÂ theÂ potentiallyÂ lifethreatening skin infection, cellulitis (30).
StaphylococcusÂ aureus withÂ methicillinÂ resistanceÂ screening:
StaphylococcusÂ aureus isÂ aÂ Gram-positiveÂ coccusÂ thatÂ isÂ largely
considered to be normal flora of the skin. However, upon breach of this
protective barrier, Staph can become highly pathogenic, particularly within
individuals having chronic disorders such as diabetes, cancer, vascular
andÂ lungÂ disease,Â eczemaÂ andÂ individualsÂ withÂ weakenedÂ immune
systems.Â InfectionsÂ ofÂ theÂ skinÂ oftenÂ goÂ untreatedÂ asÂ initialÂ infections
resembleÂ pimplesÂ orÂ spiderÂ bites,Â allowingÂ theÂ infectionÂ toÂ progressÂ to
greaterÂ degreesÂ ofÂ severity.Â InfectionsÂ areÂ furtherÂ complicatedÂ byÂ the
emergence and circulation of methicillin-resistant strains (19, 21, 32).
Clinical Benefits of Testing
MDLÂ offersÂ highlyÂ sensitiveÂ andÂ specificÂ quantitativeÂ Real-TimeÂ PCR
(qPCR) based assays for the detection of skin and soft tissue infection
associated pathogens utilizing the OneSwabÂ®
366Â Â SkinÂ &Â SoftÂ TissueÂ InfectionsÂ (SSTI)Â Panel
byÂ Real-TimeÂ PCRÂ [BacteroidesÂ fragilis,
EnterococcusÂ faecalis,Â EscherichiaÂ coli,Â Group A
Streptococcus, Group B Streptococcus, Klebsiella
species, Prevotella Groups 1 & 2, Proteus mirabilis,
PseudomonasÂ aeruginosa,Â Staphylococcus
aureus,Â methicillinÂ resistantÂ Staplyococcusa
aureusÂ (MRSA),Â CommunityÂ AssociatedÂ MRSA
Table 2. Summary of Treatment Options.
Abbreviations: PO (per OS oral) IM (intramuscular); IV (intravenous); MRSA
(Methicillin-ResistantÂ StaphylococcusÂ aureus)Â andÂ CA-MRSAÂ (CommunityassociatedÂ MRSA).Â EnterobacteriaceaeÂ includesÂ entericsÂ suchÂ as E.Â coli, Klebsiella species, and Proteus species.a Methicillin-Resistant StaphylococcusÂ aureus isolatesÂ areÂ resistantÂ toÂ the ÃŸ-lactam class of antibiotics (e.g. penicillin, ampicillin, amoxicillin, piperacillin, cephalosporins, carbepenems). For hospital-associated MRSA (HA-MRSA or MRSA), vancomycin (IV), linezolid (PO, IV), and daptomycin (IV) are effective. TheseÂ antibioticsÂ areÂ notÂ includedÂ inÂ theÂ panelÂ dueÂ toÂ veryÂ lowÂ levelsÂ of resistance.
Community-associatedÂ MRSAÂ (CA-MRSA),Â TypeÂ IVÂ SCCÂ andÂ PantonValentine Leukocidin postive, unlike HA-MRSA, are often susceptible to other non-ÃŸ-lactamÂ commonÂ antibioticsÂ suchÂ asÂ trimethoprim-sulfamethoxazole, doxycycline, and clindamycin.
StreptococcusÂ speciesÂ areÂ susceptibleÂ toÂ theÂ ÃŸ-lactamÂ classÂ ofÂ antibiotics
(e.g.Â penicillin,Â ampicillin,Â cephalosporins,Â carbepenems).Â ForÂ penicillin
allergic patients at risk for anaphylaxis, clindamycin, vancomycin, doxycycline,
fluoroquinolones can be alternatives.
ForÂ anaerobicÂ bacteria,Â metronidazoleÂ isÂ used,Â oftenÂ inÂ combination withÂ ampicillin,Â amoxicillin,Â cephalosporinsÂ withÂ anaerobicÂ activity,Â and/or fluoroquinolones.
ForÂ EnterococcusÂ spp.,Â combinationÂ therapyÂ ofÂ ampicillin,Â penicillin,Â or vancomycinÂ (forÂ susceptibleÂ strains),Â plusÂ anÂ aminoglycoside,Â isÂ usually indicatedÂ forÂ seriousÂ EnterococcalÂ infections,Â unlessÂ high-levelÂ resistance toÂ bothÂ gentamicinÂ andÂ streptomycinÂ isÂ documented;Â suchÂ combinations areÂ predictedÂ toÂ resultÂ inÂ synergisticÂ killingÂ ofÂ theÂ Enterococcus.Â High-level gentamicin resistance screening is not performed in this antibiotic susceptibility assay
1.Â Fredricks DN. 2001. Microbial Ecology of the Human Skin in Health and Disease. J
Investig Dermatol Symp Proc 6(3):167-9.
2.Â Chiller K, Selkin BA, Murakawa GJ. 2001. Skin Microflora and Bacterial Infections
of the Skin. J Investig Dermatol Symp Proc 6(3):170-4.
3.Â Moet GJ, Jones RN, Biedenbach DJ, et al.2007. Contemporary Causes of Skin
andÂ SoftÂ TissueÂ InfectionsÂ inÂ NorthÂ America,Â LatinÂ AmericaÂ andÂ Europe:Â Report
from the SENTRY Antimicrobial Surveillance Program (1998-2004). Diagn Microbiol
Infect Dis 57(1):7-13.
4.Â Dowd SE, Sun Y, Secor PR, et al.2008. Survey of Bacterial Diversity in Chronic
Wounds Using Pyrosequencing, DGGE, and Full Ribosome Shotgun Sequencing.
BMC Microbiol 8:43.
5.Â Dowd SE, Wolcott RD, Sun Y, et al.2008. Polymicrobial Nature of Chronic Diabetic
Foot Ulcer Biofilm Infections Determined Using Bacterial Tag Encoded FLX Amplicon
Pyrosequencing (bTEFAP). PLoS One 3(10):e3326.
6.Â James GA, Swogger E, Wolcott R, et al. 2008. Biofilms in Chronic Wounds. Wound
Repair Regen. 16(1):37-44.
7.Â Mangram AJ, Horan TC, Pearson ML, et al.1999. Guidelines for Prevention of
SurgicalÂ SiteÂ Infection,Â 1999.Â CentersÂ forÂ DiseaseÂ ControlÂ andÂ PreventionÂ (CDC)
HospitalÂ InfectionÂ ControlÂ PracticesÂ AdvisoryÂ Committee. AmÂ JÂ InfectÂ Control
8.Â National Pressure Ulcer Advisory Panel. Pressure Ulcer Stages Revised by NPUAP.
Accessed February 12, 2012. http://www.npuap.org/pr2.htm.
9.Â American Diabetes Association. 2011 Data from the 2011 National Diabetes Fact
Sheet (release January 26, 2011). Accessed January 26, 2012. http://www.diabetes.
10.Â Woundinfection.net. 2012. Accessed XXX. http://woundinfection.net/diabetic.html
11.Â Driver VR, Fabbi M, Lavery LA, et al. 2010. The Cost of Diabetic Foot: The Economic
Case for the Limb Salvage Team. J Vasc Surg 52(12S):17S-22S.
12.Â CaballeroÂ E,Â FrykbergÂ RG.Â 1998.Â DiabeticÂ FootÂ Infections.Â JÂ FootÂ AnkleÂ Surg
13.Â Frykberg RG. 2002. Diabetic Foot Ulcers: Pathogensis and Management. Am Fam
14.Â Park-Lee E, Caffrey C. 2009. Pressure Ulcers Among Nursing Home Residents:
United States, 2004. NCHS data brief, no. 14. Hyattsville, MD: National Center for
15.Â Mayo Clinic. Bedsores (pressure sores). Accessed January 26, 2012. http://www.
16.Â ClevelandÂ Clinic.Â LowerÂ ExtremityÂ (LegÂ andÂ Foot)Â Ulcers. AccessedÂ JanuaryÂ 26,
17.Â MikaelÂ Haggstrom.Â WoundÂ HealingÂ Phases.Â AccessedÂ JanuaryÂ 26,Â 2012. http://
18.Â BrookÂ I, etÂ al. 2011.Â BacteroidesÂ Infection.Â AccessedÂ FebruaryÂ 14,Â 2012.Â http://
19.Â DrydenÂ MS.Â 2010.Â ComplicatedÂ SkinÂ andÂ SoftÂ TissueÂ Infection.Â JÂ Antimicrob
Chemother65 Suppl 3:iii35-44.
20.Â Owens CD, Stoessel K. 2008. Surgical Site Infections: Epidemiology, Microbiology
and Prevention. J Hosp Infect70 Suppl 2:3-10.
21.Â Sapico FL, Canawati HN, Witte JL, et al.1980. Quantitative Aerobic and Anaerobic
Bacteriology of Infected Diabetic Feet. J Clin Micro 12(3):413-20.
22.Â Umeh O. 2011. Klebsiella Infections. Accessed February 14, 2012. http://emedicine.
23.Â American Academy of Pediatrics. Summaries of Infectious Diseases. In: Pickering
LK, Baker CJ, Kimberlin DW, Long SS, eds. Red Book: 2009 Report of the Committee
onÂ InfectiousÂ Diseases.Â 28thÂ ed.Â ElkÂ GroveÂ Village,Â IL:Â AmericanÂ AcademyÂ of
24.Â Struble K, Bronze MS, Jackson RL. 2011. Proteus Infections. Accessed February
14, 2012. http://emedicine.medscape.com/article/226434-overview.
25.Â SaviniÂ V,Â etÂ al.Â 2008.Â UlcerÂ InfectionÂ byÂ ESbetaL-ProducingÂ ProteusÂ mirabilis: A
Case Report. Int J Low Extrem Wounds. 7(2):99-101.
26.Â MerckÂ Manual.Â PseudomonasÂ andÂ RelatedÂ Infections.Â 2009.Â AccessedÂ February
16,Â 2012.Â http://www.merckmanuals.com/professional/infectious_diseases/gramnegative_bacilli/pseudomonas_and_related_infections.html
27.Â Lessnau K-D, Cunha BA, Dua P, et al. 2012. Pseudomonas aeruginosaInfections.
AccessedÂ FebruaryÂ 16,Â 2012. http://emedicine.medscape.com/article/226748-overview.
28.Â Bjarnsholt T, Kirketerp-Moller K, Jensen PO, et al. 2008. Why Chronic Wounds
Will Not Heal: A Novel Hypothesis. Wound Rep Reg 16:2-10.
29.Â Mayo Clinic. 2010. Impetigo. Accessed February 16, 2012. http://www.mayoclinic.
30.Â Woods, CJ, Levy CS. 2011. Streptococcus Group B Infections. Accessed February
16, 2012. http://emdicine.medscape.com/article/229091-overview.
31.Â Mayo Clinic. 2010. Cellulitis. Accessed February 16, 2012. http://www.mayoclinic.
32.Â Centers for Disease Control. Methicillin-Resistant Staphylococcus Aureus(MRSA)
Infections. Accessed February 16, 2012. http://www.cdc.gov/mrsa/.
33.Â Edwards R, Harding KG. 2004. Bacteria and Wound Healing. Curr Opin Infect Dis
34.Â LazenbyÂ GB,Â SoperÂ DE.Â 2010.Â Â Prevention,Â Diagnosis,Â andÂ TreatmentÂ of
Gynecologic Surgical Site Infections. Obstet Gynecol Clin N Am 37: 379-386.
35.Â May AK, Stafford RE, Bulger EM, et al.2011. Skin and Soft Tissue Infections: The
New Surgical Infection Society Guidelines. Surgical Infect 12: 179-184.
36.Â StevensÂ DL,Â Bisno AL,Â ChamberÂ HF,Â etÂ al.Â 2005.Â Â PracticeÂ GuidelinesÂ forÂ the
Diagnosis and Management of Skin and Soft-Tissue Infections (IDSA Guidelines).
Clin Infect Dis 41: 1373-1406.
37.Â Clinical and Laboratory Standards Institute: Performance Standards for Antimicrobial
Susceptibility Testing; Twenty-First Informational Supplement. M100-S21, 2011, Vol.
Effective Not Effective
Amoxacillin-clavulanic acidÂ PO
Clindamycin PO, IM, IV
Not for pregnancy
or children < 8yrs
Trimethoprim-sulfamethoxazole PO, IV
Ciprofloxacin PO, IV
(Levofloxacin for Strep.)
Not for pregnancy
Cefepime IM, IV
Imipenem IM, IV
Gentamicin IM, IV Combination antibiotic e