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Retrospective characterisation and outcome of canine idiopathicmesenteric purulent lymphadenitis and lymph node abscesses ata teaching hospital from 2005 to 2015

Citation for published version:Schmitz, S 2016, 'Retrospective characterisation and outcome of canine idiopathic mesenteric purulentlymphadenitis and lymph node abscesses at a teaching hospital from 2005 to 2015' Journal of Small AnimalPractice. DOI: 10.1111/jsap.12551

Digital Object Identifier (DOI):10.1111/jsap.12551

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Retrospective characterisation and outcome of canine idiopathic mesenteric purulent

lymphadenitisandlymphnodeabscessesatateachinghospitalfrom2005–2015.

SilkeSchmitz*(Dipl.ECVIM-CA,PhD,MRCVS)

SmallAnimalHospital,InternalMedicine,Justus-LiebigUniversity,Giessen,Germany

*Correspondingauthordetails:

SilkeSchmitz’saddresshasnowchangedto:

TheRoyal(Dick)SchoolofVeterinaryStudies

HospitalforSmallAnimals

EasterBushCampus

Midlothian

EH259RG

Acknowledgements:

TheauthorwouldliketothankProf.Dr.RetoNeiger,Prof.Dr.AndreasMoritzandProf.Dr.Martin Kramer for providing access to the hospital records of the different departments(internalmedicine,surgery,clinicalpathology)forthisstudy.

Sourceofsupport:

Theauthordeclaresnoconflictofinterest.Thismanuscriptwasnotsupportedbyanygrantorthirdparty.

StructuredSummary1

2

Background: Idiopathic purulent mesenteric lymphadenitis or lymph node abscesses3

(mLAd/mLAb),eventhoughrareindogs,areimportantdiseaseswhererapiddiagnosisand4

treatmentisoftheessence.Ascurrentlynotmuchknownaboutthesediseases,thisstudy5

aimedatcharacterisingmLAd/mLAbindogstodescribetypicalfeatures.6

Materialandmethods:Archivedrecordsfrom2005to2015wereretrospectivelyevaluated7

for the occurrence of mLAd/mLAb in dogs. History, physical, and clinicopathological8

abnormalitiesaswellasdiagnostictestsperformed,treatmentandoutcomewerereviewed.9

Results: 14 cases with histopathologic and/ or cytologic confirmation were identified.10

Typically,gastrointestinal(GI)signsincludingabdominalpainandhyperthermiawerepresent.11

BloodworkshowedunspecificinflammatorychangesincludingelevatedC-reactiveprotein.12

Theextentofworkupforpossibleunderlyingdiseasesvaried,butdidnotidentifyaprimary13

cause in any case.Half of bacterial cultures from lymphnodes showedgrowthof various14

organisms,e.g.E.coliorstaphylococci.Treatmentwassurgical in10/14cases,andalldogs15

weredischargedfromthehospital.Threesufferedfromarelapsebetween1-5monthsafter16

discharge,andweresuccessfullymanagedwithantibiotictreatment.17

Conclusionandclinicalrelevance: IdiopathicmLAd/mLAbisstillaninfrequentdisease,but18

clinically important. Bacterial translocation from the GI tract is a possible cause. Other19

aetiologies (gastroenteritis, pancreatitis, immune-mediated diseases, Bartonella or20

mycobacterial infection) have not been evaluated consistently enough to be ruled out.21

Thoroughandstandardiseddiagnosticworkupandtreatmentoffuturecasesisnecessaryto22

evaluatedpossiblepathogenesesandoptimaltherapeuticoptions.Surgical,symptomaticand23

antibiotic treatment led to resolution of clinical signs in the evaluated cases. Although24

recurrenceispossible,outcomewasoverallfavourable.25

Keywords26

Lymphadenopathy,intra-abdominal27

28

Introduction29

Lymphnodeabscessesorpurulentlymphadenitislimitedtotheintra-abdominal(mesenteric)30

lymphnodeshavebeenrarelydescribed indogs,withmostpublicationspresentingsingle31

casereportsorsmallcaseseries(Beaumontetal.1997;Campbell2009,Mcpherson1992).32

Intra-abdominalabscessesoccurinthepancreasspleen,liver,kidneys,ovariesandwithinthe33

retroperitonealspace(Abdellatifetal.2014;Andersonetal.2008;Agutetal.2004;Bozaet34

al.2010;Schulzetal.2006;Schwarzetal.1998).Reportedaetiologiesincludeurolithiasisand35

bacterialurinarytractinfection(Agutetal.2004;Leeetal.2009),suspectedingestedforeign36

bodies including migrating plant material (Campbell 2009; Marvel and Macphail 2013),37

remnantsuturingmaterialorswabsfromprevioussurgicalprocedures(Bozaetal.2010;Ho-38

Jungetal.2007;Rayneretal.2010),traumaticinjurytoorgans(Schulzetal.2006),andorgan39

metaplasiaorectopy(ToblemanandSinnott2014).Adiffuseinflammatorygastrointestinal40

(GI) pathology (e.g. gastroenteritis, perforated foreign body, pancreatitis) with bacterial41

translocation,peritonitisorsepsisisfrequentlyassumedincasesofdiffuseintra-abdominal42

lymphadenitis or mesenteric lymph node abscesses, but might be difficult to prove in43

individualcases(BeaumontandGlauberg1979;Macpherson1992;Schwarzetal.1998).The44

bacterial species isolated from affected lymph nodes include Staphylococcus intermedius;45

whichistypicallycolonisingtheskinandthusspeculationonthesignificanceofthisfindingor46

thepointofentryforstaphylococciisdifficult(Abdellatifetal.2014;Macpherson1992;Lee47

etal.2009).Importantdifferentialdiagnosesforlymphadenopathyorlymphadenitisinsmall48

animals aremycobacterial orBartonella sp. infections (Duncanetal. 2008;Moralesetal.49

2007;Pappalardoetal.2000;Tuckeretal.2014).However,theseinfectionstypicallyleadto50

generalisedgranulomatousorpyogranulomatouslymphadenitisindogs(Moralesetal.2007;51

Saunders andMonroe 2006). To the author’s knowledge, only one case report of intra-52

abdominalinfectionwithM.tuberculosisinadoghasbeenpublished(Engelmannetal.2014).53

Recently, a subjective increase in idiopathicmesenteric lymphadenitis/mesenteric lymph54

nodeabcesses (mLAd/mLAb) indogshasbeennotedatour teachinghospital.Dueto this55

observation,aretrospectiveanalysisofthehospital`smedicalrecordstoidentifythesecases56

anddescribetypicalfeaturesofhistoryandphysicalexamination,laboratoryabnormalities,57

treatmentandoutcomewassought.Theaimwastoidentifypossiblecommoncharacteristics58

orpathomechanismsthatmightenableearlieridentificationandtreatment.59

60

MaterialsandMethods61

Electroniccasefilesfromthe1stofJanuary2005tothe31stofDecember2015ofboththe62

hospital’sinternalmedicineandsofttissuesurgeryservicedatabaseswereevaluateda.For63

this,thesoftware`sintegratedsearchtoolwasusedtoperformsocalled“filtering”offilesfor64

different search terms. These included “lymph node(s)” combined with “*abdom* and65

“*mesent*”,respectively;andthesearchwasconductedwithineitherthesurgicalprocedure66

report,finaldiagnosis,freehandtextordischargereportsectionofthepatientfiles.Asimilar67

searchwasperformedforthesamehospital’sclinicalpathologyservice(centrallaboratory)68

databaseusingthesamesearchtermswithinthecytologyorpathologyreportsectionofthe69

files. From this initial list of cases, duplicateswere removedmanually. Patient fileswere70

excluded if the final diagnosis within either the patient`s record or the cytology or71

histopathologyreportwasnotpurulentormixedlymphadenitisorlymphnodeabscess,also72

if the location of the respective lymph node(s) was not recorded as intra-abdominal or73

mesenteric, or if themedical record was not complete (e.g. location of lymph node not74

specified,nofinaldiagnosismade)andthediagnosisofmLAb/mLAdcouldnotbeconfirmed75

retrospectively. Diagnosis was based on either cytologic and/ or histologic lymph node76

examination.77

78

Results79

Theinitialsearchyieldedatotalof4842hitscombinedinallthreedatabases.Afterremoval80

ofduplicatesandcaseswithlymphadenitis/abscessesofotherlocationsthanmesenteric,5581

casesremained.Ofthose,30caseshadtobeexcluded,asnofineneedleaspiration(FNA)or82

biopsy was performed, hence the aetiology of mesenteric lymphadenopathy remained83

unclear (enlarged lymph nodes with the suspicion of lymphadenitis were visualised on84

abdominalultrasonographyinallofthosecases). Anadditional6caseswereexcluded,as85

even though initial lymph node cytology was consistent with purulent or mixed86

lymphadenitis, histopathology revealed neoplasia/ metastasis (n =1 of each: lymphoma,87

fibrosarcoma,carcinoma,histiocyticneoplasia)or reactivehyperplasia (n=2).Finally, ina88

total of 5 cases, acquired samples were either non-diagnostic (n = 2) or another intra-89

abdominalaetiologywasidentifiedthatwaslikelyresponsibleformLAd/mLAb(pancreatitis/90

pancreaticabscessn=2,purulenthepatitisn=1),hencethesewerealsoexcluded.Thisleft91

14casesofpresumedidiopathicmLAd/mAb,whichwillbedescribed inmoredetail inthe92

followingparagraphs.93

Thedogs’signalment,treatment,follow-upandoutcomearesummarisedintable1.Median94

ageatpresentationwas41months(range6-98months)andmedianbodyweightwas19.995

kg(range4.5–36.2kg).Themaletofemaleratiowas1:1.8.TheSmallMunsterlanderbreed96

seemedsubjectivelyoverrepresentedcomparedtothenormalhospitalpatientpopulation,97

butnumbersweretoosmalltocalculateameaningfuloddsratio.Mainpresentingcomplaints98

were frequently unspecific (inappetence n = 9, hyperthermia n = 8, lethargy/ weakness/99

exerciseintolerancen=7,diffusepainn=4)orrelatedtothegastrointestinaltract(diarrhoea100

n=6,vomitingn=5).Lameness,stiffgaitandataxiawerereportedin3dogs,andin2dogs101

observedpainwasofpresumedabdominalorigin.Additionalsignswerecollapse,polyuria/102

polydipsia,mastitis,adipsia,halitosis,swollenvulva,subcutaneousmass,andcough(eachn103

= 1). Findings on physical examination were variable, but included pain on abdominal104

palpation in all cases. The median rectal temperature was 39.2°C (range 37.9 – 40.6°C),105

medianheartrate114bpm(range78–138bpm)andmedianbreathingrate36breaths/min106

(range28–66breaths/min).107

Clinicopathologicaldata(completebloodcount[CBC],serumbiochemistry[BC])fromalldogs108

aresummarisedintable2.InadditiontostandardBC(n=14),amylaseandunspecificlipase109

activitywereassessed in5dogs, caninepancreatic lipase (cPL) in4dogs (2hadanormal110

semiquantitativebed-sidetestb,twoquantitativeassessment<200pg/mlc).Fibrinogen,PT111

and aPTTweremeasured in 5 dogs each, and d-dimer concentrations in 3 (see table 2).112

Thrombelastogrammswereperformedin5dogs,4ofwhichwerenormocoagulable,and1113

hypercoagulable(dog7).C-reactiveprotein(CRP)serumlevelswereassessedin8dogsand114

wereelevatedinallbut1dog.AsCRPwasmeasuredusingtwodifferentassayswithseparate115

referencerangesandsensitivitiesacrosstheyears,amoredetailedcomparisonbetweendogs116

isdifficult.Valueswithoneassaydwere0.1,35.3,41.3,56,60.8and73.5mg/l (reference117

range0-13.33mg/l),and212and229.3µg/lwiththesecondassaye(referencerange0-14.9118

µg/l).Resultsfromvenousbloodgasanalysiswereavailableonthedayofadmissionfor5119

dogsshowingameanpHof7.35(sd0.02),HCO3of21.64mmol/l(sd2.98mmol/l),pCO2of120

39.48mmHg(sd3.55mmHg),baseexcessof-3.4(sd3.1),andalactateof2.22mmol/l(sd121

1.27mmol/l).Urinalysiswasperformedin9of14dogs(seetable3),includingbacterialurine122

culturein7(allnegative).123

Additionaldiagnostictestsperformedincludedimagingprocedureslikethoracic(n=13)and124

abdominalradiographs(n=10),abdominalultrasound(n=14),andCT/MRI(headandspine125

n=2;abdomenn=1).Cerebrospinalfluidandmultiplejointtapswereperformedinatotal126

of 4 dogs. Other diagnostics included analysis of ascitic fluid (n = 3; all septic exudates),127

bacterial culture from ascites (n = 2, both negative), culture of swabs or biopsies from128

mesentericlymphnodes/abscesses(n=6;3ofwhichwerenegative,isolatedorganismsfrom129

theothersincludedE.coli,Serratiamarcescens,Staph.aureus,Staph.epidermidis,Scc.canis,130

Prevotellasp.), joint fluidculture (n=1,negative),and faecalculture (n=1:Enterobacter131

cloacae+++,Proteussp.++,Cl.perfringens+++).Anattemptto identifyacid-fastbacterial132

speciesbyeithercultureorZiehl-Neelsenstainingoflymphnodebiopsieswasonlyspecifically133

mentionedin2cases(bothnegative).PCRsforinfectiousorganismswerenotperformedon134

anysamplefromthe14dogs,andvectorborndiseaseswereonlyinvestigatedintwodogs(1135

Leishmaniasp.serology,1PCRforBabesiasp.).136

Faecalparasitology(sedimentation/flotationandGiardiaantigen)wasperformedin2dogs,137

whichwerebothnegative.Fineneedleaspiratesofdistantsitesincludedperipherallymph138

nodes(n=1;normallymphnode/reactivehyperplasia)andsubcutaneousmasses(n=2;both139

lipomas).140

Asnocausativeagentorunderlyingdiseaseprocesswas identified inanyofthedogs,the141

tentativediagnosisof idiopathicmLAd/mLAbwasmade.Inonedog,apossibleassociation142

betweenthediseaseandthefactthatthedamsufferedfromseveresepticmastitiswhenthe143

dogwasapuppy(beforebeingweaned)waspostulated.However,acausalrelationshipwas144

difficulttoproveinthiscase.Anadditional2dogssufferedfromdegenerativeintervertebral145

discdisease(IVDD)simultaneouslytothedetectionofmLAd/mLAb(neurolocalisationL7-S1146

indog1;C1-C4indog2),butagain,acausalrelationshipbetweenthosediseasesseemed147

unlikely.TherewasnoevidenceofdiscospondylitisonCT/MRIinthesedogs.Dog2underwent148

surgical treatment for IVDD (ventral slot C2/3) 4 days after surgical intervention for the149

mLAd/mLAb and recovered uneventfully from both procedures. This dog was well and150

normothermic4and8weeksafterdischarge.Dog1wasmanagedconservativelyforIVDD151

(kennel rest, analgesics) and also recovered well. Another dog (dog 5) developed152

fibrocartilagenousembolicdisease14monthsaftermLAd/mLAbwasdiagnosed,butagain,a153

causalrelationshipseemedunlikely.154

Inanothercase(dog4)balloonvalvuloplastyforpulmonicstenosishadbeenperformeda155

monthpriortothedevelopmentofdiarrhoea,hyperthermiaandlethargy,andsubsequent156

diagnosis of mLAd/mLAb. No valvular abnormalities consistent with endocarditis were157

detected on echocardiography at any stage. Follow-up physical examination and158

echocardiography3and12monthsafter the initial valvuloplastywerealsowithinnormal159

limits.160

Dog13hadanexploratory laparotomy2monthsprior,whereremnantovariantissuewas161

removed.Thedogthendevelopedlethargy,hyperthermia,diarrhoeawithtenesmusanda162

palpablerectalmassatthetimemLAd/mLAbwaspresent(withStaph.epidermidis,Staph.163

canis, streptococci,2 typesofE.coliandPrevotella sp. isolated fromtheabdominal lymph164

nodesontwoseparateoccasions)andwassubsequentlydiagnosedwithaleiomyomadorsal165

totherectum,whichwassuccessfullyremoved.Thisdogwashospitalisedforaprolonged166

periodoftimeduetosepticperitonitis,buteventuallyrecovered.Itwasdeemedunlikelythat167

previoussurgeryortheleiomyoma,whichwaswellencapsulatedandeasytoremove,was168

responsibleformLAd/mLAb,butacausalrelationshipcannotbefullyexcluded.Twoand4169

weeksafterdischargefromthehospital,physicalexaminationwaswithinnormallimitsand170

abdominalultrasoundshowedmildfocalthickeningoftherectalwall,whichwasinterpreted171

aspost-operativechanges/scarring.172

Inthemajorityofdogs(n=10),surgicalinterventionwithremoval(n=4),biopsy(n=3)or173

debridement/ omentalisation (n = 3) of the affected mesenteric lymph nodes (or a174

combinationoftheseprocedures,n=1)wasperformed,whereas4receivedantibioticand175

supportivetreatmentalone(seetable1).Surgical findingswerevariable,but includedthe176

presenceofgeneralisedmildintra-abdominallymphadenopathyinadditiontotheaffected177

lymphnode (n = 8), generalised peritonitis (n = 5), detection of an intra-abdominalmass178

withoutconnectiontoaspecificorgan(n=4),abscessationofintra-abdominallymphnode(s)179

(n=4),smallamountsofascites(n=3), inflammationoftheintestine,describedaswhite180

generalisedplaquesontheserosalsurfaceandbleedings(n=2),andchangesofotherintra-181

abdominal organs (spleen, liver, pancreas, n = 4). The abnormal lymph nodes/ masses182

themselveswereofvariablesizes,rangingfrommultifocalbutsmall(approximately2x1cm)183

toaround6.5cmdiameter.Biopsiesfromother intra-abdominalorgansweretakeninthe184

minorityofcases.Intestinalfullthicknessbiopsiesrevealedmildlymphoplasmacytic(dog5)185

andmoderateeosinophilicenteritis(dog14),andhepaticbiopsiesshowedunspecificchanges186

(mildreactive/mixedcellularhepatitis,mild fibrosis,mildcholestasisandcongestion) in2187

cases(dogs7and12).188

Dogsreceivedavarietyofsupportivetreatmentsanddrugseitherasanadditiontosurgery189

orasasoletherapy,whicharesummarised intable4.Alldogsweredischargedalive,but190

follow-up times varied (see table 1). At least 3 dogs experienced a relapse with similar191

symptoms(from1-4monthsafterinitialdischarge),allofwhichweretreatedconservatively192

(antimicrobialdrugtherapy)withoutfurtherinvasivediagnosticsorrepeatbiopsiesandwere193

dischargedagain.194

195

Discussion196

ContrarytotheperceivedincreaseincasesofidiopathicpurulentmLAd/mLAbindogs,this197

disease entity was uncommon during time frame analysed. A search of the veterinary198

literatureonlyidentifiedsinglecasereportsorsmallcaseseries,someofwhichinotherintra-199

abdominal locations (Beaumont and Glauberg 1979; Campbell 2009; Macpherson 1992;200

MarvelandMacphail2013),making this the first larger report including14cases from10201

years.Commoncharacteristicsofthedogswiththisconditionincludedunspecificaswellas202

GIrelatedclinicalsigns,abdominalpainandpyrexia.Typicallaboratoryabnormalitieswere203

consistent with systemic inflammation (inflammatory leucogramm with left-shift, mild204

hypalbuminaemiawithmildhyperglobulinaemia,moderatehyperfibrinogenaemia,increased205

D-dimers, increased CRP) and hepatobiliary involvement in some cases (mild206

hyperbilirubinaemia and elevated alkaline phosphatase). Urinalysis results ranged from207

normaltoinflammation/infection,butbacterialurinaryculturewasnegativeinallcasesin208

whichitwasavailable.Theremainderoftheperformedinvestigationsfailedtoidentifyan209

underlyingcauseofthemLAd/mLAb,buttheextentoftheworkupvaried.Thisinconsistency210

isdue to the retrospectivenatureof thestudy (nostandardiseddiagnosticor therapeutic211

approach),differencesinpresentingcomplaintsdrivingtheinvestigations,andinavailability212

ofdiagnostictestsovertheyears.Interestingly,inonly50%oftheculturesperformedfrom213

the lymphnodes, bacterial growthwas identified. Similarly toprevious reports (Campbell214

2009; Macpherson 1992; Marvel and Macphail 2013), this included isolates typically215

associatedwiththeskin,e.g.StaphylococcusandStreptococcussp.,ortheGItract.Asmall216

amount of bacteria from theGI tract (includingmicroorganisms from the oral cavity and217

possiblyskin)migratetothemesentericlymphnodesunderphysiologicalconditions,usually218

within antigen-presenting cells (macrophages, dendritic cells) (Alexander et al. 1990;219

Dahlingeretal.1997;MacphersonandSmith2006).Thisispartoftheinnateimmunesystem220

of the GI tract (gut-associated lymphoid tissue; GALT) recognising and processing GI221

microbiota, thereby maintaining tolerance towards harmless commensal microorganisms222

(MacphersonandSmith2006).However,insituationswheretheintestineisinflamedorthe223

physiological architecture destroyed, bacterial translocation with subsequent intra-224

abdominal or systemic inflammation (systemic inflammatory response syndrome; SIRS)225

and/orsepsiscanoccur(GoddardandLeisewitz2010;Qinetal.2002;Untereretal.2015).As226

somedogsdescribedinthisreportfulfilledSIRScriteria(Gebhardtetal.2009;PurvisandKirby227

1994;Torrenteetal.2015),bacterialtranslocationorhaematologicalspreadfromadistant228

unrelated and undetected site is a possible pathogenesis. Pancreatitis – which is a valid229

differentialdiagnosisindogswithacutetosub-acuteGIsigns,pyrexiaandaninflammatory230

leucogramm–hasbeenassociatedwithbacterialtranslocationinbothhumans(Kazantsevet231

al. 1994)anddogs (Qinetal. 2002). Intestinalbiopsies toassesspossibleGIpathologyor232

comprehensive faecal examinations forpotential intestinal pathogens (bacterial, parasitic,233

viral)werenotavailable inmostof thecasespresentedhere, thereforeprimary intestinal234

inflammationorinfectioncannotberuledout.Pancreatitiswasnotdetectedinanydogbased235

onmeasurementofunspecificserumlipaseactivity,whichispartoftheroutinebiochemical236

profileofourteachinghospitalformorethan10years.However,morespecificcPL(Haworth237

etal.2014)wasonlyassessedin4cases(allwithinnormallimits).Innoneofthedogs,findings238

oftheabdominalultrasoundexaminationwereparticularlysuspiciousforpancreatitis;but239

again,itcannotbeentirelyexcluded(Xenoulis2015).Whileultrasonographicvisualizationof240

the pancreas has improved dramatically with equipment advances, the sensitivity for241

diagnosis of pancreatitis with ultrasound remains only around 70% (Hess et al. 1998;242

Shanamanetal.2013;Xenoulis2015).ThesensitivityfordiagnosisofpancreatitisusingcPL243

rangesbetween72-78%(McCordetal.2012);thereforepancreatitiscannotbeexcludedfrom244

ourpatientpopulation.245

Italsohastobeconsideredthatthebacterialspeciesisolatedfrommesentericlymphnodes246

in these casesmay not represent the initial causative agents,making speculation on the247

significanceofthesefindingsevenmoredifficult.Otherbacterialorganisms–e.g.anaerobes,248

Bartonellasp.ormycobacteria–havenotconsistentlybeeninvestigated;henceitispossible249

that they have beenmissed. However, even though Bartonella sp. (Morales et al. 2007;250

Pappalardoetal.2001;Tuckeretal.2014)andmycobacteria(Camporaetal.2011;Grooters251

etal.1995;Martinhoetal.2013;Turinellietal.2004;Zeissetal.1994)undoubtedlyhave252

their place in causing lymphadenopathy, lymphadenitis and/ or lymph node abscesses in253

dogs, the expected histopathological changes would be a granulomatous or mixed254

inflammatoryresponseratherthanpurulentinflammation(Camporaetal.2011;Drutetal.255

2014;Grootersetal.1995;Moralesetal.2007;Pappalardoetal.2000;SaundersandMonroe256

2006;Tuckeretal.2014;Turinellietal.2004;Zeissetal.1994).Inaddition,thesediseases257

usually cause multifocal or generalised lymphadenitis; and even though intra-abdominal258

lymphnodeshavebeeninvolvedinsomereportedcases(Martinhoetal.2013;Saundersand259

Monroe2006),thereisonlyonecasereportofsoleintra-abdominallymphadenitisassociated260

withM.tuberculosis(Engelmannetal.2014).Primaryimmune-mediateddiseaseleadingto261

increasedtransportordecreasedclearanceofbacteriafromthemesentericlymphnodescan262

alsonotbeexcluded.263

Themajorityofthedogsinthepresentcasereportweretreatedsurgically,mainlybecause264

mesenteric lymph nodes showed signs of abscessation on ultrasonography or septic265

peritonitiswaspresent.Thisnaturallyintroducesabiastowardsdogswithonlymild(often266

multiple) affectedmesenteric lymph nodes (lymphadenitis) and no ascites, to be treated267

conservatively. Interestingly, a number of dogs suffered relapses with lymph node268

abscessations (no ascites) where surgery was not an option for the owner, but repeat269

treatment with antimicrobials lead to resolution of clinical signs. This suggests that270

conservativemanagementofmLAd/mLAbmaybeaneffectiveoptionwhensurgery isnot271

possible,especiallyincaseswithoutsepticperitonitis.However,itdoesnotallowprediction272

ofthebestpossibletreatmentorfaircomparisonofconservativeversussurgicaltherapyin273

thesecases.Itseemsprudentthatinthepresenceofsepticperitonitisorseverelymphnode274

abscessationwithriskofrupture,surgicalinterventionisstillconsideredthebestoptionof275

therapy,untilstrongevidenceisavailablethatprovesotherwise.276

Inconclusion,thecombinationofGIsigns,specificallyabdominalpain,andpyrexiaindogs277

withmesentericlymphadenopathywarrantsathoroughandproblem-orientedapproachto278

searchforanunderlyingpathology.BacterialtranslocationfromtheGItractmaypotentially279

contributetomLAd/mLAbindogs(eitherprimaryorduetoanunderlyinginflammatoryor280

infectiousdiseaseoftheGItract,thepancreasorotherintra-abdominalorgans)butthebest281

approach to diagnostic workup and ideal treatment still needs to be defined. It can be282

assumedthatdependingontheseverityanddurationoftheseprocesses,differentstagesof283

theinflammatoryprocesswithinthelymphnodesexist(frommildsuppurativelymphadenitis284

toruptureoflymphnodeabscesses),whichrequiredifferenttreatments.Oncetheabscessis285

fullyformedorifthereisconcurrentevidenceofsepticperitonitis,surgicaltherapyseemsa286

successfulandsafetreatmentoptionwithagoodlong-termprognosis.Relapsesseemtobe287

relativelyuncommon,andiftheyoccur,canbelikelymanagedconservatively.Themostideal288

length of antibiotic treatment or the usefulness of prophylactic diagnostic or therapeutic289

interventionsremainsunknown.Prospectivestudiesinvestigatingmorecrypticpathogeneses290

more consistently (e.g. infectious diseases not routinely assessed and concurrent organ291

diseases)ordeterminingtherelevanceofisolatedbacterialorganismswouldbeuseful,asa292

primaryimmunopathogenesiswithsecondaryinfectioncannotbeexcludedatthisstage.293

294

Footnotes:295

a Easyvet Clinical Data Management System, IFS Informationssysteme GmbH, Hannover,296

Germany297

bSNAP®cPLTMTest,IDEXXlaboratories(VetMedLaborGermany),Ludwigsburg,Germany298

cSpeccPL®Test,IDEXXlaboratories(VetMedLaborGermany),Ludwigsburg,Germany299

d Gentian specific canine CRP Test (immunoturbidimetric), Scil Animal Care, Viernheim,300

Germany301

eRandoxCRPtest,RandoxLaboratoriesLtd.,Crumlin,UK302

303

304

305

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414

DogID Breed Gender Ageattimeofpresentation(months)

Diagnosisbasedon:cytology(C)histology(H)

Pre-treatment Treatment:surgical(S)conservativedrugtherapy(C)andantibioticsused

Lengthofhospitalisation/follow-up(days)

Outcome

1 CotondeTulear Mc 63 C potAmox,metamizole

C,potAmox 10/16 Alive

2 SmallMunsterlander

F 98 H Carprofen S,potAmox 10/35 Alive

3 Poodle F 58 C,H Ampicillin,dexamethasone,scopolamine

S,potAmox,enrofloxacin

7/104 Alive

4 Germanwirehairpointer

M 15 C Marbofloxacin,scopolamine,single-proteindiet,metamizole

C,marbofloxacin 5/447 Alive

5 Foxterrier M 40 C,H None S,potAmox 8/971 Alive6 Mixedbreed Fs 22 C,H Amoxicillin,

doxycyclin,metamizole

S,potAmox,enrofloxacin

8/166 Alive,recurrenceafter1month,dischargedagain

7 OldEnglishsheepdog

F 47 C,H potAmox,enrofloxacin,metamizole,carbesia

S,potAmox,enrofloxacin,metronidazole,doxycyclin

11/32 Alive

8 SmallMunsterlander

F 14 C,H Penicillin-streptomycin,scopolamine

S,potAmox 10/0 Discharged,buteuthanisedforunknownreason1yearlater

9 GordonSetter M 90 C None C,potAmox 1/14 Alive10 BorderCollie Fs 93 C None C,potAmox 3/0 Alive11 Mixedbreed F 24 C,H None S,potAmox,

enrofloxacin9/7 Alive

12 Mixedbreed Fs 41 C,H None S,potAmox,enrofloxacin

20/43 Alive,recurrenceafter5months,dischargedagain

13 Mixedbreed F 13 C,H Ciprofloxacin,metamizole

S,pradofloxacin,cephalexin

26/0 Alive

14 SmallMunsterlander

M 6 C,H Ampicillin,metamizole

S,Ampicillin,enrofloxacin,doxycyclin

5/261 Alive,recurrenceafter3months,dischargedagain

Table1:Signalement,pre-treatment,typeoftreatmentandoutcomein14dogswithidiopathicmesentericlymphadentitis/lymphnodeabcess.

Parameter Value(mean±sd) Referenceinterval

Units No.ofpatients(n/14)

WBC 24.42(±14.09) 5.48–13.74 10e9/l 14/14Neutrophils 19.91(±12.97) 2.78–8.73 10e9/l 14/14Lymphocytes 2.37(±1.04) 0.72–4.71 10e9/l 14/14Monocytes 2.28(±2.90) 0.06–0.83 10e9/l 14/14Eosinophils 0.28(±0.22) <1.47 10e9/l 14/14Basophils 0.05(±0.07) <0.11 10e9/l 14/14LUC 0.51(±0.54) <0.04 10e9/l 11/14Bandneutrophils

2.15(±2.69) <0.5 10e9/l 9/14

RBC 6.14(±1.32) 5.5–8.5 10e12/l 14/14Hgb 11.64(±3.54) 8.06–12.21 mmol/l 14/14HCT 41.5(±8.9) 39–56 % 14/14Reticulocytes 29.94(±18.76) <60 10e9/l 7/14RDW 14.27(±1.94) 10.76–12.8 % 14/14MCV 67.54(±3.67) 62.61–73.5 fL 14/14MCH 1.62(±0.19) 1.35–1.62 fmol/l 14/14MCHC 27.71(±4.25) 20.82–

23.53g/dl 14/14

Plt 273(±130) 150–500 10e9/l 14/14Urea 8.4(±7.7) 3.3–9.82 mmol/l 14/14Creatinine 103(±99) 53–122 µmol/l 14/14Sodium 145(±3) 141–146 mmol/l 14/14Chloride 109(±4) 104–112 mmol/l 14/14Potassium 3.8(±0.5) 3.35–4.37 mmol/l 14/14IonizedCalcium

1.33(±0.11) 1.23–1.43 mmol/l 13/14

Anorganicphosphorus

1.59(±0.81) 0.79–2.1 mmol/l 13/14

Ionisedmagnesium

0.55(±0.20) 0.47–0.63 mmol/l 13/14

Totalprotein 65.5(±6.0) 55.3–69.84 g/l 14/14Albumin 27.1(±5.5) 29.6–37.01 g/l 14/14Globulin 38.5(±7.0) 22.9–35.6 g/l 14/14Glucose 6.17(±7.02) 3.3–6.5 mmol/l 14/14Totalbilirubin 3.82(±1.89) 0–3.6 µmol/l 14/14Cholesterol 6.28(±1.90) 3.3–8.6 mmol/l 14/14Triglycerides 0.711(±0.68) 0.08–0.75 mmol/l 13/14ALP 308(±536) <130 U/l 14/14ALT 40(±28) <85 U/l 14/14GLDH 2(±1) <9.9 U/l 13/14CK 238(±312) <143 U/l 11/14Amylase 787(±277) <1157 U/l 5/14Lipase 67(±61) <300 U/l 4/14Fibrinogen 4.11(±1.79) 1.21–3.03 mmol/l 5/14PT 7.6(±8.1) 6.5–8.2 sec 5/15aPTT 11.3(±12.3) 9.9–14.2 sec 5/15d-dimers 0.4(±0.27) <0.1 µg/dl 3/14

Table2.Laboratoryparametersin14caninepatientswithpresumedidiopathicmesenteric

lymphadenitis/lymphnodeabscesses.Boldnumbersindicateameanoutoftherespective

referencerange.

DogID USG(>1035) pH(6.5-7.5) Bilirubin(neg) Blood/RBC(+) Glucose(Neg) Ketones(Neg) Protein(Negto+) Sediment(Neg) UPC(<0.5)3 1026 5 ++ +++ Neg Neg +++ >5/hpfRBC 1.15 1020 7.5 Neg Neg Neg Neg Neg Neg n.p.6 1038 5 Neg Neg Neg Neg + Neg n.p.7 1042 7.5 + Neg Neg Neg + Neg n.p.8 >1050 5 + +++ Neg Neg + Scarcerenal

epithelian.p.

10 1025 8 n.p. n.p. n.p. n.p. n.p. Neg n.p.11 1018 7 Neg Neg Neg Neg ++ Neg 0.412 1018 7 + +++ Neg Neg +++ >5/hpfWBCand

RBCn.p.

14 1048 6.5 Neg Trace Neg Neg ++ >5/hpfWBCandRBC

0.2

Table3.Urinalysisfrom9/14dogswithidiopathicmesentericlymphadenitis/lymphnodeabscesses.Referencerangesprovidedinbrackets.Hpf=highpowerfield;n.p.=

notperformed;Neg=negative;RBC=redbloodcells;WBC=whitebloodcells

Drugclass Activeingredient NumberofdogsAntimicrobials Amoxicillin/clavulanate 11

Enrofloxacin 6

Doxycyclin 2

Marbofloxacin 1

Ampicillin 1

Verafloxacin 1

Cephalexin 1

Metronidazole 1

Anti-inflammatories Metamizole 4

Robinacoxib 1

Analgesics Tramadol 4

Fentanyl 1

Buprenorphin 1

Tetrazepam 1

Gastroprotectants Omeprazol 4

Pantoprazol 4

Sucralfate 3

Antiemetics Maropitant 3

Metoclopramide 3

Prokinetics Prucaloprid 1

Antiparasitics Fenbendazole 1

Choleretics Ursodeoxycholicacid 1

Plateletaggregationinhibitors Clopidogrel 1

Table4.Medicaltreatmentsadministeredto14dogswithpresumedidiopathicmesenterial

lymphadenitis/lymphnodeabscesses.