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NoninfectedUlcerations
Noninfected wounds, by definition, do not require antibiotic therapy. Routine culturing of
woundsthatdonotappearclinicallyinfected(i.e.,nocellulitis,purulence,erythema)should
beavoidedbecauseevennoninfectedulcerationsarecolonizedwithmultipleorganisms.
20
The use of antibiotics to “prevent” infection is not supported by currently available
medical evidence andmay lead to the development ofresistant organisms21 that may make
subsequentinfectionsmoredifficulttotreat.Inatleastonestudy,microbialloadanddiversity
hasbeenshownnottobepredictiveofweeks-to-closureorpercentreductioninsurfacearea
perweek.22Antibioticsshouldbeusedtotreatinfections,nothealwounds.
A common misconception is that patients with diabetes do not respond with cellulitis.
Althoughtheremaybemutedresponsetosomeofthesignsofinfection,itisextremelyunlikely
thattherewouldbenoevidenceofcellulitisatall.Cellulitisisthereforeareliableindicatorof
infectioninallbutthemostarteriallycompromisedpatients.
MildInfection
ThebeliefthatallDFIsarepolymicrobialhaschanged.Decadesago,itwasthoughtthateven
mildly infected diabetic wounds harbored anaerobic bacteria such as Bacteroides fragilis,
leading to treatment with broad spectrum antibiotics even inthe face of negative anaerobic
cultures.
WenowknowthatmildlyinfecteddiabeticwoundsharborpredominantlyaerobicGrampositive cocci. Whether theinfection is mild, moderate, or severe, S. aureus and Group B
Streptococcusarefarandawaythemostcommonpathogensencountered.
Wounds with a mild infection show at least two of the signs and symptoms of a host
response.Thereisusuallylocalizedcellulitisaroundthewound thatextends<2cmfromthe
wound border. Purulent exudate may be present; however, the infection remains localized.
Thereisnodeepextensionorproximalspread.Thereisnolymphangiitisorlymphadenopathy.
There are no systemic signs or symptoms of infection, and the patient’s white blood cell
(WBC)countandbloodglucosearenotabovethepatient’susualrange.
Mildlyinfecteddiabeticulcersaretreatednodifferentlywithrespecttoantibioticchoice
anddurationcomparedwithsimilarwoundsinnondiabeticpatientsandcanusuallybetreated
on an outpatient basis with oral antibiotic therapy. Antibiotic therapy should be directed
against S. aureus and Streptococcus, with the caveat that there are increasing rates of
methicillin-resistantS.aureus(MRSA)inthesepatients.Anaerobiccoverageinthesewounds
is unnecessary. The use of broad spectrum agents such as amoxicillin/clavulanate or
moxifloxacin,whilenotwrong,canbeconsideredoverkill.
23
Some patientsmayrequire debridementorincisionand drainagefor a small abscess or
offloading ofpressure areas. It is recommended that thepatient follow upinafew daysto
review theresultsofcultureandsensitivity tests and toensure there has been anadequate
responsetotreatment.
ModerateandSevereInfections
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Moderateandsevereinfectionsareoftenclassifiedtogether.Thechoiceofantibioticstotreat
eachgroupis often similar, owing tothe similarityofthe spectrum ofinfectingorganisms.
However, moderate infections are limb threatening, whereas severe infections are life
threatening.
Accordingtothe2012IDSAguidelines,19moderateinfectionscanbedefinedasthosewith
cellulitisextending>2cmfromthewoundmarginorpenetrationofinfectionintothedeeper
tissues,such as fascia, tendon, muscle, or bone.Lymphadenopathy or lymphangiitis maybe
present.The patientis systemically well andmetabolicallystable, although there maybe a
mildelevationoftheWBCcount.Bloodglucoselevelsmaybehigherthanthepatient’susual
values.
Comparedwithamoderateinfection,thehallmarkofasevereinfectionisevidenceofa
septic state. The patient may be febrile, hypotensive, and confused or have significant
metabolicimbalance(e.g.,azotemiaandacidosis).Distinctfrommildinfections,moderateand
severe infections tend to be polymicrobial. S. aureus, including MRSA and Streptococci
(GroupB), are still thepredominant pathogens, butGram-negativeorganismsare commonly
found.
There has been some debate as to the need to direct antibiotic therapy toward Gramnegative organisms in general and Pseudomonas aeruginosa in particular. Although an
importantpathogeninrespiratorytractandurinarytractinfections,therearedatatosuggestthat
P.aeruginosa when cultured from skinand softtissueinfections may existas a commensal
ratherthanatruepathogen,andtherapydirectedagainstthisbacteriamaynotbenecessaryto
effect a cure in diabetic lower extremity skin and skin structure infections.
23,24
Anaerobic
bacteriasuchasBacteroidesfragilisaremorefrequentlyseeninthesewounds,andwhether
suspectedorcultured,itisoftenprudenttodirecttherapytowardthem.
25,26
Thisisespecially
trueinthecaseofinfectionsinwhichgasisseenonX-ray.
THEROLEOFANAEROBESINDFIS
The presence of anaerobic bacteria inDFIs is probably overestimated by most physicians.
When present in lower extremity infections, anaerobes such as Bacteroides spp. are more
commonlyseeninmoderatetosevereinfections,rarelyifeverinmildinfections,andalmost
never present as solitary organisms. Anaerobic bacteria require specialized culture media,
rapid transportto thelab, andstrictanaerobic conditionswhen cultured. Becauseof this, it
maybemore usefultoemploy16spolymerasechainreaction(PCR)andpyrosequencingto
detecttheir presence, rather than relying ontraditional culture methods. Unfortunately, as of
thiswriting,thesetestsarecostlyandnotwidelyavailable.
Thereisatimewornsaying,“allthatisgasisnotclostridia.”Althoughthepresenceofgas
insofttissueonX-raycanindeedindicatethepresenceofanaerobicbacteria,itisprobably
more often than not caused by gas-producing Gram-negative bacteria such as Klebsiella,
Proteus, or Escherichia coli rather than obligate anaerobes. There are even nonbacterial
causesof“gasintissue,”includingtheuseofhigh-pressureirrigationintheoperatingroomor
the use of hydrogen peroxide flushes employed bythe patient.In arecent literature review
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concerning the epidemiology, antibiotic susceptibility, andclinical significance ofanaerobic
isolatesinpatients with DFIs,44publishedstudies werefound,involving a total of13,012
patients.Ofthese, theincidence ofanaerobic pathogenswas only11%.27Noepidemiologic
surveytodatehasreportedaworseoutcomeforwoundsfromwhichanaerobicbacteriawere
isolatedcomparedwithno-anaerobes,withthepossibleexceptionofClostridiumspp.
28
Nonetheless, it has become standard practice by many to employ broad spectrum
antibiotics with anaerobic activity in most if not all moderate to severe DFIs. Long-term
coverageofanaerobicbacteriamaynotonlybeunnecessary,butmayhavetheunwantedside
effect of driving antibiotic resistance and increase health care costs. Antibiotics are not
withouttheiradverseevents.InarecentlypublishedstudyfromIstanbul,Turkey,almost20%
ofpatientsreceivingpiperacillin/tazobactamfor>10daysdevelopedneutropenia(neutrophil
countof<2,000cellspermm3).
29
THEPROBLEMOFDRUG-RESISTANTORGANISMSIN
DFIS
Inthepastdecade,oneoftheimportantchangesinthemicrobiologyofDFIsistheincreasing
isolationofMDROs.AnMDROcanbedefinedasanorganismwithdecreasedsusceptibility
tomultiple(usuallytwoorthree)classesofantimicrobialagentstowhichtheorganismwould
normallybesusceptible.
30
OneofthemostimportantGram-positiveMDROsisMRSA.Inasurveyof97UShospitals
conductedbetween2003 and2007, theprevalenceofMRSA inhospitalizedpatientswitha
DFIalmostdoubled,from11.6%to21.9%.
31
DespitetheprevalenceofMRSA,treatingeveryDFIforMRSAisunnecessaryandlikely
toleadtoafurtherincreaseinresistanceaswellasraisethecostofhealthcare.32Althoughthe
isolationofMRSAwouldseemtobeafactorassociatedwithtreatmentfailureinpatientswith
DFIs,33ithasnotbeendemonstratedtobeassociatedwithlongerhospitalizationorahigher
incidenceofamputations.
32,34
Infact,studiesbyHartemann-Huertieretal.35aswellasRichard
etal.36foundthatthepresenceofMDROs,mostnotablyMRSA,hadnosignificantimpacton
healingtimeofdiabeticfootwoundswhencomparedwithmethicillin-susceptibleS.aureus.
EmpiriccoverageforMRSAshouldbestartedforpatientswithknownriskfactors,andfor
thosepatientswithsevereinfectionsinwhomfailuretopromptlytreatwouldleadtolossof
lifeorlimb.
Risk factors associated with MRSA infection of foot ulcers include the presence of
MDROs,historyofanMRSADFI,andapositiveMRSAnasalculture.
32
TherearecurrentlytwonewlyapprovedantibioticstotreatMRSAinfections.Ceftaroline
isaparenteral-onlyextendedspectrumcephalosporinthatisactiveagainstMRSAandhasthe
Gram-negative activity of a third-generation cephalosporin. Tedizolid is a newer
oxazolidinone, similar tolinezolid,exceptwith once-dailydosing andwithoutthe serotonin
syndromerisk.
The other MDRO seen with an increasing incidence is extended spectrum β-lactamase
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(ESBL)–producingGramnegatives (sonamed becausetheyproduce enzymes thathydrolyze
extendedspectrumcephalosporins).TheincreaseinESBL-producingstrainsjeopardizesthe
usefulness of β-lactam agents, leading to increases in costs and treatment failures. These
organismsarebeingfoundwithincreasingfrequencyinDFIs.
37,38
ESBLs are found in many commonly encountered Gram-negative organisms including
Klebsiella, E. coli, Acinetobacter, Citrobacter, Enterobacter, Morganella, Proteus,
Pseudomonas, Salmonella, and Serratia. ESBLs can hydrolyze oxyimino cephalosporins
(ceftazidime, ceftriaxone, cefepime, cefotaxime) and monobactams (aztreonam) but cannot
hydrolyzecarbapenems(imipenem,meropenem,ertapenem).
Unfortunately, Gram-negative active agents such as aminoglycosides, trimethoprim–
sulfamethoxazole(TMP/SMX),andquinolonesmaynotbeeffectiveeither.Plasmidsw/genes
encoding for ESBLs may also carry genes conferring resistance to aminoglycosides,
TMP/SMX,andquinolones.Evenwhenplasmid-encodeddecreaseinquinolonesusceptibility
is not present, there is a strong association between quinolone resistance and ESBL
production.
Thecarbapenemshavethereforeemergedasthe“go-to”classofantibioticsfortreatment
ofESBLGram-negativeinfections,andformanyyearshaveheldthetopspotinthisregard.
Unfortunately, some Gram-negative organisms have developed resistance to even the
carbapenems. Collectivelyknown as CRE (carbapenem-resistant Enterobacteriaceae), these
organisms are resistant to not only carbapenems, but to penicillins, cephalosporins, and
monobactamsaswell.39Themostcommontypeofcarbapenemase(enzyme)currentlyseenin
theUnitedStatesisKlebsiellapneumoniacarbapenemase.However,otherenzymescapableof
inactivatingcarbapenemshavebeendiscoveredaswell;amongthemareNewDelhimetallo
β-lactamase
40,41
andVeronaintegron-encodedmetalloβ-lactamase-1.
42
Current treatment options for CRE infections are limited and include tigecycline and
colistin.Newerdrugs are underdevelopment.Onesuchdrug,avibactam, hasbeenshown to
inhibit extended spectrum β-lactamase and carbapenemase enzymes produced by Gram
negatives in much the same way that tazobactam, sulbactam, and clavulanic acid inhibit βlactamase produced byS. aureus.The addition of avibactam to existing antibiotics suchas
aztreonamandceftarolinewillresultinanewcompoundwithextendedactivityagainstawide
rangeofmultidrug-resistantGram-negativeorganisms.
DIABETICFOOTOSTEOMYELITIS
It has been estimated that approximately 15% of diabetic foot ulcers are complicated by
osteomyelitis,andinsomecentersapproximately20%ofpatientswhopresentwithaDFIhave
involvementoftheunderlyingbone.43Mostcasesofdiabeticfootosteomyelitisarechronicby
thetimetheypresent.Infectionofboneinthefootofapatientwithdiabetesusuallyoccursvia
contiguous spread from an overlying soft tissue ulceration. The presence of osteomyelitis
increases the likelihood of lower extremity amputation. Thus, accurately diagnosing and
treatingdiabetic foot osteomyelitis is ofcritical importance. Bone biopsy withculture and
histopathology is still considered the criterion standard for diagnosing diabetic foot
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osteomyelitis,whereasmagneticresonanceimaging(MRI)iscurrentlyconsideredtheimaging
modalityofchoice.
Ithaslongbeenheldthat,withthepossibleexceptionofS.aureus,thereexistslittleorno
correlationbetweenorganismsculturedfromasinustractandtheinfectingorganisminbone.
The question therefore arises as tothe reliability of swab cultures indetermining the bone
pathogen.
In his seminal study, Mackowiak et al.44 found only 44% of the sinus tract cultures
containedthe operative pathogen, withS.aureus havingthehighestcorrelation.Since then,
however,there havebeenseveral studies thatsuggestthat a carefully obtained culture ofa
sinus tract may indeed correlate well with bone cultures, depending on how they are
performed.
45–47
Bernard et al.46 demonstrated that deep sinus tractcultures in contact with
bonecorrelatewellwithbonebiopsyspecimensobtainedthroughadjacent,noninfectedskin.
The reason for this may simply be that bacteria in the superficial portion of a sinus tract
originate from skin, whereas bacteria in thedeeper portion of a sinus tract originatesfrom
bone. Bernard found that performing two consecutive deep sinus tract cultures with bone
contactaccuratelypredictedthepathogenofdiabeticfootosteomyelitisin90%ofcases.
46
Asmentioned,bonebiopsyremainsthe criterionstandardfor diagnosis. Althoughrarely
performedroutinely,abonebiopsycanyieldawealthofinformation.Apercutaneous11gaor
13gaJamshidineedlebonebiopsyissimpletodo,canbeperformedatthebedsideorinan
outpatient setting under local anesthesia, and is safe. The specimenshould be obtained by
goingthroughadjacent,noninfectedskin,ifpossible.Inadditiontoconfirmingthepresenceof
osteomyelitis, a bone biopsy can identify the causative organism and its antibiotic
susceptibilities.Inaretrospective cohortstudyof50 consecutivepatientswithdiabeticfoot
osteomyelitistreatednonsurgically,Sennevilleetal.48foundthatboneculture–basedantibiotic
therapywas the only variable significantlyassociated with remissionofinfection. There is,
however, one important caveat to performing a percutaneous bone biopsy: chronic
osteomyelitis can be a patchy disease, and there is no guarantee that a specimen of bone
harvested “byfeel” during a blindprocedure will be “on the money.” False negatives can
resultifinfectedboneismissed.Itmaythereforebeadvisabletoperformtheprocedureunder
ultrasoundguidanceinordertoincreasethechancesforapositiveyield.
TREATINGDIABETICFOOTOSTEOMYELITIS
Osteomyelitisisstillconsideredbymanytobeprimarilyasurgicaldisease.
The long-held standard (and, for some, dogmatic) approach to treating diabetic foot
osteomyelitishasbeentoaggressivelyresectallinfectedanddevitalizedbone,andtofollow
up with6 weeks of parenteral antibiotic therapy directed against a bone biopsy–recovered
pathogen.
Surgicalremovalofallinfectedboneprobablygivesthebestchanceforacure,asleaving
infected bone behind increases the possibility for recurrence. Factors that favor surgical
intervention includemajor bonedestruction,acuteinfectionsrequiringdrainage,problemsin
limb perfusion, the presence of MDROs, and contraindication for or patient refusal of
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prolongedantibiotictherapy.
Thesurgeon,inanattempttopreservegaitandfunction,mayoptforpartialresectionrather
thanaggressivelypursuing amputation.However,patientswithpositivemarginsforresidual
osteomyelitisaftersurgicalresectionhavebeenfoundtobeatgreaterriskfortreatmentfailure,
including the need for more proximal amputation despite the longer duration of antibiotic
therapy.
49
Treating osteomyelitiscantherefore be likenedtotreatingcertainformsofcancer.Wide
excision and removal of all affected bone is optimal. Residual affected bone requires
chemotherapy(antibiotics).Aslongasthereremainsinfectedbone,thereremainsthechance
forrecurrence.Inthecaseofincompleteexcision,remissionmaybethebestthatcanbehoped
for.
Thenotionthatdiabeticfootosteomyelitisisalwaysasurgicaldiseaseischanging.
There are instanceswhensurgeryisnot a viableoption,suchas whenitisthe patient’s
choicetoavoidsurgeryorcomorbiditiesconferanunacceptablyhighrisk.Insuchsituations,
and when there are no contraindications to prolonged antibiotic therapy, medical-only
(nonsurgical)managementmaybeconsidered.Arecentsystematicreviewofpatientstreated
for diabetic foot osteomyelitis found that there is currently no evidence that surgical
debridementoftheinfectedboneisroutinelynecessary,noraretheresufficientdatatosupport
thesuperiorityofanyparticularantibioticagentorrouteofdelivery.50Zeunetal.51conducted
a retrospective study of consecutive patients with diabetes presenting to a tertiary center
between2007and2011withfootosteomyelitisinitiallytreatedwithnonsurgicalmanagement.
Almosttwo-thirdsofpatientspresentingwithosteomyelitishealedwithoutundergoingsurgical
boneresectionortherequirementforfurtherantibiotictherapy.
The evidence for selecting an arbitrary 6-week duration of treatment is weak, largely
resting on the results of experimental studies of acute staphylococcal osteomyelitis in
rabbits
52,53
and observations of the time it takes for bone healing to occur. Applying a
standardizedregimentoeverypatientmayendupovertreatingsome,andundertreatingothers.
Likewise,therearecurrentlynodatatoindicatethesuperiorityorinferiorityofanyparticular
route of administration (oral vs. parenteral) or any antibiotic over another for treating
osteomyelitis.Forsome,thismayseemcounterintuitive.
Overthepastfewyears,therehavebeenanumberofstudiestosupporttheuseoforal(as
opposed to parenteral) antibiotics as the sole therapy in the treatment of diabetic foot
osteomyelitis, andtodatethereare nostudies thatappear tofavor oneparticular antibiotic
overanother.Themostimportantfactorsarethattheyhavehighbioavailabilityandareactive
againsttheinfectingorganism.Highlybioavailableantibioticsthatareeffectiveinthepresence
ofbiofilm54and canenterhostcells15have changedthewaywethinkabouttreatingchronic
osteomyelitis and may make nonsurgical management feasible in some cases. This is a
somewhaticonoclasticviewbecauseparenteralantibioticshaveremainedformany(forbetter
orworse)theperceivedgoldstandardoftreatment.Despiteemergingevidencetothecontrary,
manycliniciansstilldoggedlyclingtothenotionthatparenteralissuperiortooralfortreating
chronic bone infection. Adherence to such dogma leads to overutilization of parenteral
antibiotics(whichshouldbebestreservedfortreatingacuteinfection),increaseshealthcare
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Table4-2.
costs (increased length of hospital stay, placement of peripherally inserted central catheter
lines,infusionnurses,materialsassociatedwithIVmedsetc.),andpresentsthepossibilityof
infectionoftheIVlineitself.
SuggestedRoute,Setting,andDurationofAntibioticTherapy,
byClinicalSyndrome
SiteofInfection,by
SeverityorExtent RouteofAdministration Setting DurationofTherapy
Soft-TissueOnly
Mild Topicalororal Outpatient 1–2wk;mayextendupto4
wkifslowtoresolve
Moderate Oral(orinitialparenteral) Outpatient/inpatient 1–3wk
Severe Initialparenteral,switchto
oralwhenpossible
Inpatient,thenoutpatient 2–4wk
BoneorJoint
Noresidualinfectedtissue
(e.g.,postamputation)
Parenteralororal — 2–5d
Residualinfectedsoft
tissue(butnotbone)
Parenteralororal — 1–3wk
Residualinfected(but
viable)bone
Initialparenteral,then
consideroralswitch
— 4–6wk
Nosurgery,orresidual
deadbone
postoperatively
Initialparenteral,then
consideroralswitch
— ≥3mo
ReprintedfromLipskyBA,BerendtAR,CorniaPB,etal.2012InfectiousDiseasesSocietyofAmericaclinical
practiceguidelineforthediagnosisandtreatmentofdiabeticfootinfections.ClinInfectDis.2012;54(12):e132–e173,
withpermission.
In a retrospective study by Embil et al.,55 remission was achieved in over 80% of 93
episodesofdiabeticfootosteomyelitistreatedwithoralantibioticagents,78%ofwhomhad
nobonedebridementorresection.Gameetal.56notedsimilarresults,witharemissionrateof
over82%notedinpatientstreatedwithantibioticsalone,comparedwith78%inthosetreated
withantibioticsandonlyminoramputation.
Recent studies also suggest the optimal length of treatment may even be significantly
shorter than oncethought. Toneetal.57 compared 6- versus 12-week duration of antibiotic
treatmentatfiveFrenchgeneralhospitals.Remissionwasobtainedin26(65%)patients,with
no significantdifferences betweenpatientstreated for6versus12weeks.Patients received
oralantibioticsforeitherallorasamajorpartoftheirtreatment.
Regardless of the mode or duration of therapy, patientswhoachieveremissionmustbe
carefullymonitoredforatleast1yearbecausetheymaydeveloparecurrenceofosteomyelitis
despite “appropriate” treatment. Algorithms are needed that would reliably predict which
patients would be most responsive to nonsurgical treatment, and which could receive
exclusivelyoral antibiotic therapy. Currently, theIDSA Clinical Practice Guidelines forthe
DiagnosisandTreatmentofDFIsareusefulforestimatingthelengthoftherapyrequiredbased
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ontheextentofresectionandviabilityofaffectedbone(Table4-2).19Inlightofnewstudies,it
willbeinterestingtoseehowtheIDSArecommendationswillchangeintheirnextincarnation.
OTHERLOWEREXTREMITYINFECTIOUS
COMPLICATIONSOFSYSTEMICDISEASE
SEPTICEMBOLIZATIONTOTHEFEETANDTOES
FROMINFECTIVEENDOCARDITIS
Peripheral embolization to the feet and toes from a proximal source of infection has been
describedinpatientswithinfectiveendocarditis.Thromboemboliccomplicationsoccurwhen
thevegetationsadherenttotheendocardiumorheartvalvesfragmentandseedtodistalsites—
including the lower extremities.58 This can result in focal necrotizing lesions or painful
localizederythema andswelling.59 Staphylococcus andStreptococcus are the most common
organismsresponsibleforinfectiveendocarditis,withStrepaccountingforthemajorityofall
cases.
The extracardiac, physical findings of infective endocarditis may be extensive60 and
include Osler nodes(painful)andJaneway lesions(painless).61 Janewaylesionshave been
described on the palms and soles.62 Osler nodes have also been described in the foot in
patientswithenterococcalendocarditisandS.aureusendocarditis.63Splinterhemorrhagesof
the toenails as well as the fingernails may be seen in subacute bacterial endocarditis and
shouldbedifferentiatedfromsplinterhemorrhagesofmicrotrauma.
REACTIVEARTHRITIS
Heelpainisoneofthemostcommonfootcomplaintsthatdrivespatientstoseekmedicalcare.
Moreoftenthannot,itisofbiomechanicaloriginandtheresultofthepulloftightplantar
fascia (or Achilles tendon in the case of retrocalcaneal pain) from its attachment on the
calcaneus.Thediagnosisofreactivearthritismustbeincludedinthedifferentialforcasesof
heelpainwhenthesymptomsarebilateralandrefractorytotreatment.
Reactivearthritis(oncecommonlyreferredtoasReitersyndrome)isconsideredaformof
spondyloarthritis.Itisanimmune-mediated,sterilesynovitiscausedbyahostresponsetoan
extra-articular slow bacterial infection, producing arthritis without infecting the jointitself.
Causative organisms of reactive arthritis include Chlamydia, Salmonella, Shigella,
Campylobacter,Ureaplasma,andYersiniaspecies.
64
Genitourinary tract infection with Chlamydia trachomatis is the more commonly
recognizedcause of reactive arthritis in developed countries andhas been identified in the
United States as the preceding infection in 42% to 69% of patients with urogenic reactive
arthritis.
65
Reactivearthritisis distinguishedby theclassictriadofsymptomsbestcharacterizedby
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medical studentsasthepatientwho“can’tsee”(conjunctivitis), “can’tpee” (urethritis),and
“can’tclimb a tree” (arthritis). It is important to note that onlyabout one-third of patients
presentwithallthreecomponents.
66
Additional manifestations include dactylitis, keratoderma blennorrhagicum, and nail
changesormaypresentwitharecentonsetofdiarrheaorurinarytractinfection.Constitutional
symptomsmayincludefever,malaise,fatigue,andweightloss.Obtainingathoroughmedical
historyisthereforeessential.
Radiographic evidence of reactive arthritis is notpresentineverycase. An unusual or
bifurcateplantarcalcanealspuroftensuggeststhattheheelpainisnotofbiomechanicalorigin.
Thecalcaneusmayexhibitafluffyperiostitis(theso-called“lover’sheel”implyingasexually
transmittedetiology)withapoorlydefined,frayedappearanceattheinsertionoftheplantar
aponeurosisandAchillestendon.RadiographicevidenceofReitersyndromeispresentinonly
about25%to50%ofpatients.
67
Theclinicalcourseofreactivearthritisisunpredictableandvariable.Insomepatients,the
diseasetakesamorechroniccourse.Inothers,initialattacksmaylastfromafewmonthstoa
yearormore,withrelapsesoccurringafterlongdisease-freeintervals.
Reactivearthritisisthoughttobelinkedtothehumanleukocyteantigen(HLA)-B27.
68
HLA-B27 has become an overused diagnostic test, however, as not every HLA-B27–
positivepatientwilldevelopReitersyndrome.69Synovialfluidanalysisrevealsinflammatory
changes,includingelevated WBCcount,turbidity,poorviscosity, andpoormucinclottests.
Synovialglucoselevel isnotsignificantlyreducedasitisinsepticarthritis.Gramstainsof
synovialfluidarenegative,asarecultures.
Diagnosis of reactive arthritis is supported by isolation of an infectious entity from a
nonarticular site.However,becausethisis rarelyachieved, anincreasedantibodytiter ofa
suspectedorganism often serves as a sufficientdiagnostic criteriontospecify theetiologic
agent.Intra-articularbacteria,whenpresent,arenonculturable;however,microbialDNAand
RNAhavebeendetectedinthejointsofpatientswithreactivearthritis.
65,70
OSTEOARTICULARTUBERCULOSIS
Tuberculosis(TB)isaliveandwellinourmodernworld.One-thirdoftheworld’spopulation
is infected with TB. In 2014, 9.6 million people around the world became sick with TB
disease.Therewere1.5millionTB-relateddeathsworldwide.71OsteoarticularTBisperhaps
oneofthemostfrequentlymisdiagnosedinfectiousdiseasesofbone.
TBisachronicdiseasecausedbyMycobacteriumtuberculosis.Transmissioncommonly
occurs by inhalation of aerosolized droplets of respiratory secretions from a patient with
activepulmonaryTB.TBhasbeennamedthesecondgreatimitatoraftersyphilisbySievers
72
becauseofitsmultipleandunusualpresentations.
Clinical symptoms of active pulmonary TB include fever, weight loss, and productive
cough often with bloody sputum. Patients with skeletal TB may have no active pulmonary
diseaseandhencenosystemicsymptomsotherthanpainattheaffectedsite.Anegativechest
X-raydoesnotexcludethediagnosis,nordoesanonreactivepurifiedproteinderivative(PPD)
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skin test. Peripheral skeletal TB, however, can exist without evidence of pulmonary
involvementeitherclinicallyorradiographically.73Patientswithabnormalitiesoftheimmune
system(suchasadvancedhumanimmunodeficiencyvirus[HIV]disease),advancedage, and
even overwhelming tuberculous infection may have a false-negative PPD skin test.
73,74
Quantiferon-TBGold(QFT-G;Cellestis,Ltd.,Carnegie,Australia)isusefulfordetectingboth
activeandlatentinfection.
Peripheral skeletal TB is caused by subsequent dissemination of M. tuberculosis by
hematogenousspreadorlymphaticdrainageearlyinthecourseoftheinfection.
Skeletal involvement is rare. Foot involvement is even rarer
75,76
and is estimated to
account for just 10% of osteoarticular TB and 0.1% to 0.3% of all patients with
extrapulmonarydisease.77Theinitiallesioniseitherintheboneorinthesynovium,andone
subsequentlyinfectstheother.78Itcanoccuratanyage.Bozkurtetal.79presentedacaseofTB
osteomyelitisofthemedialcuneiformina3-year-oldchild.
The evolution of skeletal TB is subtle: pain is often the presenting symptom. Early
radiographic signs are nonspecific and mimic osteoarthritis. Lesions may remain silent for
yearswithoutsignificantprogressionuntilreactivationoccursviatraumaorasimilarevent.
80
Itisthisslowindolentprogressioncoupledwithitsabilitytomimicotherdiseasestatesthat
allowsanaccuratediagnosistobedelayed.
Vertebral lesions (Pott disease) may cause symptoms of radiculopathy. Lumbosacral
involvementmaycausenumbness,tingling,andweaknessofthelowerextremities.
Whenfoundinthefoot,itmostcommonlyoccursinthecalcaneusandthetarsalbones.
77
Thetypical radiographicpresentationisoroftennonspecific andcharacterizedby juxtaarticularosteoporosis,peripheralosseouserosions,andgradualjointspacenarrowing,known
asthe Phemistertriad.
78,81,82
MRIisacceptedasthe imaging modalitymostusefulinaiding
diagnosis and revealing the extent of the disease.73 Tuberculomas can be synovial (rare),
osseous(frequent),orarticular(indicativeofalatestage)78andpresentwithorwithoutsinus
tractsorulceration.
The cornerstone of diagnosis of osteoarticular TB depends on demonstration of M.
tuberculosisoneitherahistologicstudy orculture.Molecular diagnosticssuch as TB-PCR,
line probe assays, or nucleic acid amplification tests have also been shown to be useful
diagnostictools.
83
One of the most useful procedures for the diagnosis of TB arthritis is the synovial
membrane biopsy. A definitive diagnosis is based on identification of M. tuberculosis in
granulomas, synovial fluid, or synovial membrane. Biopsy should be taken from the
granulomatous or cystic area or from immediately adjacent synovium.77 Samples can be
harvestedbyeitheropenbiopsyorCT-guidedpercutaneousneedleaspiration.
Itisprudentforthe cliniciantoorderacid-faststainsandcultures onboneandsynovial
membranebiopsies.Acid-fastorganismsgrowslowly.Culturereportsmaytakeseveralweeks
to return. Acid-fast stains may be ordered to aid in the empiric diagnosis in the interim.
Molecular diagnostics in TB has enabled rapid detection of M. tuberculosis complex in
clinicalspecimens.
84
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