Reading list.indd - The British Society for Antimicrobial Chemotherapy

122 Pages·2009·2.87 MB·English

Management of the diabetic foot
Difficult to treat Scottish Intercollegiate Guidelines
CLICK HERE
Network, Management of diabetes.
infections SIGN 2001, guidelines 55
Diagnosis and treatment of diabetic foot
CLICK HERE
infections
Clinical Infectious Diseases 2004; 39:885-
910
Wound microbiology and approaches to
CLICK HERE
wound management
Clinical Microbiology Review 2001; 14:244-
269
Culture of percutaneous bone biopsy
CLICK HERE
specimens for diagnosis of diabetic foot
osteomyelitis: concordance with ulcer
Educational
swab cultures
Clinical Infectious Diseases 2006; 42: 57-62
Workshops
Diagnostic accuracy of the physical
CLICK HERE
2009 examination and imaging tests for
osteomyelitis underlying diabetic foot
ulcers: meta-analysis.
Clinical Infectious Diseases 2008; 47:519-27
Venues throughout the UK
October - November 2009
Probing to bone in infected pedal ulcers: a
CLICK HERE
clinical sign of underlying osteomyelitis in
diabetic patients
The Journal of the American Medical
Association 1995; 273:721-3
READING LIST
Diabetic foot ulcer classifi cation system
CLICK HERE
for research purposes: a progress report
on criteria for including patients in
research studies.
Diabetes/metabolism research and reviews
2004; 20 (supplement 1): S90-95
Fungal infection of the diabetic foot: two
CLICK HERE
ditinct syndromes
Diabetic Medicine 2001; 18:567-72
Rifampicin-ofl oxacin oral regimen for the
CLICK HERE
treatment of mild to moderate diabetic
foot osteomyelitis
Journal of Antimicrobial Chemotherapy
2001; 48:927-30
Treating foot infections in diabetic
CLICK HERE
patients: a randomized, multicenter, open-
label trail of Linezolid versus ampicillin-
sulbactam/amoxicillian-clavulanate
Clinical Infectious Diseases 2004; 38:17-24
Difficult to treat Ertapeenem versus peperacillin/ CLICK HERE
tazobactam for diabetic foot infections
infections (SIDESTEP): prospective, randomized,
controlled, double-blinded, multicentre
trial
Lancet 2005; 366:1695-703
Daptomycin for treating infected diabetic
CLICK HERE
foot ulcers: evidence from a randomized,
controlled trial comparing daptomycin
with vancomycin or semi-synthetic
penicillins for complicated skin-structure
infections
Journal of Antimicrobial Chemotherapy
2005; 55:240-5
Cost-minimization analysis and audit of
Educational CLICK HERE
antibiotic management of bone and joint
infections with ambulatory teicoplanin,
Workshops
in-patient care or outpatient oral linezolid
therapy
2009 Journal of Antimicrobial Chemotherapy
2003; 51: 391-396
Practice guidelines for outpatient
Venues throughout the UK CLICK HERE
parenteral antimicrobial therapy
October - November 2009
Clinical Infectious Diseases 2004; 38:
1651-72
Prosthetic Joint Infections
READING LIST Diagnosis and management of prosthetic
CLICK HERE
joint infection
BMJ 2009; 338:b1773, doi: 10.1136/bmj.
b1773
One hundred and twelve infected
CLICK HERE
arthroplasties treated with ‘DAIR’
(debridement, antibiotics and implant
retention): antibiotic duration and
outcome
Journal of Antimicrobial Chemotherapy
2009 June; 63 (6): 1264-71
Two-stage revision of infected hip
CLICK HERE
arthroplasty using a shortened post-
operative course of antibiotics
Archives of orthopaedic and trauma
surgery 2009 Apr; 129 (4): 489-94
Prosthetic Joint Infections
CLICK HERE
The New England Journal of Medicine 2004;
351: 1645-1654
Difficult to treat Is there a role for extended antibiotic CLICK HERE
therapy in a two-stage revision of the
infections infected knee arthroplasty?
Journal of Bone Joint Surgery 2005 Feb; 87
(2): 171-4
Prospective evaluation of criteria for
CLICK HERE
microbiological diagnosis of prosthetic
joint infection at revision arthroplasty
Journal of Clinical Microbiology 1998; 36:
2932-2939
Vascular Graft Infections
Correlation between reduced daptomycin
CLICK HERE
susceptibility and vancomycin
resistance in vancomycin-intermediate
Educational
staphylococcus aureus
Antimicrobial Agents and Chemotherapy;
Workshops
2006 Mar: 1079-1082
2009 Failures in clinical treatment of
CLICK HERE
staphylococcus aureus infection with
daptomycin are associated with
alterations in surface charge, membrane
Venues throughout the UK
phospholipid asymmetry and drug
October - November 2009
binding
Antimicrobial Agents and Chemotherapy;
2008 Jan: 269-278
Detection of aortic graft infection by
CLICK HERE
READING LIST fl uorodeoxyglucose positron emission
tomography: comparison with computed
tomographic fi ndings
Journal of Vascular Surgery; vol 42, no 5:
919-925
Prosthetic vascular graft infection: A risk
CLICK HERE
factor analysis using a case-control study
Journal of Infection 2006; 53: 49-55
CLINICALMICROBIOLOGYREVIEWS,Apr.2001,p.244–269 Vol.14,No.2
0893-8512/01/$04.0010 DOI:10.1128/CMR.14.2.244–269.2001
Copyright©2001,AmericanSocietyforMicrobiology.AllRightsReserved.
Wound Microbiology and Associated Approaches to
Wound Management
P.G.BOWLER,1*B.I.DUERDEN,2,3ANDD.G.ARMSTRONG4,5
ConvaTecGlobalDevelopmentCenter,Deeside,Flintshire,1DepartmentofMedicalMicrobiology,UniversityofWales
CollegeofMedicine,Cardiff,2PublicHealthLaboratoryService,London,3andDepartmentofMedicine,
ManchesterRoyalInfirmary,Manchester,4UnitedKingdom,andDepartmentofSurgery,
SouthernArizonaVeteransAffairsMedicalCenter,Tucson,Arizona5
INTRODUCTION.......................................................................................................................................................245
WOUNDTYPES.........................................................................................................................................................245
WOUNDMICROBIOLOGY.....................................................................................................................................246
MicrobialColonization..........................................................................................................................................246
FactorsPredisposingtoMicrobialProliferation................................................................................................246
WoundInfection......................................................................................................................................................247
Surgicalwoundinfections..................................................................................................................................248
Acutesofttissueinfections................................................................................................................................250
Bitewoundinfections.........................................................................................................................................250
Burnwoundinfections.......................................................................................................................................250
Diabeticfootulcerinfections............................................................................................................................250
Leganddecubitus(pressure)ulcerinfections...............................................................................................251
SignificanceofMicroorganismsinWounds........................................................................................................251
Quantitativemicrobiology:significanceofmicrobialnumbers....................................................................251
Qualitativemicrobiology:significanceofspecificmicroorganisms.............................................................252
MICROBIOLOGICALANALYSISOFWOUNDS................................................................................................254
Wound-SamplingMethods....................................................................................................................................254
Woundtissuesampling......................................................................................................................................254
Woundfluidsampling........................................................................................................................................254
SpecimenTransport...............................................................................................................................................256
AnalysisofWoundSpecimens..............................................................................................................................256
Gas-liquidchromatographyformalodorousspecimens................................................................................257
Gramstain...........................................................................................................................................................257
Cultureofwoundspecimens.............................................................................................................................257
Reportingofmicrobiologicalresults................................................................................................................258
CONTROLOFMICROBIALPOPULATIONSINWOUNDS............................................................................258
AntimicrobialMethodsofTreatment..................................................................................................................259
Antibiotics............................................................................................................................................................259
(i)Acutewounds.............................................................................................................................................259
(ii)Chronicwounds........................................................................................................................................260
(iii)Complementarytherapy.........................................................................................................................260
(iv)Roleofthemicrobiologylaboratoryinguidingantibiotictreatmentinwoundmanagement.....260
Antiseptics............................................................................................................................................................261
Alternativeantimicrobialtherapies..................................................................................................................261
Hyperbaricoxygentherapy................................................................................................................................262
NonantimicrobialMethodsofTreatment............................................................................................................263
Debridement........................................................................................................................................................263
(i)Surgicaldebridement................................................................................................................................263
(ii)Autolyticandenzymaticdebridement...................................................................................................263
(iii)Biosurgicaldebridement........................................................................................................................263
Pressurereductioninwounds...........................................................................................................................263
(i)Off-loading..................................................................................................................................................263
(ii)Vacuum-assistedwoundclosure.............................................................................................................264
InfectionControl.................................................................................................................................................264
CONCLUSIONS.........................................................................................................................................................264
REFERENCES............................................................................................................................................................265
*Corresponding author. Mailing address: ConvaTec GDC, First
Avenue, Deeside Industrial Park, Deeside, Flintshire CH5 2NU,
UnitedKingdom.Phone:[phone].Fax:[phone].
E-mail:[email protected].
244
VOL.14,2001 WOUND MICROBIOLOGY 245
INTRODUCTION There is also debate about whether a wound should be
sampledforculture,thevalueofwoundsamplingindetermin-
Fromamicrobiologicalperspective,theprimaryfunctionof
ing the cause of infection and subsequent treatment, and the
normal,intactskinistocontrolmicrobialpopulationsthatlive
sampling technique required to provide the most meaningful
on the skin surface and to prevent underlying tissue from
data. Regarding the role of the microbiology laboratory, con-
becoming colonized and invaded by potential pathogens. Ex-
siderationmustbegiventotherelevanceofculturingpolymi-
posureofsubcutaneoustissuefollowingalossofskinintegrity
crobialspecimens,thevalueofidentifyingoneormoremicro-
(i.e.,awound)providesamoist,warm,andnutritiousenviron-
organisms, and which microorganisms (if any) should be
mentthatisconducivetomicrobialcolonizationandprolifer-
assayed for antibiotic susceptibility. By questioning and justi-
ation. However, the abundance and diversity of microorgan-
fyingtheneedtosampleandperformmicrobiologicalanalyses
ismsinanywoundwillbeinfluencedbyfactorssuchaswound
on any problematic wound, long-term savings in cost, labor,
type,depth,location,andquality,theleveloftissueperfusion,
andtimetoboththewoundmanagementteamandthemicro-
and the antimicrobial efficacy of the host immune response.
biology laboratory could be considerable. In this respect, the
Whereasthemicrofloraassociatedwithclean,surgicalwounds
valueoftheGramstainasaquickandinexpensiveadditional
would be expected to be minimal, the presence of foreign
oralternativetestisalsoworthyofconsideration.
materialanddevitalizedtissueinatraumaticwoundislikelyto
Although appropriate systemic antibiotics are considered
facilitate microbial proliferation unless early prophylactic an-
essential for the treatment of nonhealing, clinically infected
tibiotic treatment and surgical debridement is implemented
wounds, there is debate about the relevance and use of sys-
(201).
temic and topical antibiotics and of topical antiseptics in the
Since wound colonization is most frequently polymicrobial
treatment of nonhealing, noninfected wounds. Other, nonmi-
(25,27,44,166,226),involvingnumerousmicroorganismsthat crobiologicalapproachestocontrollingpotentiallypathogenic
are potentially pathogenic, any wound is at some risk of be- microbialpopulationsinwoundsmustalsobeconsideredpart
coming infected. In the event of infection, a wound fails to ofamultidisciplinarywoundmanagementeffort.
heal,thepatientsuffersincreasedtrauma,treatmentcostsrise, Inviewofthefears,uncertainties,andcontroversiesregard-
and general wound management practices become more re- ingtheroleofmicroorganismsinwounds,thisreviewaimsto
source demanding. An analysis of postsurgical wound infec- capturecurrentopinion,evaluatetheroleofthemicrobiologist
tions following head and neck surgery demonstrated an in- and the microbiology laboratory in wound management, and
creaseintheaveragehospitalizationperiodfrom14dayswhen clarify the relevance of treatment and treatment options in
wounds healed without complication to 24 days when the controllingmicrobialcolonizationandinfectioninwounds.
wounds became infected (118). In a similar analysis of 108
postsurgicalwounds,Zoutmanetal.(249)concludedthat10.2
WOUNDTYPES
dayspercasewasdirectlyattributabletowoundinfectionand
that the associated hospital cost was $3,937 per infected pa- Wounds can be broadly categorized as having either an
tient. acute or a chronic etiology. Acute wounds are caused by ex-
Thus,concernamonghealthcarepractitionersregardingthe ternaldamagetointactskinandincludesurgicalwounds,bites,
risk of wound infection is justifiable not only in terms of in- burns, minor cuts and abrasions, and more severe traumatic
creasedtraumatothepatientbutalsoinviewofitsburdenon woundssuchaslacerationsandthosecausedbycrushorgun-
financial resources and the increasing requirement for cost- shot injuries (60). Irrespective of the nature of the cutaneous
effective management within the health care system. From a injury,acutewoundsareexpectedtohealwithinapredictable
clinicalperspective,fearsassociatedwithwoundinfectionhave timeframe,althoughthetreatmentrequiredtofacilitateheal-
paralleled the increasing use of occlusive dressings since the ingwillvaryaccordingtothetype,site,anddepthofawound.
1960s.Theprimaryfunctionofdressingssuchaspolyurethane The primary closure of a clean, surgical wound would be ex-
films, polyurethane foams, and hydrocolloids is to maintain a pected to require minimal intervention to enable healing to
moist and optimal environment for wound healing. Although progress naturally and quickly. However, in a more severe
they have been reported to encourage microbial proliferation traumaticinjurysuchasaburnwoundorgunshotwound,the
inwounds(95,128),theinfectionrateislowerunderocclusive presence of devitalized tissue and contamination with viable
dressingsthanunderconventionaldrydressings(24,113)and (e.g., bacterial) and nonviable foreign material is likely to re-
woundhealingisnotimpaired(95). quire surgical debridement and antimicrobial therapy to en-
Although microorganisms are responsible for wound infec- ablehealingtoprogressthroughanaturalseriesofprocesses,
tion, widespread controversy still exists regarding the exact including inflammation and granulation, to final reepithelial-
mechanisms by which they cause infection and also their sig- izationandremodeling.
nificance in nonhealing wounds that do not exhibit clinical In marked contrast, chronic wounds are most frequently
signsofinfection.Oneschoolofthoughtisthatthedensityof caused by endogenous mechanisms associated with a predis-
microorganismsisthecriticalfactorindeterminingwhethera posing condition that ultimately compromises the integrity
wound is likely to heal (100, 102, 151, 196, 202). However, a ofdermalandepidermaltissue(60).Pathophysiologicalab-
second school of thought argues that the presence of specific normalitiesthatmaypredisposetotheformationofchronic
pathogens is of primary importance in delayed healing (59, wounds such as leg ulcers, foot ulcers, and pressure sores
130,149,181,216,217),whileyetothershavereportedmicro- include compromised tissue perfusion as a consequence of
organismstobeofminimalimportanceindelayedhealing(4, impaired arterial supply (peripheral vascular disease) or im-
70,80,95,98,214,237). paired venous drainage (venous hypertension) and metabolic
246 BOWLER ET AL. CLIN.MICROBIOL.REV.
diseases such as diabetes mellitus. Advancing age, obesity, the microbial population in both acute and chronic wounds
smoking, poor nutrition, and immunosuppression associated (25, 27, 28, 33–38, 41–45, 64, 80, 98, 143, 166, 185, 213, 226).
with disease (e.g., AIDS) or drugs (e.g., chemotherapy or ra- OnthebasisofthestudiesreviewedinTable1,whichinvolved
diationtherapy)mayalsoexacerbatechroniculceration.Pres- detailedmicrobiologicalanalysesofclinicallynoninfected(i.e.,
sure or decubitus ulcers have a different etiology from other colonized) wounds of varied etiology, anaerobes constituted,
chronic wounds in that they are caused by sustained external onaverage,38%ofthetotalnumberofmicrobialisolatesper
skin pressure, most commonly on the buttocks, sacrum, and study. It should be emphasized that the studies reported did
heels.However,theunderlyingpathologyoftencontributesto not investigate specifically the effect of microorganisms on
chronicity,andinthissituation,pressuresores,likeallchronic woundhealing.
woundtypes,healslowlyandinanunpredictablemanner. Recognition of the fact that anaerobes are too often over-
looked,althoughmanyarepotentiallyhighlyvirulent,hasled
WOUNDMICROBIOLOGY expertsinthefieldtodefinemembersofthisgroupofbacteria
as being “the secret pathogens” (74) and “invisible villains”
(18). Nichols and Smith (175) reported that endogenous an-
MicrobialColonization
aerobic bacteria were the likely cause of postoperative infec-
Exposedsubcutaneoustissueprovidesafavourablesubstra- tionswhenwoundspecimensfailedtoyieldbacterialgrowthon
tumforawidevarietyofmicroorganismstocontaminateand routineculture.
colonize,andiftheinvolvedtissueisdevitalized(e.g.,ischemic, Thefailuretorecognisetheprevalenceofanaerobicbacteria
hypoxic, or necrotic) and the host immune response is com- inwoundsmaybeduetoseveralreasons.(i)Anaerobesarenot
promised, the conditions become optimal for microbial growth. regarded as being detrimental to normal wound healing (70,
Wound contaminants are likely to originate from three main 80, 150, 217). (ii) Compared with aerobic and facultative mi-
sources: (i) the environment (exogenous microorganisms in the croorganisms, the culture, isolation, and identification of an-
airorthoseintroducedbytraumaticinjury),(ii)thesurrounding aerobicbacteriaismoretime-consuming,labor-intensive,and
skin (involving members of the normal skin microflora such as expensiveandisoftendeemedtobetoodemandingformany
Staphylococcus epidermidis, micrococci, skin diphtheroids, and diagnosticmicrobiologylaboratories.Therelevanceofcultur-
propionibacteria),and(iii)endogenoussourcesinvolvingmucous ingspecimensforanaerobicbacteriaisdiscussedin“Microbi-
membranes (primarily the gastrointestinal, oropharyngeal, and ological analysis of wounds” below. (iii) Since anaerobes are
genitourinarymucosae)(65).Thenormalmicroflorasofthegut, often perceived to die rapidly in air, the method of specimen
theoralcavity,andthevaginaarebothdiverseandabundant,and collection and transportation to the laboratory is assumed to
thesesources(particularlytheoralandgastrointestinalmucosae) be critical for maintaining viability and for effective culture.
supplythevastmajorityofmicroorganismsthatcolonizewounds. However, many of the frequent wound colonizers, including
Detailed microbiological analyses of wounds demonstrate close Bacteroides,Prevotella,Porphyromonas,andPeptostreptococcus
correlationsbetweenthespeciesfoundinthenormalfloraofthe spp.,willsurviveforseveraldaysinthepresenceofair(17,26,
gutororalcavityandmicroorganismspresentinwoundsinclose 99, 142). Consequently, the methods for sampling and trans-
proximitytothosesites(33–35,43,46).Whereasaminor,healing portation are probably less critical than the microbiological
woundmayallowsufficienttimeforaonlyrelativelysmallnumber methodsusedtoensureeffectiveisolationofanaerobicbacte-
ofskincontaminantstotakeresidence,thecontinuedexposureof ria.However,thisdoesnotimplythatspecimencollectionand
devitalizedtissueassociatedwithaslowlyhealingchronicwound transport should be performed without the utmost care and
islikelytofacilitatethecolonizationandestablishmentofawide meticulousprocedures.
varietyofendogenousmicroorganisms.Dentalplaque,thegingi- Bothacuteandchronicwoundsaresusceptibletocontami-
valcrevice,andthecontentsofthecoloncontainapproximately nation and colonization by a wide variety of aerobic and an-
1011to1012microorganisms/goftissue,ofwhich,upto90%of aerobicmicroorganisms,asindicatedinTable2.
theoralmicroflora(16)andupto99.9%ofthecolonicmicroflora
(105)areanaerobes.Inviewofthissituation,itisreasonableto FactorsPredisposingtoMicrobialProliferation
predictthatwoundswithasufficientlyhypoxicandreducedenvi-
ronmentaresusceptibletocolonizationbyawidevarietyofen- Surgicalwoundswillhealrapidlyifbloodperfusionismax-
dogenousanaerobicbacteria.However,todate,widespreadopin- imized, thus delivering oxygen, nutrients, and cells of the im-
ionamongwoundcarepractitionersisthataerobicorfacultative mune system to the site of injury and providing minimal op-
pathogens such as Staphylococcus aureus, Pseudomonas aerugi- portunityformicroorganismstocolonizeandproliferate(110).
nosa,andbeta-hemolyticstreptococciaretheprimarycausesof This situation is exemplified by wounds in the anus, which,
delayedhealingandinfectioninbothacuteandchronicwounds. despitebeingsusceptibletogrossmicrobialcontamination,are
Suchopinionhasbeenformedonthebasisofreferencedcom- verywellperfusedandrarelybecomeinfected(110).Theprob-
mentsandstudiesperformedlargelyduringthelasttwodecades abilityofwoundhealingisextremelyhighifthetissueoxygen
thathaveinvestigatedtheroleofmicroorganismsinwoundheal- tension(pO )is.40mmHg,buthealingisunlikelytooccur
2
ing(58,59,81,94,146,182,216,217,238;D.J.Leaper,Editorial, at levels of ,20 mm Hg (110). In well-perfused periwound
J.WoundCare7:373,1998).Acommonoversightintheseand tissue, reported oxygen tensions of 60 to 90 mm Hg compare
other studies and opinions is that the culture and isolation of withlevelsofnearzeroincentraldeadwoundspace(176).
anaerobic bacteria was minimal or omitted, whereas when In contrast, chronic, nonhealing wounds are frequently hy-
wounds are investigated by appropriate microbiological tech- poxic (218) as a consequence of poor blood perfusion (isch-
niquesanaerobesarefoundtoformasignificantproportionof emia), and host and microbial cell metabolism contributes
VOL.14,2001 WOUND MICROBIOLOGY 247
TABLE 1. Studiesinvolvingadetailedanalysisoftheaerobicandanaerobicmicrobiologyofnoninfectedwoundswithoutspecifically
investigatingtheroleofmicroorganismsinwoundhealing
Studydescription No.ofmicrobialisolates
Author(reference) Predominantisolates
(no.ofwounds) (%thatwereanaerobes)
Louieetal.1976(143) Microbiologyof20diabetic 116(45) Bacteroidesspp.,Peptostreptococcusspp.,
ulcers(scrapingsofulcerbed Proteusspp.
andwoundedge)
Brooketal.1981(46) 392specimenstakenfromburn 580(23) S.epidermidis,S.aureus,alpha-hemolytic
sitesin180children streptococci,Propionibacteriumacnes,
Peptostreptococcusspp.,Bacteroidesspp.
Sapicoetal.1986(213) 49specimensfrom25pressure 130(24) Bacteroidesspp.,coliforms,P.aeruginosa
sores
Brook1987(33) Aspiratesfromhumanand 59fromanimalbites(37); S.aureus,Peptostreptococcusspp.,Bacte-
animalbitewoundsin39 97fromhumanbites(55) roidesspp.(inbothwoundgroups)
children
Brooketal.1990(42) Analysisof584woundsfrom 1,470(62) Bacteroidesspp.,Peptostreptococcusspp.,
manysites S.aureus,Clostridiumspp.,Fusobacte-
riumspp.
Brook1991(37) Analysisofdecubitusulcersin 132(40) S.aureus,Peptostreptococcusspp.,B.fragi-
58children lisgroup,P.aeruginosa
Hanssonetal.1995(98) Analysisoflegulcerswithout 325(22) S.aureus,Enterococcusfaecalis,Enter-
clinicalsignsofinfectionin58 obactercloacae,Peptostreptococcusmag-
patients nus
Brooketal.1998(44) 43swabspecimensfromchronic 97(34) S.aureus,Peptostreptococcusspp.,B.fragi-
legulcersin41patients lisgroup
Bowleretal.1999(28) Swabspecimensfrom30 110(36) S.aureus,coliforms,coagulase-negative
noninfectedlegulcerswithout staphylococci,fecalstreptococci,Pepto-
clinicalsignsofinfection streptococcusspp.
further to a lowering of the local pO . Oxygen tensions of stratedinthecolon,wherevaluescanbeaslowas2250mV,
2
between 5 and 20 mm Hg have been recorded in nonhealing compared with approximately 1150 mV in normal tissue and
wounds (218), and values of less than 30 mm Hg have been upto1250mVincirculatingblood.Althoughsomeanaerobes
recorded in infected and traumatized tissue (164); this corre- have been reported to survive in an aerated broth culture
lateswithareportedpO requirementofapproximately30mm medium that was maintained at low E (73), other investiga-
2 h
Hg for active cell division (111). Thus, cell death and tissue tions have demonstrated that several intestinal pathogens
necrosiscausedbytissuehypoxiaoranoxiaarelikelytocreate (Clostridium perfringens, Bacteroides fragilis, and Peptostrepto-
idealgrowthconditionsformembersofthewoundmicroflora, coccusmagnus)wereinhibitedinthepresenceofoxygenatan
includingfastidiousanaerobesthatwillproliferateasresidual E of250mV(73).Also,thetoleranceofanaerobestoE is
h h
oxygen is consumed by facultative bacteria. Such interaction influencedbypH,asdemonstratedbyC.perfringens,whichhas
betweenmicroorganismswasrecognizedaslongagoas1915by a growth-limiting E of 130 mV at pH 7.8 but can survive at
h
Alexander Fleming in his studies on gunshot wounds during 1250mVatpH6.0(73).
the First World War (63). As well as being essential for cell Althoughopinionisconflictingregardingtheimportanceof
growth and wound healing, oxygen is a critical component of the redox potential in supporting the growth of anaerobic
therespiratoryburstactivityinpolymorphonuclearleukocytes bacteria, a wound environment that has a low oxygen tension
(PMNs), resulting in the intracellular production of highly (hypoxiaoranoxia)andalowredoxpotentialwillfacilitatethe
potentantimicrobialmetabolites.Asignificantreductioninthe developmentofpolymicrobialaerobic-anaerobicpopulations.
killing capacity of PMNs at a pO of ,30 mm Hg has been
2
reported (107), and in this respect, poorly perfused wound WoundInfection
tissueisconsideredtobefarmoresusceptibletoinfectionthan
arewoundsinvolvingwell-perfusedtissue(176). Infectionoccurswhenvirulencefactorsexpressedbyoneor
Although many endogenous anaerobes survive prolonged moremicroorganismsinawoundoutcompetethehostnatural
periods of exposure to air (17, 26, 99, 142, 230) and tolerate immunesystemandsubsequentinvasionanddisseminationof
oxygentensionsupto60mmHg(8%oxygen)(184),theredox microorganismsinviabletissueprovokesaseriesoflocaland
(oxidation-reduction)potential(E )oftissueisalsoimportant systemic host responses. Characteristic local responses are a
h
for their survival (11). Generally, a low E (measured in mil- purulentdischargeorpainfulspreadingerythemaindicativeof
h
livolts) favors the growth of anaerobic bacteria, as demon- cellulitisaroundawound(186).Theprogressionofawoundto
248 BOWLER ET AL. CLIN.MICROBIOL.REV.
TABLE 2. Aerobicandanaerobicisolatesfromacuteandchronicwoundsofvariedetiologya,b
Aerobicandfacultativemicroorganisms Typeofwound Anaerobicbacteria Typeofwound
Coagulase-negativestaphylococci A,C Peptostreptococcusasaccharolyticus A,C
Micrococcussp. C Peptostreptococcusanaerobius A,C
Staphylococcusaureus A,C Peptostreptococcusmagnus A,C
Beta-hemolyticstreptococcus(groupC) A Peptostreptococcusmicros A,C
Beta-hemolyticstreptococcus(groupG) C Peptostreptococcusprevotii A,C
Streptococcusspp.(fecal) A,C Peptostreptococcusindolicus C
Streptococcusspp.(viridans) A,C Peptostreptococcussp. A,C
Corynebacteriumxerosis C Streptococcusintermedius C
Corynebacteriumsp. A,C Clostridiumperfringens A,C
Bacillussp. A Clostridiumclostridioforme A,C
Clostridiumcadaveris A,C
Escherichiacoli A,C Clostridiumbaratii C
Escherichiahermanii A Clostridiumsepticum A
Serratialiquefaciens C Clostridiumhistolyticum A,C
Klebsiellapneumoniae A,C Clostridiumtertium A
Klebsiellaoxytoca A,C Clostridiumramosum C
Enterobactercloacae A,C Clostridiumsporogenes A,C
Enterobacteraerogenes C Clostridiumdifficile C
Citrobacterfreundii C Clostridiumbifermentans A
Proteusmirabilis A,C Clostridiumlimosum A
Proteusvulgaris C Eubacteriumlimosum C
Providenciastuartii A Propionibacteriumacnes A,C
Morganellamorganii C
Acinetobactercalcoaceticus A,C Bacteroidesfragilis A,C
Pseudomonasaeruginosa A,C Bacteroidesureolyticus A,C
Stenotrophomonasmaltophilia A Bacteroidesovatus A
Sphingobacteriummultivorum C Bacteroidesuniformis A,C
Bacteroidesstercoris C
Candidaparapsilosis A Bacteroidescapillosus C
Candidakrusei A Bacteroidesthetaiotaomicron C
Bacteroidescaccae C
Prevotellaoralis A,C
Prevotellaoris A,C
Prevotelladisiens A
Prevotellabivia C
Prevotellabuccae C
Prevotellasp. A
Prevotellacorporis A,C
Prevotellaintermedia A
Prevotellamelaninogenica C
Porphyromonasasaccharolytica A,C
Gram-negativepigmentedbacillus A,C
Fusobacteriumnecrophorum C
Veillonellaspp. A
aAdaptedfromreference27withpermissionofthepublisher.
bAcutewounds(A)includedprimarilycutaneousabscessesandpostsurgicalwounds;chronicwounds(C)includedprimarilylegulcers,footulcersandpressuresores.
Atotalof367isolateswereculturedfromthe106wounds(61acutewoundsand45chronicwounds).
an infected state is likely to involve a multitude of microbial ulcers (36 and 49%, respectively); a correlation between the
andhostfactors,includingthetype,site,size,anddepthofthe incidence of anaerobic bacteria and wound infection is thus
wound,theextentofnonviableexogenouscontamination,the evident.
levelofbloodperfusiontothewound,thegeneralhealthand Surgicalwoundinfections.Theriskofinfectionisgenerally
immune status of the host, the microbial load, and the com- based on the susceptibility of a surgical wound to microbial
binedlevelofvirulenceexpressedbythetypesofmicroorgan- contamination (196). Clean surgery carries a 1 to 5% risk of
isms involved. Most acute and chronic wound infections in- postoperativewoundinfection,andindirtyproceduresthatare
volve mixed populations of both aerobic and anaerobic significantlymoresusceptibletoendogenouscontamination,a
microorganisms, and this is demonstrated in Table 3, which 27%riskofinfectionhasbeenestimated(174).TheGuideline
collatessomeofthepublishedliteratureregardingthemicro- for Prevention of Surgical Site Infection, 1999 issued by the
biologyofavarietyofinfectedwoundtypes. CentersforDiseaseControlandPreventionclassifiedsurgical
The overall average percent frequencies of anaerobic bac- wound infections as being either incisional (involving skin,
teria in noninfected and infected wounds, based on data pre- subcutaneous tissue, or deeper fascia and muscle tissue) or
sentedinTables1and3,are38and48%,respectively.These organ/space, involving any internal organs or anatomical
numberscompareverycloselywiththoseobservedbyBowler spaces(151).Examplesofthelatterincludesurgeryassociated
and Davies (28) specifically in noninfected and infected leg withthelargeintestineandtheheadandneck,whereextensive
VOL.14,2001 WOUND MICROBIOLOGY 249
TABLE 3. Studiesinvolvingadetailedmicrobiologicalanalysisoftheaerobicandanaerobicmicrobiologyofinfectedwounds
Studydescriptionand No.ofmicrobialisolates
Author(reference) Predominantisolates
no.ofwounds (%thatwereanaerobes)
Sandersonetal.1979(212) Anaerobesin65purulentpost- 179(54) E.coli,Bacteroidesspp.,Peptostreptococcus
appendectomywounds(swab spp.
samples)
Brooketal.1981(46) Analysisof209cutaneousabscesses 467(58) S.aureus,Streptococcusspp.,E.coli,
inchildren Bacteroidesspp.
Wheat1986(243) Analysisof131infecteddiabetic 538(21) Peptostreptococcusspp.,Enterococcusspp.,
footulcersin130patients Staphylococcusspp.
Brook1989(34) 89specimensfrompostsurgical 235(55) E.coli,Bacteroidesspp.,Peptostreptococcus
abdominalwoundinfections spp.,Clostridiumspp.
Brook1989(36) Specimensfrom74patientswith 87(22) S.epidermidis,S.aureus,coliforms,
postthoracotomysternalwound Peptostreptococcusspp.
infections
Brook1989(35) AnalysisofpusfromaBartholin’s 67(64) Bacteroidesspp.,Peptostreptococcusspp.,
abscessin28patients E.coli
Brooketal.1990(42) Analysisof676cutaneousabscesses 1,702(65) Bacteroidesspp.,Peptostreptococcusspp.,
S.aureus,Clostridiumspp.,
Fusobacteriumspp.
Johnsonetal.1995(116) Swabsamplesfrom43diabeticfoot 285(36) Peptostreptococcusspp.,Prevotellaspp.,
ulcers(46infectedsites) Bacteroidesspp.(emphasison
anaerobes)
Brook1995(38) Analysisofpusfromgastrostomy 102(44) E.coli,Peptostreptococcusspp.,
sitewoundinfectionsin22 Enterococcusspp.,Bacteroidesspp.,
children S.aureus
Summanenetal.1995(226) Comparisonofthemicrobiologyof 304(43)fromIVDU; S.aureus,“Streptococcusmilleri,”
softtissueinfectionsinIVDUa 222(48)from Peptostreptococcusspp.,Prevotellaspp.,
andnon-IVDU(160abscesses non-IVDU Bacteroidesspp.,Streptococcuspyogenes
sampled)
Brook1996(39) Microbiologyofspecimensfrom8 21(62) Peptostreptococcusspp.,Streptococcus
childrenwithnecrotizingfasciitis pyogenes,Bacteroidesspp.
DiRosaetal.1996(64) Roleofanaerobesin300 639(23) Clostridiumspp.,Bacteroidesspp.,
postoperativewoundinfections Peptostreptococcusspp.(emphasison
anaerobes)
Mousa1997(166) Swabsamplesofburnwoundsfrom 377(31) P.aeruginosa,S.aureus,Bacteroidesspp.,
127patients Peptostreptococcusspp.,Klebsiellaspp.
Brooketal.1997(43) Analysisofperirectalabscessesin44 456(72) B.fragilisgroup,Peptostreptococcusspp.,
patients Prevotellaspp.,S.aureus,Streptococcus
spp.
Brooketal.1998(45) Analysisof368specimensfrom340 711(63) B.fragilisgroup,Peptostreptococcusspp.,
traumapatientswithwound Clostridiumspp.,S.aureus,Prevotella
infection spp.
Brook1998(40) Analysisof175specimensfrom166 521(70) Peptostreptococcusspp.,Prevotellaspp.
childrenwithinfectedtraumatic Fusobacteriumspp.,S.aureus,B.fragilis
wounds group
Pathareetal.1998(185) Pusortissuespecimensfrom252 775isolates(29) Staphylococcusspp.,Streptococcusspp.,
diabeticfootinfections Peptostreptococcusspp.
Bowleretal.1999(28) Swabsamplesof44infectedleg 220isolates(49) Peptostreptococcusspp.,coliforms,
ulcers(basedonclinicalsigns) coagulase-negativestaphylococci,
pigmentedandnonpigmentedgram-
negativebacteria(anaerobes),fecal
streptococci
aIVDU,intravenousdruguser.
endogenous wound contamination, and hence a higher prob- and9.4%in1,770operations(238).Inthelasttwostudies,the
abilityofwoundinfection,islikely. infectionratesrangedfrom1.5%(57)and5.9%(238)follow-
With the exception of clean operative procedures, surgical ingcleansurgeryto40%(57)and52.9%(238)followingcon-
wound infections are recognized as having a polymicrobial taminated surgery. Despite the frequency and prevalence of
etiology,involvingbothaerobicandanaerobicmicroorganisms endogenous anaerobes in surgical wound infections (Table
(Table 3) (2, 35, 36, 38, 64, 175, 212), and intra-abdominal 3), the Centers for Disease Control and Prevention guideline
infectionsnormallyreflectthemicrofloraoftheresectedorgan for the prevention of surgical site infection has recognized
(34, 175). Reported wound infection rates following orthope- S.aureus,coagulase-negativestaphylococci,Enterococcusspp.,
dic surgery are relatively low (2 to 6.8%) (20, 61, 223), and Escherichia coli, P. aeruginosa, and Enterobacter spp. as the
similar studies, involving a large number of generalized post- most frequently isolated pathogens (151). Unfortunately, this
operativewoundtypes,havereportedoverallinfectionratesof view has been based on only two published reports that pro-
3.4% in 5,129 operations (1), 4.7% in 62,939 operations (57), vidednoindicationoftheinclusionofanaerobicbacteriology
250 BOWLER ET AL. CLIN.MICROBIOL.REV.
in the associated studies, and hence the data may have been tridial myonecrosis (since it involves muscle invasion and is
biasedinfavorofaerobicandfacultativemicroorganisms(50, associatedwithahighermortalityrate)andothernon-muscle-
154).Incontrast,Rotsteinetal.(207)emphasizedthepolymi- associatedsofttissueinfections.
crobialnatureofalmostallsurgicalinfectionsandcommented The management of necrotizing soft tissue infections re-
that the critical importance of aerobic-anaerobic mixtures in quires early diagnosis, aggressive and, if necessary, repeated
theseinfectionshadreceivedrelativelylittleattention. debridement,andantibiotictherapy(12,69,191).Hyperbaric
Minimizing the incidence of postoperative wound infection oxygen (HBO) therapy is also believed by many to facilitate
relies on adequate asepsis and antisepsis and preservation of wound healing (12, 69), although its use is controversial (53,
thelocalhostdefenses(109).Asepsisinvolvestheutilizationof 69,165).HBOtherapyisdiscussedinmoredetailin“Control
effective infection control procedures (e.g., air filtration, skin of microbial populations in wounds” (below). The pilonidal
barrier garments, disinfection) to minimize exogenous micro- sinusisanothertypeofacutewoundthatissusceptibletofecal
bialcontaminationduringsurgery.Antisepsisinvolvestheuse contaminationandinfection;Bascom(18)reportedthatanaer-
ofskinantisepticsontheoperativesiteandalso,inthecaseof obes were the true and invisible causative microorganisms.
dirty surgical procedures, administration of prophylactic anti- Surgicalreshapingofthewoundtoprovideimprovedoxygen-
biotics at a time point just prior to surgery that will ensure ationisoftenrequired(18).
adequate tissue levels of antibiotic during surgery. As part of Bite wound infections. The reported infection rate for hu-
the surgical procedure, endogenous and exogenous microbial man bite wounds ranges from 10 to 50% depending on the
contamination must be minimized by ensuring good aseptic, severity and location of the bite, and up to 20% of dog bites
skilledsurgicaltechniquesandminimizingthedurationofsur- and 30 to 50% of cat bites become infected (92). Brook (33)
gery, while also optimizing the local wound conditions (97). reportedthat74%of39humanandanimalbitewoundscon-
This primarily involves removing any devitalized tissue to re- tained a polymicrobial aerobic-anaerobic microflora, with S.
establishbloodflowtothewoundarea(2),therebymaintain- aureus,Peptostreptococcusspp.,andBacteroidesspp.beingthe
ingadequateperfusiontoenablethedeliveryofimmunecells, predominantisolatesinbothwoundtypes.
oxygen,andnutrientsandreducingthemicrobialload. Duetothecomplexnatureoftheoralmicroflorainhumans
Acute soft tissue infections. Acute soft tissue infections in- and animals, the majority of bite wounds harbor potential
cludecutaneousabscesses,traumaticwounds,andnecrotizing pathogens,manyofwhichareanaerobes.Aswellasthecom-
infection. Microbiological investigations have shown that S. monanaerobesinbothhumanandanimalbitewounds,suchas
aureusisthesinglecausativebacteriuminapproximately25to Bacteroides,Prevotella,Porphyromonas,andPeptostreptococcus
30%ofcutaneousabscesses(41,158),andthesameorganism spp.(83),lesscommonpotentialpathogenssuchasPasteurella
hasalsobeenrecognizedasbeingthemostfrequentisolatein multocida, Capnocytophaga canimorsus, Bartonella henselae,
superficialinfectionsseeninhospitalAccidentandEmergency andEikenellacorrodensmayalsobeinvolved(75).
Departments (180). However, other studies have demon- Management of bite wounds is likely to involve high-pres-
strated that approximately 30 to 50% of cutaneous abscesses sure irrigation to reduce the microbial load, debridement of
(41,42,226),50%oftraumaticinjuriesofvariedetiology(40, devitalizedtissue,andantibiotictreatmentforhigh-riskwounds
45), and 47% of necrotizing soft tissue infections (69) have a suchaspunctures(75,82).
polymicrobialaerobic-anaerobicmicroflora. Burnwoundinfections.Infectionisamajorcomplicationin
Necrotizing soft tissue infections occur with different de- burn wounds, and it is estimated that up to 75% of deaths
greesofseverityandspeedofprogression;theyinvolvetheskin following burn injury are related to infection (200, 239). Al-
(e.g.,clostridialandnonclostridialanaerobiccellulitis),subcu- though exposed burned tissue is susceptible to contamination
taneous tissue to the muscle fascia (necrotizing fasciitis), and by microorganisms from the gastrointestinal and upper respi-
muscletissue(streptococcalmyositisandclostridialmyonecro- ratorytracts(239),manystudieshavereportedtheprevalence
sis).S.aureushasbeendescribedasbeingthesinglepathogen of aerobes such as P. aeruginosa, S. aureus, E. coli, Klebsiella
intwopatientswithrapidlyprogressingnecrotizingfasciitisof spp., Enterococcus spp., and Candida spp. (13, 132, 154, 200,
thelowerextremity(199),andinastudyofnecrotizingfasciitis 239).Inotherstudiesinvolvingmorestringentmicrobiological
in eight children, Brook (40) reported the presence of pure techniques, anaerobic bacteria have been shown to represent
Streptococcus pyogenes in two patients and a mixed predomi- between11and31%ofthetotalnumberofmicrobialisolates
nance of Peptostreptococcus spp., S. pyogenes, B. fragilis, C. fromburnwounds(46,166,197).Whiletheaerobesisolatedin
perfringens,E.coli,andPrevotellaspp.intheothers.Potentia- the latter studies were similar to those reported previously,
tionofinfectionbymicrobialsynergisticpartnershipsbetween predominant anaerobic burn wound isolates were Peptostrep-
aerobes, such as S. aureus and S. pyogenes, and nonsporing tococcus spp., Bacteroides spp., and Propionibacterium acnes
anaerobes has been recognized in various types of nonclos- (46, 166). Mousa (166) also reported the presence of Bacte-
tridialcellulitisandnecrotizingfasciitis(40,122). roides spp. in the wounds of 82% of patients who developed
Theclassificationofnecrotizingsofttissueinfectionsiscom- septicshockandconcludedthatsuchmicroorganismsmayplay
plex and is based on (i) the assumed causative microorgan- asignificantroleinburnwoundsepsis.
ism(s),(ii)theinitialclinicalfindings,(iii)thetypeandlevelof Managementofinfectioninburnwoundsinvolvestheuseof
tissueinvolved,(iv)therateofprogression,and(v)thetypeof topical and systemic antimicrobial agents, aggressive debride-
therapy required (12). However, Elliot et al. (69) argued that ment of dead tissue, maximization of the immune response,
theclassificationofsuchinfectionsserveslittleclinicalpurpose andprovisionofadequatenutrition(147).
because the prognosis and treatment are the same and, con- Diabeticfootulcerinfections.Plantarulcersassociatedwith
sequently, differentiation is required only between pure clos- diabetes mellitus are susceptible to infection due to the high