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ImportedSkinDiseases ImportedSkin Diseases EDITEDBY
WilliamR.Faber MD,PhD
EmeritusProfessorofTropicalDermatology
DepartmentofDermatology
AcademicMedicalCenter
UniversityofAmsterdam
Amsterdam,theNetherlands
RoderickJ.Hay DM,FRCP,FRCPath
ProfessorofCutaneousInfection
KingsCollegeLondon London,UK
BernardNaafs MD,PhD
VisitingProfessor RegionalDermatologyTrainingCenter(RDTC) Moshi,Tanzania;and
InvitedProfessor InstitutoLaurodeSouzaLima(ILSL) Bauru,Brazil;and
Consultant
StichtingTropen-Dermatologie Munnekeburen,theNetherlands
SECONDEDITION
A John Wiley & Sons, Ltd., Publication
Thiseditionfirstpublished2013 C 2006byElsevier;2013byJohnWiley&Sons,Ltd.
Wiley-BlackwellisanimprintofJohnWiley&Sons,formedbythemergerofWiley’sglobal Scientific,TechnicalandMedicalbusinesswithBlackwellPublishing.
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LibraryofCongressCataloging-in-PublicationData
Importedskindiseases/editedbyWilliamR.Faber,RoderickJ.Hay,BernardNaafs.–2nded. p.;cm.
Includesbibliographicalreferencesandindex. ISBN978-0-470-67226-6(hardback:alk.paper)
I.Faber,WilliamRichard,1940-II.Hay,R.J.(RoderickJ.),1947-III.Naafs,B.(Bernard) [DNLM:1.SkinDiseases–diagnosis.2.SkinDiseases–epidemiology.3.DiseaseTransmission, Infectious.4.EmigrationandImmigration.5.RareDiseases–diagnosis.6.Travel.WR141] 616.5–dc23
2012021653
AcataloguerecordforthisbookisavailablefromtheBritishLibrary. Wileyalsopublishesitsbooksinavarietyofelectronicformats.Somecontentthatappearsinprint maynotbeavailableinelectronicbooks.
Coverimage:mainimage C iStockphoto.com/Petrovich9 Smallimages(lefttoright)withkindpermissionfromtheauthorsofChapter3(image1);Chapter 14(image2);Chapter10(images3)
CoverdesignbyMeadenCreative Setin9.5/13ptMeridienbyAptara R Inc.,NewDelhi,India
12013
WilliamR.FaberMD,PhD studiedmedicineattheUniversityofLeiden. Thereafter,hewasamedicalofficerinUgandaandpracticedasageneralpractitionerintheNetherlands.HewastrainedasadermatovenereologistattheBinnengasthuis,Amsterdam(ProfessorDrR.H.Cormane). HecompletedhisPhDfromtheUniversityofAmsterdam.Thereafter,he wasaconsultantdermatologistattheMeanderMedischCentrum,Amersfoort,andProfessorinTropicalDermatologyattheAcademicMedical Centre(AMC),UniversityofAmsterdam,Amsterdam,theNetherlands. Atpresent,heisEmeritusProfessorofTropicalDermatologyatUniversity ofAmsterdam.
BernardNaafsMD,PhD wastrainedasadermatovenereologistbyProfessorCormaneattheBinnengasthuisinAmsterdam.Heworkedduring1974–1979inEthiopiaandduring1983–1986inZimbabwe.For 14years,hehasdividedhistimebetweentheNetherlands(Antonius hospital,EmmeloordandDiaconessenhuis,annexSteenwijk),andthe developingcountries,particularly,eachyear3monthsattheRegional DermatologyTrainingCentreinMoshi,Tanzania,and3monthsatthe InstitutoLaurodeSouzaLima,Bauru,SP,Brazil.
RoderickJ.HayDM,FRCP,FRCPath istheChairmanoftheInternationalFoundationforDermatology,ConsultantDermatologist,SkinInfectionClinic,KingsCollegeHospital,London,andProfessorofCutaneous Infection,KingsCollegeLondon.HeisEmeritusProfessorofDermatology,QueensUniversityBelfast(QUB)andHonoraryProfessorintheClinicalResearchUnit,LondonSchoolofHygieneandTropicalMedicine.He waspreviouslyHeadoftheSchoolofMedicineandDentistryandDeanof theFacultyofMedicineandHealthSciences,QueensUniversityBelfast. Beforethis,hewasMaryDunhillProfessorofCutaneousMedicineatthe StJohnsInstituteofDermatology,London.Hecurrentlycoordinatesthe dermatologysubmissionfortheGlobalBurdenofDiseaseProject(WHO).
Contributors,ix
1 Introduction,1
W.R.Faber,R.J.Hay,&B.Naafs
2 PrecautionsandProtection,4
W.R.Faber,R.J.Hay,&B.Naafs
3 PigmentaryDisordersinBlackSkin,8
J.P.W.vanderVeen&L.Nieuweboer-Krobotova
4 DifferencebetweenPigmentedandNonpigmentedSkin,19 B.Naafs
5 InfluenceoftheNewEnvironmentontheSkin,31
S.Badeloe&H.E.Menke
6 FungalInfections,45
R.J.Hay
7 MycobacterialInfections,64
W.R.Faber
8 Leprosy,79
B.Naafs&W.R.Faber
9 BuruliUlcer,94
D.S.Walsh,W.M.Meyers,&F.Portaels
10 UlceratingPyodermas,107
J.E.Zeegelaar
11 Rickettsioses,114
P.A.Kager&H.G.Schipper
12 ViralDiseases,123
R.M.Mays,R.A.Gordon,S.Javed,J.M.Wilson,W.J.LaPolla, N.A.Kjar,&S.K.Tyring
13 SexuallyTransmittedInfections,149 M.Waugh&H.J.C.deVries
14 EndemicTreponematoses,162
H.J.H.Engelkens
15 AmericanTegumentaryLeishmaniasis,171
C.Talhari,J.A.deOliveiraGuerra,A.Chrusciak-Talhari, P.R.L.Machado,&S.Talhari
16 Leishmaniasis:OldWorld,189
F.Vega-L ´ opez
17 Onchocerciasis/Filariasis,205
M.E.Murdoch
18 Schistosomiasis,226
A.M.Polderman&L.vanLieshout
19 Tungiasis,234
H.Feldmeier&J.Heukelbach
20 CutaneousLarvaMigrans,243
J.Heukelbach&H.Feldmeier
21 Myiasis,252
R.Kapoor,T.A.McGraw,&D.M.Elston
22 PersistentInsectBites,264
C.L.M.vanHees
23 BeetleDermatitis,273
M.Glatz&P.Schmid-Grendelmeier
24 AquaticSkinDisorders,283
M.T.W.Gaastra
25 GeographicDistribution,293
W.R.Faber,R.J.Hay,&B.Naafs
26 ClinicalProblems,296
W.R.Faber,R.J.Hay,&B.Naafs
Index,299
Contributors SadhannaBadeloeMD,PhD Dermatovenerologist DepartmentofDermatology MedicalCentreHaaglanden TheHague,theNetherlands
AnnetteChrusciak-TalhariPhD Dermatologist Fundac ¸ aodeMedicinaTropicalDr.Heitor VieiraDourado Manaus,Brazil
JorgeAugustodeOliveira GuerraPhD
Infectologist Fundac ¸ aodeMedicinaTropicalDr.Heitor VieiraDourado Manaus,Brazil
HenrydeVriesMD,PhD ProfessorofSkinInfections DepartmentofDermatology AcademicMedicalCenter UniversityofAmsterdam Amsterdam,theNetherlands
DirkElstonMD Director AckermanAcademyofDermatopathology NewYork,NY,USA
HermanJ.H.EngelkensMD,PhD DepartmentofDermatologyandVenereology IkaziaHospital Rotterdam,theNetherlands
WilliamR.FaberMD,PhD EmeritusProfessorofTropicalDermatology DepartmentofDermatology AcademicMedicalCenter UniversityofAmsterdam Amsterdam,theNetherlands
HermannFeldmeierMD,Ph.D. ProfessorofTropicalMedicine InstituteofMicrobiologyandHygiene Charit ´ eUniversityMedicine Berlin,Germany
MennoT.W.GaastraMD Dermatologist CentrumOosterwal ClinicforDermatologyandFlebology Alkmaar,theNetherlands
MartinGlatzMD ResidentinDermatology DepartmentofDermatology UniversityHospitalofZurich Zurich,Switzerland
RachelA.GordonMD ClinicalResearchFellow CenterforClinicalStudies DepartmentofDermatology UniversityofTexasMedicalSchool Houston,TX,USA
RoderickJ.HayDM,FRCP,FRCPath ProfessorofCutaneousInfection KingsCollegeLondon London,UK
JorgHeukelbachMD,MScIH,PhD ProfessorofEpidemiology DepartmentofCommunityHealth SchoolofMedicine FederalUniversityofCear ´ a Fortaleza,Brazil;and AdjunctProfessor AntonBreinlCentreforPublicHealth andTropicalMedicine SchoolofPublicHealth TropicalMedicineandRehabilitationSciences JamesCookUniversity Townsville,Australia
SabaJavedBS MedicalStudent UniversityofTexasMedicalSchoolatHouston Houston,TX,USA
PietA.Kager
EmeritusProfessorofTropicalMedicine DepartmentofMedicine DivisionofInfectiousDiseases,UnitofTropical Medicine AcademicMedicalCenter UniversityofAmsterdam Amsterdam,theNetherlands
RogerKapoorMD,MBA DermatologyResident DermatologyDepartment MassachusettsGeneralHospital HarvardMedicalSchool Boston,MA,USA
NatalieA.KjarBS MedicalStudent UniversityofTexasMedicalSchool Houston,TX,USA
WhitneyJ.LaPollaMD DermatologyResident CenterforClinicalStudies DepartmentofDermatology UniversityofTexasMedicalSchool Houston,TX,USA
LisettevanLieshoutPhD AssociateProfessor HumanParasitology LeidenUniversityMedicalCenter Leiden,theNetherlands
PauloRobertoLima MachadoPhD Dermatologist UniversityHospitalProf.EdgardSantos UniversidadeFederaldaBahia Salvador,Brazil
RanaM.MaysMD
Fellow
InternalMedicineAttendingClinicalResearch DepartmentofDermatology BaylorCollegeofMedicine Houston,TX,USA
TimothyA.McGrawMD ChiefofDermatology U.S.AirForceAcademy,CO,USA
HenkE.MenkeMD,PhD Dermatologist HistoryofMedicineDepartment JuliusCenterforHealthSciencesand PrimaryCare UniversityMedicalCenter(UMC) Utrecht,theNetherlands
WayneM.MeyersMD,PhD FormerChief MicrobiologyDivision ArmedForcesInstituteofPathology Washington,DC,USA
MicheleE.MurdochBSc,FRCP ConsultantDermatologist WatfordGeneralHospital Watford,UK
BernardNaafsMD,PhD VisitingProfessor RegionalDermatologyTrainingCenter(RDTC) Moshi,Tanzania;and InvitedProfessor InstitutoLaurodeSouzaLima(ILSL) Bauru,Brazil;and Consultant
StichtingTropen-Dermatologie Munnekeburen,theNetherlands
L.Nieuweboer-KrobotovaMD Head,Outpatient’sClinic NetherlandsInstituteforPigmentDisorder AcademicMedicalCenter UniversityofAmsterdam Amsterdam,theNetherlands
AntonM.PoldermanPhD AssociateProfessorofParasitology(Retired) LeidenUniversityMedicalCenter Leiden,theNetherlands
Franc¸oisePortaelsPhD EmeritusProfessor FormerHead MycobacteriologyUnit DepartmentofBiomedicalSciences InstituteofTropicalMedicine Antwerp,Belgium
HansG.SchipperMD,PhD Retired,staffmember DepartmentofInternalMedicine AcademicMedicalCenter UniversityofAmsterdam Amsterdam,theNetherlands
PeterSchmid-GrendelmeierMD Head,AllergyUnit AssociateProfessorofDermatology DepartmentofDermatology UniversityHospitalofZurich Zurich,Switzerland
CarolinaTalhariPhD ProfessorofDermatology FacultyofMedicine StateUniversityofAmazonas Manaus,Brazil
Sin ´ esioTalhariPhD ProfessorofDermatology FacultyofMedicine StateUniversityofAmazonas Manaus,Brazil
StephenK.TyringMD,PhD Director CenterforClinicalStudies AssociateProfessor DepartmentofDermatology UniversityofTexasMedicalSchool Houston,TX,USA
J.P.W.vanderVeenMD,PhD Director
NetherlandsInstituteforPigmentDisorders AcademicMedicalCenter UniversityofAmsterdam Amsterdam,theNetherlands
ColetteL.M.vanHeesMD Dermatologist ConsultantTropicalDermatology DepartmentofDermatology ErasmusMedicalCenter Rotterdam,theNetherlands
FranciscoVega-LopezMD,PhD ProfessorandConsultant
DermatologistattheDermatologyDepartment UniversityCollegeHospitalandtheHospitalfor TropicalDiseases London
DouglasS.WalshMD,MS DepartmentofImmunologyandMedicine UnitedStatesArmyMedicalComponent ArmedForcesResearchInstituteofMedical Sciences(USAMC-AFRIMS) Bangkok,Thailand and AdjunctAssociateProfessorofDermatology UniformedServices UniversityoftheHealthSciences(USUHS) Bethesda,MD,USA
MichaelWaughMB,FRCP,FAChSHP EmeritusConsultant GenitourinaryMedicine LeedsGeneralInfirmary Leeds,UK;and FormerHon.SeniorLecturer FacultyofMedicine UniversityofLeeds Leeds,UK
JaniceM.WilsonBS MedicalStudent UniversityofTexasMedicalSchool Houston,TX,USA
JimE.ZeegelaarMD,PhD DepartmentofDermatology Flevoziekenhuis Almere,theNetherlands
CHAPTER1 Introduction WilliamR.Faber1 ,RoderickJ.Hay2 ,&BernardNaafs3,4,5
1 DepartmentofDermatology,UniversityofAmsterdam,Amsterdam,theNetherlands
2 KingsCollegeLondon,London,UK
3 RegionalDermatologyTrainingCenter(RDTC),Moshi,Tanzania
4 InstitutoLaurodeSouzaLima(ILSL),Bauru,Brazil
5 StichtingTropen-Dermatologie,Munnekeburen,theNetherlands
Internationaltourismisoneofthelargestandfastestgrowingeconomic sectorsintheworldwithcontinuousexpansionanddiversification,and manynewdestinations,oftentolessprivilegedareas.
Internationaltouristvisitsin2010wereestimatedtobe940million, andareexpectedtoincreaseby4–5%in2011.In2020,1.6billioninternationalvisitsareexpected.Expenditureoninternationaltourismhad reached $919bn(€693bn)in2010.Internationaltourismisthefourth globalexportcategoryandaccountsfor30%ofworldexportsofcommercialservices.Itisestimatedtocontribute5%totheworldwidegross domesticproduct[1].
Astheworlddevelopsintoaglobalvillage,peopletraveldailyfromcontinenttocontinentandinfectiousdiseasesmaytravelwiththem.Onthe onehand,someonewithaninfectionacquiredunder“tropical”conditions abroadmayvisitthehealthservicesinEuropeorNorthAmericawithin 24hoursofhisorherdeparturefromthecountryvisited.Ontheother hand,insomediseases,clinicalsignsandsymptomsmaydevelopweeksto monthsafterreturn,sotherelationshipwiththepasttravelisnotobvious.
Therearethreemainreasonswhypatientswith“tropicalorexoticskin diseases”havebeenseenmorefrequentlyinrecentyears.
First,leisuretimeinaffluentsocietiesisincreasing,andmoreandmore people,includingthoseintheolderagegroups,takeholidaysinfar-off places.Moreandmoreadventureholidaysarebeingtakentoplaceswhere theriskofacquiringadiseaseismuchgreaterthaninamoreprotected environment.
Second,therearelargeimmigrantgroupsinmostWesterncountries, originatingfromothercontinents.Theymaypresentwithskindiseases monthsoryearsaftersettlingintotheirnewhomecountry.Also,these
ImportedSkinDiseases,SecondEdition.EditedbyWilliamR.Faber, RoderickJ.HayandBernardNaafs. C 2013JohnWiley&Sons,Ltd.Published2013byJohnWiley&Sons,Ltd.
peoplemayregularlyvisittheirfamilyintheircountryoforiginand acquireaskindisease.
Third,thereisagroupofprofessionaltravelersvisiting,regularlyorfor alongperiods,countriesinothercontinents;thisincludesmembersofthe militarygoingfortrainingorpeace-keepingmissions.
Skindiseasesarefoundinaconsiderablenumberoftravelers.Itwas reportedthatamong2004patientsattendinganInstituteforTropical MedicineinBerlin,Germany,14%oftheconsultationswereforskin diseases[2].FromtheUnitedStatesofAmerica,a2-yearsurveyof784 travelerstodevelopingcountriesreportedskinproblemsduringtravelin 8%ofthetravelers.In3%ofthemtheseproblemscontinuedorhadan onsetwithin14daysafterreturn[3].Of12,437travelerstoNepal,12.44% werefoundtohaveskindiseasesinwhichbacterialskindiseases,fungalskindiseases,scabies,and“skinallergy”werethemostprevalent[4].
Morerecently,inastudyfrom30GeoSentinelsites,whicharespecialized travelortropicalmedicineclinics,oftravelersreturningfromsixdevelopingregionsoftheworld,itwasfoundthatdermatologicaldisordersranked thirdinfrequency[5].
FrenchresearchersreportedinaprospectivestudyofFrenchtravelers totropicalcountries,ofwhom38%hadvisitedsub-SaharanAfrica,that themostcommondiagnosesin269patientswerecutaneouslarvamigrans (25%)andpyoderma(18%),followedbyinsectbites,myiasis,tungiasis, urticaria,feverandrash,andcutaneousleishmaniasisin10%orless.In 39%ofthepatientstheskinlesionsdevelopedafterthereturntoFrance. Themedianonsetafterdeparturefromthetropicswas7days(range0–52 days)[6].Themostcommonskin-relateddiagnosesin4595patientsseen inGeoSentinelclinicswerecutaneouslarvamigrans(9.8%),insectbites (8.2%),skinabscess(7.7%),andsuperinfectedinsectbites(6.8%)[7].
Thisbookhasbeenwrittenandillustratedforthehealthprofessionals livinginwesternEuropeandNorthAmericainordertohelpinthediagnosisandmanagementofpatientswithdiseasesacquiredinanother,often tropical,environment.Inthisrespect,thebookdealswithskindiseases thatarenotcommonintheWesternworld.
Awidespectrumofimportedskindiseases,themajorityinfectiousin origin,iscovered.Sexuallytransmittedinfectionsaswellasdermatological diseasesarealsodiscussed.
Skinsignsmayprovideacluetothediagnosisofsometimeslifethreateningsystemicinfections,andshouldthereforeberecognizedas soonaspossiblebytheattendingphysician.Astravelthesedaysisoften notonlyterrestrialbutalsoinvolveswaterexposureintheoceanorrivers, achapteronaquaticskindisordersisincluded.
Thebookalsodealswithemergingdiseasessuchascutaneous leishmaniasis,whichisbeingdiagnosedwithincreasingfrequencyin
travelersandalsointhemilitarysector,andBuruliulcer,whichisstill rareintravelers.
Theinfluenceofenvironmentalfactors,thecharacteristicsofpigmented skin,whichinfluencetheclinicalexpressionofdiseasesinthecoloredskin, anddisordersofthepigmentarysystemitselfarealsoaddressed.Tables andflowchartsofimportantclinicalconditionsandtherelationshipof thoseskindiseasestothedifferentgeographicalareaswillbehelpfulin thediagnosisandmanagementofpatientswithimportedskindiseases.
Thecontributionsoftheauthors,allexpertsintheirrespectivefields,are greatlyappreciated.
References 1UNWTO(2011)TourismHighlights2011edition,WorldHealthOrganization.
2Harms,G.,Dorner,F.,Bienzle,U.&Stark,K.(2002)Infectionsanddiseasesafter travelling. DeutscheMedizinischeWochenschrift, 127,1748–1753.
3Hill,D.R.(2000)HealthproblemsinalargecohortofAmericanstravellingtodevelopingcountries. JournalofTravelMedicine, 7,259–266.
4Caumes,E.,Brucker,G.,Brousse,G.,Durepaire,R.,Danis,M.&Gentilini,M.(1991) Travel-associatedillnessin838FrenchtouristsinNepalin1984. TravelMedicineInternational, 9,72–76.
5Freedman,D.O.,Weld,L.H.,Kozarsky,P.E. etal. (2006)GeoSentinelsurveillancenetworkspectrumofdiseaseandrelationtoplaceofexposureamongillreturnedtravelers. TheNewEnglandJournalofMedicine, 354,119–130.
6Caumes,E.,Carriere,J.,Gwermonpieze,G.,Bricaire,F.,Danis,M.&Gentilini,M. (1995)Dermatosesassociatedwithtraveltotropicalcountries:aprospectivestudyof thediagnosisandmanagementof269patientspresentingtoatropicaldiseaseunit. ClinicalInfectiousDiseases, 20,542–548.
7Lederman,E.R.,Weld,L.H.,Elyazar,I.R.F. etal. (2008)Dermatologicconditionsofthe illreturnedtraveler:ananalysisfromtheGeoSentinelSurveillanceNetwork. InternationalJournalofInfectiousDiseases, 12,593–602.
PrecautionsandProtection WilliamR.Faber1 ,RoderickJ.Hay2 ,&BernardNaafs3,4,5
1 DepartmentofDermatology,UniversityofAmsterdam,Amsterdam,theNetherlands
2 KingsCollegeLondon,London,UK
3 RegionalDermatologyTrainingCenter(RDTC),Moshi,Tanzania
4 InstitutoLaurodeSouzaLima(ILSL),Bauru,Brazil
5 StichtingTropen-Dermatologie,Munnekeburen,theNetherlands
Keypoints
Ajourneytoatropicalcountrymustbeadequatelyplannedinadvance Certaingroupsoftravelersaremoreatrisk Measuresshouldbetakentodiminishtheinfluenceofsunexposure Measuresshouldbetakentopreventinsectbites
Introduction
Whenplanningajourneytoatropicaldestination,thevisitorshould contact,dependingonthelocalcircumstances,aninstitutionsuchasthe publichealthservice,atravelclinic,ortropicaldiseasedepartmentsat (university)hospitalsinordertogetproperadviceonrequiredvaccinationsandprophylaxissuchasmalariaprophylaxis.Thisconsultation shouldtakeplacemorethan8weeksbeforedepartureandthisisespeciallyadvisableforpeoplewithpreexistingdiseasesandthoseoncomplex orimmunosuppressivetreatmentssuchasbiologicals.Theadvicegivenin thefollowingtextisspecificallyrelatedtotheskinandtravelersshould rememberthattakingmalarialprophylaxisandduecareindrinkingwater andeatinglocallyareallkeytopreventingillnesswhileabroad.
Amedicalkitisadvisablefordestinationswithsignificanthealthrisks, andcouldcontainthefollowingitemsforthetreatmentofskinproblems [1]:
Antisepticwoundcleanseroralkalinesoap
Bandages
Insectrepellent ImportedSkinDiseases,SecondEdition.EditedbyWilliamR.Faber, RoderickJ.HayandBernardNaafs.
C 2013JohnWiley&Sons,Ltd.Published2013byJohnWiley&Sons,Ltd.
Strongsteroidcream(touseonceortwiceonsunburnandinsectbites)
Antihistaminetablets
Steriledressing
Sunscreen
Tweezers
Adhesivestripstoclosesmallwounds
Andaccordingtodestinationandcircumstancesoftravel: Antibioticstargetingthemostfrequentinfectionsintraveler’santibacterialointment
Antifungalpowder
Mosquitonetandinsecticidetotreatfabrics(clothes,nets,curtains)
Oneshouldalsobeacquaintedwithclimaticconditionsduringtravel.In general,underconditionsofhighhumiditysuchasintropicalrainforest areasandduringmonsoonseasons,fungalandbacterialskininfections areprevalent.Whereasinsemiaridandaridareas,sun-exposure-related problemsaremorecommon.
Sunexposure UVB(wavelength280–315nm)andUVA(wavelength315–400nm)can bothhaveadverseeffectsontheskin.UVBcaninduceaskinburndependingontheexposureandskintype.Polymorphouslighteruption,solar urticaria,andphototoxicandphotoallergicreactionsmayalsooccur.PhototoxicreactionsaremediatedbyUVBandcommonlyresultfrominteractionwithdrugssuchascertaintetracyclines,thiazines,quinolones, andNSAIDs;also,phototoxicreactionsthroughlocalcontactwithfurocoumarinsinplantsandperfumesmayoccur.Photoallergicreactionsare generallymediatedbyUVA,andcausedbyphotoallergensincosmetics, antiseptics,sunscreens,andcertaindrugs.
Precautionsandprotectivemeasurestobetakenareasfollows[2]: Avoidexposuretothesuninthemiddleoftheday,whentheUVintensityisgreatest.
Donotoverexertyourselfonthefirstfewdaysafterarrivalinaveryhot climate.Heatexhaustionandpricklyheat(miliaria)arecommon.
Wearclothingthatcoversarmsandlegs(coveringtheskinwithclothing ismoreeffectiveagainstUVthanapplyingasunscreen).
WearUV-protectivesunglassesofwraparounddesignplusawidebrimmedsunhat.
Applyabroad-spectrumsunscreenofsunprotectionfactor(SPF)15 + liberallyonareasofthebodynotprotectedbyclothingandreapply frequently.
Takeparticularcaretoensurethatchildrenarewellprotected—babies shouldbeprotectedfromthesunbutalsobedressedinlightlooseclothing.
Avoidexposuretothesunduringpregnancy.
Takeprecautionsagainstexcessiveexposurewhileonorinwateroron snow.
CheckthatmedicationbeingtakenwillnotleadtosensitivitytoUV radiation.
Ifadverseskinreactionshaveoccurredpreviously,avoidanyexposure tothesunandavoidanyproductsthathavepreviouslycausedthe adversereactions.
Dophysicalexercisesduringairtravel,andwhenolderwearelastic stockings,topreventdeepvenousthrombosis.Elasticstockingsmay alsopreventthemildorsubclinicallowerlegedemacommontotravel intropicalclimate,whichmaypredisposetoinfectedminortraumaor insectbites.
Insects Thebiteorstingofaninsect,andalsonearlyallarthropods,cannotonly leadtopersistentinsectbitereactions,butcanalsobethesourcefortransmissionofinfectiousdiseaseslike(cutaneous)leishmaniasis,chikungunya andotherviraldiseases,rickettsioses,andLymedisease.
Precautionsandprotectivemeasurestobetakenareasfollows[2]:
Protectiveclothing
Insectrepellentsofwhich N,N-diethyl-3-methylbenzamide(DEET)is mostwidelyusedbutotheragentsarealsoavailable[3]
Mosquitonets
Mosquitocoils
Aerosolsprays
Certaingroupsoftravelersaremoreatriskofacquiringtravel-related diseasessuchasthefollowing[4]:
Visitorstofriendsandrelatives.ImmigrantsinWesterncountries increasinglytraveltotheircountryoforigintovisitfriendsandrelatives.Itappears,thatasaconsequenceoftheplacestheyvisitandthe waytheyparticipateinthelocallifestyle,theyareatanincreasedrisk ofexposure.Theyalsoarelesslikelytotakeprotectivemeasures. TravelerswithHIV/AIDSmayhaveincreasedsusceptibilitytotropical diseases.Theyhavereducedimmuneresponsetosomevaccines,and areatriskofseverereactionstolivevaccines.Accesstomedicalservice duringtravelmaybesubstandard.
Patientsontreatmentwithbiologicalsand/oronimmunosuppressive drugs.Anincreasingnumberofimmunocompromisedpersonstravelto (sub)tropicalregions,alsobecausenewtherapeuticmodalitiesenable suchundertaking.Immune-mediatedinflammatorydiseasessuchas rheumatoidarthritis(RA),inflammatoryboweldisease(IBD),andpsoriasis,sharecommongeneticproblemscharacterizedbycytokinedysregulation.Immunosuppressiveorimmunomodulatoryagentsareused totreattheirdisorders.Both,diseaseandtreatment,haveimplications forvaccination,awell-establishedstrategytopreventcertainimportantinfectiousdiseasesintravelerstothetropics.Liveattenuatedvaccines,suchasforyellowfever,arecontraindicatedinthesepatients, whereasinactivatedvaccinesaresafebutmightrequireassessmentof theimmuneresponse.Thesetravelers,andalsothosewithotherunderlyingconditionssuchasHIVdiseaseorsplenicdysfunction,shouldseek expertpretraveladviceasfarinadvanceaspossible[5,6].
References 1InternationalTravelandHealth(2011)Healthrisksandprecautions:generalconditions,Ch1.WorldHealthOrganization.
2InternationalTravelandHealth(2011)Environmentalhealthrisks,Ch3.World HealthOrganization.
3Katz,T.M.,Miller,J.H.&Hebert,A.A.(2008)Insectrepellents:historicalperspectives andnewdevelopments. JournaloftheAmericanAcademyofDermatology, 58,865–871.
4InternationalTravelandHealth(2011)Specialgroupsoftravellers,Ch9.World HealthOrganization.
5CenterforDiseaseControlandPrevention(2012)CDCHealthInformationforInternationalTravel.
6Rahier,J.-F.,Moutschen,M.,VanGompel,A. etal. (2010)Vaccinationsinpatients withimmune-mediatedinflammatorydiseases. Rheumatology, 49,1815–1827.
PigmentaryDisorders inBlackSkin J.P.W.vanderVeen&L.Nieuweboer-Krobotova
NetherlandsInstituteforPigmentDisorders,UniversityofAmsterdam,Amsterdam,theNetherlands
Keypoints
Dark-skinnedpeoplemoreoftenseekmedicalattentionforpigmentproblemsthan Caucasiansdo.
DarkskinoftenshowsunevenpigmentationpatternslikeVoight’sdemarcationlines.
Darkskinreadilyreactstoevenminortraumaandinflammationwithpigmentation shifts,mostoftenhyperpigmentation.
SomepigmentarydisorderslikeOta-,Ito-andHorinevusanddermatosispapulosa nigraareseenmoreoftenindarkerskintypes.
DiagnosticpitfallsareHorinevusversusmelasmaandprogressivemacularhypomelanosisversuspityriasisversicolor.
Ubiquitouspigmentdisorderslikevitiligoaremoreconspicuousinblackskinandpose biggerproblemsregardingqualityoflife.
Melanomainblack-skinnedpeoplemostlypresentsinanacrallentiginousgrowth patternatanadvancedstagebecauseofdiagnosticdelay.
Introduction
Westernsocietiesarebecomingincreasinglymultiracialandsoisthe patientpopulationinmedicalpractice,especiallyinlargemetropolitan areas.
Pigmentproblemscanbeverydisturbingforpatientswithdarkskin, especiallywhenhugecontrastswiththeconstitutionalskincoloremerge, suchascanbeseeninblackswithvitiligo.However,pigmentproblems thatmightnotappearsignificantatfirstsightcanhaveimportantculturallydeterminedpsychosocialconnotationsindark-skinnedpatientsand should,therefore,alwaysbetakenseriouslybytheirdoctors.
Inthischapter,normalpigmentaryvariationsandanumberofcommon pigmentdisordersindarkskinhavebeendescribed.
ImportedSkinDiseases,SecondEdition.EditedbyWilliamR.Faber, RoderickJ.HayandBernardNaafs.
C 2013JohnWiley&Sons,Ltd.Published2013byJohnWiley&Sons,Ltd.
Normalvariationsinethnicskin
Voigt’sorFutcher’slines Atotaloffivelinesofdemarcationbetweendarkerandlighterskinareas, theso-calledVoigt’sorFutcher’slines,havebeendescribed.Theselines canbefoundontheupperarmanteromedially,theposteriorportionof thelowerlimb,thepresternalarea,theposteromedialareaofthespine, andthebilateralaspectofthechest.About75%oftheAfricanAmerican populationhasatleastonepigmentarydemarcationline[1].
Hyperpigmentationattheextensorside ofthejoints (Figure3.1)
Stretchingoftheskinatthejointscanpossiblybeamechanicaltriggerfor themelanocytes.Arthritismayalsocausethishyperpigmentation.
Nailpigmentation Nailpigmentationmanifestsaslongitudinallineardarkbandsinthenail plate,whichoccursespeciallyonthethumbsandindexfingers[2].The pigmentationisusuallyabsentatbirthandincreaseswithage.Nailpigmentationismostlyseeninblackswithaverydarkcomplexion.It isimportanttodifferentiatetheselesionsfrommalignantmelanoma, nevusandpigmentationsecondarytodrugs,chemicalsandpostirradiation changes.
Familialperiorbitalhyperpigmentation (Figure3.2)
Periorbitalhyperpigmentationisacommonfindinginotherwisehealthy peopleandhasbeendescribedasanautosomaldominanthereditarydisorder[3].Thehyperpigmentationusuallystartsduringchildhoodinthe
lowereyelidsandprogresseswithagetoinvolvetheentireperiorbitalarea. Periorbitalhyperpigmentationcanalsobefoundineveryskintypeasan atopicstigma.
Oralpigmentation Oralpigmentationisusuallyseenonthegingivae.Thehardpalate, buccalmucosa,andtonguearelessfrequentlyinvolved.Theselesions shouldbedistinguishedfromconditionslikesecondarysyphilis,malignant melanoma,anddrugeruptions.Unlikenailpigmentation,theskincolor cannotpredictthelikelihoodoforalpigmentation[1].
Palmarandplantarhyperpigmentation Macularhyperpigmentationiscommonlyseenonpalmsandsolesof blackpatients.Theyvaryinshapeandaremottledinappearance.Clinically,thesemustbedifferentiatedfrompalmar/plantarlesionsofsyphilis, ephelides,nevi,andmelanoma.
Whereinpatientswithfairskinpigmentedlinesinthepalmscanbea clinicalfeatureofAddison’sdisease,thisisanormalvariationinpeople withdarkskin.
Mongolianspot (Figure3.3)
Thisisthemostcommoncongenitalhyperpigmentation,occurringin approximately80–100%oftheAsianandblacknewborns.Itisaform ofdermalmelanocytosisinwhichmelanocyteshavebeenarrestedintheir fetalmigrationfromtheneuralcresttotheepidermis.Thegray-bluemacularlesionsvaryinsizebutusuallyoccupylessthan5%ofthebodysurface. Themostcommonlocationsarethesacrum,buttocks,andback.
Figure3.2 Familialperiorbitalhyperpigmentation
ThemajorityofMongolianspotsintensifyincolorduringthefirstyear oflifefollowedbygradualdisappearance.Bytheageof10,virtuallyall Mongolianspotsdisappear[4].
Abnormalhyper-andhypopigmentations NevusofOta,nevusofIto,andHorinevus (Figure3.4)
Theseneviareseeninallraces,butaffectmostlyAsianpeople.Nevusof Otaornevusfuscocoeruleusophtalmomaxillarisisadermalmelanocytic hamartomathatpresentsasabluishhyperpigmentationwithinthedistributionofthefirstandsecondbranchofthetrigeminalnerve[5].Very oftenthescleraearealsoinvolved.Histologicallyandclinicallythelesions
Figure3.3 Mongolianspot
Figure3.4 NevusofOtawitheyeinvolvement
resembleMongolianspotsbutare,unlikethelattercondition,notselflimiting.
Thepigmentedspotsusuallyappearinchildhoodandincreaseinnumberandextenttobecomeconfluentinsomeareas.Thedistributionis usually,butnotalways,unilateral.Malignanttransformationhasbeen reportedinveryrareinstances.ThenevusofItoinvolvestheacromioclavicularregionandtheupperchestandissimilartothenevusofOtain itshistology.
AcquiredbilateralnevusofOta-likemacules(ABNOM)hasfirstbeen describedbyHori etal. in1984andisalsoknownasHorinevus[6].The conditionischaracterizedbytheappearanceofsmall,butlateralsoconflatinggrayishbrownmaculesintheface,mostlybilateralinthemalar regions.LikeinnevusofOta,thehistologyischaracterizedbydermal melanocytosis.ItismostseenineasternAsiainwomenintheir30s andlater.ABNOMshouldbedifferentiatedfrommelasma.Wood’slamp assistedinspectionofthelesionsoftenprovidestheclue[7].
AlltheselesionscanbetreatedfairlysuccessfulwithQ-switchedpigmentlasers[8],thoughpostinflammatoryhyper-andhypopigmentation occureasilyindarkerskinwarrantingprecautionarylikepre-andposttreatmentbleachingregimens[7]andlasertherapy[9].
Transientneonatalpustularmelanosis Transientneonatalpustularmelanosis(TNPM)canbeseenin2–5%of blacknewborns[10].
Thecharacteristiclesionsconsistofverysuperficialvesicopustuleswithoutanysignoferythemaandrupturedpustules,resultinginhyperpigmentedpapuleswithasurroundingcolleretteofscaleinthefirstphase. Thoughalwayspresentatbirth,thelesionscanbeeasilyoverlookedand noticedforthefirsttimeseveraldaysafterbirth.
Thelesionsusuallyare2–3mmindiameterandcanappeareverywhere onthebody,groupedorsolitary.Thehead,neck,back,fingers,andtoes arepredilectionsites.
Inthepustulesneutrophilsbutnobacteriacanbedemonstrated.
ThedifferentialdiagnosisofTNPMincludesdiseaseslikeerythematoxicumandstaphylococcalimpetigo,whichcanbedifferentiatedbythetypicalclinicalappearanceandthehistory.Theactivevesiculopustulesdisappearindays,butthehyperpigmentedmaculesslowlydisappearinweeks toseveralmonths.
Ashydermatosis AshydermatosisisseenworldwidebutismostcommoninLatin AmericaandAsia.Itisseensomewhatmorefrequentlyinwomen thaninmenandhasnoagepreference.Clinicalmanifestationsinclude
asymptomatic,slate-grayorviolaceoushyperpigmentedmaculesdistributedmostcommonlyoverthetrunkandproximalextremitiesandless frequentoverthefaceandneck.Themaculesvaryinsizeandshapeand occasionallydemonstrateanerythematousraisedborderinitsearlystages. Inthosecases,thetermerythemadyschromicumperstanshasbeencoined [11].Thedifferentialdiagnosisshouldincludelichenplanuspigmentosus, macularamyloidosis,leprosy,andfixeddrugeruption.
Theetiologyofashydermatosisremainsunknown.Atthistime,no evidence-basedtreatmentisavailable.
Dermatosispapulosanigra (Figure3.5) Thesesmall,darklypigmentedpapulesareregardedasavariantofseborrhoickeratoses.TheywereoriginallydescribedinAfricanAmericansbut areseenindarkerskinnedpeopleofmanyraces.Theincidenceofthis hereditaryconditioninblackpeoplerisesfromabout5%inthefirstdecade tomorethan40%bythethirddecade,andisratherhigherinfemalesthan inmales.
Thepapulesareoftennumerousinthemalarregionsandontheforeheadandmayoccurontheneckandtrunk.Thelesionscanbetreatedwith curettage,electrodesiccationorlaser,allwithexcellentoutcomes[12].
Carehastobetakennottoaffectthenormalsurroundingskininorder topreventthepredictableinductionofpostinflammatoryhyperpigmentation(PIH).
Figure3.5 Dermatosispapulosanigra
Pityriasisversicolor Tineaversicolororpityriasisversicolorisoneofthemostcommonpigmentarydisordersworldwide.Itappearstobemoreprevalentintheblack population[13],andintropicalregions,itoccurswithaprevalenceas highas40%.Itiscausedbyovergrowthofcommensal Malassezia yeasts andaffectsmostcommonlythetrunk.Patientshavemanyslightlyscalingmaculesandpatches,whichcanhave,asimpliedbythenameversicolor,manydifferentcolorssuchasyellowish-brown,paleyellow,or dark-brown,occasionallyreddishorpinkishappearinghypopigmentedor hyperpigmented[14].Thereisnocorrelationbetweenpigmentaryvariationandskincolor.
Antifungaltherapiesusuallycurethedisease,butthepigmentchanges willdisappearonlyslowlyandrecurrencescanoccur.
Melasma Melasmaischaracterizedbyirregular,usuallysymmetricalbrownpatches onsun-exposedskin.Themalarprominences,theforehead,theupperlip, thenose,andthechinarethemostcommonsitesofinvolvement,but otherareasliketheneckandforearmscanalsobeaffected.Melasmais notexclusivelyadisorderofthedarkerskintypes,butitappearstobefar morecommoninHispanics,Asians,andblacks.Etiologicfactorsinclude geneticandhormonalinfluences(pregnancy,birthcontrolpills),exposure toUV-radiation,cosmetics,phototoxicdrugs,andantiseizuremedication. Currenttreatmentoptionsincludetheuseofsunblocks,hypopigmenting agents,andchemicalpeels[15].
Postinflammatoryhyperpigmentation PIHisoneofthemostcommonpigmentarydisordersindarkskin.Inflammatoryskinconditionslikeinfections,bullousandpustulardisorders, phototoxiceruptions,papulosquamousdisorders,andmedicalinterventions(lasertherapy,chemicalpeels,anddermabrasion)canallcausethe increasedpigmentationseeninpostinflammatoryhyperpigmentation.The twoprocessesinvolvedareepidermalhyperpigmentationand/ordermal hyperpigmentation(incontinentiapigmenti).Thehyperpigmentedareas correspondwiththedistributionoftheoriginaldermatosis.Blacksseem tohavemorefollicularskinproblems,andpost-acnehyperpigmentations inthefaceareverycommon.InepidermalPIH,thelesionsarelighter brownandwellcircumscribed,ascomparedwiththedarkergray,poorly circumscribedlesionsinpredominantlydermallesions.DermalPIHcan takeyearstofadeawaytonormal,whereasepidermalPIHusuallydisappearsin6–12months[16].Sunexposure,chemicals,andcertaindrugscan aggravatePIH.Theprimarygoaloftherapyistreatmentoftheunderlying
inflammatorydisease.Furthermore,treatmentofPIHshouldalways includethedailyuseofsunscreen.Inaddition,resurfacingmodalitiesand manytopicalagentshavebeenusedincludingkeratolytics,retinoids,corticosteroids,anddepigmentingagents.However,cautionisnecessaryas manyoftheseagentscaninduceirritationmakingtheproblemworse [17,18].
Postinflammatoryhypopigmentation Postinflammatoryhypopigmentationiscausedbyvariouscutaneous inflammatorydiseases.Thelonguseofpotentcorticosteroids,chemical peelings,andmedicalinterventions(laser,peels)canalsoplayarole[19]. AsinPIH,theconfigurationanddistributionreflectstheoriginaldermatosis.Inpostinflammatoryhypopigmentation,themelanocytesreact withdecreasedmelaninproductionafteraninflammationortrauma.Sunlightexposureorphoto(chemo)therapymayleadtorepigmentation withinmonths.Preventionofthetriggercausingthehypopigmentationis important.
Pityriasisalba Pityriasisalbaisaneczematousdisorderoftenoccurringinchildrenwith anatopicbackgroundanddryskin.Thelesionsaretypicallyhypopigmented,scaly,andasymptomatic,andcommonlyaffectthefacebutcan alsobeseenonneck,arms,andtrunk.Mostofthepatientsarechildren between6and16yearsofage.Inmanycases,itishardlynoticeableon whiteskin;thedisordercanbeveryconspicuousinblack-skinnedchildren.Sunexposureinconjunctionwithtopicalsteroidsorcalcineurin inhibitorsandcorrectionofthexerosiscutisisusuallyeffective[20]. Recurrencescanoccurthough.
Idiopathicguttatehypomelanosis Oneofthemostcommontypesofhypomelanosisinelderlypeopleisidiopathicguttatehypomelanosis(IGH).Anincidenceofmorethan60%has beenreported.IGHappearsasnumeroushypopigmentedsmallmacules (1–10mm)onsun-exposedareas,suchasthebackofthehands,forearms,legs,andoccasionallyontheface,abdomen,andtrunk.Thisdermatosisaffectsallraces,ismorefrequentinwomen,andtendstoincrease inincidencewithage.Theetiologyandpathogenesisarenotwellunderstood,butsincethelesionsappearmainlyonsunexposedareas,actinic damagemaybeacausalfactor[21].Anotherfactormightberepetitive microtrauma(“Bodyscrubbing”)[22].Forwidespreadlesions,noeffective treatmentsareavailable.Insomecasesthough,autologouspunch-grafting canbequiteeffective(personalexperienceLN-K).
Vitiligo Vitiligoischaracterizedbythedestructionofskinmelanocytesleadingto thedevelopmentofwell-defineddepigmentedchalkwhitemacules,which canbepresentonanysiteofthebody,butareusuallyseenonsitesof stretchandpressure,inbodyfoldsandaroundbodyorifices(e.g.,mouth). Thediseaseisseenallovertheworldandinallskintypes,affectingapproximately0.5–1%ofthepopulation.
Inmanypatientswithactivevitiligo,theKoebnerphenomenoncanbe observed;newlesionsappearoninjuredorirritatedskin.
Itisimportanttodifferentiatebetweengeneralizedvitiligo,themost commonformwithlesionsdistributedinamoreorlesssymmetricalway andsegmentalvitiligo,moreseeninchildren,wherelesionsdevelopina unilateralandusuallylimitedway[23].
Generalizedvitiligoisconsideredtobeanautoimmunediseaseandis associatedwithotherautoimmunediseaseslikethyroiddisease,type-1 diabetes,andsoon.Inmanypatients,itrunsachroniccoursewithstable periodssometimeswithpartlyrepigmentationinterchangedbyrelapses leadingtomoreandlargerlesions.
Segmentalvitiligoshowsarapidcoursethatstopsinacoupleofyears, leadingtostablespotsrefractorytotheusualmedicaltherapieslikephototherapy,topicalsteroids,andcalcineurininhibitors.Ontheotherhand, graftingtechniquesthatreplenishthereservoirofmelanocytesbygrafts fromanotherbodyregionareverysuccessfulinthesepatients,leadingto alastingrecoveryinmostofthem.
Understandingly,vitiligoindark-skinnedpatientsismuchmoredisfiguringthaninwhites,leadingtoamorequality-of-lifeissues[24].Because oftheresemblancetoleprosy,vitiligopatientsinareaswithendemiclepra oftensufferfromsocialexclusion.
Melanoma Darkskinisbetterprotectedfromsunlight,makingsun-inducedcancers lessprevalent.Blackshaveanincidenceofmalignantmelanoma5–18 timeslessthanwhites.However,atthismomentthereisatrendtoward increasedskincancerratesinmostethnicgroups[25,26].Theprognosisof melanomaisrelatedtothestageofthediseaseatthetimeofpresentation.
AfricanAmericansdiagnosedwithmelanomahaveaworseprognosisthan whitesbecausetheyareinitiallyseenwithamoreadvanceddisease[27] andthesameisfoundinotherblack-skinnedpopulations[28].
Anothersignificantdifferenceistheprimarytumorlocation.Themost commontypeofmelanomafoundinAfricanAmericanstypeistheacral lentiginousgrowthpattern,whereasinwhites,thetrunkisthemostcommonsite[29,27].
Progressivemacularhypomelanosis Progressivemacularhypomelanosisischaracterizedbynonscaly,nonitchy, ill-definedhypopigmentedmaculesontheskin.Themaculesoccuronthe frontandthebackofthetrunk(lessfrequentontheface,theneckandthe upperextremities)andareconfluentinandaroundthemidline.Itoccurs inyoungadultsofbothsexesbutmoreofteninwomenandcanbefound allovertheworld,especiallyinblackpopulations.Probably,itiscausedby avariantof Propionibacteriumacnes andcanbeeffectivelytreatedbytopical therapyincluding5%benzoylperoxidegelandclindamycinlotion[30].
Acknowledgments:Theauthorsdidnotreceiveresearchgrantsorotherfinancial supportforwritingtheirchapter.
References 1McMichael,A.J.(1999)AreviewofcutaneousdiseaseinAfrican-Americanpatients. DermatologyNursing, 11 (1),35–43.
2Henderson,A.L.(1983)Skinvariationsinblacks. Cutis, 32,376–3774.
3Burton,EsterlyN.,Baselga,E.&Drolet,B.A.(2006)Geneticepidermalsyndromes: localizedhyperpigmentation:periorbitalhyperpigmentation.In:J.J.Nordlund,R.E. Boissy,V.J.Hearing etal. (eds), ThepigmentarySystem:PhysiologyandPathophysiology, 2ndedn,pp.879–880.BlackwellPublishing,Oxford.
4Lee,S.J.,Hann,S.-K.&Im,S.(2006)Aquiredandcongenitaldermalhypermelanosis:sacralspotofinfancy.In:J.J.Nordlund,R.E.Boissy,V.J.Hearing etal. (eds), ThePigmentarySystem:PhysiologyandPathophysiology,2ndedn,pp.1003–1006.BlackwellPublishing,Oxford.
5Chan,H.H.,Lam,L.K.,Wong,D.S. etal. (2001)NevusofOta:anewclassification basedontheresponsetolasertreatment. LasersinSurgeryandMedicine, 28,267–272.
6Hori,Y.,Kawashima,M.,Oohara,K.&Kukita,A.(1984)Acquired,bilateralnevus ofOta-likemacules. JournaloftheAmericanAcademyofDermatology, 10,961–964.
7Park,J.M.,Tsao,H.&Tsao,S.(2009)AquiredbilateralnevusofOta-likemacules(Horinevus):etiologicandtherapeuticconsiderations. JournaloftheAmerican AcademyofDermatology 61,88–93.
8Polder,K.D.,Landau,J.M.,Vergilis-Kalner,J. etal. (2011)Lasereradicationofpigmentedlesions:areview. DermatologicSurgery, 37,572–595.
9Wang,C.C.&Chen,C.K.(2011)EffectofspotsizeandfluenceonQ-switched alexandritelasertreatmentforpigmentationinAsians:arandomized,double blinded,split-facecomparativetrial. TheJournalofDermatologicalTreatment (Epub aheadofprint).
10Mebazaa,A.,Khaddar,Kort,R.,Cherif,F. etal. (2011)M ´ elanosepustuleuse n ´ eonataletransitoire. ArchivesdeP ´ ediatrie, 18,291–293.
11Zaynoun,S.&Rubeiz,N.(2008)Ashydermatoses—acriticalreviewoftheliterature andaproposedsimplifiedclinicalclassification. InternationalJournalofDermatology, 47,542–544.
12Garcia,M.S.,Azari,R.&Eisen,D.B.(2010)Treatmentofdermatosispapulosanigra in10patients:acomparisontrialofelectrodesiccation,pulseddyelaser,andcurettage. DermatologicSurgery, 36,1968–1972.
13Child,F.J.,Fuller,L.C.,Higgins,E.M.&DuVivier,A.W.(1999)Astudyofthespectrumofskindiseaseoccurringinablackpopulationinsouth-eastLondon. British JournalofDermatology, 141,512–517.
14Swartz,R.A.(2004)Superficialfungalinfections. Lancet, 364,1173–1182.
15Rajaratnam,R.,Halpern,J.,Salim,A.&Emmett,C.(2010)Interventionsfor melasma. CochraneDatabaseofSystematicReviews 7(7):CD0035.
16Lacz,N.L.,Vafaie,J.,Kihiczak,N.I.&Schwartz,R.A.(2004)Postinflammatory hyperpigmentation:acommonbuttroublingcondition. InternationalJournalofDermatology, 43 (5),362–365.
17Grimes,P.E.(2009)Managementofhyperpigmentationindarkerracialethnic groups. SeminarsinCutaneousMedicineandSurgery, 28,77–85.
18Davis,E.C.&Callender,V.D.(2010)Postinflammatoryhyperpigmentation:Areview oftheepidemiology,clinicalfeatures,andthetreatmentoptionsinskinofcolor. The JournalofClinicalandAestheticDermatology, 3,20–31.
19Vachiramon,V.&Thadanipon,K.(2011)Postinflammatoryhypopigmentation. ClinicalandExperimentalDermatology 36 (7),708–714.
20Jadotte,Y.T.&Janniger,C.K.(2011)Pityriasisalbarevisited:perspectivesonan enigmaticdisorderofchildhood. Cutis, 87,66–72.
21Kim,S.K.,Kim,E.H.,Kang,H.Y. etal. (2010)Comprehensiveunderstandingofidiopathicguttatehypomelanosis:clinicalandhistopathologicalcorrelation. International JournalofDermatology, 49,162–166.
22Shin,M.K.,Jeong,K.H.,Oh,I.H. etal. (2011)Clinicalfeaturesofidiopathicguttate hypomelanosisin646subjectsandassociationwithotheraspectsofphotoaging. InternationalJournalofDermatology, 50,798–805.
23Taıeb,A.&Picardo,M.(2009)Clinicalpractice:vitiligo. NewEnglandJournalof Medicine, 360,160–916.
24Linthorst,HomanM.W.,Spuls,P.I.,DeKorte,J. etal. (2009)Theburdenofvitiligo: patientcharacteristicsassociatedwithqualityoflife. JournaloftheAmericanAcademy ofDermatology, 61,411–420.
25Halder,M.H.&Ara,C.J.(2003)Skincancerandphotoaginginethnicskin. DermatologicClinics, 21,725–732.
26Rouhani,P.,Pinheiro,P.S.,Sherman,R. etal. (2010)Increasingratesofmelanoma amongnonwhitesinfloridacomparedwiththeUnitedStates. ArchivesofDermatology, 146,741–746.
27Rouhani,P.,Hu,S.&Kirsner,R.S.(2008)Melanomainhispanicandblackamericans. CancerControl, 15,248–253.
28 Hore, T.,Robinson,E.&Martin,R.C.(2010)MalignantmelanomaamongstMaori andNewZealandEuropeans,2000–2004. WorldJournalofSurgery, 34,1788–1792.
29Byrd,K.M.,Wilson,D.C.,Hoyler,S.S.&Peck,G.L.(2004)Advancedpresentationof melanomainAfricanAmericans. JournaloftheAmericanAcademyofDermatology, 50, 21–24.
30Relyveld,G.N.,Menke,H.E.&Westerhof,W.(2007)Progressivemacularhypomelanosis:anoverview. AmericanJournalofClinicalDermatology, 8,13–19.
CHAPTER4 DifferenceBetweenPigmented andNonpigmentedSkin BernardNaafs
RegionalDermatologyTrainingCenter(RDTC),Moshi,Tanzania InstitutoLaurodeSouzaLima(ILSL),Bauru,Brazil StichtingTropen-Dermatologie,Munnekeburen,theNetherlands
Keypoints
Themajordifferencesbetweencoloredskinandwhiteskinareinthefollowing. Theclinicalexpressionoferythema,anearabsenceofitindarkskin
Thede-,hypo-,andhyperpigmentationofdarkerskinsinstead Thelargercohesionbetweenthekeratinocytesinthecoloredskin
Agreatertendencyofthecoloredskintolichenification
Agreatertendencytokeloidformationinthenonwhiteskin
Agreaterriskofepidermalskincancersinthewhiteskin
VitaminDproduction,hinderedbymelaninincoloredskin
Introduction Whileinothermedicalspecialtiestheclinicalpresentationofdiseases hardlydiffersbetweenthedifferentraces,indermatologytheaspectof askinconditionisdecidedlydifferentincoloredskinthanitisinlight Caucasianskin.Skindiseasesareexpresseddifferentlyindifferentskins [1].Forinstanceerythema,rednessasasignofinflammation—thehallmarkofEuropean-Americandermatology—isdifficulttoappreciateina pigmentedskin.Pigmentchangesdominatethepicture[1].
Racesaredifferentduetogeneticdifferencesthatmanifestthemselves inbodybuild,formofheadandface,andlengthandshapeofmusclesand bones,butevenmoreinthecoloroftheskin,andthecolorandformof thehair(Figure4.1).Untilrecentlymostpublicationsonethnicdifferences indermatologywerenotwellresearchedanddidnotmakeallowancesfor differentclimaticorsocioeconomiccircumstances[2].Butmoreandmore
ImportedSkinDiseases,SecondEdition.EditedbyWilliamR.Faber, RoderickJ.HayandBernardNaafs.
C 2013JohnWiley&Sons,Ltd.Published2013byJohnWiley&Sons,Ltd.
Figure4.1 WorldwidedistributionofindigenousskincolorsaccordingtotheVonLuschan’sChromaticscale(courtesyUniversityof Amsterdam)
Figure4.2 (a,b)Tineaimbricata:absenceoferythemainthedarkskin
ithasbecomeclearthatsomeofthedifferencesareimportantbecausethey influencetheclinicalpresentationofskindiseases[1,3–6].
Erythema Duetotheoverlyingpigmentation,erythema,asignofinflammation, isnoteasilyvisibleinablackskin(Figure4.2).Therefore,palpationis evenmoreimportantintheexaminationofpigmentedskinthanitisin whiteskin.Duringpalpationtheothersignsofinflammation,calor(heat, warmth),tumor(swelling),anddolor(pain,tenderness)canbeappreciated.Sometimeserythemamaymanifestasadarkviolethue.Theconditionerythrodermaisnotclearlyvisibleassuchintheblackskinandcan onlybeappreciatedasexfoliativedermatitis.
Pigmentchanges Pigmentchanges(de-,hypo-,andhyperpigmentation)dominatetheclinicalpictureinthedermatologyofthepigmentedskin.
Depigmentation canbeseenduringtheextremedesquamationthat mayoccurwhenpsoriasisistreatedaggressively,orwhenthereisatotal disruptioninthetransferofmelanosomes[7],ashappensinsomeforms ofcutaneouslupuserythematosus(Figure4.3).Themelanocyteitselfcan disappearduetocytotoxicityinautoimmunediseasessuchasvitiligo[8]or asaresultoftoxicsubstancesasseeninsomeleucodermas(cheaprubber).
Hypopigmentation canbeduetoanincreaseddesquamationofthe skin.Theturnoverofkeratinocytesisincreased,whereasthepigment synthesisisnot,sothateachkeratinocytecontainslesspigment.Inanepidermisofthesamethicknessthisresultsinhypopigmentation.Thiscanbe seeninpityriasisalba,whichisprobablyamildformofatopicdermatitis,
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Prunusdomestica 1. Jour. Hort. N. S. 17:228. 1869. 2. Lange Allgem. Garten. 2:419. 1879. 3. Oberdieck Deut. Obst. Sort. 432. 1881. 4. Lauche Deut. Pom. 19, Pl. IV. 1882. 5. Hogg Fruit Man. 692. 1884. 6. Mathieu Nom. Pom. 420. 1889. 7. Gaucher Pom. Prak. Obst. 94, Pl. 1894. 8. Soc. Nat. Hort. France Pom. 550 fig. 1904. 9. Cat. Cong. Pom. France 468, fig. 1906. 10. Baltet Cult. Fr. 490, fig. 328. 1908.
Althan’s Reine Claude 6, 7. Althann’s Reine Claude 2, 3, 4, 6. Althahn’s Rote Reine-Claude 6, 7. Althann’s Reine Claude 7. Count Althann’s Gage 5. Count Althann’s Gage 6, 7. Graf Althan’s Reine-Claude 6. Graf Althann’s Reine-Claude 7. Hathen’s Red Gage 1. Reine-Claude Rouge de Hathen 1. Reine-Claude d’Althann 5, 6, 7. Reine-Claude Comte Althan 5, 6. ReineClaude de Comte Hathem 5, 6. Reine-Claude du Comte Hathem 6, 7. Reine-Claude du Comte d’Althan 8. Reine-Claude Althan’s 5, 6, 7. ReineClaude Comte d’Althan 6. Reine-Claude d’Althan 8. Reine-Claude d’Althan 6, 7, 10. Reine-Claude Rouge Comte Althan 6, 7. Reine-Claude Rouge du Comte Hethau 6. Reine-Claude rouge du comte Hethan 7. Reinette Claude Comte d’Althan 9. Reinette Claude d’Althan 9.
Altham is an excellent plum for dessert or home use. The color is a trifle too dull for market purposes and yet it is better colored than McLaughlin, which sells fairly well. The fruit is the type of the last named plum but is later. In Europe this variety is well known and highly esteemed for its quality, but unfortunately it is almost unknown in America. The variety is well worth trial in this country as a fine plum of the Reine Claude group. Altham is a seedling of Reine Claude, raised by Herr Prochaska, gardener to Count Michael Joseph Althann, of Swoyschitz, in Bohemia. It was noted in the English JournalofHorticulture for 1869 as a new plum sent out by Thomas Rivers.
Tree of medium size, upright-spreading, dense-topped, productive; leafscars prominent; leaves folded upward, obovate, two and one-quarter inches wide, nearly four inches long, very thick, leathery; margin doubly crenate, with few, small, dark glands; petiole thick, with from one to four globose, yellowish-green glands on the stalk; season of bloom intermediate, short; flowers appearing after the leaves, one inch across,
yellowish at the apex of the petals; borne on lateral buds and spurs, singly or in twos.
Fruit mid-season; one and one-half inches by one and five-eighths inches in size, oblate, strongly truncate at the base, compressed; color dark purplish-red over a yellow ground, covered with thick bloom; dots russet surrounded with a dark red ring; stem adhering strongly to the pulp; flesh light golden-yellow, firm but tender, sweet, mild, pleasant; very good to best; stone semi-clinging, seven-eighths inch by five-eighths inch in size, flattened, irregular-oval, with pitted surfaces, contracted at the base into a short oblique neck; ventral suture prominent, heavily furrowed, often with distinct wing; dorsal suture wide, deep.
AMERICA AMERICA Prunusmunsoniana× Prunustriflora
1. Burbank Cat. 3. 1898 2. Vt. Sta. Bul. 67:5. 1898, 3. Rural N. Y . 59:706. 1900. 4. Vt. Sta. An. Rpt. 14:273. 1900. 5. Mich. Sta. Bul.
205:37 1903. 6. Del. Penin. Hort. Soc. Rpt. 36. 1905. 7. Ohio Sta. Bul. 162:254, 255. 1905. 8. Ga. Sta. Bul. 68:8, 35. 1905.
America is illustrated and described in full chiefly because it is the most promising cross between Prunus munsoniana and Prunus triflora. The fruit of the variety is unusually attractive in appearance, golden-yellow with a red cheek and waxy lustre turning currant-red when ripe, ships exceptionally well and is of very good quality for cooking, but is without merit as a dessert plum. The trees are large, very vigorous, as hardy as either of its parents or possibly more so, and enormously productive. The qualities of fruit and tree are such that the variety ought to succeed in commercial plantations where any but the hardiest native plums are cultivated. America is almost phenomenally free from rot, considering its parentage.
This variety is one of Luther Burbank’s productions, grown from a seed of Robinson fertilized by pollen from Abundance. It was introduced by the originator in 1898 and has been since that time well tested at several places in the eastern states and is very generally well spoken of for a plum of its kind for the East.
Tree large, vigorous, spreading, somewhat open-topped, hardy, very productive; branches roughish and with cracked bark, slightly zigzag, dark ash-gray, with numerous, conspicuously raised lenticels; branchlets willowy, long, with short internodes, green with a reddish tinge changing to dark chestnut-red, glossy, glabrous, with numerous, small, raised lenticels; leaf-buds small, short, conical, free.
Leaves folded upward, broadly lanceolate, peach-like, one and one-half inches wide, three and one-fourth inches long, thin; upper surface reddish late in season, smooth and glossy, with deeply grooved midrib; lower surface light green, sparingly pubescent along the midrib and larger veins which are more or less red; apex taper-pointed, base abrupt, margin finely and doubly crenate and with numerous, small, dark glands; petiole one-half inch long, tinged red, pubescent along one side, glandless or with one or two small globose, reddish glands on the upper part of the stalk.
Blooming season intermediate and long; flowers appearing after the leaves, one-half inch across, white; borne in clusters on short lateral spurs and buds, in pairs or in threes; pedicels five-sixteenths inch long, slender, pubescent, green; calyx-tube greenish, obconic, glabrous; calyx-lobes
obtuse, with a trace of red along the margin, glandular-serrate, glabrous, with marginal hairs, erect; petals small, roundish, entire, tapering abruptly to narrow claws; anthers yellowish; filaments three-sixteenths inch long; pistil glabrous, longer than the stamens.
Fruit early, season of medium length; one and three-eighths inches in diameter, roundish-oval, halves equal; cavity shallow, flaring; suture shallow, a distinct line; apex roundish; color clear, dark, currant-red over golden-yellow, mottled, with thin bloom; dots numerous, small, whitish, inconspicuous; stem slender, one-half inch long, glabrous, adhering to the fruit; skin thin, bitterish, separating readily from the pulp; flesh yellow, juicy, fibrous, somewhat tender, sweet, not high in flavor; fair in quality; stone clinging, seven-eighths inch by one-half inch in size, oval, pointed, with pitted surfaces, broadly ridged along the ventral suture; dorsal suture grooved.
AMERICAN Prunusdomestica 1. Oregon Sta. Bul. 61:17, 18. 1900.
American Seedling 1.
American originated with a Mr. Peterson of Elkton, Douglas County, Oregon, as a sprout from an old tree. It has never been extensively disseminated, but seems to be a variety of considerable promise. The fruit as grown on the Station grounds resembles Hand rather closely; is large for a plum of its type, is a handsome golden color, is high in quality and will probably keep and ship well. Too little is known of its tree-characters to recommend it unqualifiedly.
Tree above medium in size, vigorous, round-topped, dense, productive; branches numerous; branchlets thick, marked by grayish scarf-skin; leaves flattened, oval or obovate, two and one-quarter inches wide, four and one-half inches long, dark green; margin serrate or crenate; blooming season intermediate, short; flowers appearing after the leaves, one and three-eighths inches across, singly or in twos, fragrant.
Fruit mid-season; very large, roundish-oblate, truncate, golden-yellow, indistinctly streaked with green, mottled, covered with thin bloom; flesh
light golden-yellow, tender, sweet, pleasant flavor; good to very good; stone clinging, one inch by three-quarters inch in size, broadly oval, flattened, surfaces pitted; dorsal suture wide, deep.
AMERICAN EAGLE Prunusamericana 1. Cornell Sta. Bul. 38:36. 1892. 2. Am. Pom. Soc. Cat. 37. 1899. 3. Can. Exp. Farms Rpt. 105. 1900. 4. Waugh Plum Cult. 142. 1901. 5. Can. Exp. Farm Bul. 43:28. 1903. 6. Ohio Sta. Bul. 162:254, 255. 1905.
Of the origin of this very good Americana variety little is known except that it probably came from Missouri, as it was introduced, in the fall of 1859, by the Osceola Nursery Company, Osceola, Missouri. Although an old variety it was not listed by the American Pomological Society until 1899. In regions where Americana plums are grown, American Eagle ought to be better known, its chief defect being the dull color of the fruit.
Tree vigorous, spreading; leaves large; petiole glandular. Fruit midseason; large, varies from roundish-oval to nearly oblate, dark red, covered with thick bloom; stem short, pubescent; flesh yellow, juicy, fibrous, sweet, aromatic, with characteristic Americana flavor; of good quality; stone clinging, three-eighths inch by one-half inch in size, roundish, turgid, conspicuously winged; surface smooth.
AMES AMES
Prunusamericana× Prunustriflora
1. Vt. Sta. An. Rpt. 12:220. 1899. 2. Ia. Hort. Soc. Rpt. 112. 1899. 3. Ia. Sta. Bul. 46:261. 1900. 4. Waugh Plum Cult. 203. 1901. 5. Budd-
Hansen Am. Hort. Man. 293. 1903. 6. S. Dak. Sta. Bul. 93:9. 1905. 7. Ill. Hort. Soc. Rpt. 422. 1905. 8. RuralN. Y . 65:730. 1906. De Soto × Oregon No. 36. Japan HybridNo. 32.
Though Ames has been known to the public scarcely ten years, its good qualities have given it relatively high rank among Americana plums with which it must be compared. Though supposed to be a cross between Prunus americana and Prunus triflora, the variety shows few, if any, traces of the Triflora parentage, except, possibly in the shape and color of the fruit. The variety is distinguished from other Americana plums by reddish dots on the fruit instead of the yellowish dots commonly found on the plums of this species. The fruit of Ames is very attractive in color, the quality is fair, it keeps and ships well and it is fairly free from rot, characters which make it desirable where the native plums are grown.
This variety was produced by Professor J. L. Budd[204] of Ames, Iowa, by crossing De Soto with pollen of a “large Japanese plum received from Oregon.” For a long while it was known as De Soto × Oregon No. 3 and as Japan Hybrid No. 3, but was named Ames by Professor John Craig, now of Cornell University.
Tree of medium size, spreading, dense-topped, hardy, productive; branches roughish, thorny, the trunk shaggy, dark ash-brown, with numerous, large, raised lenticels; branchlets willowy, thick, long, with long internodes, green changing to dark chestnut-red, glossy, glabrous, thickly strewn with conspicuous, large, raised lenticels; leaf-buds small, short, obtuse, plump, appressed.
Leaves falling early, flattened, oval, two inches wide, four inches long; upper surface dark green, glabrous, slightly rugose; lower surface light green, pubescent; apex taper-pointed, base abrupt, margin coarsely serrate, the serrations ending in hair-like tips, eglandular; petiole seveneighths inch long, slender, pubescent, tinged red, glandless or with from one to three globose, greenish-red glands.
Blooming season medium in time and length; flowers appearing after the leaves, nearly one inch across, white; borne in clusters on lateral buds and spurs, in threes or fours; pedicels one-half inch long, slender, glabrous, greenish; calyx-tube green, campanulate, glabrous; calyx-lobes
narrow, somewhat acute, reflexed, pubescent on the inner surface, the margin faintly pubescent and with a trace of red; petals small, oval, somewhat dentate, tapering below to long, narrow, slightly hairy claws; anthers yellowish; filaments five-sixteenths inch long; pistil glabrous, equal to the stamens in length, frequently defective.
Fruit mid-season, one and seven-sixteenths inches by one and five sixteenths inches in size, ovate or oval, sides compressed, halves equal; cavity shallow, narrow, flaring; suture a line; apex roundish; color light to dark red over a yellow ground, covered with thin bloom; dots numerous, small, brownish-red; stem slender, glabrous; skin medium in thickness and toughness, adhering; flesh golden-yellow, juicy, coarse, fibrous, tender and melting, semi-sweet; of fair quality; stone nearly free, one inch by five-eighths inch in size, irregular-oval, flattened and elongated at the base, abruptly pointed at the apex, very smooth; ventral suture winged and furrowed; dorsal suture acute.
APPLE 1. Burbank Cat. 2. 1898. 2. Vt. Sta. Bul. 67:6. 1898. 3. Vt. Sta. An. Rpt. 12:220. 1899. 4. Am. Gard. 21:36. 1900. 5. Waugh Plum Cult. 203.
